Essentials of Clinical and Periodontics

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Procedure on Live Periodontal Surgery Essentials of Clinical Periodontology and Periodontics

THIRD EDITION

Shantipriya Reddy BDS MDS (Periodontia) Professor and Head Department of Periodontics Dr Syamala Reddy Dental College and Hospital Bengaluru, Karnataka, India

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Essentials of Clinical Periodontology and Periodontics

© 2011, Shantipriya Reddy

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First Edition: 2006 Second Edition: 2008 Third Edition: 2011 ISBN 978-93-5025-037-2 Typeset at JPBMP typesetting unit Printed at To My late grandfather, who had believed in my abilities, it is because of whom I chose this profession My grandmother, for her constant support My father and mother, for always being there My uncle for his continuous encouragement My husband for his unique mentorship My daughter and son for being so understanding

PREFACE TO THE THIRD EDITION

I am extremely happy to present the third edition of Essentials of Clinical Periodontology and Periodontics. In planning the third edition, a firm commitment has been made to provide a thorough and complete text. An attempt has been made to revise and update all the chapters. The highlight of the edition is introduction of KNOW MORE section which contains latest additional information pertaining to each chapter. Conscious attempt has been made not to disturb the clarity and simplicity of the main text which had gained immense popularity amongst the students. The edition also provides an add on, Manual of Clinical Periodontics which will guide the students in recording case history and performing clinical examination so as to arrive at a proper diagnosis and treatment planning. Also, special emphasis was given to instrumentation which will instruct the students in their clinical work. While describing all these, we have not only mentioned what steps are to be followed but also how to carry out these steps with the help of various illustrations and photographs. I am grateful to all my colleagues and students who have helped me with their valuable suggestions, which in turn enabled me to write the edition in a more understandable fashion. I hope this book will help the students and practitioners in understanding periodontics in a simplified manner.

Shantipriya Reddy PREFACE TO THE FIRST EDITION

The basic text when conceived in the year 2003 has been written in an attempt to make our understanding of accessible to the undergraduate students, general practitioners and dental hygienists. The Essentials of Clinical Periodontology and Periodontics is a learning textbook intended to serve the needs of several groups of dental care professionals and is written with credibility and readability maintained at every level. Undergraduate students especially will find it useful in integrating the concepts they have been taught in a more elaborate way. Clarity and simplicity in language has been my objective while writing this book. The organization of the chapters and the key points with review questions at the end of every chapter serve as a programmed-guide for the reader. The text can be of help for the academicians to re-think the modes of presenting information and also as a model to test whether the students have grasped the concepts they have been taught and are able to use them in a practical manner. All the efforts have been made to make the text as accurate as possible and the information provided in the text was in accordance with the standards accepted at the time of publication. In order to attain these goals, suggestions as well as critiques from many students and clinicians have been received and utilized. Much of the style in the textbook is compact with adequate bibliographies. The reader is advised to use them to gain greater depth of knowledge. The way of periodontist is hard and the book will reflect the difficulty of that path. I hope that the textbook will fulfill all the requirements and expectations of the students and practitioners as this is a special branch of our profession. The field of periodontics remains a work in progress.

Shantipriya Reddy ACKNOWLEDGMENTS

Any book requires the help and assistance of others in order to be completed successfully. First and foremost, I would like to thank Dr Deepti Sinha for drawing the excellent diagrams inserted in the book. Special thanks must go to all my colleagues Dr Prasad MGS, Dr Amudha D and Dr Jaya for their contribution in writing Manual of Clinical Periodontics. I owe a deep sense of gratitude to all my postgraduate students (Dr Ravi Kumar Jirali, Dr Chaitali Agrawal, Dr Soumya Kambali, Dr Shweta Kumari, Dr Nirjhar Bhowmik, Dr Hrishikesh Asutkar) who have helped me relentlessly, while writing the edition. I would like to extend my special thanks to Dr Jeeth Rai, Dr Satish, Dr Keshav, Dr Shabeer, Dr Anilkumar for being so generous in helping me to collect the clinical photographs used in various editions. My heartfelt thanks to Dr Srinivas K for writing the chapters Desquamative and Oral Malodor in the edition. I am also very grateful to Dr Deepak Daryani for providing me with some of the excellent photographs published in the edition. I would also like to thank Dr Ashwath (Smart design navigator) for helping me with animation photographs of various suturing techniques. The excellent cooperation of the publisher is also greatly acknowledged.

PROLOG

HISTORICAL BACKGROUND OF PERIODONTOLOGY Various forms of gingival and periodontal diseases have affected the human race since the dawn of history. In the earlier historical records, almost all the writings have information regarding the diseases affecting oral cavity and majority of it is about periodontal diseases.

Early Civilizations

Summerians of 3,000 BC first practiced . Babylonians and Assyrians, who also have suffered from periodontal diseases, have treated themselves using gingival massage combined with various herbal medications. Research on embalmed bodies of the ancient Egyptians pointed out that periodontal disease was the most common of all the diseases. Medical writings of the time Ebers Papyrus had many references to gingival diseases and also contain various prescriptions for strengthening the teeth and . The medical works of ancient India, Susruta Samhita and Charaka Samhita describe severe periodontal disease with loose teeth and purulent discharge from the gingiva and the treatment advised was to use a stick that is bitter for cleaning teeth. Periodontal disease was also discussed in Ancient Chinese books. The oldest book written in 2,500 BC describes various conditions affecting oral cavity. Gingival inflammation, periodontal abscesses and gingival ulcerations are described in detail. They were among the earliest people to use the to clean the teeth.

Middle Ages

The systematic therapeutic approach was not developed until the middle ages. This was a period of golden age of Arabic science and medicine. Avicenna and Albucasis made a refined, novel approach to surgical work. Albucasis had a clear understanding of as etiology of periodontal disease and described the technique of removing it. He had also developed a set of scalers for removing calculus. He also wrote in detail on other treatment procedures like extraction of teeth, splinting loose teeth with gold wire, etc.

18th Century

Modern dentistry was developed in 18th century. Pierre Fauchard in 1678 who is rightly considered as Father of Modern Dentistry designed periodontal instruments and described the technique in detail. His book The Surgeon Dentist published in 1728 presented all aspects of dental practice (i.e. restorative dentistry, prosthodontics, oral surgery, periodontics and orthodontics). Fauchard wrote in that, confections and sweets destroy the teeth by sticking to the surfaces producing an acid. John Hunter (1728-93) known as an anatomist, surgeon and pathologist of 18th century wrote a book entitled The Natural History of the Human Teeth describing the anatomy of the teeth and their supporting structures with clear illustrations. Thomas Berdmore (1740-85) known as Dentist to His Majesty published the Treatise in the disorders and deformities of the teeth and gums. He not only offered detailed descriptions of instrumentation but also stressed on prevention. xii

19th Century A German born dentist, Leonard Korecker in his paper Philadelphia Journal of Medicine and Physical Sciences mentioned the need for oral hygiene by the patient, to be performed in the morning and after every meal using an astringent powder and a toothbrush. Levi Spear Parmly was considered the Father of Oral Hygiene and the Inventor of . The name Pyorrhea Alveolaris was used to describe periodontal disease. John W Riggs was the first individual to limit his practice to periodontics and was considered the first specialist in this field. Periodontitis was known as Riggs disease. Several major developments took place in the second half of the 19th century starting the era called modern medicine. PROLOG The first was the discovery of anesthesia and second scientific breakthrough was made by Louis Pasteur who established the Germ Theory of Disease. The third scientific finding was the discovery of radiographs by Wilhelm Roentgen. Also the late 19th century has witnessed a proper understanding of the pathogenesis of periodontal disease based on histopathologic studies. GV Black in 1899 gave the term gelatinous microbic plaque and described its relationship to caries. Xenophon recognized ANUG in 4th century BC Salomon Robicsek developed a surgical technique called .

20th Century Early 20th century witnessed major changes in the treatment of periodontal disease. Gottlieb published extensive microscopic studies of periodontal diseases in humans. It was realized that, removal of calculus and other deposits was not enough. In addition, removal of periodontal pockets was necessary to control the disease. Leonard Widman and Newman described flap surgery for the removal of periodontal pockets. Removal of bone was considered essential at that time. After World War II, the focus was on periodontal research and this led to a better understanding of the pathological, microbiological and immunological aspects of periodontal disease. The first workshop in periodontology was conducted in 1951. It was realized at that time, scientific methods should be introduced in the periodontal research. Subsequent workshops conducted in periodontics have witnessed significant scientific contributions in the field of periodontics.

JOURNALS OF PERIODONTOLOGY The various journals of periodontology available are:

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials • The Journal of Periodontology by Robert J Genco. • Journal of Periodontal Research by Isao Ishikawa, Jorgen Slots, Maurizio Tonetti • Journal of Clinical Periodontology by Jan Lindhe. • Periodontology 2000 by Jorgen Slots. • International Journal of Periodontics and Restorative Dentistry in India by Myron Nevins. • Journal of Indian Society of Periodontology. CONTENTS

PART I: THE NORMAL 3. Periodontal Structures in Aging Humans ...... 29 1. Anatomy and Development of the Structures General Effects of Aging ...... 29 of Periodontium...... 3 Skin ...... 29 External Anatomic Features ...... 3 Bone ...... 29 Development of Periodontium ...... 4 Age Changes in the Periodontium ...... 29 Early Development of ...... 4 Gingiva and other Areas of the Oral Mucosa ... 29 Later Development of Cementum ...... 5 Periodontal Ligament and Age Changes Development of ...... 6 in the Periodontium ...... 30 Changes in the Alveolar Bone and Cementum. 30 2. Biology of Periodontal Tissues ...... 8 Bacterial Plaque and Immune Response ...... 30 The Gingiva ...... 8 Effects of Aging on the Progression Macroscopic Features ...... 8 of Periodontal Diseases ...... 30 Microscopic Features ...... 10 Effects of Treatment on the Aging Individuals ...... 30

TOOTH-SUPPORTING STRUCTURES Periodontal ligament ...... 16 PART II: CLASSIFICATION AND EPIDEMIOLOGY Definition ...... 16 OF PERIODONTAL DISEASES Structure ...... 16 4. Classification Systems of Periodontal Diseases .. 35 Development of Principal Fibers Need for Classification ...... 35 of Periodontal Ligament ...... 18 Current Classification Systems of Structures Present in the Connective Tissue .... 19 Periodontal Diseases ...... 35 Functions of Periodontal Ligament ...... 20 World Workshop in Clinical Clinical Considerations ...... 20 Periodontics (1988) ...... 35 Alveolar bone...... 21 Genco (1990) ...... 36 Definition ...... 21 Ranney (1993) ...... 36 Parts of Alveolar Bone ...... 21 European Workshop in Periodontology (1993) 36 Composition of Alveolar Bone...... 22 Classification of Periodontal Disease and Osseous Topography ...... 22 Condition...... 36 Fenestrations and Dehiscences...... 22 Periosteum and Endosteum ...... 23 5. Epidemiology of Gingival and Remodeling and Resorption ...... 23 Periodontal Diseases ...... 42 Blood Supply to the Bone ...... 24 Epidemiology ...... 42 Clinical Considerations ...... 24 Definition ...... 42 Cementum ...... 24 Types of Epidemiologic Research ...... 42 Definition ...... 24 Aims of Epidemiology ...... 43 Classification...... 24 Index ...... 43 Functions ...... 25 Definition ...... 43 Composition ...... 25 Purposes and Uses of an Index ...... 43 Thickness of Cementum ...... 25 Characteristics of an Index...... 44 Cementoenamel Junction ...... 25 Indices Used to Assess the Cemental Resorption and Repair ...... 25 Periodontal Problems ...... 44 xiv

Indices Used to Assess Gingival Inflammation ...... 45 Indices Used to Assess Treatment Needs ...... 52 Papillary Marginal Attachment (PMA) Gingival Periodontal Index ...... 52 Index by Schour and Massler (1944) ...... 45 Community Periodontal Index of Treatment Gingivitis Component of the Needs by Ainamo and Associates ...... 53 Periodontal Disease ...... 45 Periodontal Treatment Need System Gingival Index by Loe H by Bellini HT ...... 53 and Sillness J (1963) ...... 45 Indices of Gingival Bleeding ...... 45 PART III: ETIOPATHOGENESIS Indices used to Measure Periodontal Destruction ... 46 Russell’s Periodontal Index by 6. Periodontal Microbiology () ...... 57 CONTENTS Russell AL (1956) ...... 46 Definition ...... 57 Periodontal Disease Index by Dental Plaque ...... 57 Sigurd P Ramfjord (1959) ...... 47 Plaque ...... 57 Extent and Severity Index by Carlos Biofilms ...... 57 and Coworkers...... 48 Dental Plaque as a Biofilm ...... 57 Radiographic Approaches to Types of Dental Plaque ...... 58 Measure Bone Loss ...... 48 Supragingival Plaque ...... 58 Indices used to Measure Plaque Accumulation ...... 48 Subgingival Plaque ...... 58 Plaque Component of Periodontal Composition of Dental Plaque ...... 59 Disease Index by Ramfjord ...... 48 Formation/Development of Dental Plaque ...... 59 Simplified Oral Hygiene Index by Bacterial Adherence ...... 60 Greene and Vermillion (1964) ...... 48 Growth and Accumulation of Bacteria ...... 60 Turesky-Gilmore-Glickman Modification Structural and Microscopic Properties of Plaque .... 61 of the Quigley Hein Plaque Index (1970) . 49 Supragingival Plaque ...... 61 Plaque Index by Sillness and Loe (1964)...... 50 Clinical Significance of Plaque...... 61 Modified Navy Plaque Index ...... 50 Subgingival Plaque ...... 62 Indices ...... 50 Microbial Specificity of Periodontal Diseases ...... 62 Patient Hygiene Performance Index (PHP) Specific Plaque Hypothesis ...... 62 by Podshadley and Hadley ...... 50 What makes plaque pathogenic?...... 62 Plaque Weight ...... 51 Microorganisms Associated with Plaque-free Score by Grant, Stern and Everett 51 Periodontal Diseases ...... 63 Plaque Control Record by O’Leary ...... 51 Bacteria Associated with Periodontal Indices used to Measure Calculus ...... 51 Health and Disease ...... 63 Calculus Component of the Simplified Health ...... 63

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Oral Hygiene Index by Greene and Chronic Gingivitis ...... 63 Vermillion...... 51 Calculus Component of the 7. Calculus and other Etiological Factors ...... 70 Periodontal Disease Index by Ramfjord .... 51 Calculus ...... 70 Probe Method of Calculus Assessment Definition ...... 70 by Volpe and Associates ...... 52 Types ...... 70 Calculus Surface Index by Ennever Structure ...... 70 and Coworkers...... 52 Composition ...... 71 Marginal Line Calculus Index by Differences between Supragingival and Mühlemann and Villa ...... 52 Subgingival Calculus ...... 72 xv

Attachment to the Tooth Surface ...... 72 Histologic Changes ...... 95 Formation of Calculus ...... 72 Other Properties ...... 97 Pathogenic Potential of Calculus Role of the Trauma from Occlusion in the in Periodontal Diseases ...... 73 Progression of Periodontal Disease ...... 97

Other Contributing Etiological Factors Pathologic Tooth Migration ...... 98 CONTENTS including Food Impaction ...... 73 Pathogenesis ...... 99 Iatrogenic Factors ...... 73 Other Causes ...... 99 Food Impaction ...... 75 Calculus...... 79 10. Role of Systemic Diseases in the Etiology Other Contributing Etiological Factors ...... 79 of Periodontal Diseases ...... 101 Classification of Stains ...... 79 Dietary and Nutritional Aspects of Extrinsic Stains ...... 80 Periodontal Disease...... 101 Intrinsic Stains ...... 80 The Consistency of Diet ...... 101 Protein Deficiency and 8. Host Response: Basic Concepts ...... 82 Periodontal Disease ...... 102 Role of Saliva in the Host Defence ...... 82 Vitamins and Periodontal Disease ...... 102 Gingival Epithelium ...... 83 Effects of Hematological Disorders Gingival Crevicular Fluid ...... 83 on Periodontium ...... 103 Complement ...... 83 White Blood Cell Disorders ...... 103 Classical Pathway ...... 83 Neutropenias ...... 103 Alternative Pathway ...... 83 Leukemia ...... 104 The Inflammatory Cell Response ...... 84 Thrombocytopenic Purpura...... 104 Neutrophils ...... 84 Disorders of WBC Function...... 105 Neutrophil Disorders Associated Red Blood Cell Disorders ...... 105 with Periodontal Diseases ...... 86 Metabolic and Endocrine Disorders ...... 106 Periodontal Diseases Associated Diabetes Mellitus and Periodontal Disease .... 106 with Neutrophil Disorders ...... 86 Thyroid Gland ...... 107 Functions of Macrophages in the Gingiva, Pituitary Gland ...... 107 Crevice and Pocket...... 86 Parathyroid Glands ...... 107 Immunological Mechanisms ...... 88 Gonads ...... 107 Type I: Anaphylactic Reactions ...... 89 Cardiovascular Diseases ...... 109 Type II: Cytotoxic Reactions ...... 89 Arteriosclerosis ...... 109 Type III: Immune Complex or Congenital Heart Disease ...... 109 Arthus Reactions ...... 89 Antibody Deficiency Disorders ...... 109 Type IV: Cell-mediated or Acquired Immunodeficiency Syndrome ...... 109 Delayed Hypersensitivity ...... 90 Other Systemic Diseases ...... 109 Immunology of Periodontal Disease ...... 90 Bismuth Intoxication ...... 109 Lead Intoxication ...... 110 9. Trauma from Occlusion...... 94 Mercury Intoxication...... 110 Physiologic Adaptive Capacity of the Other Chemicals ...... 110 Periodontium to Occlusal Forces ...... 94 Psychosomatic Disorders ...... 110 Trauma From Occlusion (TFO) ...... 94 Definition and Terminology ...... 94 11. Oral Malodor...... 111 Types ...... 95 Classification of Halitosis ...... 111 Signs and Symptoms ...... 95 Genuine Halitosis ...... 111 xvi

Pseudohalitosis ...... 112 15. Host Modulation in Periodontal Therapy ...... 131 Halitophobia ...... 112 Introduction...... 131 Etiology ...... 112 Specific Aspects of Disease Pathogenesis Causes for Physiologic Halitosis ...... 112 as Potential Targets for Host Modulation ...... 131 Causes for Pathologic Halitosis ...... 112 Regulation of Immune and Diagnosis of Halitosis ...... 112 Inflammatory Responses ...... 131 Treatment and Management of Oral Malodor ...... 113 Excessive Production of Matrix Summary ...... 114 Metalloproteinases (MMPs)...... 132 Role of MMPs in Human Periodontal 12. Pathogenesis of Periodontal Diseases ...... 116 Diseases...... 132 CONTENTS Role of Bacterial Invasion ...... 116 Production of Arachidonic Acid Metabolites...... 132 Role of Exotoxins ...... 117 Regulation of Bone Metabolism ...... 133 Role of Cell Constituents ...... 117 Role of Enzymes ...... 117 PART IV: PERIODONTAL PATHOLOGY Evasion of Host Responses ...... 117 Section 1: Gingival Diseases The Host Derived Bone Resorbing Agents ...... 118 Cytokines ...... 118 16. Defence Mechanisms of the Gingiva ...... 137 Other Inflammatory Mediators...... 119 Defence Mechanisms ...... 137 Role of Cytokines ...... 119 Nonspecific Protective Mechanisms ...... 137 Specific Protective Mechanism ...... 138 13. Periodontal Medicine ...... 121 Sulcular Fluid...... 138 Era of Focal Infection ...... 121 Anatomy of Gingival Crevice or Sulcus ...... 138 Periodontal Disease and Coronary Significance of and Fluid .... 139 Heart Disease/Atherosclerosis ...... 122 Significance of Gingival Vasculature and Effect of Periodontal Infection...... 123 Crevicular Fluid ...... 139 Ischemic Heart Diseases ...... 123 Permeability of Sulcular and Periodontal Infection and Stroke ...... 124 Junctional Epithelium ...... 139 Periodontal Disease and Diabetes Mellitus...... 124 Methods of Collection...... 140 Role of Periodontitis in Pregnancy Outcome...... 124 Composition of Gingival Crevicular Periodontal Disease and Chronic Fluid (GCF) ...... 141 Obstructive Pulmonary Disease ...... 125 Clinical Significance ...... 144 Periodontal Disease and Acute Respiratory Infection ...... 126 17. Gingival Inflammation ...... 147 Periodontal Medicine in Clinical Practice ...... 126 Stage I Gingivitis: The Initial Lesion ...... 147 Stage II Gingivitis: The Early Lesion ...... 148

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials 14. Smoking and Periodontal Diseases ...... 128 Stage III Gingivitis: The Established Lesion ...... 148 Effect of Smoking on the Prevalence and Stage IV Gingivitis: The Advanced Lesion ...... 149 Severity of Periodontal Disease ...... 128 Progression from Health to Periodontitis ...... 149 Effect of Smoking on the Etiology and Pathogenesis of Periodontal Disease ...... 128 18. Clinical Features of Gingivitis ...... 151 Microbiology ...... 128 Types of Gingivitis ...... 151 Immunology ...... 129 Depending on the Course and Duration ...... 151 Physiology ...... 129 Depending on the Distribution ...... 151 Effect of Smoking on the Response to Clinical Findings ...... 151 Periodontal Therapy ...... 129 Gingival ...... 152 Effect of Smoking Cessation...... 129 Color Changes in the Gingiva ...... 153 xvii

Changes in the Consistency of Gingiva ...... 153 Intraoral Signs and Symptoms ...... 176 Changes in the Size of the Gingiva ...... 155 Oral Symptoms ...... 176 Surface Texture ...... 155 Extraoral Signs and Symptoms ...... 176 Changes in the Position of Gingiva...... 156 Clinical Course ...... 177

Changes in Gingival Contour ...... 158 Etiology ...... 177 CONTENTS Histopathology ...... 178 19. ...... 159 Diagnosis...... 178 Classification ...... 159 Treatment ...... 178 Inflammatory Enlargement ...... 160 Acute Herpetic Gingivostomatitis (AHG) ...... 179 Acute Inflammatory Enlargement ...... 160 Clinical Features ...... 179 Chronic Inflammatory Enlargement ...... 161 Etiology ...... 180 Noninflammatory Gingival Histopathology ...... 180 Enlargement (Fibrotic Gingival Enlargement)...... 162 Diagnosis...... 181 Phenytoin-induced Gingival Hyperplasia ...... 162 Differential Diagnosis ...... 181 Treatment of Drug-associated Treatment ...... 181 Gingival Enlargement ...... 164 Recurrent Aphthous Stomatitis (RAS) ...... 181 Idiopathic Gingival Fibromatosis ...... 165 Pericoronitis ...... 182 Combined Enlargement ...... 165 Definition ...... 182 Enlargement Associated with Systemic Types ...... 182 Diseases or Conditions...... 165 Clinical Features ...... 182 Conditioned Enlargement...... 167 Acute Pericoronitis ...... 182 Enlargement in Pregnancy ...... 167 Enlargement in Puberty ...... 168 21. Periodontal Diseases in Children and Vitamin C Deficiency ...... 168 Young Adolescents...... 185 Plasma Cell Gingivitis ...... 168 Anatomic Considerations in Children ...... 185 Nonspecific Conditioned Enlargement Changes in Gingiva ...... 185 (Granuloma Pyogenicum) ...... 169 Cementum ...... 186 Systemic Disease Causing Periodontal Ligament ...... 186 Gingival Enlargement ...... 169 Alveolar Bone ...... 186 Granulomatous Diseases ...... 171 Histopathology of Gingivitis in Children ...... 186 Neoplastic Enlargement (Gingival Tumor) ...... 171 Microbiology of Periodontal Benign Tumors of the Gingiva ...... 171 Diseases in Children ...... 186 Malignant Tumors of the Gingiva ...... 171 Classification of Periodontal False Enlargement ...... 173 Diseases in Children ...... 186 Underlying Osseous Lesions ...... 173 Gingival Lesions ...... 186 Underlying Dental Tissues ...... 173 Periodontal Lesions ...... 186 Periodontitis Associated with Systemic Disease ... 186 20. Acute Gingival Infections ...... 175 Gingival Lesions ...... 186 Classification of various Acute Types of Periodontitis ...... 189 Gingival Lesions ...... 175 Periodontitis Associated with Syndromes ...... 191 According to Manson ...... 175 Necrotizing Ulcerative Gingivitis (NUG) ...... 176 22. ...... 194 Terminology ...... 176 Classification ...... 194 Clinical Features ...... 176 Clinical Features ...... 195 xviii

Histopathology ...... 195 Pathogenesis ...... 204 Diagnosis ...... 195 Summary of Pathogenesis ...... 207 Therapy ...... 196 Histopathology ...... 207 Diseases Clinically Presenting Changes in the Soft Tissue Wall...... 207 as Desquamative Gingivitis ...... 196 Microtopography of the Lichen Planus...... 196 Gingival Wall of the Pocket ...... 208 Clinical Features ...... 196 Periodontal Pocket as a Healing Lesion ...... 208 Histopathology ...... 196 Pocket Contents ...... 208 Differential Diagnosis ...... 196 Changes in the Root Surface Wall...... 208 Treatment and Prognosis ...... 196 Periodontal Disease Activity ...... 209 CONTENTS Cicatricial Pemphigoid ...... 197 Periodontal Cyst ...... 209 Clinical Features ...... 197 Determination of Pocket Depth ...... 209 Histopathology ...... 197 Treatment of Periodontal Pocket...... 210 Differential Diagnosis ...... 197 Treatment and Prognosis ...... 197 24. Bone Loss and Patterns of Bone Destruction ... 213 Bullous Pemphigoid ...... 197 Normal Anatomy of Alveolar Bone ...... 213 Clinical Features ...... 197 Mechanism of Bone Formation and Histopathology ...... 197 Bone Destruction ...... 214 Treatment ...... 197 Local Factors ...... 214 Linear IgA Disease ...... 197 Systemic Factors ...... 215 Oral Lesions ...... 198 Factors Determining Bone Histopathology ...... 198 Morphology in Periodontal Disease...... 216 Differential Diagnosis ...... 198 Normal Variation in Alveolar Bone ...... 216 Treatment ...... 198 Bone Destruction Patterns in Periodontal Disease 216 Dermatitis Herpetiformis ...... 198 Horizontal Bone Loss...... 216 Clinical Features ...... 198 Vertical or Angular Defects ...... 216 Histopathology ...... 198 Osseous Craters ...... 217 Treatment ...... 198 Bulbous Bony Contours ...... 217 Pemphigus Vulgaris ...... 198 Reversed Architecture ...... 218 Clinical Features ...... 198 Ledges ...... 218 Histopathology ...... 198 Furcation Involvements...... 218 Differential Diagnosis ...... 198 Prevalence and Distribution of Bone Defects Treatment ...... 199 in Moderate Adult Periodontitis ...... 218 Drug Reaction or Eruptions ...... 199

Diseases Clinically Presenting as 25. ...... 220 Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Desquamative Gingivitis...... 199 Definition ...... 220 Diagnostic Criteria for Chronic Periodontitis ...... 220 Clinical Features ...... 220 Section 2: Periodontal Diseases Microbiological Features ...... 221 23. The Periodontal Pocket ...... 203 Radiographic Features...... 221 Definition ...... 203 Types ...... 221 Classification ...... 203 Disease Distribution ...... 221 Clinical Features ...... 204 Disease Severity ...... 221 Signs ...... 204 Nature of Disease Progression ...... 222 Symptoms ...... 204 Risk factors for Disease ...... 222 xix

General Concept for Etiology of Necrotizing Ulcerative Periodontitis ...... 237 Chronic Periodontitis ...... 223 Necrotizing Stomatitis ...... 238 CDC Surveillance Care Classification (1993) 238 26. ...... 225 Most Common Oral and Periodontal

Localized Aggressive Periodontitis/Localized Manifestations of HIV Infection ...... 238 CONTENTS Juvenile Periodontitis ...... 225 Management...... 238 Historical Background ...... 225 Treatment of and Clinical Features ...... 226 Necrotizing Ulcerative Gingivitis ...... 238 Radiographic Findings ...... 227 Treatment of Necrotizing Ulcerative Histopathology/Microscopic Features ...... 228 Periodontitis ...... 238 Bacteriology ...... 228 Treatment of Necrotizing Stomatitis ...... 239 Immunology ...... 228 Treatment ...... 228 29. Diagnosis of Periodontal Diseases ...... 240 Generalized Aggressive Periodontitis ...... 228 Periodontal Diagnosis ...... 240 Clinical Characteristics ...... 229 Principles of Diagnosis ...... 240 Radiographic Findings ...... 229 Clinical Diagnosis ...... 240 Risk Factors for Aggressive Forms Key Stages of Periodontal Diagnosis ...... 240 of Periodontitis ...... 229 Clinical Diagnosis with Detailed Case History Recording ...... 241 27. Necrotizing Ulcerative Periodontitis, Case History Proforma ...... 242 Refractory Periodontitis and Periodontitis Chief Complaint ...... 242 as a Manifestation of Systemic Disease ...... 231 Oral Hygiene Methods ...... 242 Necrotizing Ulcerative Periodontitis (NUP) ...... 231 Clinical Examination...... 243 Non-AIDS Type Necrotizing Gingival Status ...... 243 Ulcerative Periodontitis...... 231 Investigations ...... 244 AIDS-Associated Ulcerative Periodontitis..... 232 Diagnosis...... 244 Refractory Periodontitis ...... 232 Treatment Plan ...... 245 Etiology ...... 232 Clinical Features ...... 232 30. Determination of Prognosis ...... 246 Treatment ...... 233 Definition of Prognosis ...... 246 Periodontitis as a Manifestation of Determination of Prognosis ...... 246 Systemic Disease ...... 233 Factors for Determination of Prognosis ...... 247 Papillon-Lefévre Syndrome ...... 233 Overall Versus Individual Tooth Prognosis...... 250 Chédiak-Higashi Syndrome (CH Syndrome) . 233 Overall Prognosis ...... 250 Down’s Syndrome (Mongolism, Trisomy 21) 234 Individual Tooth Prognosis ...... 250 Hypophosphatasia ...... 234 Relationship between Diagnosis and Prognosis ... 251 Neutropenia ...... 234 Prognosis for Patients with 251 Leukocyte Adhesion Deficiency ...... 234 Prognosis for Patients with Periodontitis ...... 251 28. AIDS and the Periodontium ...... 236 Re-evaluation of Prognosis after Phase I Therapy 252 HIV Opportunistic Infections ...... 236 Classification of Periodontal Diseases 31. Related Risk Factors Associated with Associated with HIV Infection ...... 236 Periodontal Diseases ...... 254 Linear Gingivitis ...... 237 Definition ...... 254 Necrotizing Ulcerative Gingivitis (NUG) ...... 237 Risk Factors for Periodontal Disease ...... 254 xx

Risk Determinants/Background Characteristics 34. Rationale for Periodontal Treatment ...... 268 for Periodontal Disease ...... 255 Objectives of Periodontal Therapy ...... 268 Risk Indicators for Periodontal Disease ...... 255 Factors which Affect Healing ...... 269 Risk Markers/Predictors ...... 255 Local Factors ...... 269 Clinical Risk Assessment for Periodontal Disease 255 Systemic Factors ...... 269 Demographic Data ...... 256 Healing after Periodontal Therapy ...... 269 Medical History...... 256 Dental History ...... 256 35. Periodontal Instrumentarium ...... 272 Clinical Examination...... 256 Periodontal Instruments ...... 272 Classification of Periodontal Instruments ...... 272 CONTENTS 32. Various Aids including Advanced Diagnostic Techniques ...... 257 Section 2(A): Nonsurgical Therapy Aids Used in Clinical Diagnosis ...... 257 Periodontal Probes ...... 257 36. Principles of Periodontal Instrumentation Aids Used in Radiographic Diagnosis ...... 259 including ...... 280 Orthopantamograph (OPG) ...... 259 Accessibility (Positioning of Patient Xeroradiography ...... 259 and Operator) ...... 280 Advanced Radiographic Techniques ...... 259 Neutral Seated Position for the Clinician ...... 280 Aids in Microbiological Diagnosis ...... 260 Patient’s Position ...... 280 Microbiology and Disease Progression ...... 260 Visibility, Illumination and Retraction ...... 281 Speciation Techniques...... 262 Dental Mirror ...... 281 Methods/Aids in Immunological Condition of Instruments (Sharpness) ...... 282 Diagnosis ...... 262 Advantages of Sharpness ...... 282 Immunofluorescence ...... 262 Maintaining a Clean Field...... 282 Latex Agglutination ...... 262 Instrument Stabilization ...... 282 Enzyme-linked Immunosorbent Instrument Grasp ...... 282 Assay (ELISA) ...... 262 Finger Rest ...... 283 Flow Cytometry ...... 263 Instrument Activation ...... 284 Biochemical Diagnosis ...... 263 Adaptation ...... 284 Prostaglandins ...... 263 Angulation...... 285 Collagenase ...... 263 Lateral Pressure ...... 285 Other Diagnostic Aids ...... 263 Strokes ...... 285 N-benzoyl-DL-arginine 2-naphthylamide Principles of Scaling and Root Planing ...... 286 (BANA) ...... 263 Scaling...... 286 Filter Separation Enzyme Root Planing...... 286 Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Immunoassay (FSEIA) ...... 263 Ultrasonic Instruments ...... 287 Polymerase Chain Reaction (PCR) ...... 264 Equipment and Armamentarium for Ultrasonic and Sonic Instrumentation ...... 288 33. Treatment Plan ...... 266 Aerosol Production ...... 289 Sequence of Therapeutic Procedures ...... 266 Preliminary Phase or Emergency Phase ...... 266 37. Plaque Control ...... 291 Phase I Therapy (Etiotropic Phase) ...... 266 Definition of Plaque Control...... 291 Phase II Therapy (Surgical Phase) ...... 266 Goals of Plaque Control Measures ...... 291 Phase III Therapy (Restorative Phase) ...... 267 Rationale ...... 291 Phase IV Therapy (Maintenance Phase) ...... 267 Basic Approaches for Plaque Control ...... 291 Preferred Sequence of Periodontal Therapy ...... 267 Mechanical Plaque Control ...... 291 xxi

Brushing Techniques ...... 293 According to Design of the Flap/ Chemical Plaque Control ...... 297 Management of the Papilla ...... 327 Incisions ...... 327 Section 2(B): Surgical Therapy Horizontal Incisions ...... 327

Crevicular Incision ...... 328 CONTENTS 38. Principles of Periodontal Surgery ...... 302 Vertical Incision ...... 328 Indications of Periodontal Surgery ...... 302 Flap Techniques for Pocket Therapy...... 329 Contraindications of Periodontal Surgery ...... 302 Modified Widman Flap ...... 331 General Principles of Surgery ...... 302 Undisplaced Flap...... 332 Preparation of the Patient ...... 302 Palatal Flap...... 334 General Conditions that are Common Apically-displaced Flap ...... 336 to all Procedures ...... 303 Distal Molar Surgery ...... 336 Suturing Techniques ...... 304 Healing after Flap Surgery ...... 337 Complications during Surgery ...... 311 Healing after Full Thickness Flap ...... 339 Complications during the First Postoperative Week ...... 311 42. Osseous Surgery ...... 340 Hospital Periodontal Surgery ...... 312 Definition ...... 340 39. Gingival Curettage ...... 314 Rationale ...... 340 Definition ...... 314 Terminology ...... 340 Types ...... 314 Types of Osseous Surgery ...... 341 Rationale ...... 314 Resective Osseous Surgery ...... 341 Indications...... 315 Indications ...... 341 Procedure ...... 315 Contraindications ...... 341 Basic Technique ...... 315 Examination Prior to Surgery...... 341 Other Techniques ...... 315 Methods...... 342 Healing after Scaling and Curettage ...... 316 Technique ...... 342 Clinical Appearance after Scaling and Curettage . 316 Vertical Grooving ...... 342 Radicular Blending ...... 342 40. Gingivectomy ...... 318 Flattening of the Interproximal Bone ...... 342 Definitions ...... 318 Gradualizing Marginal Bone ...... 342 Prerequisites ...... 318 Healing after Surgery ...... 343 Indications...... 318 Reconstructive Osseous Surgery...... 343 Contraindications ...... 319 Evaluation of New Attachment Types of Gingivectomy ...... 319 and Bone Regeneration ...... 343 Surgical Gingivectomy...... 319 Nongraft-associated New Attachment...... 344 Gingivectomy by Electrosurgery ...... 323 Graft-associated New Attachment ...... 346 Laser Gingivectomy ...... 323 Gingivectomy by Chemosurgery...... 324 43. Mucogingival Surgery ...... 351 Definition ...... 351 41. Periodontal Flap ...... 325 Mucogingival Problems ...... 351 Indications/Objectives of Flap Surgery...... 325 Objectives, Indications and Contraindications Definition ...... 326 of Mucogingival Surgery ...... 351 Classification ...... 326 Objectives ...... 351 According to the Placement of Flap Indications ...... 352 after Surgery ...... 326 Contraindications ...... 352 xxii

Techniques to Increase the Width of Effects of Periodontitis on the Dental Pulp ...... 391 Attached Gingiva ...... 352 Endoperiolesions...... 391 Gingival Extension Operation ...... 352 Classification ...... 391 Free Soft Tissue Autograft ...... 352 Microbiological Findings ...... 392 The Classic Technique ...... 352 Diagnosis and Treatment ...... 392 Apically-displaced Flap ...... 356 Treatment ...... 394 Other Techniques for Widening the Zone of Attached Gingiva ...... 358 46. Splints in Periodontal Therapy ...... 395 Free Gingival Autograft ...... 367 Definition ...... 395 Subepithelial Connective Tissue Graft ...... 368 Harmful Aspects ...... 395 CONTENTS Procuring the Graft from the Donor Site...... 368 Beneficial Aspects ...... 395 Guided Tissue Regeneration Technique Objectives of Splinting ...... 395 for Root Coverage ...... 372 Classification of Splints ...... 396 Indications ...... 372 According to the Period of Stabilization ...... 396 Modifications ...... 372 According to the Type of Material ...... 396 Operations for Removal of Frena ...... 372 According to the Location on the Tooth ...... 396 Indications ...... 373 Various commonly used Splints ...... 396 Techniques for the Removal of the Frenum ... 373 Principles of Splinting ...... 396 Indications and Contraindications of Splinting .... 396 PART V: TREATMENT Indications ...... 396 OF PERIODONTAL DISEASES Contraindications ...... 397 Advantages ...... 397 44. Furcation Involvement and its Management .... 381 Disadvantages ...... 397 Definition ...... 381 Etiology ...... 381 47. Dental Implants: Periodontal Considerations .. 398 Primary Etiologic Factor ...... 381 Terminology ...... 398 Classification ...... 383 Historical Background ...... 399 Clinical Features ...... 385 The Ancient Era (Before 1000 AD) ...... 399 Clinically ...... 385 The Medieval Era (1000 to 1799 AD)...... 399 Microscopically ...... 385 The Foundation Era (1800 to 1910 AD) ...... 399 Prognosis...... 385 The Modern Era (1910 to 1978 AD) ...... 399 Treatment ...... 385 The Contemporary Era (1978 Till Date) ...... 399 Traditional Treatment Procedures ...... 386 Biological Considerations of Implants...... 399 Reconstructive and Regenerative Soft Tissue Implant Interface ...... 399

Treatment Procedures ...... 386 Bone Implant Interface...... 400 Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Indications and Contraindications for Biomaterials used for Implants ...... 400 Root Resection and Separation ...... 387 Metals and Alloys...... 400 Indications ...... 387 Inert Ceramics ...... 400 Contraindications ...... 387 Calcium Phosphate Ceramics ...... 400 Bioactive and Biodegradable Ceramics ...... 400 45. Pulpoperiodontal Problems ...... 390 Polymers...... 400 Pathways of Communication between Classification of Implants ...... 401 Pulp and Periodontium...... 390 Based on the Shape and Form ...... 401 Effects of Pulpal Disease on the Periodontium ..... 390 Based on Surface Characteristics ...... 401 xxiii

Classification of Implant Systems...... 401 49. Occlusal Evaluation and Therapy in the Treatment Planning ...... 401 Management of Periodontal Disease ...... 412 Clinical Assessment ...... 401 Terminology ...... 412 The Absolute Requirements for Clinical Evaluation of Occlusion ...... 412 Treating Implant Patients ...... 401 Temporomandibular Disorders (TMDs) ...... 412 CONTENTS Indications for Implant Therapy...... 401 Management of Trauma from Occlusion ...... 413 Absolute Contraindications for Possible Requirements for Occlusal Stability ...... 413 Implant Treatment ...... 402 Occlusal Therapy ...... 413 Surgical Procedures ...... 402 Healing following Implant Surgery ...... 404 50. The Role of Orthodontics as an Adjunct Different Phases of Healing ...... 404 to Periodontal Therapy ...... 415 Rationale for Orthodontic Treatment Peri-implant Complications ...... 404 in Periodontal Therapy ...... 415 Peri-implant Diseases...... 404 Reducing Plaque Retention ...... 415 Types of Peri-implant Diseases ...... 404 Improving Gingival and Osseous Form ...... 415 Clinical Features ...... 405 Facilitating Prosthetic Replacements ...... 416 Diagnosis...... 405 Improving Esthetics ...... 416 Probing ...... 405 Use of Orthodontics as an Adjunct Radiographs ...... 405 to Overall Treatment ...... 416 Microbial Monitoring...... 405 Indications and Contraindications Management and Maintenance ...... 405 of Orthodontic Therapy ...... 416 Indications ...... 416 48. Maintenance Phase Contraindications ...... 416 (Supportive Periodontal Treatment) ...... 408 Timing of Orthodontic Procedures Importance of Maintenance Phase ...... 408 in Periodontal Treatment ...... 416 Rationale for Supportive Iatrogenic Effects Associated Periodontal Therapy ...... 408 with Orthodontic Treatment ...... 417 Causes for Recurrence of Periodontal Disease ..... 408 Root Resorption ...... 417 Goals of Supportive Effects of Orthodontic Bands on the Periodontal Treatment ...... 408 Periodontium ...... 417 Objectives of Maintenance Phase ...... 409 Microbiology around Orthodontic Bands ...... 417 Parts of Maintenance Phase ...... 409 Effects of Orthodontics on Dentition with Part–I: Examination Normal Height of Attachment Apparatus ...... 417 (Approximate Time –7 Min) ...... 409 Dentition with Reduced Height of Part–II: Treatment Attachment Apparatus ...... 417 (Approximate Time – 35 Min) ...... 410 Response of the Periodontal Ligament Part–III: Schedule Next Procedure...... 410 to Orthodontic Forces ...... 417 Sequence of Maintenance Visits ...... 410 Determination of Maintenance 51. Periodontal-Restorative Inter-relationship ...... 419 Recall Intervals ...... 410 Margins of the Restorations ...... 419 Procedures to be Performed at Recall ...... 410 Rules for Margin Placement ...... 419 Management of Particular Type of Restorative Margins Encroaching on Recall Patients ...... 410 the Biologic Width ...... 420 xxiv

Methods to Correct Biological 53. Questionnaire for Clinical Case Discussion ...... 432 Width Violation ...... 420 Questions ...... 432 Crown Contour ...... 420 Questions Related to Periodontal Hypersensitivity to Dental Materials ...... 420 Instruments and Treatment ...... 433 Proximal Contact and Embrasure ...... 420 Questions and Answers ...... 433 Pontic Design ...... 421 Mouthbreathing ...... 434 Tonguethrusting ...... 434 52. Drugs Used in Periodontal Therapy ...... 423 Cigarette Smoking...... 434 Classification of Various Drugs used Bruxism ...... 435 Mechanical Plaque Control ...... 435 CONTENTS in Periodontal Therapy ...... 423 Chemical Plaque Control ...... 435 Depending on Antimicrobial Efficacy Scrub Technique ...... 436 and Substantivity ...... 423 Roll Technique ...... 436 Chemicals used for Supragingival Bass Method...... 436 Plaque Control ...... 424 Modified Bass Method ...... 436 Phenols ...... 424 Modified Stillman Method ...... 436 Quaternary Ammonium Compound ...... 424 Charter’s Technique ...... 436 Antibiotics used in Periodontal Therapy...... 424 Changes in Epithelium ...... 444 Systemic Administration of Antibiotics ...... 424 Changes in Connective Tissue ...... 444 Local Administration of Antibiotics ...... 425 Classification of Furcation Involvement ...... 448 Tetracyclines ...... 425 Grading of Mobility ...... 449 Metronidazole ...... 426 Complete Blood Count...... 451 Penicillins ...... 427 Advantages of OPG ...... 453 Dosage...... 427 Disadvantages of OPG ...... 453 Non-steroidal Anti-inflammatory Advantages of IOPA...... 453 Drugs (NSAIDs) ...... 427 Disadvantages of IOPA ...... 453 Actions of Flurbiprofen ...... 427 Nonsurgical Instruments ...... 455 Mechanism of Action of NSAID ...... 427 Surgical Instruments...... 455 Local Drug Delivery Systems ...... 427 Characteristics of a Scaler ...... 455 Local Administration of Antibiotics and Characteristics of Curette ...... 456 Antimicrobial Agents ...... 428 Supragingival Scalers ...... 456 Vehicles for Local Delivery ...... 428 Subgingival Scalers ...... 456 Methods of Delivery of Finger rest ...... 457 Chemotherapeutic Agents ...... 429 Advances in Diagnostic Instruments ...... 459 Currently Available Local Drug Delivery

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Advances in Root Planing Instruments ...... 459 Systems in Periodontal Therapy ...... 430 Frequently used Local Antimicrobials Glossary ...... 461 with Dosage Specification ...... 430 Conclusion ...... 430 Index ...... 481

1 ChapterChapter

Anatomy and Development of the Structures of Periodontium

 EXTERNAL ANATOMIC FEATURES • Later Development of Cementum  DEVELOPMENT OF PERIODONTIUM • Development of Junctional Epithelium • Early Development of Cementum

INTRODUCTION 2. Specialized mucosa: It covers the dorsum of the tongue. 3. Lining mucosa: It is the oral mucous membrane that The term periodontium arises from the Greek word peri lines remainder of the oral cavity. Among all the meaning around and odont meaning tooth, thus it can be structures of the periodontium, only the gingiva is visible simply defined as the “tissues investing and supporting the clinically. The gingiva is divided anatomically into free teeth”. The periodontium is composed of the following or marginal, attached and interdental gingiva. The border tissues namely alveolar bone, root cementum, periodontal or groove between marginal and attached gingiva is ligament (supporting tissues) and gingiva (investing tissue). called as a free gingival groove, a shallow depression The various diseases of the periodontium are collectively on the faciogingival surface that roughly corresponds termed as periodontal diseases. Their treatment is referred to the base of the gingival sulcus. The junction between to as periodontal therapy. The clinical science that deals the attached gingiva and alveolar mucosa is called as with the periodontium in health and disease is called mucogingival line or junction (Fig. 1.1). periodontology. The branch of dentistry concerned with The normal gingiva is pink in color (salmon coral pink) prevention and treatment of periodontal disease is termed and accumulation of melanin pigmentation is normal. The periodontics or periodontia. surface of the gingiva exhibits an orange peel-like appearance referred to as . In health, the gingiva EXTERNAL ANATOMIC FEATURES completely fills the embrasure spaces between the teeth and The oral mucosa consists of three zones: is known as the interdental gingiva. In the posterior teeth, 1. Masticatory mucosa: It includes the gingiva and the where the contact areas between the teeth are usually broad, covering of the hard palate. the interdental gingiva consists of two papillae, facial and

4 PART I

Fig. 1.1: Surface characteristics of the Fig. 1.2: Root sheath of Hertwig clinically-normal gingiva

lingual which are connected by the col. The significance of col is that, it is made up of nonkeratinized epithelium and hence represents the most frequent site for initiation of disease process.

The Normal Periodontium Normal The DEVELOPMENT OF PERIODONTIUM To understand the development of periodontal tissues one has to have a clear understanding of the root formation. Development of cementum and roots of the teeth starts once the formation of enamel is completed. The outer and inner epithelia together form the epithelial root sheath of Hertwig, which is responsible for determining the shape of the root.

Early Development of Cementum The outer and inner epithelial layers become continuous (without stratum intermedium or stellate reticulum) in the area of the future cementoenamel junction and form a two- Fig. 1.3: Proliferation of root sheath and further dentine layered sheath, which grows into the underlying formation in an apical direction mesenchyme. The apical portion of the root sheath remains constant whereas the coronal portion, which is associated Once the crown formation is complete the cells of the with dentin and cementum formation moves in the direction inner enamel epithelium loose their ability to form enamel of the oral cavity. The root sheath bends horizontally at the and is called reduced enamel epithelium. They retain the level of future cementoenamel junction forming the ability to induce perimesenchymal cells to differentiate into epithelial diaphragm, following which the cervical opening odontoblasts and to proceed with the formation of predentin becomes smaller (Figs 1.2 and 1.3). and dentin. 5

After the dentin formation is completed, certain changes occur in the root sheath. Recent studies have shown that, the epithelial cells of the root sheath produce a layer on the root dentin, which is 10 μm thick, has a

hyaline appearance and contains fine granules and fibrils. 1 CHAPTER This layer is called the hyaline layer of Hopewell Smith or intermediate cementum. The epithelial cells of the root sheath secrete enamel proteins such as amelogenin or enameloids. The root sheath at this stage becomes discontinuous and enables the surrounding follicular mesenchyme to come in contact with the amelogenin. These follicular cells then differentiate into cementoblasts Periodontium of Structures the of Development and Anatomy and deposit the organic matrix of cementum on the root surface (Figs 1.4 and 1.5). Fig. 1.4: Fragmentation of root sheath

Later Development of Cementum

Cementoblasts are cuboidal cells that are arranged on the outer surface of the hyaline layer. These cells are responsible for the deposition of the organic matrix of cementum, which consists of proteoglycan ground substance, intrinsic collagen fibers and is followed by subsequent mineralization of the organic matrix (Fig. 1.6). Mineralization starts with the formation of a thin layer called cementoid. Mineral salts are derived from the tissue fluid containing calcium and phosphate ions and are deposited as hydroxyapatite crystals. The disintegrated Hertwig’s root sheath slowly moves away from the root surface and remain in the periodontal ligament as epithelial cell rests of Malassez. The periodontal ligament forms from the dental follicle soon after root Fig. 1.5: Follicular cells and fibers contact dentine surface formation begins. Before a tooth erupts, fibers from the follicle are incorporated in the cementum and they lie parallel to the root surface. Once the tooth erupts, the fibers are arranged in an oblique manner and are regarded as the precursor of the periodontal ligament fibers. As the cementum continues to increase in thickness, more fibers become incorporated into the cementum and eventually called as Sharpey’s fibers, when periodontal ligament becomes established. Alveolar bone forms around the periodontal ligament. With continuous bone deposition the periodontal ligament space gradually becomes narrower. The Fig. 1.6: Early deposition of matrix 6

surface of the enamel called primary enamel cuticle. The inner enamel epithelium after laying down enamel reduces to a few layers of flat cuboidal cells, which is then called as reduced enamel epithelium. It covers the entire enamel surface extending till the cementoenamel junction. During eruption, the tip of the tooth approaches the oral mucosa leading to fusion of the reduced enamel epithelium with the oral epithelium. As the crown emerges into the oral cavity

PART I the former ameloblasts that are in contact with the enamel get transformed into junctional epithelium. Coronally, the junctional epithelium is continuous with the oral epithelium. As the tooth erupts, the reduced enamel epithelium grows shorter gradually. A shallow groove, the gingival sulcus may develop between the gingiva and the tooth surface. Fig. 1.7: Advanced formation of cementum Hence, the ameloblasts pass through two phases, in one develops during the eruption of the teeth and cells they form enamel and in the other phase they help in responsible for bone formation are osteoblasts (Fig. 1.7). formation of primary epithelial attachment or junctional epithelium. When the junctional epithelium forms from the Development of Junctional ameloblasts it is called primary epithelial attachment. Epithelium (Fig. 1.8) Junctional epithelium that forms after surgical therapy takes When the enamel formation is complete the ameloblasts its origin from the basal cells of oral epithelium instead of

The Normal Periodontium Normal The become shorter, and they leave a thin membrane on the ameloblasts. This is called secondary epithelial attachment.

Fig. 1.8: Development of junctional epithelium 7

REVIEW QUESTIONS

1. The periodontium is composed of alveolar bone, root 1. Define periodontology and periodontics. cementum, periodontal ligament (supporting tissue) and gingiva (investing tissue). 2. What are the parts of periodontium?

2. The gingiva is the only structure of the periodontium that 3. Describe the development of structures of periodontium. 1 CHAPTER is clinically visible and anatomically it can be divided into marginal, attached and interdental gingiva. 3. The junction between the marginal and attached gingiva BIBLIOGRAPHY is called free gingival groove, whereas the junction between the attached gingiva and alveolar mucosa is 1. Jansen BG, Van Rensburg. Oral Biology, Chapter 8. Quintessence called as . Publishing Co Ltd, 1995;301-7. 4. Once the dentin formation is completed, the root sheath 2. Varma BRR, Nayak RP. Current Concepts in Periodontics, becomes discontinuous and allows the surrounding mesenchyme to come in contact with the products of the Chapter 2. Arya Publishing, 2002;4-8. epithelial cells of the root sheath, i.e. amelogenin. These 3. Bhasker SN. Orbans, Oral Histology and Embryology, 10th Periodontium of Structures the of Development and Anatomy follicular cells then differentiate into cementoblasts, edition. CBS Publishers and Distributers, New Delhi, 41-4. fibroblasts and osteoblasts by which cementum, 4. Tencate. Oral Histology, Development, Structure and Function, periodontal ligament fibers and alveolar bone are 3rd edition. Jaypee Brothers Medical Publishers, 228-43. deposited. 5. Fusion of the oral epithelium along with the reduced enamel epithelium gives rise to the junctional epithelium or epithelial attachment. 2 ChapterChapter

Biology of Periodontal Tissues

 THE GINGIVA  ALVEOLAR BONE • Macroscopic Features • Definition • Microscopic Features • Parts of Alveolar Bone  TOOTH-SUPPORTING STRUCTURES • Composition of Alveolar Bone  PERIODONTAL LIGAMENT • Osseous Topography • Definition • Blood Supply to the Bone • Structure • Clinical Considerations Cellular Composition  CEMENTUM Extracellular Components • Definition • Development of Principal Fibers of • Classification Periodontal Ligament • Functions • Structures Present in the Connective Tissue • Composition • Functions of Periodontal Ligament • Thickness of Cementum • Clinical Considerations • Cementoenamel Junction • Cemental Resorption and Repair

INTRODUCTION root fits. The main function of the gingiva is to protect the surrounding tissues from the oral environment. Periodontium is the functional unit of tissues supporting the tooth including gingiva, the periodontal ligament, the THE GINGIVA cementum and the alveolar process. The tooth and periodontium are together called as the dentoperiodontal Macroscopic Features unit. The main support of the tooth is provided by the The gingiva is that part of the oral mucosa (masticatory periodontal ligament, which connects the cementum of the mucosa) that covers the alveolar process of the jaws and root to the alveolar bone or tooth socket, into which the surrounds the necks of the teeth. Anatomically, the gingiva 9

is divided into—marginal, attached and interdental gingiva Gingival Sulcus (Fig. 2.1). It is defined as the space or shallow crevice between the Marginal Gingiva or Free Gingiva or tooth and the free gingiva, which extends apical to the junctional epithelium. It is V-shaped and barely permits the

Unattached Gingiva 2 CHAPTER entrance of a . Under normal or ideal It is defined as the terminal edge or border of the gingiva conditions it is about 0 mm (seen only in germ free animals). surrounding the teeth in a collar-like fashion. In some cases, The so-called probing depth of a clinically-normal gingival it is demarcated apically by a shallow linear depression sulcus in humans is 2 to 3 mm (Fig. 2.3). called the free gingival groove. Though the marginal gingiva is well-adapted to the tooth surface, it is not attached to it Attached Gingiva (Fig. 2.2).

It is defined as that part of the gingiva that is firm, resilient Tissues Periodontal of Biology and tightly-bound to the underlying periosteum of the alveolar bone. On the facial aspect it extends up to the loose and movable alveolar mucosa, from which it is demarcated by the mucogingival junction. The width of attached gingiva is the distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or the periodontal pocket. It varies in different areas of the mouth, greater in the maxilla than mandible, least width in the mandibular first premolar area, greatest width in the maxillary incisor region. The width of attached gingiva increases with age and in Fig. 2.1: Normal gingiva in health supraerupted teeth.

Interdental Gingiva

Usually, occupies the gingival embrasure. There are three parts of interdental gingiva, facial papilla, lingual papilla and col, which is a valley-like depression that connects the

Fig. 2.2: Anatomic land marks of gingiva Fig. 2.3: Sulcus depth in healthy gingiva 10

facial and lingual papilla. The lateral borders and tips of the interdental papilla are formed by continuation of marginal gingiva and the intervening portion by the attached gingiva. In the presence of diastema the interdental papilla will be absent (Figs 2.4 and 2.5).

Microscopic Features The gingiva consists of a central core of connective tissue

PART I covered by stratified squamous epithelium. Three types of epithelium exists in the gingiva. 1. The oral or outer epithelium (keratinized epithelium) (Fig. 2.6). 2. The 3. The junctional epithelium (nonkeratinized epithelium) (Fig. 2.7). In the keratinized epithelium, the principal cell type is the keratinocyte, which can synthesize keratin. The process of keratinization involves a sequence of biochemical and morphological events that occur in a cell as it migrates from the basal layer towards the cell surface.

The nonkeratinized epithelium contains clear cells, The Normal Periodontium Normal The which include melanocytes, Langerhans cells, Merkel cells and lymphocytes. Fig. 2.5: ‘COL’ in various types of contacts The oral epithelium has the following cell layers: 1. Basal layer (Stratum basale or Stratum germinativum). 2. Spinous layer (Stratum spinosum). 3. Granular layer (Stratum granulosum). 4. Keratinized cell layer (Stratum corneum).

Fig. 2.4: Absence of interdental papilla in diastema cases Fig. 2.6: Orthokeratinized epithelium 11

The basal cells possess the ability to divide, it is in the basal layer that the epithelium is renewed and therefore this is also called as stratum germinativum. When two daughter cells have been formed by cell division an adjacent “older”

basal cell is pushed into the spinous cell layer and starts as 2 CHAPTER a keratinocyte, to traverse the epithelium. It takes approxi- mately one month for a keratinocyte to reach the outer epithelial surface where it becomes desquamated from the stratum corneum. The basal cells are separated from the connective tissue by a basement membrane. In light microscopy this membrane appears as a zone approximately 1 μm wide and Tissues Periodontal of Biology reacts positively to a PAS stain (periodic acid Schiff stain), which indicates the presence of carbohydrates (glycoproteins) in the basement membrane. In electron micrograph, immediately beneath the basal cell, an Fig. 2.7: Nonkeratinized epithelium approximately 400 Å wide electrolucent zone can be seen which is called lamina lucida. Beneath the lamina lucida an There are three distinct differences between the oral electron dense zone – lamina densa is observed. From the sulcular epithelium, oral epithelium and the junctional lamina densa so-called anchoring fibrils project in fan- epithelium: shaped fashion into the connective tissue. The epithelial a. The size of the cells in the junctional epithelium is, cells facing the lamina lucida contain a number of electron relative to the tissue volume, larger than in the oral dense, thicker zones called hemidesmosomes. The sulcular epithelium. hemidesmosomes are involved in the attachment of the b. The intercellular space in the junctional epithelium is, epithelium to the underlying basement membrane. comparatively wider than in the oral epithelium. Stratum spinosum consists of large cells with short c. Granular layer, which is seen in the oral epithelium, is cytoplasmic processes resembling spines. Since they are absent in sulcular and junctional epithelium. arranged at regular intervals they give the cells a prickled Morphologic Characteristics of the Different appearance. The cells are attached to one another by Areas of Gingival Epithelium numerous desmosomes (pairs of hemidesmosomes), which are located between the cytoplasmic processes of adjacent Oral or outer epithelium: It covers the crest and outer surface cells. of the marginal gingiva and the surface of the attached Composition of a desmosome: It consists of two adjoining gingiva. It is keratinized or parakeratinized or combination hemidesmosomes separated by a zone containing electron of both. Keratinization varies in different areas in the dense granulated material (GM). In addition, outer and inner following order: Palate (most keratinized), gingiva, ventral leaflets of the cell (OL, IL) and the attachment plaque (AP), aspect of the tongue and cheek (least keratinized). The represent granular and fibrillar material in the cytoplasm keratinized epithelium of the gingiva consists of four layers, (GM) (Fig. 2.8). namely stratum basale, stratum spinosum, stratum granulosum and stratum corneum. Stratum granulosum: Electron dense keratohyalin bodies The cells of the basal layer are either cylindrical or begin to occur, these granules are believed to be related to cuboidal and are in contact with the basement membrane. the synthesis of keratin. Here, there is conversion of cells 12

they do not undergo keratinization. However, the surface cells are flattened and exhibit a tendency towards partial keratinization in response to physical stimulation. Normally, there are no regular rete pegs in sulcular epithelium but they form during the inflammation of the lateral wall. Junctional epithelium: Denotes the tissue that joins to the tooth on one side and to the oral sulcular epithelium and connective tissue on the other. It forms the base of the sulcus. PART I It has been examined in detail by several investigators, many hypothesis have been put forward to explain the mode of attachment of the epithelium to the tooth surface. Prior to the Gottlieb concept, it was believed generally, that the gingival soft tissues were closely opposed, but not organically united to the surface of the enamel. This concept Fig. 2.8: Composition of a desmosome was based on the clinical finding that the gingiva could be easily deflected from the tooth surface during to “acellular” structure bordered by a cell membrane instrumentation. However, experimental and clinical indicating keratinization of the cytoplasm of the observations have led Gottlieb to the concept that the soft keratinocyte. tissues of the gingiva are organically united to the enamel surface. He termed it as “epithelial attachment”. Although Stratum corneum: The cytoplasms of the cells in this layer it was accepted generally, the concept did not explain how The Normal Periodontium Normal The are filled with keratin and the entire nucleus is lost. But in exactly junctional epithelium attaches to the root surface parakeratinized epithelia, the cells contain remnants of (Fig. 2.9). nuclei. Waerhaug in 1952, based on his observations presented Keratinization is considered as a process of diffe- the concept of the “epithelial cuff, he concluded that the rentiation rather than degeneration. The keratinocytes while gingival tissues are closely apposed, but not organically traversing from the basal layer to the epithelial surface united to the tooth surface. In 1962, Stern showed that the undergoes certain changes. attachment to the tooth surface is through hemidesmosomes. a. From the basal layer to the granular layer both the This was supported by extensive studies conducted by number of tonofilaments in the cytoplasm and the Schroeder and Listgarten, they revealed that there is a number of desmosomes increase significantly. structural continuity between the tooth surface and b. In contrast, the number of organelles such as epithelium. These studies by Schroeder and Listgarten states mitochondria, lamellae of rough endoplasmic reticulum that the epithelium-tooth interface was observed to be and Golgi apparatus decrease. similar to the epithelium-connective tissue interface and that Oral sulcular epithelium: The soft tissue wall of the is by hemidesmosome and basal lamina. A basal lamina is gingival sulcus is lined coronally with sulcular epithelium, always interposed between epithelial cells and crown or root extending from the to the junctional surface, and the epithelial cells are united to the basal lamina epithelium. It is made up of basal and prickle cell layer. by hemidesmosomes. The sulcular epithelium resembles the oral/gingival The junctional epithelium is attached to the tooth surface epithelium in all respects with the exception that it does not by internal basal lamina and to the gingival connective become fully keratinized. Although it contains keratinocytes tissue by an external basal lamina. The internal basal lamina 13 HPE 2 CHAPTER

Fig. 2.9: Concepts of epithelial attachment Biology of Periodontal Tissues Periodontal of Biology

consists of a lamina densa (adjacent to the enamel) and a formation and interdigitation. Junctional epithelial cells, lamina lucida to which hemidesmosomes are attached. especially those near the base of the gingival sulcus, appear Various studies have also shown that junctional epithelial to have phagocytic capacity. cells are involved in the production of laminin and play a The structural features of junctional epithelium indicate key role in the adhesion mechanism. The attachment of the that it is highly permeable. Leukocytes and lymphocytes junctional epithelium to the tooth surface is reinforced by within junctional epithelium are seen even in clinically the . Hence the junctional epithelium and healthy gingiva. The densities of desmosomes that gingival fibers are considered as a functional unit, referred interconnect the cells are considerably less than that of oral to as the dentogingival unit. epithelia and represents wider intercellular junctions.

General structural features of junctional epithelium: Epithelium-Connective Tissue Interface It consists of a collar like band of stratified squamous non keratinizing epithelium. Thickness varies from three or four Histological sections have demonstrated that, the rete pegs layers in early life and increases with age up to 15 to 20 of epithelial cells project deeply into the connective tissue layers at the base of the gingival sulcus, and only 1 or 2 leading to the formation of a series of interconnecting cells at the most apical portion. The length of the junctional epithelial ridges. Basement membrane seems to form a epithelium ranges from 0.25 to 1.35 mm. The cells are continuous sheet that connects the epithelium and arranged into basal and suprabasal layers and they do not connective tissue. Electron microscope reveals a faintly have granular layer or cornified layers. They exhibit unusual fibrillar structure, called as the basal lamina, which is a part cytologic features and differ significantly from other oral of the basement membrane. This structure has lamina lucida epithelia. Three zones in junctional epithelium have been adjacent to the basal epithelial cells and lamina densa described, apical, coronal and middle. Apical is for towards connective tissue. Basal lamina is produced by germination, middle is for adhesion and coronal is adjacent epithelial cells and is made up of collagenous permeable. proteins and proteoglycans binded together into a totally- The basal cells are cuboidal or in some cases, flattened. insoluble complex. It also contains laminin and fibronectin. They contain slightly more rough endoplasmic reticulum Fibrils measuring 20 to 40 nm in diameter seem to extend and lysosomal content. The content of mitochondria of the from the basal cells through the basal lamina and into the cells as they migrate toward and along the tooth surface lamina propria of the connective tissue. These structures decreases. Cells of the suprabasal layer especially those called as anchoring fibrils are supposed to bind the basal adjacent to the tooth surface exhibit complex microvillus cells, basal lamina and connective tissue together (Fig. 2.10).

14 PART I

Fig. 2.10: Structure of the junction between epithelium and connective tissue

Supra-alveolar Connective Tissue

The connective tissue supporting the oral epithelium is Fig. 2.11: The principal group of fibers termed as the lamina propria and for descriptive purpose it can be divided into two layers: The functions of gingival fibers are the following: a. The superficial papillary layer—associated with the a. It braces the marginal gingiva firmly against the tooth. epithelial ridges. b. It helps to withstand the forces exerted by mastication. b. Deeper reticular layer—that lies between the papillary c. It unites the free gingiva to the root cementum and the layer and the underlying structures. adjacent attached gingiva.

The term reticular here means net-like and refers to the The arrangement of gingival fibers is described as The Normal Periodontium Normal The arrangement of collagen fibers. In the papillary layer, the principal group of five bundles and secondary group of collagen fibers are thin and loosely-arranged and many minor fibers consisting of six sets (Fig. 2.11). capillary loops are present. The reticular layer is dominated The principal group fibers are: by collagen arranged in thick bundles. 1. Dentogingival fibers: They project from the cementum The lamina propria consists of cells, fibers, blood vessels in a fan-like conformation towards the crest and outer embedded in amorphous ground substances. surface of the marginal gingiva. They provide support I. Cells: Different types of cells present are: to the gingiva by attaching it to the tooth. a. Fibroblast 2. Alveolar gingival fibers: They extend from the b. Mast cells periosteum of the alveolar crest coronally into the lamina c. Macrophages propria. Their function is to attach the gingiva to the d. Inflammatory cells. alveolar bone. II. Fibers: The connective tissue fibers are produced by 3. Dentoperiosteal fibers: They arise from the cementum fibroblasts and can be divided into: near the cementoenamel junction and insert into the a. Collagen fibers periosteum of the alveolar bone and protect the b. Reticulin fibers periodontal ligament. c. Oxytalan fibers 4. Circular fibers: They surround the tooth in a cuff or d. Elastin fibers. ring like fashion and course through the connective Collagen type I form the bulk of the lamina propria and tissue of the marginal and attached gingiva. provide the tensile strength to the gingival tissues. Type II 5. Trans-septal fibers: They are located interproximally, collagen is seen in the basement membrane. they extend from cementum of one tooth to the 15

cementum of the neighboring tooth. Their function is to Extracellular matrix/ground substance: It is produced by protect the interproximal bone and maintain tooth-to- fibroblasts, followed by mast cells and other components tooth contact. derived from the blood. The matrix is the medium in which Fibers of the secondary group (Fig. 2.12) are: the connective tissue cells are embedded and is essential 1. Periosteogingival fibers: They extend from the for the maintenance of the normal function of the connective 2 CHAPTER periosteum of the alveolar bone to the attached gingiva. tissue. Thus, the transportation of water, electrolytes, They help to attach the gingiva to the alveolar bone. nutrients, metabolites, etc. to and from the individual 2. Interpapillary fibers: They are seen in the interdental connective tissue cells occurs with in the matrix. gingiva extending in a faciolingual direction and support The main constituents of connective tissue matrix the gingival papilla. are protein polysaccharide matrix. These complexes are 3. Transgingival fibers: These are seen in and around the normally differentiated into proteoglycans and glyco- teeth with in the attached gingiva. They maintain the proteins. The proteoglycans contains glycosaminoglycans, Tissues Periodontal of Biology alignment of teeth in the arch. e.g. chondroitin sulfate, heparin sulfate, hyaluronic acid, 4. Intercircular fibers: They extend from the cementum etc. The proteoglycans act as a molecular filter and in on distal surface of a tooth splaying buccally and addition, play an important role in the regulation of cell lingually around the next tooth and are inserted on the migration in the tissue. Due to their structure and hydration, mesial surface. the macromolecules exert resistance and hydration, towards 5. Intergingival fibers: They are seen within the attached deformation. Hence, when gingiva is suppressed, the gingiva adjacent to the basement membrane extending macromolecule become deformed, when the pressure is mesiodistally. They provide support and contour for the eliminated the macromolecules regain their original form. attached gingiva. Thus, the macromolecules are of importance for the 6. Semicircular fibers: They extend from the mesial surface resilience of the gingiva. of a tooth to the distal surface of same tooth in a half circle. 7. Oxytalan fibers: They are present in all connective tissue Blood Supply, Lymphatics and Nerves structures of the periodontium. The function of these fibers is yet unknown. Three major sources of blood supply to the gingiva 8. Elastin fibers: Elastin fibers are only present in (Fig. 2.13) has been described: connective tissue of the gingiva and periodontal 1. Supraperiosteal arterioles: Overlying the alveolar bone ligament. They are also seen in the connective tissue of along the facial and lingual surfaces, sends branches to alveolar mucosa in large numbers. the surrounding tissue.

Fig. 2.12: Secondary group of fibers Figs 2.13 A and B: Blood supply to gingiva. Arterioles penetrating the interdental bone (A), supraperiosteal arterioles (B) 16

2. Vessels of the periodontal ligament: They extend into a. Osteoblasts the gingiva and anastamose with the capillaries in the b. Fibroblasts sulcus area. c. Cementoblasts 3. Arterioles emerging from the crest of the interdental 2. Resorptive cells septa. a. Osteoclasts Lymphatic drainage of the gingiva brings in the b. Cementoclasts lymphatics of the connective tissue papillae. It progresses c. Fibroblasts to the periosteum of the alveolar process and then to regional 3. Progenitor cells

PART I lymph nodes (mainly submaxillary group). 4. Other epithelial cells Nerve supply to gingiva is derived from fibers arising Epithelial cell rests of Malassez from nerves in the periodontal ligament and from the labial, 5. Connective tissue cells buccal and palatal nerves. Mast cells and macrophages.

Characteristics of a Synthetic Cell TOOTH-SUPPORTING STRUCTURES 1. Should be actively-synthesizing ribosomes PERIODONTAL LIGAMENT 2. Increase in the complement of rough endoplasmic reticulum and Golgi apparatus Definition 3. Large open faced or vesicular nucleus containing Tooth-supporting structures include, the periodontal prominent nucleoli. ligament, cementum and alveolar bone. The periodontal Osteoblasts: Covers the periodontal surface of the alveolar ligament is a connective tissue structure that surrounds the bone. Alveolar bone contains endosteum and a periosteum. The Normal Periodontium Normal The root and connects it with the bone. In the past, periodontal A periosteum contains at least two distinct layers, cambium ligament has been described by many terms. Among these layer or cellular layer and a fibrous layer. A cellular layer is are desmodont, gomphosis, pericementum, alveolodental present on the periodontal surface of the alveolar bone. ligament and periodontal membrane. Since it is a soft connective tissue providing continuity between two Fibroblasts: It is the most prominent connective tissue cell mineralized connective tissues, the term periodontal (65% of total cell population). Periodontal ligament fibro- ligament appears to be more appropriate. blasts are phenotypically different from gingival fibroblasts. In the coronal direction, the periodontal ligament is They consist of subtypes with distinct phenotypes and found continuous with the lamina propria of the gingiva and to synthesize higher quantities of chondroitin sulfates and communicates with the marrow spaces of the alveolar bone lesser quantities of heparan sulfate and hyaluronan sulfate. through Volkmann’s canals. The main function of the fibroblasts is the production of various types of fibers and it is also instrumental in the Structure synthesis of the connective tissue matrix. The fibroblast is a stellate or spindle-shaped cell which produce The periodontal ligament space has the shape of an hourglass • Collagen fibers and is narrowest at the mid-root level. The width of • Reticulin fibers periodontal ligament is approximately 0.25 mm ± 50 • Oxytalan fibers percent. • Elastin fibers Various stages in the production of collagen fibers are Cellular Composition as follows: Cells of periodontal ligament are categorized as: The first molecule released by fibroblasts is tropo- 1. Synthetic cells collagen which contains three polypeptide chains interwined 17 to form a helix. Tropocollagen molecules are aggregated role of these cells is not known. When certain pathologic longitudinally to form protofibrils, which are subsequently conditions are present, cells of the epithelial rests can laterally-arranged in parallel to form collagen fibrils. undergo rapid proliferation and can produce a variety of Collagen fibers are bundles of collagen fibrils. cysts and tumors of the jaws.

Cementoblasts are seen lining the cementum. 2 CHAPTER Mast cells: These are relatively small, round or oval cell Resorptive Cells having a diameter of almost 12 to 15 μm. The cells contain numerous cytoplasmic granules with small or round nucleus. Osteoclasts: These are the cells that resorb the bone and The granules have been shown to contain heparin and tend to be large and multinucleated. The precursor cells of histamine. The physiologic role of heparin in mast cells does the osteoclasts are circulating monocytes. The characteristic not appear to be clear. Whereas mast cell histamine plays a features of osteoclasts are the plasma membrane of the cell role in the inflammatory reaction and they have been shown lying adjacent to the bone that has been actively undergoing Tissues Periodontal of Biology to degranulate in response to antigen-antibody formation resorption is raised in characteristic folds and is termed as on their surface. ruffled or striated border. Macrophages may also be present in the ligament. They Fibroblasts: It must be made clear that the fibroblasts may are capable of phagocytosis. be capable of both synthesis and resorption. The fibroblasts responsible for resorption contain fragments of collagen that Extracellular Components appear to be undergoing digestion. The presence of these cells indicates resorption of fibers occurring during either 1. Fibers: disease or physiological turnover or remodeling of • Collagen periodontal ligament. • Oxytalan 2. Ground substance: Cementoclasts: The main observation in this is that • Proteoglycans cementum is not remodeled in the fashion of alveolar bone • Glycoproteins and periodontal ligament, but that it undergoes continual deposition during life. However, resorption of cementum Periodontal fibers: The most important elements of the occurs in certain circumstances and in these instance periodontal ligament are the principal fibers. These fibers cementoclasts are located in Howship’s lacunae. are collagenous in nature and are arranged in bundles, they follow a wavy course. The terminal portion of these principal Progenitor cells: Little is known about these cells. It is fibers that insert into the cementum and bone are termed believed that, generally, as and when the need arises, the Sharpey’s fibers. Collagen is a specific, high molecular daughter cell after the division differentiates into the weight protein to which a small number of amino acids are functional type of connective tissue cells. attached, the most important of which are glycine, proline Epithelial cell rests of Malassez: They are found close to and hydoxyproline. Collagen is synthesized by fibroblasts, cementum. These cells are first described by Malassez in chondroblasts, osteoblasts, odontoblasts and other cells. 1884 and are remnants of the epithelium of Hertwig’s Several types of collagen have been demonstrated. The epithelial root sheath. The epithelial cell rests persists as a principal fibers are composed primarily of Type I collagen, network, strands, island or tubule like structures near and whereas reticular fibers are made up of Type III collagen. parallel to the surface of the root. Type IV collagen is seen in the basal lamina. Electron microscope observation shows that the The principal fibers of periodontal ligament (Fig. 2.14) epithelial cell rests exhibits tonofilaments and they are are arranged in six groups that develop sequentially in the attached to one another by desmosomes. The physiologic developing root. They are: 18

other well-formed fiber bundles, that inter-digitate at right angles or splay around and between the regular fiber bundles. These fibers are associated with blood vessels and nerves of the periodontal ligament. Although periodontal ligament does not contain mature elastin, two immature forms have been described, the so-called oxytalan fibers and elaunin. It was suggested that, they provide elastic properties to periodontal ligament. There are also reticulate

PART I fibers, which are fine, immature collagen fibers with a lattice like arrangement. In addition to the above fiber types, small collagen fibers arranged in all directions, forming a plexus have also been reported. They are closely-associated with principal fibers Fig. 2.14: Principal fiber groups in periodontal ligament and are termed as the indifferent fiber plexus.

• Trans-septal group Ground substance: The space between cells, fibers, blood • Alveolar crest, horizontal, oblique, apical and inter- vessels and nerves in the periodontal space is occupied by radicular fibers. ground substance. The ground substance is made up of two major groups of substances. Glycosaminoglycans such as Trans-septal group: They may be considered to belong to hyaluronic acid, proteoglycans and glycoproteins such as the gingiva because they do not have osseous attachment. fibronectin and laminin. It also has high water content (70%).

Alveolocrestal group: They extend obliquely from the The Normal Periodontium Normal The cementum just beneath the junctional epithelium to the Development of Principal Fibers of alveolar crest. Their function is to retain tooth in socket, Periodontal Ligament (Fig. 2.15) resist lateral tooth movement and protect deeper periodontal The principal fibers develop in conjunction with the eruption ligament structure. of the tooth. The fibroblasts surrounding the developing Horizontal group: Extend from cementum to the alveolar root produce collagen fibers. These fibers are seen in the bone at right angles to the long axis of the tooth. periodontal space without a specific orientation. As and Oblique group: They are the largest group in the periodontal when the tooth erupts, the orientation of the fibers alters. ligament; extend coronally in an oblique direction from the 1. First small, fine brush-like fibrils are seen arising from cementum to the bone. They resist axially directed forces. the root cementum and projecting into the periodontal ligament space. Apical group: They originate from cementum of root apex, 2. Similar fibers are seen on the surface of the bone but splaying apically and laterally into the bone of the alveolar only in thin, small numbers. fundus. Their main function is it prevents tooth tipping; 3. Later on, the number and thickness of fibers originating resists luxation, protects blood, lymph and nerve supply to from the bone increase and elongate. They radiate the tooth. towards the loose connective tissue in the midportion Inter-radicular fibers: Extends from cementum of of the periodontal ligament. bifurcation areas, splaying from apical into furcal bone. 4. The fibers originating from the cementum also increase It resists luxation and also tipping and torquing. in length and thickness and fuses with the fibers Secondary fibers of periodontal ligament: In addition to originating from the alveolar bone in the periodontal the principal fiber groups, periodontal ligament contains ligament space. 19 HPE 2 CHAPTER

Fig. 2.16: Periodontal blood supply Tissues Periodontal of Biology

Blood vessels: Periodontal ligament is supplied by branches derived from three sources dental, inter-radicular and interdental arteries (Fig. 2.16). 1. Dental artery before it enters apical foramen gives off branches to the periodontal ligament which also supplies the pulp. 2. The inter-radicular artery gives off branches in the alveolar process that supplies the periodontal ligament Fig. 2.15: Development of periodontal ligament fibers through the cribriform plate. (principal) 3. Interdental artery emerges from the crest of the alveolar 5. They mature progressively towards the root apex as the bone and supplies the coronal part of the periodontal eruption progresses. When the tooth, following eruption, ligament. reaches contact in occlusion and starts to function, the Lymphatic vessels are seen to follow the path of blood principal fibers become organized in bundles and run vessels in the periodontal ligament. continuously from bone to cementum. Nerve supply: In an unerupted tooth, the developing For long, it was believed that this middle portion where periodontal ligament is supplied by fine, unmyelinated nerve the splicing of fibers from cementum and bone takes place, it fibers. Whether this persists after the tooth is erupted is not forms the intermediate plexus. These plexus were thought to known. Periodontal ligament is mainly supplied by the play a significant role in orientation and adjustment of fibers dental branches of the alveolar nerve through the apical during eruption and functional movement of teeth. But recent perforations of the tooth socket or from the cribriform plate. investigations have revealed that, in humans these plexus Many studies have proved that periodontal ligament is richly disappears once the fusion of cemental and osseous fibers supplied by mechanoreceptors whose cell bodies are located are completed. in the trigeminal ganglion. These receptors provide sense of touch, pressure, pain, and proprioception during Structures Present in the Connective Tissue mastication. 1. Blood vessels Cementicles are calcified masses adherent to or detached 2. Lymphatics from the root surface. They may be developed from calcified 3. Nerve innervation epithelial rests, calcified Sharpey’s fibers, and calcified 4. Cementicles thrombosed vessels within the periodontal ligament. 20

Functions of Periodontal Ligament transmitted to the tooth, the extracellular fluid is pushed The following functions of periodontal ligament have been from the periodontal ligament into the marrow spaces explained: through the cribriform plate. After the depletion of the tissue 1. Physical fluids, the bundle fibers absorb the shock and tighten. This → → 2. Formative and remodeling leads to blood vessel stenosis arterial back pressure → 3. Nutritional and sensory function. ballooning of the vessels Tissue replenishes with fluids.

Physical Function Formative and Remodeling Function

PART I The physical functions of the periodontal ligament are: Cells of the periodontal ligament have the capacity to control a. Provides soft tissue “casing” in order to protect the the synthesis and resorption of the cementum, ligament and vessels and nerves from injury due to mechanical forces. alveolar bone. Periodontal ligament undergoes constant b. Transmit the occlusal forces to the bone. Depending on remodeling; old cells and fibers are broken down and the type of force applied, axial force when applied causes replaced by new ones. stretching of oblique fibers of periodontal ligament. Transmission of this tensional force to the alveolar bone Nutritional and Sensory Function encourages bone formation rather than bone resorption. Since periodontal ligament has a rich vascular supply it But when horizontal or tipping force is applied the tooth provides nutrition to the cementum, bone and gingiva. rotates around the axis, at first the tooth movement is Periodontal ligament is supplied by nerve fibers that can within the confines of the periodontal ligament. When transmit sensation of touch, pressure and pain to higher a greater force is applied, displacement of facial and centers. The nerve bundle follows the course of blood vessel lingual plates may occur. The axis of rotation, in single-

The Normal Periodontium Normal The and enters the periodontal ligament from periapical area rooted teeth is located in the area between the apical through channels from the alveolar bone. These bundles and middle third of the root. In multirooted teeth, the divide into single myelinated fibers, which later on lose axis of rotation is located at the furcation area. their myelin sheath and end in one of the four types of neural c. Attaches the teeth to the bone termination. d. Maintains the gingival tissues in their proper relationship • Free endings, carry pain sensations to the teeth. • Ruffini-like mechanoreceptors located in the apical area e. Shock absorption resists the impact of occlusal forces. • Meissners corpuscles are also mechanoreceptors located Two theories have been explained for the mechanism primarily in the mid-root region. of tooth support. • Spindle-like pressure and vibration endings, located a. Tensional theory mainly in the apex. b. Viscoelastic theory Pain sensation is transmitted by small diameter nerves, Tensional theory: According to it the principal fibers of temperature by intermediate type; pressure by large periodontal ligament plays a major role in supporting the myelinated fibers. tooth and transmitting forces to the bone. When forces are applied to the tooth, principal fibers unfold and straighten Clinical Considerations and then transmit the forces to the alveolar bone, causing The primary role of periodontal ligament is to support the elastic deformation of the socket. tooth in the bony socket. Its thickness varies in individuals Viscoelastic theory is based on the fact that, the fluid and in different teeth in the same person. Periodontal movement largely controls the displacement of the tooth, ligament is shaped like an hourglass and is narrowest in the with fibers playing a secondary role. When the forces are middle region of the root and thus seems to be the fulcrum 21 of physiological movement. In connection with the physiological mesial migration of the teeth, the periodontal ligament is thinner on the mesial root surface than on the distal surface.

Due to acute trauma to the periodontal ligament or in 2 CHAPTER accidental blows, many pathological changes will be produced, such as fracture or resorption of cementum and alveolar bone. Hence there will be loss of alveolar bone and widening of periodontal ligament, which results in the tooth becoming loose. When the trauma is removed repair usually will take place. Fig. 2.17: Alveolar bone structure Tissues Periodontal of Biology Orthodontic Tooth Movement The cortical plates consist of compact bone, in Depends on the resorption and formation of both bone and which the lamellae are often arranged circumferentially periodontal ligament. These activities can be stimulated by around blood vessels forming Haversian systems, which are properly regulated pressure and tension. If the movement the internal mechanisms that bring a vascular supply to of the tooth is within physiological limits, the compression bones that are too thick to be supplied only by surface of the periodontal ligament on pressure side results in bone vessels. The cortical plates and the bone lining the socket resorption, where as on the tension side bone apposition is meet at the alveolar crest, usually 2 mm below the seen. Application of the large forces results in the necrosis cementoenamel junction. of periodontal ligament and alveolar bone. The bone lining the socket is also compact bone and If gingivitis is not controlled or treated, it will invariably can be known as any of the following: extend to the periodontal ligament and bone and produces 1. , since bundles of Sharpey’s fibers from the the destruction of the same. Once they are destroyed, it is periodontal ligament are embedded in it. difficult for them to regenerate and therefore the diseases 2. The cribriform plate, because it is perforated by of periodontal ligament are often irreversible. numerous vascular channels. 3. Alveolar bone proper, as it provides direct bony support ALVEOLAR BONE for the teeth. 4. Lamina dura, which is radiographically seen as a dense Definition plate. It is that portion of the maxilla and mandible that forms and Cancellous bone: It consists of narrow irregular bony supports the tooth socket (alveoli). It is formed when the trabeculae, which, by branching and uniting forms a network tooth erupts, in order to provide osseous attachment to the of spaces between the trabeculae. There is a considerable forming periodontal ligament and gradually disappears after variation in the proportions of compact to cancellous bone the tooth is lost. in different regions of the jaws and in different tooth surfaces. For example: In relation to lower anterior teeth, Parts of Alveolar Bone (Fig. 2.17) i.e. lower incisors, there is a thin bone that consists of an Alveolar bone consists of the following: outer cortical plate and the bone lining the socket with no 1. Inner and outer cortical plate. intervening cancellous bone. In contrast, the buccal and 2. The bone lining the socket. interdental bone of molars is relatively thick and cancellous 3. An interior portion of cancellous bone. bone may predominate. 22

As the diameter of the tooth root gradually decreases in b. Osteoclasts: They are large multinucleated giant cells. an apical direction, there is a corresponding increase in the They originate from hematopoietic tissue and are formed thickness of alveolar bone with increase in cancellous bone by the fusion of mononuclear cells of asynchronous being present. These variations are important to note because populations. Generally they are found in bay like they influence the pattern and progression of bone loss in depressions in the bone called Howship’s lacunae. The destructive forms of periodontal diseases. part of the cell in contact with bone shows a convoluted Roentgenogram permits the classification of trabecular surface and a ruffled border from which hydrolytic patterns of the alveolar process into two main types: enzymes are believed to be secreted. The ruffled border

PART I • In type I, the interdental and inter-radicular trabeculae is surrounded by a clear zone, which contains cytoplasm are regular, horizontal and are arranged in a ladder-like exclusively and is believed to be associated with binding pattern. (Common in mandible) of cells to the bone surface and isolation of areas of • In type II, irregularly arranged numerous interdental and resorptive activity. inter-radicular trabeculae are seen most commonly in c. Osteocytes: Alveolar bone is formed during foetal maxilla. growth by intramembranous ossification and consists of a calcified matrix with osteocytes enclosed within a Composition of Alveolar Bone space called lacunae. The osteocytes extend processes It has two basic constituents: into canaliculi that radiate from the lacunae. The main a. The cells consist of osteoblasts, osteoclasts, and osteocytes. function of these canaliculi is to bring oxygen and b. Extracellular matrix consists of 65 percent inorganic and nutrients to the osteocytes through the blood and remove 35 percent organic matter. metabolic waste products. The inorganic component is composed of minerals such The main cells responsible for bone resorption are

The Normal Periodontium Normal The as calcium, phosphate along with hydroxyl, carbonate, osteoclasts, on rare occasions bone resorption by osteocytes citrate and trace amounts of other ions, such as sodium, has been reported which is called as osteocytic osteolysis. magnesium and fluorine. The minerals are in the form of hydroxyapatite crystals. Osseous Topography The organic matrix consists of 90 percent of type I The anatomy of the alveolar bone varies from patient to collagen, with small amounts of non-collagenous proteins patient. Normally it conforms to the root prominence, with such as osteocalcin, osteonectin, bone morphogenetic intervening depressions that taper towards the margin. The proteins, proteoglycans, and glycoproteins. factors that affect the height and thickness of the facial and Cellular Components lingual bony plates are alignment of the teeth, angulation of the root to the bone and the occlusal forces. a. Osteoblasts: They are cuboidal cells with well-developed When the teeth are in a labial version, the margin of the rough endoplasmic reticulum, a large Golgi apparatus, bone is located more apically and is thinned to a knife-edge and secretory vesicles. It synthesizes bone matrix as compared to the teeth in proper alignment. When teeth (osteoid), type I collagen and regulate its mineralization. are in a lingual version, the facial bony plate is thicker than Each osteoblast carries out a cycle of matrix synthesis normal and the margin is blunt, rounded and horizontal after which it is either buried as an osteocyte or remains rather than arcuate. on the surface as a resting or inactive osteoblast. Osteoblasts are derived from the progenitor cells at sites Fenestrations and Dehiscences (Fig. 2.18) of bone formation. These progenitor cells belong to the mesenchymal cell family. In contrast, osteoclasts Fenestrations are isolated areas in which the root surface is originate from blood–borne monocytes. covered only by the periosteum and gingiva, but in these 23

tissue is constantly changing in its internal organization, it retains approximately the same form from childhood through adult life. Haversian systems (osteons) are the internal mechanisms that bring vascular supply to bones too thick

to be supplied only by surface vessels. Bone deposition by 2 CHAPTER osteoblasts is balanced by resorption brought about by osteoclasts during tissue remodeling and repair. Osteoblasts, lay down nonmineralized bone matrix called osteoid, while new osteoid is being deposited, the Fig. 2.18: Fenestration and dehiscence older osteoid becomes mineralized. Bone resorption is a complex process and appears as eroded bone surfaces, situations, the marginal bone remains intact. When the Tissues Periodontal of Biology namely Howship’s lacunae. It has been suggested that bone marginal bone is also denuded, the defect is called resorption at any site is a chemotactic phenomenon. This dehiscence. is, initiated by the release of some chemotactic factors like These defects are seen more often on the facial bone interleukin-1 and 6, which attract the monocytes to the target than on the lingual, and are more common in anterior teeth site. Osteoblasts release Leukemia inhibiting factor (LIF), than on the posterior. The etiologies of these defects are not which coalesce monocytes to form multinucleated clear; some of the predisposing factors are root prominence, osteoclasts, which then resorb bone. malposition, and teeth in labial version with thin bony plates. During bone resorption three processes occur: The diagnosis of these defects is important as it may affect a. Decalcification the outcome of the surgical treatment. b. Degradation of matrix c. Transport of soluble factors to the extra cellular fluid. Periosteum and Endosteum Since calcified matrix is resistant to proteases of all The tissue covering the outer surface of bone is termed as kinds, bone must first be decalcified. This is achieved at periosteum, where as the tissue lining the internal bone the ruffled border of the osteoclasts by secretion of some cavities is called endosteum. The periosteum consists of acids such as citric acid and lactic acid, which chelate bone, two layers, the inner layer, next to the bone surface, consists the low pH leads to increase in solubility of hydroxyapatite. of bone cells that have the potential to differentiate into The next step is degradation of matrix, takes place by osteoblasts and an outer layer which is more fibrous collagenase enzymes and other proteases like cathepsin-B. containing blood vessels and nerves. Collagenolysis occurs outside the osteoclast. Finally, the The endosteum is composed of a single layer of break down products of bone are transported to the osteoprogenitor cells and a small amount of connective tissue. extracellular fluids and to the blood vascular system. Tencate described the following sequence of events Remodeling and Resorption during bone resorption: During both embryonic bone development and the entire a. Attachment of osteoclasts to the mineralized bone pre-adult period of human growth, bone is being formed surface. very rapidly, primarily on the periosteal surface. Simul- b. Creation of a sealed acidic environment, which taneously, bone is being destroyed along the endosteal demineralizes the bone and exposes the organic matrix. surface and at focal points along the periosteal surface (bone c. Degradation of exposed organic matrix by the action of modeling). enzymes such as acid phosphatase and cathepsine. Bone growth occurs by apposition of an organic matrix d. Sequestering of mineral ions and amino acids within that is deposited by osteoblasts. Although the alveolar bone the osteoclasts. 24

Blood Supply to the Bone The vessels enter the interdental septa through nutrient canals together with veins, nerves, and lymphatics. The alveolar arteries sends off branches through periodontal ligament and enter the marrow spaces through the perforations in the cribriform plate.

Clinical Considerations PART I Bone although one of the hardest tissue of human body, is biologically a highly plastic tissue. Bone is resorbed on the side of pressure and apposed on the side of tension. It has been shown that on the pressure side there is an increase in the level of cyclic adenosine monophosphate (cAMP) in cells, which may play a role in bone resorption. The most frequent and harmful change in the alveolar process is that which is associated with periodontal diseases. The bone resorption caused by periodontal diseases is usually symmetrical, occurs in episodic manner, and is both of the horizontal and vertical type. Once lost, this bone is very difficult to regenerate. Regeneration of just a few

The Normal Periodontium Normal The millimeters of bone that has been lost is the greatest Fig. 2.19: Acellular/cellular cementum challenge to the periodontists across the world. Table 2.1: Differences between acellular and CEMENTUM cellular cementum Acellular cementum Cellular cementum Definition a. Forms during root Forms after the eruption Cementum is a calcified avascular mesenchymal tissue that formation of the tooth and in response to functional demands forms the outer covering of the anatomic root. It provides b. Does not contain any cells Contains cementocytes anchorage mainly to the principal fibers of periodontal c. Seen at the coronal Seen at a more apical portion of root portion of root ligament. Two sources of collagen fibers can be found in d. Formation is slow Deposition is more rapid the cementum: e. Arrangement of collagen Collagen fibers are 1. Sharpey’s (extrinsic) fibers which are formed by the fibers are more organized irregularly arranged fibroblasts. Classification 2. Fibers belonging to the cementum matrix per se (intrinsic) produced by cementoblasts. Depending on location, morphology and histological Two types of cementum were described earlier: appearance, Shroeder and Page have classified cementum a. Acellular cementum/primary cementum (Fig. 2.19). as: b. Cellular cementum/secondary cementum. a. Acellular afibrillar cementum (AAC): It contains only The differences between the acellular and cellular the mineralized ground substance. It does not contain cementum are given in Table 2.1. collagen fibers nor does it exhibit entrapped cemento- 25

cytes. It is a product of cementoblasts and is found almost Composition exclusively on the enamel near the cementoenamel The cementum is composed of both inorganic (46%) and junction with a thickness of 1 to 15 μm. organic matter. The organic matrix is chiefly composed of b. Acellular extrinsic fiber cementum (AEFC): By 90 percent Type I collagen, 5 percent Type III collagen and HPE 2 CHAPTER definition it is composed primarily of Sharpey’s fibers noncollagenous proteins like enamel proteins, adhesion of periodontal ligament but does not contain molecules like tenascin and fibronectin, glycosaminoglycans cementocytes. Developmentally they come to occupy like chondroitin sulfate, dermatan sulfate and heparan sulfate the coronal one half of the root surface. Its thickness is which constitute the remaining organic matrix. between 30 and 230 μm. c. Cellular mixed stratified cementum (CMSC): It harbors Thickness of Cementum both intrinsic (cementoblasts derived) and extrinsic

Formation of cementum is a continuous process, Tissues Periodontal of Biology (fibroblast derived) fibers and may contain cells. In the formative rate of which varies throughout life. humans it is seen in the apical third of the roots, apices It is most rapid at the apical regions. At the coronal half the and furcation areas. Its thickness varies from 100 to 1000 thickness varies from 16 to 60 μm (almost the thickness of μm. hair) and at the apical third it varies from 150 to 200 μm. It d. Cellular intrinsic fiber cementum (CIFC): It contains is thicker in the distal surfaces as compared to the mesial only intrinsic fibers secreted by cementoblasts and not surfaces and this can be explained by functional stimulation by the periodontal ligament fibroblasts. In humans it following mesial migration. fills the resorption lacunae. Hypercementosis or cemental hyperplasia is a prominent e. Intermediate cementum (or) the hyaline layer of Hope thickening of the cementum. It can be localized or Well Smith: It is an ill-defined zone extending from pre- generalized. It may appear as a generalized thickening of cementoenamel junction to the apical 1/3rd of the root. the cementum, with nodular enlargement at the apex or as It appears to contain cellular remnants of Hertwig’s spike like projections (cemental spikes). The etiology of Sheath embedded in calcified ground substance. The hypercementosis is not very well understood. The spike like significance of this layer is that, it contains enamel like projections could be as a result of excessive tension from proteins, which helps in attachment of cementum to orthodontic appliance or occlusal forces. The generalized dentin. It has been observed by many that, when this type may be associated with a variety of situations, like layer is removed during root planing procedure, the teeth without antagonists, in teeth with chronic pulpal and resultant reparative cementum that is formed will not periapical infections. Hypercementosis of the entire be attached firmly on the dentin. dentition may be seen in patients with Paget’s disease.

Functions Cementoenamel Junction (Fig. 2.20) a. Primary function of cementum is to provide anchorage At the cementoenamel junction three types of relationships to the tooth in its alveolus. This is achieved through the may exist. In about 60 to 65 percent of cases, the cementum collagen fiber bundles of the periodontal ligament, overlaps the enamel, in about 30 percent of cases, end-to- whose ends are embedded in cementum. end relationship of enamel and cementum is seen and in b. Cementum also plays an important role in maintaining 5 to 10 percent, the cementum and enamel fail to meet. occlusal relationships, whenever the incisal and occlusal surfaces are abraded due to attrition, the tooth supra Cemental Resorption and Repair erupts in order to compensate for the loss and deposition Cemental resorption may be caused by local, systemic or of new cementum occurs at the apical root area. idiopathic factors. Local conditions that contribute to 26

3. Microscopically, the gingival epithelium is divided into keratinized, i.e. oral epithelium and non-keratinized, i.e. junctional and sulcular epithelium. 4. The keratinized epithelium of the gingiva consists of four layers, namely stratum basale, stratum spinosum, stratum granulosum and stratum corneum. 5. The granular layer, which is seen in the oral epithelium is absent in sulcular and junctional epithelium. 6. Junctional epithelium is attached to the tooth surface by hemidesmosomes and basal lamina. 7. Lamina propria/gingival connective tissue consists of

PART I cells, fibers, and blood vessels, embedded in the extracellular matrix. Tooth-supporting Structures Fig. 2.20: Configuration of cementoenamel junction Periodontal Ligament 1. Periodontal ligament is a connective tissue structure that cemental resorption are trauma from occlusion, orthodontic surrounds the root and connects it with the bone. 2. It consists of cells and extra-cellular substances. tooth movement, pressure from erupting teeth, cysts and 3. Cellular components are categorized as synthetic cells, tumors, teeth without functional antagonist, periapical resorptive cells, progenitor cells, epithelial cells and disease and periodontal disease. Systemic conditions that connective tissue cells. 4. Extracellular matrix is composed of fibers like collagen, may predispose to cemental resorption are calcium oxytalan and ground substance with proteoglycans and deficiency, hypothyroidism and Paget’s disease. glycoproteins. The resorptive process may not necessarily be a 5. The principal fibers of periodontal ligament are arranged in six groups, i.e. trans-septal group, alveolar crest group, continuous process; it may alternate with periods of repair horizontal, oblique, apical and inter-radicular group. The Normal Periodontium Normal The and deposition, which can be demarcated by formation of 6. In the connective tissue other structures like blood reversal line. Remodelling of cementum requires the vessels, nerves, and lymphatics are also present. 7. Functions of periodontal ligament are explained under presence of viable connective tissue and can occur even in physical function, formative and remodelling function, non-vital teeth. nutritive and sensory function. Cementum is not exposed to the oral environment 8. Finally any trauma to the periodontal ligament can result in the loss of alveolar bone and widening of ligament but because it is covered by alveolar bone and gingiva. In cases once the trauma is removed, repair usually takes place. of and as a consequence of loss of 9. When the inflammation extends from the gingiva to the attachment in pocket formation, cementum can become periodontal ligament, destruction of periodontal structures will result, which is difficult to regenerate, hence the exposed to the oral environment. Once exposed, organic disease of periodontal ligament are often irreversible. substances, inorganic ions and bacteria penetrate the Alveolar Bone sufficiently permeable cementum. Caries of the cementum 1. Alveolar bone is that portion of the maxilla and mandible may also develop. that forms and supports the tooth sockets. 2. It consists of inner and outer cortical plate, the bone lining the socket and an interior portion of cancellous bone. 3. It has two basic constituents (a) cells like osteoblasts, osteoclasts, and osteocytes, (b) extracellular matrix made The Gingiva up of 65 percent inorganic and 35 percent organic. 1. The gingiva is that part of the oral mucosa that covers Inorganic is composed of calcium, phosphate along with the alveolar process of the jaws and surrounds the necks some trace elements. Organic matrix consists of of the teeth. 90 percent Type I collagen with small amounts of non- 2. Anatomically it is divided into marginal, attached and collagenous proteins such as osteonectin, osteocalcin, interdental gingiva. bone morphogenetic proteins, etc. 27

4. Fenestrations are isolated areas in which the root surface (Melanocytes, Langerhans cells, Merkel’s cells and is covered only by periosteum and gingiva, but the inflammatory cells). In histologic sections the zone marginal bone remains intact. When marginal bone is around their nucleus appears lighter than that in the also involved, the defect is called dehiscence. surrounding keratin-producing cell. Hence they are 5. Bone resorption occurs by three processes—(a) named clear cells. decalcification, (b) degradation of matrix and (c) transport • Melanocytes are pigment synthesizing cells and are 2 CHAPTER of soluble factors to the extracellular fluid. responsible for the production of melanin. The Cementum Langerhans cells are believed to play a role in the defence mechanisms of the oral mucosa whereas 1. Cementum is a calcified avascular mesenchymal tissue Merkel’s cells have been suggested to have a sensory that forms the outer covering of the anatomic root. function. 2. Acellular cementum forms during root formation and is seen at the coronal portion of the root, whereas cellular Periodontal Ligament cementum forms after eruption of the tooth and is seen Progenitor cells are also seen in the cellular components apically on the root. Tissues Periodontal of Biology 3. The cementum consists of 46 percent inorganic matter of periodontal ligament. They are basically undifferen- and the rest 90 percent organic being, Type I collagen tiated mesenchymal cells which have the capacity to and the remaining consists of non-collagenous proteins. differentiate into either formative cells or resorptive cells 4. Three types of relationships of cementum may exist at depending on the external signaling. Hence, presence of the cementoenamel junction. In 60 to 65 percent of cases, these cells in the periodontal ligament gives it the potential cementum overlaps the enamel, in 30 percent, edge-to- for regenerative phase of healing following periodontal edge butt joint exists and in 5 to 10 percent, the cementum disease. and enamel do not meet. Cementum Development and acquired anomalies of cementum KNOW MORE ... Enamel projections: Most commonly seen in the mandibular furcation areas, when amelogenesis does not cease before the formation of root, there enamel Gingiva projections may form over a portion of root. • Normally, the gingiva extends from marginal gingiva to the mucogingival junction but on the palatal surface Enamel pearls: They are globule like structures of enamel it merges with the palatal mucosa. Hence there is no seen in the cervical portion of the root surface. When mucogingival line present on the palate. Hertwig’s root sheath fails to detach from the dentin • It was observed that, clinically a free gingival groove surface, cementogenesis may proceed. This will result in is present only in about 30-40 percent of adults and is large pearls. positioned at a level corresponding to the level of Cementicles: They are globular masses of cementum, cementoenamel junction (CEJ). may be found lying either in periodontal ligament or • The free gingival groove is most pronounced in the attached to a root surface. They may have originated from mandibular incisor and premolar regions on the buccal calcified epithelial cell rests of Malassez or calcified surfaces and least seen in the mandibular molar and Sharpey’s fibers. maxillary premolar regions. Ankylosis: Fusion of the cementum and alveolar bone • Width of attached gingiva increases with age. Since with obliteration of the periodontal ligament is termed as the mucogingival junction remains stable throughout ankylosis. It occurs in teeth with cemental resorption which life, the increasing width of the gingiva may be due to may represent a form of abnormal repair. the occlusal wear and supraeruption of the teeth. • Functions of width of attached gingiva are: (a) It holds Alveolar Bone/Process the marginal gingiva in position, (b) allows for proper deflection of food, (c) provides mechanical and Bone marrow: In embryos and newborn, the bone cavities functional stability. are filled with red hematopoietic marrow, which gradually • Microscopically in the keratinized epithelium, undergoes physiologic changes and gets replaced by keratinocytes comprise about 90% of the total cell yellow inactive type of marrow. In the oral cavity mostly population. The oral epithelium contains the non- we see yellow type of marrow with occasional foci of red keratinocytes which are also called “clear cells” bone marrow. 28

REVIEW QUESTIONS 2. Jan Lindhe. Clinical Periodontology and Implant Dentistry. 4th edition. Blackwell Munksgaard Publication 2003. The Gingiva 3. Jansen Van Rensburg. Oral biology. Quintessence Publishing Co. Inc. 1995. 1. Describe the microscopic and macroscopic features of 4. Newman, Takei, Fermin A Carranza. Clinical periodontology, gingiva. 9th edition, WB Saunders Co. 2002. 2. Discuss the development, structure and mode of 5. Thomas M Hassell. Tissues and cells of the periodontium. attachment of junctional epithelium. Periodontol 2000;3:1993. 3. Describe the blood supply to the gingiva. Tooth-supporting Structures PART I 4. Describe various gingival fiber groups with illustrations. Periodontal Ligament Tooth-supporting Structures 6. Jan Lindhe. Clinical Periodontology and Implant Dentistry, IV Periodontal Ligament edition, Blackwell Munksgaard publication, 2003. 7. Newman, Takei, Fermin A Carranza. Clinical periodontology, 1. Describe the development, structure and composition IX edition, WB Saunders Co, 2002. of periodontal ligament. 8. Thomas M Hassell. Tissues and cells of the periodontium, Periodontol 2000; 3:1993. 2. Enumerate various principle fibers of periodontal ligament with the help of illustrations. Alveolar Bone 3. Discuss in detail the functions of periodontal ligament. 9. Tencate AR. Oral histology, Development, Structure and Alveolar Bone Function, 5th edition, Mosby Publication. 10. Grant, Stern, Listgarten. Periodontics, VI edition, Mosby

The Normal Periodontium Normal The Discuss the alveolar bone with reference to the following: Publication, 1998. 1. Structure, composition and parts of alveolar bone. 11. Manson JD, Meley B. Outline of Periodontics III edition, British 2. Fenestration and dehiscence. Library Cataloguing in Publication Data, 1995. 12. Jan Lindhe. Clinical Periodontology and Implant Dentistry, 4th 3. Resorption and remodeling. edition, Blackwell Munksgaard Publication, 2003. 13. Newman, Takei, Fermin A Carranza. Clinical Periodontology, Cementum 9th edition, WB Saunders Co., 2002. Discuss cementum with reference to the following: 1. Structure and composition of cementum. Cementum 2. Cementoenamel junction. 14. Tencate AR. Oral Histology, Development, Structure and 3. Hypercementosis. Function, IIIrd edition, St. Louis: CV Mosby Company, 1989. 4. Classification. 15. Jansen Van Rensburg BG. Oral Biology, Quintessence Books, Chicago, 1995. 16. Bhaskar SN. Orbans, Oral Histology and Embryology, 11th BIBLIOGRAPHY edition, St. Louis CV Mosby company. 17. Newman, Takei, Fermin A Carranza. Clinical Periodontology, The Gingiva 9th edition, WB Saunders and Co., 2002. 1. Tencate AR. Oral Histology, Development, Structure and 18. Schroeder HF. Oral Structural Biology, Thieme Medical Function. 5th edition, Mosby Publication. Publishers, Inc. New York, 1991. 3 ChapterChapter

Periodontal Structures in Aging Humans

 GENERAL EFFECTS OF AGING • Changes in the Alveolar Bone and Cementum  AGE CHANGES IN THE PERIODONTIUM • Bacterial Plaque and Immune Response • Gingiva and other Areas of the Oral Mucosa  EFFECTS OF AGING ON THE PROGRESSION OF • Periodontal Ligament and Age Changes in the PERIODONTAL DISEASES Periodontium  EFFECTS OF TREATMENT ON THE AGING INDIVIDUALS

GENERAL EFFECTS OF AGING e. With age water content of bone is reduced, the mineral crystals are increased in size and collagen fibers are Skin thickened. a. The dermis and epidermis are thinned b. Keratinization is diminished AGE CHANGES IN THE c. Blood supply is diminished PERIODONTIUM (FIG. 3.1) d. Degeneration of nerve endings occur e. Capillaries appear to become more fragile which may Gingiva and other Areas of the Oral Mucosa result in hemangiomas after minor traumas f. Tissue elasticity is decreased. 1. Decreased keratinization. 2. Reduced or unchanged amount of stippling. Bone 3. Decreased connective tissue cellularity. a. Undergoes osteoporosis with aging 4. Decreased oxygen consumption—which may reflect b. The bone is rarified, trabeculae are reduced in number upon the metabolic activity. and cortical plates are thinned 5. Increased width of attached gingiva. c. Vascularity is reduced and lacunar resorption is more 6. Greater amounts of intercellular substances. prominent 7. Atrophy of the connective tissue with loss of elasticity. d. Increased susceptibility to fracture 8. Increase in the number of mast cells. 30

PART I Fig. 3.1: Aging of the periodontium

Periodontal Ligament and Age Changes in the Periodontium Fig. 3.2: Periodontal changes associated with aging 1. Decrease in vascularity. 2. Decrease in mitotic activity. 3. Decrease in fibroblasts. 2. Some studies have shown a qualitative change in the 4. Collagen fibers and mucopolysaccharides are decreased. subgingival flora, it has been speculated that a shift 5. Increase in elastic fibers and arteriosclerotic changes occurs in certain periodontal pathogens with age, are seen. including increase in number of enteric rods, 6. Both increase and decrease in the width of the and decreased role for periodontal ligament is seen. The periodontal ligament Actinobacillus actinomycetemcomitans. Some age-

width is increased as a result of less number of teeth related changes have been shown to affect the host The Normal Periodontium Normal The supporting the entire functional load and decrease in its response, but there is no evidence to show that these width is associated with reduced strength of the changes correlate with periodontitis in elderly patients. masticatory musculature and continuous deposition of cementum and bone. EFFECTS OF AGING ON THE PROGRESSION OF PERIODONTAL Changes in the Alveolar Bone and Cementum DISEASES

1. Osteoporosis. The conclusions drawn from the various studies are 2. Decreased vascularity. strikingly consistent and show that, age has either no effect 3. Reduction in metabolic rate and healing capacity. or provides a small and clinically insignificant increased 4. Resorption activity is increased and the rate of bone risk of loss of periodontal support. Therefore, age has been formation is decreased. suggested to be not a true risk factor but a background or 5. Continuous deposition of cementum occurs with age and an associated factor for periodontitis. greater irregularity in the surface of both the cementum and alveolar bone facing the periodontal ligament is EFFECTS OF TREATMENT ON THE seen. AGING INDIVIDUALS The few studies that have been done so far have clearly Bacterial Plaque and demonstrated that in spite of certain changes in the Immune Response (Fig. 3.2) periodontium with aging, no differences in response to 1. Plaque accumulation has been suggested to increase with nonsurgical or surgical treatment have been shown for age. periodontitis. 31

REVIEW QUESTIONS

KNOW MORE ... 1. Describe the age changes in the periodontium. 2. Role of aging on the progression of periodontal diseases.

Age Changes in the Perodontium 3 CHAPTER With increasing age, the gingival connective tissue becomes coarser and denser. BIBLIOGRAPHY Tissue culture studies of gingival fibroblasts from older individuals exhibits reduction in the rate of proliferation, 1. JD Manson, B Meley. Outline of Periodontics, Third edition decrease in the quantity and quality of proteoglycans with 1995, British Library Cataloguing in Publication Data. 2. Newman, Takei, Fermin A, Carranza. Clinical Periodontology, reduced protein and collagen production.

9th edn, WB Saunders, 2002. Periodontal Structures in Aging Humans Aging in Structures Periodontal

4 ChapterChapter

Classification Systems of Periodontal Diseases

 NEED FOR CLASSIFICATION  SYNOPSIS OF TYPES AND CHARACTERISTICS  CURRENT CLASSIFICATION SYSTEMS OF OF GINGIVAL DISEASES PERIODONTAL DISEASES  SYNOPSIS OF TYPES AND CHARACTERISTICS • Gingivitis OF PERIODONTAL DISEASES • Periodontitis

NEED FOR CLASSIFICATION • Chronic (adult) gingivitis • Acute necrotizing ulcerative gingivitis. • For the purpose of diagnosis, prognosis and treatment planning. Periodontitis • To understand the etiology and pathology of the diseases of the periodontium. • Adult Periodontitis: • For logical, systematic separation and organization of Possible subgroups: knowledge about disease. – High risk • Facts can be filed for future references. – Normal risk • Helps to communicate among clinicians, researchers, – Refractory periodontitis educators, students, epidemiologists and public health • Early Onset Periodontitis: workers. – Localized juvenile periodontitis – Rapidly progressive periodontitis CURRENT CLASSIFICATION SYSTEMS OF – Prepubertal periodontitis PERIODONTAL DISEASES * Localized * Generalized World Workshop in – Periodontitis associated with systemic diseases. Clinical Periodontics (1988) World Workshop in Clinical Periodontics (1989) Gingivitis I. Adult periodontitis. • Childhood gingivitis II. Early onset periodontitis. 36

• Prepubertal • Early onset periodontitis: – Generalized or localized – Localized early onset periodontitis • Juvenile – Neutrophil abnormality – Generalized or localized – Generalized early onset periodontitis, neutrophil • Rapidly progressive periodontitis abnormality, immunodeficient III. Periodontitis associated with systemic diseases • Early onset periodontitis-related to systemic disease: • Down’s syndrome – Leukocyte adhesion deficiency, hypophosphatasia, • Diabetes – Type I Papillon-Lefevre syndrome, neutropenias, leukemias, • Papillon-Lefévre syndrome

PART II Chediak-Higashi syndrome, AIDS, diabetes mellitus • AIDS and other diseases type-I, trisomy-21, histiocytosis X, Ehlers-Danlos IV. Necrotizing ulcerative periodontitis syndrome (type VIII) V. Refractory periodontitis. • Early onset periodontitis, systemic determinants Genco (1990) unknown • Periodontitis in adults. • Necrotizing ulcerative periodontitis • Periodontitis in juveniles – Systemic determinants unknown – Localized form – Related to HIV – Generalized form – Related to nutrition • Periodontitis with systemic involvement • – Primary neutrophil disorders – Secondary or associated neutrophil impairment. European Workshop in Periodontology (1993) – Other systemic diseases • Adult periodontitis • Miscellaneous conditions. • Early onset periodontitis • Necrotizing periodontitis Ranney (1993) All the above-mentioned classification systems have Gingivitis been widely used by clinicians and research scientists throughout the world, unfortunately they have been many • Gingivitis, plaque/bacterial induced shortcomings including: • Non-aggravated 1. Considerable overlap in disease categories. • Systemically-aggravated by sex hormones, drugs, 2. Absence of a gingival disease component. systemic diseases 3. Inappropriate emphasis on age of onset of disease and • Necrotizing ulcerative gingivitis • Systemic determinants unknown rates of progression. • Related to HIV 4. Inadequate or unclear classification criteria. • Gingivitis, non-plaque induced Hence, the need for a revised classification system for

Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification • Associated with skin diseases, allergy and infections. periodontal diseases was emphasized and in 1999, the international workshop had considered designing a new Periodontitis classification system. • Adult periodontitis Classification of Periodontal – Non-aggravated Disease and Condition – Systematically-aggravated (neutropenias, leuke- mias, lazy leukocyte syndrome, AIDS, diabetes By AAP 1999 (International Workshop for Classification mellitus, Crohn’s disease, Addison’s disease). of Periodontal Disease). CHAPTER 4 Classification Systems of Periodontal Diseases 37 : allergic agent antimicrobial rinse, supportive periodontal therapy excision of pyogenic granuloma alternative medications, supportive periodontal therapy Gingivitis associated with dental plaque only a. local contributing factors. Without b. local contributing factors With Gingival diseases modified by systemic factors: a. Associated with endocrine system: 1. 2. not cause loss of clinicalattachment factors, supportive of interproximal papilla periodontal therapy therapy periodontal brushing periodontal therapy swelling of , according to Varies Identification and elimination , infectious agent or control of infectious : These diseases pallidum

, histoplasmosis chemotherapy Table 4.1: Synopsis of types and characteristics of gingival diseases of gingival types and characteristics 4.1: Synopsis of Table Candida Treponema Neisseria gonorrhoeae plaque—retention factors does swelling, bleeding, correct plaque retentive pemphigoid trauma as on eating and supportive therapy, hormonal influencegranuloma pyogenic possible periodontal therapy, Dental plaque-induced gingival diseases may occur on a periodontium with no attachment loss or on one with attachment loss that is stable and not progressing. fungal origin streptococcal species, agent, appropriate specific bacteria or Gingival disease of Acute necrotizinggingivitis be Bacterial plaque, may Desquamativegingival disease redness, Pain, gingival AIDS at any age associated with swelling, bleeding, necrosis Skin diseases, lichen planus, and cicatricial pemphigus antimicrobial rinse, supportive , plaque control, Gingivitis associated redness, epithelial Gingival systemicwith systemicof Manifestation Gentle plaque control, with pain denudation, diseases Dependent on diseases in gingiva and symptomatic palliative Gingivitis associatedpregnancywith plaque, local Bacterial plaque, retentive factors,disease systemic of systemic disease, Treatment Drug-induced redness and Gingival gingival enlargementcyclosporine phenytoin, drugs, bleeding, swelling, Calcium channel blocking Debridement and plaque plaque control, atraumatic Allergic reaction control, supportive Gingival enlargement Local allergensHerpeticgingivostomatitis Debridement and plaque Herpes type I virus control, surgical excision, use of Gingival redness and and elimination Identification Pain, vesicle formation, and symptomatic Palliative ulceration medication antiviral therapy, Types of gingivalTypes disease CausesGingivitis plaque, local Bacterial Signs and symptoms Gingival redness and Treatment plaque control, Debridement, A. Gingival Disease (Table 4.1) Gingival Disease (Table 38

i. Puberty-associated gingivitis i. Lichen planus ii. Menstrual cycle-associated gingivitis ii. Pemphigoid iii. Pregnancy-associated iii. Pemphigus vulgaris – Gingivitis iv. Erythema multiforme – Pyogenic granuloma v. Lupus erythematosus iv. Diabetes mellitus-associated gingivitis vi. Drug induced b. Associated with blood dyscrasias: vii. Others i. Leukemia-associated gingivitis b. Allergic reactions:

ii. Others i. Dental restorative materials PART II 3. Gingival diseases modified by medications: – Mercury a. Drug-influenced gingival diseases – Nickel i. Drug-influenced gingival enlargements. – Acrylic ii. Drug-influenced gingivitis – Others – Oral contraceptive-associated gingivitis ii. Reactions attributable to: – Others – Toothpaste’s or dentifrices 4. Gingival diseases modified by malnutrition: – Mouthrinses or a. Ascorbic acid deficiency gingivitis – Chewing gum additives b. Others – Foods and additives B. Nonplaque-induced gingival lesions: iii. Others 1. Gingival diseases of specific bacterial origin. 6. Traumatic lesions (factitious, iatrogenic, or accidental) a. Neisseria gonorrhoeae a. Chemical injury b. Treponema pallidum b. Physical injury c. Streptococcal species c. Thermal injury d. Others 7. Foreign body reactions 2. Gingival diseases of viral origin 8. Not otherwise specified (NOS). a. Herpes virus infections • Primary herpetic gingivostomatitis Chronic Periodontitis (Table 4.2) • Recurrent oral herpes a. Localized — Less than 30 percent of sites • Varicella zoster involved or, b. Others b. Generalized — More than 30 percent of sites 3. Gingival diseases of fungal origin involved. a. Candida species infections; generalized gingival c. Slight — 1 to 2 mm . candidiasis d. Moderate — 3 to 4 mm clinical attachment loss

Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification b. Linear gingival erythema and, c. Histoplasmosis e. Severe — More than 5 mm clinical attachment d. Others. loss. 4. Gingival lesions of genetic origin a. Hereditary gingival fibromatosis Aggressive Periodontitis b. Others 5. Gingival manifestations of systemic conditions a. Localized–slight, moderate or severe a. Mucocutaneous lesions: b. Generalized. CHAPTER 4 Classification Systems of Periodontal Diseases 39 Contd... periodontal surgery, supportive periodontal surgery, periodontal therapy periodontal surgery, supportive periodontal therapy supportive dontal surgery, periodontal therapy periodontal origin, endodontic and periodontal therapy or extraction may be necessary generalized or localizedchemotherapy, antimicrobial of bone support of firstmolars and incisors.Generalized juvenile based on microbial analysis, periodontitis: generalized loss of support throughout possible regenerative surgery, dentition supportive periodontal therapy local plaque retentive factorslocal plaque retentive andsuch as dental calculus periodontal generalized with restorationsfaulty cessation, scaling and pockets, bone and clinical root planing, correction of attachment loss, may be host response,possible impaired by periods of remission, may local plaque retentive factors smoking smoking cessation, bacteria, possible impaired hostresponse, smoking therapy and supportive generalized or localized be cessation smoking analysis, debridement, possible therapy periodontal or genetic disorders debridement, possible perio- Actinobacillus actinomycetemcomitans tissue tooth support supportive periodontal therapy Table 4.2: Synopsis of types and characteristics of periodontal diseases of periodontal and characteristics of types Synopsis 4.2: Table Aggressiveperiodontitis Bacterial plaque, superinfection bacteria, with specific periodontal Severe and rapid periodontalfollowedpossibly destruction therapy antimicrobial Specific, analysis, based on microbial periodontitisRefractory Bacterial plaque, superinfection,typeany of disease Progression of antimicrobial, Specific, periodontalspecific, with Periodontitis as a ofmanifestation diseasessystemic despite good conventional Associated with disorders of the Generalized and localized based on microbial therapy blood or blood forming organs such as neutropenia, leukemiadisease, systemic of Treatment forms of severe destruction of bone and connective atraumatic plaque control, antimicrobial rinse, Juvenile periodontitis:localized andautosomalmajor Probably generalized Localized juvenile, gene effect and infection with periodontitis: typically loss Scaling and root planing, specific antimicrobial therapy Types of periodontalof Types disease CausesChronic periodontitis smoking, Bacterial plaque, progressionslow Overall smoking Plaque control, Signs and symptoms Treatment Periodontitiswithassociated endodontic lesions or May be of endodontic periodontal origin Periodontal pocket of extending to area If primarily of endodontic therapy endodontic origin, endodontic lesion alone, if primarily of 40

Contd...

Types of periodontal Causes Signs and symptoms Treatment disease

Periodontal abscess Subgingival bacteria Painful, acute swelling of Nonsurgical or surgical periodontal tissues associated debridement, antibiotic with deep periodontal pocket therapy, regeneration of lost periodontal support is often

a possibility PART II Acute necrotizing Immunocompromised, Pain, rapid loss of bone Debridement, atraumatic periodontitis may be associated and tooth support associated plaque control, analgesic with HIV with gingival and medication, antimicrobial rinse, bony necrosis supportive periodontal therapy

Periodontitis as a Manifestation of b. Periodontal abscess Systemic Diseases c. Pericoronal abscess a. Associated with hematological disorders: Periodontitis Associated with Endodontic Lesions i. Acquired neutropenia ii. Leukemias Combined periodontic—endodontic lesions. iii. Others b. Associated with genetic disorders: Developmental or Acquired Deformities and i. Familial and cyclic neutropenia Conditions ii. Down’s syndrome a. Localized tooth-related factors that modify or predispose iii. Leukocyte adhesion deficiency syndrome to plaque-induced gingival diseases/periodontitis. iv. Papillon-Lefévre syndrome i. Tooth anatomic factors v. Chediak-Higashi syndrome ii. Dental restorations/appliances vi. Histiocytosis syndrome iii. Root fractures vii. Glycogen storage disease iv. Cervical root resorption and cemental tear viii. Infantile genetic agranulocytosis b. Mucogingival deformities and conditions around teeth: ix. Cohen syndrome i. Gingival/soft tissue recession, facial or lingual x. Ehlers-Danlos syndrome (Types IV and VIII) surfaces, interproximal (papillary) xi. Hypophosphatasia ii. Lack of keratinized gingiva Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification xii. Others iii. Decreased vestibular depth iv. Aberrant frenum/muscle position Necrotizing Periodontal Diseases v. Gingival excess: a. Necrotizing ulcerative gingivitis – Pseudopocket b. Necrotizing ulcerative periodontitis. – Inconsistent gingival margin – Excessive gingival display Abscesses of the Periodontium – Gingival enlargement a. Gingival abscess vi. Abnormal color CHAPTER 4 Classification Systems of Periodontal Diseases 41 BIBLIOGRAPHY “periodontitis as a manifestation of systemic a manifestation “periodontitis as diseases”. diseases”. “necrotizing periodontal and “developmental endodontic lesions” “periodontal and conditions are included. or acquired deformities” WB Saunders Company, 2002. WB Saunders Company, Ann Periodontol 1999; periodontal diseases and conditions. 4:1-6. dontology 2000;1993:2-13. periodontalAnnals of Periodontology diseases and condition. 1999;4(1). 1. edition. Newman, Clinical Periodontology Ninth Carranza Jr. 2. for Armitage, Development of a classification system Gary C. 3. RR. Classification of periodontal diseases. Perio- Ranney 4. Development of classification systems for Robert JG. c. periodontitis entity for refractory No separate d.has been designed for classification Separate e. is replaced with “Necrotizing ulcerative periodontitis” f. abscess”, Additional categories like, “periodontal KNOW MORE ... i. Primary i. horizontal ridge deficiency. and/or Vertical periodontitis” and “early onset periodontitis” with periodontitis” and “early onset periodontitis” “aggressive periodontitis”. v. Decreased vestibular depth ii. Secondary occlusal trauma. ii. gingival/keratinized tissue Lack of iv. Aberrant frenum/muscle position vi. Abnormal color iii. tissue enlargement Gingival/soft ridges: a.separate section on gingival disease. There is a b. “Adult periodontitis” is being replaced with “chronic Changes Made in the Classification Proposed by Changes Made in the Classification International Workshop (1999) c.on edentulous and conditions deformities Mucogingival d. Occlusal trauma: 5 ChapterChapter

Epidemiology of Gingival and Periodontal Diseases

 DEFINITION, TYPES AND AIMS OF • To Assess Gingival Inflammation EPIDEMIOLOGY • To Measure Periodontal Destruction  DEFINITION, USES AND CHARACTERIS- • To Measure Plaque Accumulation • To Measure Tooth Mobility TICS OF AN INDEX • To Measure Calculus  VARIOUS INDICES USED TO STUDY • To Assess Treatment Needs PERIODONTAL PROBLEMS

EPIDEMIOLOGY a. Incidence rate: This is defined as the number of new Definition cases occurring in a defined population during a specific period of time. Study of health and disease in populations and how the states b. Prevalence rate: This refers to all current cases (new are influenced by heredity, biology, physical and social and old) existing at a given point in time or over a period environmental ways of living. of time in a given population. Types of Epidemiologic Research Two types are described: a. Point prevalence a. Descriptive studies b. Analytical studies b. Period prevalence c. Experimental epidemiology Longitudinal Studies Descriptive Studies The observations are repeated in the same population over These are used to observe and document the occurrence, a prolonged period of time by means of follow-up progression and distribution of a disease or condition in examinations. populations, in relation to host and environmental factors (when, where and who). Uses Measurement of disease: Incidence can be obtained from i. To study the natural history of disease and its future “Longitudinal studies” and prevalence from “cross-sectional” outcome. studies. ii. For identifying the risk factors of disease. 43

iii. For finding out the incidence rate or rate of occurrence c. To provide the data essential for the planning, of new cases. implementation and evaluation of services for the prevention, control and treatment of disease. Disadvantage

They are difficult to organize and time consuming as INDEX 5 CHAPTER compared to cross-sectional studies. Definition

Cross-sectional Studies These are numerical values describing the relative It is the simplest form of an observational study. It is status of the population on a graduated scale with based on a single examination of a cross-section of definite upper and lower limits, which are designed population at one point of time (It is also known as to permit and facilitate comparisons with other populations

prevalence study). and are classified by the same criteria and methods. Diseases Periodontal and Gingival of Epidemiology Uses Purposes and Uses of an Index i. It is more useful for chronic (long-term diseases) as compared to acute (short-term) diseases. For Individual Patients ii. It gives information about the distribution of a disease An index can: in a population rather than its etiology. i. Provide individual assessment to help a patient to recognize an oral problem. Analytical Studies ii. Reveal the degree of effectiveness of present oral It includes two distinct types: hygiene practices. a. Case control study iii. Motivate the person in preventive and professional b. Cohort study care for the elimination and control of oral disease. iv. Evaluate the success of an individual and professional Case control or retrospective study: The study precedes treatment over a period of time by comparing index backwards from effect to cause. scores. Cohort study: It is a prospective study (incidence study or longitudinal study), which is usually undertaken to obtain, In Research additional evidence to refute and support the existence of An index is used to: an association between the suspected cause and disease. i. Determine the baseline data before the experimental factors are introduced. Experimental Epidemiology ii. Measure the effectiveness of specific agents for It is used to test hypothesis further by introducing a preventive the prevention, control and treatment of oral conditions. or therapeutic agent and comparing the outcome in the test iii. Measures the effectiveness of mechanical devices for subjects with concurrent observations in control groups. personal care, such as, , interdental cleaning devices or water irrigators. Aims of Epidemiology In Community Health Three main aims have been proposed: a. To describe the distribution and size of disease problems An index: in human populations. i. Can show the prevalence and trends of incidence, of b. To identify the etiological factors in the pathogenesis of a particular condition occurring within a given disease. population. 44

ii. Provides a baseline data to show the existing dental Indices Used to Measure health practices. Periodontal Destruction iii. Assesses the needs of a community and compares the a. Russell’s periodontal index. effects of a community program and evaluates the b. Periodontal disease index by Ramfjord. results. c. Extent and severity index by Carlos and co-workers. Characteristics of an Index d. Radiographic approaches to measure bone loss. i. GBI—Gingival bone count index by Dunning and 1. It should be simple to use and accurate. Leach. 2. It should require minimal equipment and expenses. PART II ii. PSI—Periodontal severity index by Adams and 3. It should have clear-cut criteria, which are readily Nystrom. understandable. 4. It should be as free as possible from subjective Indices Used to Measure Plaque Accumulation interpretation. 5. It should be reproducible by the same examiner or a. Plaque component of periodontal disease index by different examiners. Ramfjord. 6. Be amenable to statistical analysis, have validity and b. Simplified oral hygiene index by Greene and Vermillion. reliability. c. Turskey-Gillmore-Glickman modification of the 7. Not require an excessive amount of time to complete. Quigley-Hein plaque index. 8. Not cause patient discomfort or be otherwise unacceptable d. Plaque index by Sillness and Loe. to a patient. e. Modified navy plaque index. f. Patient hygiene performance index by Podshadley and Indices Used to Assess the following Haley. Periodontal Problems g. Plaque weight. h. Plaque free score by Grant, Stern and Everett. 1. The degree of inflammation of the gingival tissues. i. Plaque control record by O’leary. 2. The degree of periodontal destruction. 3. The amount of plaque accumulated. Indices Used to Measure Calculus 4. The amount of calculus present. 5. In addition, indices are developed to assess the treatment a. Calculus component of simplified oral hygiene index needs. by Greene and Vermillion. b. Calculus component of the periodontal disease index Indices Used to Assess Gingival Inflammation by Ramfjord. c. Probe method of calculus assessment by Volpe and a. PMA index by Schour and Massler. associates. b. Gingivitis component of the periodontal disease. Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification d. Calculus surface index by Ennever and coworkers. c. Gingival index by Loe and Sillness. e. Marginal line calculus index by Mühlemann and Villa. d. Indices of gingival bleeding. i. Sulcus bleeding index (SBI) of Mühlemann and Indices Used to Assess Treatment Needs Mazor. ii. Papillary bleeding index by Mühlemann. a. Gingival periodontal index. iii. Bleeding points index by Lennox and Kopczy K b. Community periodontal index of treatment needs by iv. Interdental bleeding index by Caton and Polson. Ainamo and associates. v. Gingival bleeding index by Ainamo and Bay. c. PTNS—Periodontal treatment need system by Belini HT. 45

INDICES USED TO ASSESS Gingival Index by Loe H and Sillness J (1963) GINGIVAL INFLAMMATION This index was solely developed for the purpose of assessing the severity of gingivitis and its location in four possible Papillary Marginal Attachment (PMA) Index by areas. Schour and Massler (1944) 5 CHAPTER

The basic philosophy used in the development of the PMA Method index was very similar to the DMF index, i.e. the number The severity of gingivitis is scored on all surfaces of all of gingival units affected were counted rather than the teeth, or selected teeth, or on selected surfaces of all teeth, severity of the inflammation. A gingival unit is divided into or, selected teeth. The tissues surrounding each tooth are three component parts: divided into four gingival scoring units:

i. Papillary gingiva (P) • Distal facial papillae, Diseases Periodontal and Gingival of Epidemiology ii. Marginal gingiva (M) • Facial margin, iii. Attached gingiva (A) • Mesial facial papillae, The presence or absence of inflammation on each • Entire lingual gingival margin. gingival unit is recorded as 1 or 0 respectively. The P, M, A A blunt instrument is used for recording the scores based numerical values for all the teeth are added separately and on the following criteria: then added together to express the PMA index score per 0 — No inflammation person. The developers of this index eventually added a 1 — Mild inflammation, no bleeding elicited on probing severity component for assessing gingivitis, the papillary 2 — Moderate inflammation, bleeding on probing units (P) were scored on a scale of 0 to 5, and the marginal 3 — Severe inflammation (M) and attached gingiva were scored on a scale of 0 to 3. The scores around each tooth are added and divided by four to arrive at the score for that particular tooth. Total all Gingivitis Component of the the teeth scores and divide it by the number of teeth. This Periodontal Disease provides the gingival index score per person. The numerical values are correlated as follows: The periodontal disease index (PDI) is similar to PI, in that; 0.1 to 1.0 — Mild gingivitis both are used to measure the presence and severity of 1.1 to 2.0 — Moderate gingivitis periodontal disease. The PDI does so by combining the 2.1 to 3.0 — Severe gingivitis assessments of gingivitis and gingival sulcus depth on six selected teeth (# 3, 9, 12, 19, 25 and 28). This group of Indices of Gingival Bleeding teeth frequently referred to as the Ramfjord teeth, have been tested as reliable indicators for the various regions of the Sulcular Bleeding Index by oral cavity. Calculus and plaque are also examined to assist Mühlemann and Son (1971) in formulating a comprehensive assessment of periodontal The purpose of the index is to locate areas of the gingival status. sulcus that bleed upon gentle probing and thus recognize A numerical score for the gingival status component of and record the presence of early inflammatory gingival the PDI is obtained by adding the values for all the gingival disease. Four gingival units are scored systemically for each units and dividing it by the number of teeth present. This tooth: the labial and lingual marginal gingiva (M units) and index has been used in epidemiological surveys, longitudinal the mesial and distal papillary gingiva (P units). The probe studies and clinical trials. is held parallel with the long axis of the tooth and 30 seconds 46

after probing; scoring is done based on the criteria, which lingual surfaces of each tooth. A periodontal probe is drawn ranges from 0 to 5. Each of the four gingival units is scored horizontally through the gingival crevice of a gradient, and 0 to 5. Scores for the four units are added and divided by the gingiva is examined for bleeding after 30 seconds. four. Adding the scores of the undivided teeth and dividing them by the number of teeth can determine the sulcus- Interdental Bleeding Index by Caton and Polson bleeding index. The index utilizes a triangle-shaped toothpick made of soft, Scoring criteria: pliable wood to stimulate the interproximal gingival tissue. 0 — Normal appearing gingiva, no bleeding upon probing The interproximal cleaner is inserted horizontally between

PART II 1 — No color or contour changes, but bleeding on probing the teeth from the facial surface, depressing the interproximal 2 — Bleeding on probing, color change (reddening), no papillae by up to 2 mm. The wooden cleaner is inserted and edema and contour changes removed four times, and the presence or absence of bleeding 3 — Bleeding on probing, color change, mild within 15 seconds is noted. The score is determined by inflammatory edema dividing the number of bleeding sites by the number of sites 4 — Bleeding on probing, color change, severe evaluated. inflammatory edema. 5 — Spontaneous bleeding on probing, color change, very Gingival Bleeding Index by Ainamo and Bay severe inflammatory edema with or without The index was developed as an easy and suitable way for ulceration. the practitioner to assess a patient’s progress in plaque control. The presence or absence of gingival bleeding is Papillary Bleeding Index by Mühlemann HR (1977) determined by gentle probing of the gingival crevice with a It is based on bleeding elicited, following gentle probing of periodontal probe. The appearance of the bleeding within the interdental papilla. A blunt periodontal probe is carefully 10 seconds indicates a positive score, which is expressed inserted into the gingival sulcus at the base of the interdental as a percentage of the total number of gingival margins papilla on the mesial aspects, and then moved coronally to examined. the papilla tip. This is repeated on the distal aspect of the same papilla. The intensity of any bleeding thus provoked INDICES USED TO MEASURE will be recorded on a scale of 0 to 4. PERIODONTAL DESTRUCTION Scoring criteria: 0 — No bleeding Russell’s Periodontal Index by Russell AL (1956) 1 — A single discrete bleeding point appears The index was intended to estimate deeper periodontal 2 — Several isolated bleeding points or a single fine line disease by measuring the presence or absence of the gingival of blood appears inflammation and its severity, pocket formation and

3 — The interdental triangle fills with blood shortly after masticatory function. Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification probing All the teeth present are examined. All of the gingival 4 — Profuse bleeding occurs after probing, blood flows tissues surrounding each tooth are assessed for gingival immediately into the marginal sulcus. inflammation and periodontal involvement. Russell chooses the scoring values (0, 1, 2, 6, 8) in order to relate the stages Bleeding Points Index by Lennox and Kopczy K of the disease in an epidemiological survey to the clinical conditions observed. The index was developed to assess a patient’s oral hygiene performance. It determines the presence or absence of Sum of individual scores PI score per person = ———————————— gingival bleeding interproximally and on the facial and Number of teeth present 47

Since only a mouth mirror and no calibrated probe or Clinical Conditions and Periodontal Scores radiographs is used while performing the PI examination, Clinical conditions Group PI scores Stage of disease the results tend to underestimate the true level of periodontal Clinically-normal 0 to 0.2 disease. The number of periodontal pockets without obvious supportive tissues supragingival calculus is also underestimated in the Simple gingivitis 0.3 to 0.9 5 CHAPTER periodontal index. Beginning of des- 0.7 to 1.9 Reversible tructive–periodontal Scoring Criteria disease Established destructive 1.6 to 5.0 Irreversible Score Criteria and scoring Additional X-ray criteria periodontal disease for field studies followed in the clinical test Terminal disease 3.8 to 8.0 Irreversible 0 Negative: There is neither Radiographic overt inflammation in the appearance is Uses Diseases Periodontal and Gingival of Epidemiology investing tissues nor loss essentially normal of function due to des- i. Epidemiological surveys. truction of supporting ii. More data can be assembled using periodontal index. tissues 1 Mild gingivitis: There is iii. Used in the National Health Survey (NHS). an overt area of inflam- mation in the free gingiva, Periodontal Disease Index by but this area does not Sigurd P Ramfjord (1959) circumscribe the tooth 2 Gingivitis: Inflammation This index is a clinician’s modification of the Russell’s completely circumscribing periodontal index for epidemiological surveys of periodontal the tooth, but there is no disease. Emphasis is placed on the recording of the apparent break in the attachment level of the periodontal disease relative to the epithelial attachment 4 Used when radiographs There is early notch-like cementoenamel junction. are available resorption of alveolar Only six selected teeth are scored for assessment of the crest periodontal status of the oral cavity, which are 1, 6, 21, 24, 6 Gingivitis with pocket There is horizontal bone 36, 41, 44. The first step is scoring of the gingival status. formation: The epithelial loss involving the entire attachment has been alveolar crest, up to half The gingiva around the teeth is dried superficially by gently broken and there is a of the length of the tooth dabbing it with absorbing cotton. Changes in color, pocket. There is no root consistency, contour; evidence of ulceration of gingiva is interference with normal evaluated by a periodontal probe. The next step is recording masticatory functions, the of the crevice depth related to a cementoenamel junction. tooth is firm and has not drifted. There is hori- For this purpose a University of Michigan 0 probe is used. zontal bone loss involving The end of probe should be placed against the enamel surface the entire alveolar crest, coronally to the margin of the gingiva and minimal force is up to half of the length applied in an apical direction maintaining tooth contact. The of the tooth root crevicular measurements are recorded in the following 8 Advanced destruction with There is advanced bone manner. Distance from free gingival margin to the bottom loss of masticatory func- loss, involving more than of the gingival crevice or pocket on the buccal and mesial tion: The tooth may be one-half of the length of loose, may have drifted, tooth root, infrabony aspect of the each tooth. The buccal measurements should may sound dull on per- defects, widening of be made at the middle of the buccal surfaces and the mesial cussion and may be periodontal ligament, measurement should be made at the buccal aspect of the depressible in socket root resorption. interproximal contact area. 48

The scoring criteria ranges from 0 to 6. The PDI score The Periodontitis Severity Index for the individual can be obtained by adding the scores for by Adams and Nystrom each tooth examined and then, dividing by the number of The index assesses the presence or absence of periodontitis teeth examined. The PDI score will range from 0 to 6. as the product of clinical inflammation and interproximal bone loss determined radiographically using a modified Scoring Criteria schei ruler. 0 — Absence of inflammation 1 — Mild to moderate inflammatory gingival changes not INDICES USED TO MEASURE PLAQUE ACCUMULATION PART II extending all around the tooth 2 — Mild to moderately severe gingivitis extending all Plaque Component of Periodontal around the tooth Disease Index by Ramfjord 3 — Severe gingivitis, characterized by marked redness, tendency to bleed and ulceration The index is used on the six teeth selected by Ramfjord 4 — Gingival crevice in any of the four measured areas (teeth number 3, 9, 12, 19, 25 and 28) after staining with (mesial, distal, buccal, lingual), extending apically Bismarck brown solution. The criteria is to measure the to the CEJ, but not more than 3 mm presence and extent of plaque on a scale of 0 to 3, looking 5 — Gingival crevice in any of the four measured areas specifically at all interproximal facial and lingual surfaces extending apically, 3-6 mm from the CEJ of the index teeth. The scoring criteria is as follows: 6 — Gingival crevice in any of the four measured areas 0 — No plaque present. extending apically more than 6 mm from the CEJ 1 — Plaque present on some but not all interproximal, buccal and lingual surfaces of the tooth. Extent and Severity Index by 2 — Plaque present on all interproximal buccal and Carlos and Coworkers lingual surfaces, but covering less than one half of the surfaces. In this newer model, periodontal disease is viewed as a 3 — Plaque extending over all interproximal, buccal and chronic process with intermittent periods of activity and lingual surfaces, and covering more than one half of remission that affects individual teeth and sites around the these surfaces. teeth at different rates within the same mouth. It uses a Only fully-erupted teeth are scored and missing teeth periodontal probe (NIDR probe) to determine attachment should not be substituted. levels. The ESI score is a bivariate statistic. It expresses the Total score percentage of sites that exhibit disease. ESI is based on probe Plaque score of an individual = ————————— measurements (at the mesiobuccal, interproximal and Number of teeth examined midbuccal locations on all teeth excluding molars and at the mesiobuccal interproximal and midbuccal of the mesial Uses root of molars) at 14 sites in half of the maxillary arch and at Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification Suitable for: 14 sites in the contralateral mandibular arch. Attachment level a. Longitudinal studies of periodontal disease. measurements are made using the Ramfjord criteria. b. Epidemiological surveys. c. Clinical trials of preventive or therapeutic agents. Radiographic Approaches to Measure Bone Loss Simplified Oral Hygiene Index by Gingival Bone Count Index by Dunning and Leach Greene and Vermillion (1964) This index records the gingival condition on a scale of The OHI-S measures the surface area of the tooth that is 0 to 3 and the level of the crest of the alveolar bone. covered by debris and calculus. It consists of two components: 49 a. Debris index-simplified (DI-S). placing a dental explorer into the distal gingival crevice b. Calculus index-simplified (CI-S). and drawing it subgingivally from the distal contact area to the mesial contact area. Scoring is done according to the Scoring Criteria for DI-S criteria. The CI-S score per person is obtained by totaling the calculus scores per tooth surface and dividing it by the 5 CHAPTER 0 — No debris or stain present. number of surfaces examined. The OHI-S score per person 1 — Soft debris covering not more than one-third of the is the total of DI-S and CI-S scores per person. The clinical tooth surface or the presence of extrinsic stains levels of oral cleanliness for debris that can be associated without other debris, regardless of surface area with groups (DI-S, CI-S) scores are as follows: covered. Good — 0.0 to 0.6 2 — Soft debris, covering more than one-third but not Fair — 0.7 to 1.8

more than two-thirds of the exposed tooth surface. Diseases Periodontal and Gingival of Epidemiology 3 — Soft debris, covering more than two-thirds of the Poor — 1.9 to 3.0 exposed tooth surface. The clinical levels of oral hygiene that can be associated with group OH1-S scores are as follows: Scoring Criteria for CI-S Good — 0.0 to 1.2 Fair — 1.3 to 3.0 0 — No calculus present. Poor — 3.1 to 6.0 1 — Supragingival calculus covering not more than one- third of the exposed tooth surface. Turesky-Gilmore-Glickman Modification of the 2 — Supragingival calculus covering more than one-third, Quigley Hein Plaque Index (1970) but not more than two-thirds of the exposed tooth surface or the presence of the individual flecks of Plaque is assessed on the facial and lingual surfaces of all subgingival calculus around the cervical portion of of the teeth after using a disclosing agent. A plaque score the tooth or both. per person is obtained by totaling all the plaque scores and 3 — Supragingival calculus covering more than two- dividing it by the number of surfaces examined. This system thirds of the exposed tooth surface or a continuous of scoring plaque is relatively easy to use because of the heavy band of subgingival calculus around the objective definitions of each numerical score. The strength cervical portion of the tooth, or both. of this plaque index is its application to longitudinal studies and clinical trials of prevention and therapeutic agents. Method Scoring Criteria Each component is assessed on a scale of 0 to 3. Only a mouth mirror and a Shepherd’s Crook or sickle-type dental 0 — No plaque explorer, and no disclosing agent are used for examination. 1 — Separate flecks of plaque at the cervical margin of The six tooth surfaces examined are No 3, 8, 14, 24 (Facial the tooth surface) and No 19, 30 (Lingual surfaces). Each tooth 2 — A thin, continuous band of plaque (up to 1 mm) at surface is divided horizontally into gingival, middle and the cervical margin incisal thirds. For the DI-S, a dental explorer is placed on 3 — A band of plaque wider than 1 mm but covering less the incisal third and moved towards the gingival third and than one-third of the crown scores are awarded according to the criteria. The DI-S score 4 — Plaque covering at least one-third but less than two- per person is obtained by totaling the debris score per the thirds of the crown tooth surface and dividing it by the number of surfaces 5 — Plaque covering two-thirds or more of the examined. The CI-S assessment is performed by gently crown. 50

Plaque Index by Sillness and Loe (1964) Procedure It is unique among the indices used for assessment of plaque Each tooth surface is divided into gingival, middle and because it ignores the coronal extent of plaque on the tooth incisal third. Gingival 3rd is divided into two halves surface area and assesses only the thickness of plaque at (horizontally) both the gingival halves are again divided the gingival area of the tooth. longitudinally into distal, middle and mesial thirds. The middle 3rd is divided into distal and mesial halves. The Method incisal 3rd is not subdivided, thereby emphasizing more of gingival two-thirds of the tooth. The evaluation or scoring is done on the entire dentition or

PART II Total scores per on selected teeth. The surfaces examined are the four gingival tooth surface areas of the tooth, i.e. the distofacial, facial, mesiofacial and Modified navy plaque index = —————————— lingual surfaces. A mouth mirror, light source, a dental Number of explorer and air-drying of the teeth and gingiva are used in surfaces examined the scoring of this index. Only plaque of the cervical third of Tooth Mobility Indices the tooth is evaluated with no attention to plaque that has extended to the middle or incisal thirds. Miller’s Index (1938)

Scoring Criteria 1. The first distinguishable sign of movement. 2. The movement of the tooth which allows the crown to 0 — No plaque in the gingival area deviate within 1 mm of its normal position. 1 — A film of plaque adhering to the free gingival margin 3. Easily noticeable and allows the tooth to move more and adjacent area of the tooth. The plaque may be than 1 mm in any direction or to be rotated or depressed recognized only by running a probe across the tooth in the socket. surface 2 — Moderate accumulation of soft deposits within the Glickman’s Index (1972) gingival pocket and on the gingival margin and/or adjacent tooth surface that can be seen by naked eye • Grade I—Slightly more than normal 3 — Abundance of soft matter within the gingival pocket • Grade II—Moderately more than normal and/or on the gingival margin and adjacent tooth • Grade III—Severe mobility faciolingually and/or mesio- surface. distally combined with vertical displacement. The score for the area is obtained by totaling the four scores per tooth and dividing it by four. The plaque index Patient Hygiene Performance Index (PHP) score for the person is obtained by adding the plaque index by Podshadley and Hadley scores per tooth and dividing by the number of teeth Advantages examined.

Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification i. It was the first index developed for the sole purpose Modified Navy Plaque Index of assessing an individual’s performance in removing debris after tooth brushing instruction. Advantage ii. It is easy to use and can be performed. It is of value in assessing health education programs and the iii. For individual patient education. ability of the individuals to perform oral hygiene practices. Selection of Teeth and Surfaces A variation of the modified navy plaque index is the DMPI (Distal mesial plaque index), which places more emphasis Six surfaces of the six teeth (3, 8, 18, 19, 24 and 30) are on the gingival, interproximal areas of a tooth. selected. 51

It records presence or absence of debris as 1 or 0 Calculations respectively. Plaque-free score = Total the number of teeth present and Total debris score total the number of surfaces with plaque PHP = ______No of teeth scored Number of 5 CHAPTER Suggested Nominal Scale plaque-free scores Plaque-free score = ————————— × 100 Rating Number of available surfaces Excellent — score Good — 0.1 to 1.7 Plaque Control Record by O’Leary Fair — 1.8 to 3.4 Similar to plaque-free score by Grant, Stern and Everett.

Poor — 3.5 to 5.0 Diseases Periodontal and Gingival of Epidemiology

Plaque Weight Interpretations Although 0 percent is ideal, less than 10 percent has been 1. Sand-blasted standardized mylar foils attached to the suggested as a guideline in periodontal therapy. After initial lingual surface of lower anterior teeth are weighed on therapy, when a patient reached 10 percent level of plaque removal after a set time. control necessary periodontal and restorative procedures are 2. Removal of plaque directly from the tooth and initiated. In comparison, a similar evaluation using a plaque- subsequent weighing is less precise but simpler than the free score record would mean a goal of over 90 percent or foil techniques. better plaque-free score before the surgical phase of treatment should be undertaken. Plaque-free Score by Grant, Stern and Everett INDICES USED TO MEASURE CALCULUS Purpose Calculus Component of the Simplified Oral To determine the location, number and percentage of plaque- Hygiene Index by Greene and Vermillion— free surfaces for individual motivation and instruction. Discussed in Plaque Index

Selection of Teeth and Surfaces Calculus Component of the Periodontal Disease Index by Ramfjord All erupted teeth are included; four surfaces are recorded for each tooth (facial, lingual, mesial and distal). Advantages 1. It has a high degree of examiner reproducibility. Procedure 2. It can be performed quickly and has the best application Apply disclosing agent and examine each tooth surface for in epidemiological surveys and longitudinal studies. evidence of plaque and record the surfaces in red color. Procedure Papillary Bleeding on Probing Six teeth are examined (3, 9, 12, 19, 25 and 28). Four Total the number of small circles marked for bleeding. For surfaces are recorded (facial, lingual, mesial, distal) with a person with 32 teeth there are 30 interdental areas. The the help of an explorer and score ranges from 0 to 3. mesial or distal of tooth adjacent to an edentulous area is 1. Supragingival plaque extending not more than 1 mm probed and counted. 2. Moderate amount of supragingival and subgingival calculus 52

3. Abundance of supragingival and subgingival calculus Marginal Line Calculus Index Total number by Mühlemann and Villa of scores Calculus index for an individual = ———————— Purpose Number of teeth To assess the supragingival calculus along the margins of the gingiva. It only scores the supragingival calculus formed Probe Method of Calculus in the cervical area along the marginal gingiva on the lingual Assessment by Volpe and Associates side of the four mandibular incisors.

PART II Advantages and Disadvantages INDICES USED TO ASSESS It has been shown to possess a high degree of interexaminer TREATMENT NEEDS and intraexaminer reproducibility. However, excessive training under a experienced investigator is required to Gingival Periodontal Index master it. It assesses three components of periodontal disease: gingival status, periodontal status, and collectively materia alba, Purpose calculus and overhanging restorations. The maxillary and It is used for longitudinal studies. mandibular arches are each divided into three segments: the six anterior teeth, the left posterior teeth, and the right Method posterior teeth. The lingual surfaces of six mandibular teeth are measured Objective in millimeter divisions with the help of graduated periodontal probe. The primary objective in using this index is to determine the tooth or surrounding tissues with the severest condition Calculus Surface Index by within each of the six segments. Each segment is assessed Ennever and Coworkers for each of the three components of periodontal disease described previously. Objective Specific Criteria It is to determine rapidly whether a specific agent has any effect on reducing or preventing supragingival or The specific criteria for the gingival status components of subgingival calculus. the GPI are as follows: Four mandibular incisors are examined for the presence 0 — Tissue tightly adapted to the teeth, firm consistency or absence by visual and tactile examination. with physiologic architecture.

1 — Slight to moderate inflammation, as indicated by Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification Scoring Criteria changes in color and consistency, involving one or more teeth in the same segment but not completely 1. Calculus not exceeding 0.5 mm in width or thickness surrounding any one tooth. 2. Calculus not exceeding 1 mm 3. Calculus exceeding more than 1 mm in width and 2 — The above changes occur either singly or combined thickness. completely encircling one or more teeth in a segment. 53

3 — Marked inflammation, as indicated by loss of surface d. Pocket 4 or 5 mm continuity (ulceration), spontaneous hemorrhage, e. Pocket more than 6 mm loss of faciolingual continuity or any interdental Treatment needs: papilla, marked deviation from normal contour, 0 No treatment neede recession and clefts. 1 Oral hygiene needs improvement 5 CHAPTER The area with the highest score determines the gingival 2 Oral hygiene improvement and professional scaling score for the entire segment, and the gingival status for the 3 Oral hygiene improvement, professional scaling and oral cavity is obtained by dividing the sum of the gingival complex treatment. scores by the number of segments. Advantages Community Periodontal Index of Treatment The value of CPITN is that it permits rapid examination of Needs by Ainamo and Associates Diseases Periodontal and Gingival of Epidemiology a population to determine periodontal treatment needs. Procedure The periodontal treatment needs are recorded for sextants. Disadvantages Third molars are not included except when they are 1. A great deal of useful information is lost when only the functioning in place of second molars. The treatment need worst score per sextant is recorded. in a sextant is recorded only when two or more teeth are 2. CPITN underestimates the pockets greater than 6 mm present and are not indicated for extraction. If only one in older age groups and overestimates the need for functioning tooth is remaining in the maxilla, the jaw would scaling in younger age groups. be recorded as one sextant. Missing sextants are indicated with a diagonal line Periodontal Treatment Need System through the appropriate box. The index teeth to be examined by Bellini HT are as follows: It attempts to place individuals into one of the four classes WHO Numbering American Equivalent based on treatment procedures relative to time requirements. It considers the presence or absence of gingivitis and plaque, 17, 16 11 26, 27 2, 3 8 14, 15 and the presence of pockets 5 mm or deeper in each quadrant 47, 46 31 36, 37 31, 30 25 18, 19 of mouth. The worst findings from these teeth surfaces are Criteria for periodontal treatment need system is recorded. WHO probe is used. described in Table 5.1.

Criteria Table 5.1: Criteria for periodontal treatment need system Periodontal status: PTNS Unit Plaque Calculus Inflam- Pocket classification and/or mation depth a. Healthy periodontium overhangs b. Bleeding observed directly or by using mouth mirror. Class-0 Mouth No No No No c. Calculus felt during probing, but entire blunt area of Class-A Mouth Yes No Yes <5 mm the probe is visible. Class-B Quadrant Yes Yes Yes <5 mm Class-C Quadrant Yes Yes Yes >5 mm 54

3. Moderate mobility—up to approximately 2 mm of buccolingual movement KNOW MORE ... 4. Severe mobility—more than 2 mm of movement.

1. Point prevalence Nyman’s Index (1975) Number of all current cases at a given point of time Degree 0 – Normal to less than 0.2 mm mobility = ______× 100 Degree 1 – Horizontal/mesiodistal mobility of 0.2 to 1 mm Estimated population at the same time Degree 2 – Horizontal/mesiodistal mobility of 1 to 2 mm Period prevalence Degree 3 – Horizontal/mesiodistal mobility exceeding

Number of all existing cases of specified 2 mm and/or vertical mobility. PART II disease at a given point of time = ______× 100 Flezar’s Index (1980) Estimated population at risk M0 – Firm tooth M – Slight increased mobility Other Tooth Mobility Indices 1 M2 – Definite to considerable increase in mobility but Prichard’s Index (1972) no impairment of function M3 – Extreme mobility, a loose tooth that would be 1. Slight mobility incomparable in function. 2. Moderate mobility 3. Extensive movement in a lateral or mesiodistal direction combined with vertical displacement in the BIBLIOGRAPHY alveolus 4. Signs can be used for added refinement. 1. Esther M Wilkins. Clinical Practice of the Dental Hygienist, 8th edition. Wolters Kluwer Company. Wasserman’s Index (1973) 2. Newman Takei, Fermin A Carranza. Clinical Periodontology, 1. Normal 9th edn WB Saunders, 2002. 2. Slight mobility—less than 1 mm of buccolingual 3. Soben Peter: Essentials of Preventive and Community dentistry,

movement Arya (MEDI), Publishing House. Classification and Epidemiology of Periodontal Diseases Periodontal of Epidemiology and Classification

6 ChapterChapter

Periodontal Microbiology (Dental Plaque)

 DEFINITION  CLINICAL SIGNIFICANCE OF PLAQUE  DENTAL PLAQUE AS A BIOFILM  MICROBIAL SPECIFICITY OF PERIODONTAL  TYPES OF DENTAL PLAQUE DISEASES  COMPOSITION OF DENTAL PLAQUE  WHAT MAKES PLAQUE PATHOGENIC  FORMATION/DEVELOPMENT OF DENTAL  MICROORGANISMS ASSOCIATED WITH PLAQUE PERIODONTAL DISEASES  STRUCTURAL AND MICROSCOPIC  BACTERIA ASSOCIATED WITH PERIODONTAL PROPERTIES OF PLAQUE HEALTH AND DISEASE

DEFINITION Biofilms Biofilms are defined as “Matrix—enclosed bacterial Dental Plaque populations adherent to each other and or/to surface or Dental Plaque is an adherent intercellular matrix consisting interfaces (by Costerton). According to the recent data primarily of proliferating microorganisms, along with a (Widerer and Charaklis 1989), biofilm is defined as the scattering of epithelial cells, leukocytes and macrophages. relatively undefinable microbial community associated with a tooth surface or any other hard, non-shedding material. Plaque Plaque can also be defined as the soft deposits that form the DENTAL PLAQUE AS A BIOFILM biofilm adhering to the tooth surface or other hard surfaces Structurally, dental plaque is now considered to be a biofilm in the oral cavity, including removable and fixed of complex and dynamic microbial community. It contains restorations. Dental Plaque is a host-associated biofilm. areas of high and low bacterial biomass interlaced with 58

aqueous channels of different sizes, which are the nutrient channels for bacterial colonization. The intercellular matrix forms a hydrated gel in which bacteria can survive and proliferate. Hence, biofilm adheres firmly to the tooth surface and is resistant to mechanical removal, as well as antibiotics.

TYPES OF DENTAL PLAQUE Based on its relationship to the gingival margin, plaque is

PART III differentiated into two categories, supragingival and subgingival plaque (Table 6.1). Supragingival plaque is further differentiated into: Fig. 6.1: Supragingival plaque Coronal plaque, which is in contact with only the tooth surface, and Marginal plaque, which is associated with the tooth surface at the gingival margin. Subgingival plaque can be further differentiated into: • Attached plaque • Unattached subgingival plaque

Etiopathogenesis • Attached plaque can be tooth, epithelium and/or connective tissue associated.

Supragingival Plaque (Fig. 6.1)

It can be detected clinically only after it has reached a certain thickness. Small amounts of plaque can be visualized by using disclosing agents. The color varies from grey to yellowish-grey to yellow. The rate of formation and location

of plaque vary among individuals and is influenced by diet, Fig. 6.2: Subgingival plaque bacteria associated with tooth age, salivary factors, oral hygiene, tooth alignment, systemic surface and periodontal tissues diseases and host factors. Tooth-associated Subgingival Plaque Subgingival Plaque (Figs 6.2 and 6.3) The structure is similar to the supragingival plaque. The It is usually thin, contained within the gingival sulci or flora is dominated by Gram-positive cocci, rods, filamentous periodontal pocket and thus cannot be detected by direct bacteria and some/few Gram-negative cocci and rods. This observation. Its presence can be identified only by running flora is associated with calculus formation, root caries and the end of a probe around gingival margin (Table 6.2). root resorption.

Table 6.1: Differences between supragingival and subgingival plaque Supragingival plaque Subgingival plaque 1. Matrix 50% Matrix Little or no matrix 2. Flora Mostly Gram-positive Mostly Gram-negative 3. Motile bacteria Few Common 4. Anaerobic/Aerobic Aerobic unless thick Highly anaerobic areas present 5. Metabolism Predominantly carbohydrates Predominantly proteins 59

Table 6.2: Characteristics of subgingival plaque Sl. No. Tooth-associated subgingival plaque Epithelium-associated plaque

1. Gram-positive bacteria predominates Gram- positive and Gram-negative bacteria. 2. Does not extend to junctional epithelium Extends to junctional epithelium. HPE 6 CHAPTER 3. May penetrate cementum May penetrate epithelium and connective tissue. 4. Associated with calculus formation and root caries Associated with gingivitis and periodontitis.

250 million bacteria. Other than bacteria, mycoplasma, fungi, protozoa and viruses may be present. The material among the bacteria in dental plaque is termed as inter-

microbial/cellular matrix. It contains organic and inorganic Plaque) (Dental Microbiology Periodontal portions. The organic matrix is composed of protein— polysaccharide complex produced by microorganisms. Carbohydrates in the form of levans (fructans) provides mainly energy while glucans (dextran) provide not only energy, but also act as the organic skeleton of plaque. Other carbohydrates are galactose and rhamnose. Glycoproteins provide the protein component and small amounts of lipids

Fig. 6.3: Subgingival plaque and calculus are also present. Inorganic components include, primarily calcium, phosphorus with small amounts of magnesium, potassium and sodium. Epithelium-associated Subgingival Plaque This type of plaque is loosely adherent because it lacks the FORMATION/DEVELOPMENT interbacterial matrix and is in direct association with the OF DENTAL PLAQUE gingival epithelium, extending from the gingival margin to Pellicle is the initial organic structure that forms on the the junctional epithelium. This plaque predominantly surfaces of the teeth and artificial prosthesis. The first stage contains Gram-negative rods and cocci, as well as a large in pellicle formation involves adsorption of salivary proteins number of flagellated bacteria and Spirochetes. to apatite surfaces. This results from the electrostatic ionic Connective Tissue-associated Plaque interaction between hydroxyapatite surface which has negatively charged phosphate groups that interacts with It is usually demonstrated in ANUG and localized aggressive opposite charged groups in the salivary macromolecules. periodontitis patients. The clinical significance is unclear. The mean pellicle thickness varies from 100 nm at 2 hours The unattached plaque can be seen anywhere. Thus, the to 500 to 1,000 nm. tooth-associated subgingival plaque is most important in The transition from pellicle to dental plaque is extremely calculus formation, root caries and slowly progressive rapid. The first components include mainly cocci with small periodontal destruction, whereas unattached bacterial number of epithelial cells and PMNL’s, they form a component is associated with rapid periodontal destruction. monolayer within a few hours, and the attached bacteria proliferate and form small colonies of cocci. With time other COMPOSITION OF DENTAL PLAQUE types of microorganisms proliferate and form different Bacteria + Intercellular matrix = Dental plaque microcolonies. Bacteria make up approximately 70 to 80 percent of total Hence, in dental plaque development, two adhesion material. One mg of dental plaque is estimated to contain processes are required. First, bacteria must adhere to the 60

pellicle surface and become sufficiently attached to withstand oral cleansing forces. Second, they must grow and adhere to each other to allow plaque accumulation.

Bacterial Adherence During initial adherence, interactions occur mainly between specific bacteria and the pellicle. They are:

PART III Bacterial Attachment via Electrostatic Interactions Fig. 6.5: Bacterial attachment via hydrophobic interactions Oral bacteria bear an overall net negative charge, negatively- charged components of the bacterial surface and negatively- charged components of pellicle become linked by cations such as calcium (Fig. 6.4).

Bacterial Attachment via Hydrophobic Interactions These interactions are based on the close structural fit

between molecules on the pellicle and bacterial surfaces. Etiopathogenesis The nature of the hydrophobicity of the cell is not clearly known. The contributing factor might be lipoteichoic acid (LTA), which may provide a long hydrophobic area (Fig. 6.5). Fig. 6.6: Bacterial attachment via Bacterial Attachment via Specific Lectin-like specific lectin-like interactions Substances (Fig. 6.6) Adhesion and attachment (Fig. 6.7) occurs between: Lectins in the bacterial surfaces recognize specific • Bacteria and clean tooth surface carbohydrate structure in the pellicle and become linked. • Bacteria and pellicle • Bacteria and same species • Bacteria and different species • Bacteria and matrix. Next step in plaque formation is:

Growth and Accumulation of Bacteria

Once the bacteria is adhered to the pellicle, subsequent growth leads to bacterial accumulation and increased plaque mass. Dental plaque growth (Fig. 6.8) depends on: a. Growth via adhesion of new bacteria b. Growth via multiplication of attached bacteria. Fig. 6.4: Bacterial attachment The initial bacteria that colonize the pellicle surface are via electrostatic interactions mostly gram-positive facultative microorganisms such as 61

HPE 6 CHAPTER Periodontal Microbiology (Dental Plaque) (Dental Microbiology Periodontal

Fig. 6.7: Role of saliva in the development and maturation of dental plaque

Fig. 6.9: Bacterial succession in dental plaque

morphologic arrangement of the flora in supragingival plaque described as “corncob” formations, characterized by central core consisting of rod-shaped bacterial cells, e.g. and coccal cells, e.g. streptococci which attaches along the surface of the rod-shaped cell. The subgingival plaque differs from supragingival plaque, in that it contains many large filaments with flagella and is rich in Spirochetes. Tooth-associated plaque is similar Fig. 6.8: Growth of dental plaque to supragingival plaque; whereas tissue-associated plaque is covered with flagellated bacteria without a well-defined Actinomyces viscosus and Streptococcus sanguis, as the extracellular matrix and numerous bristle—brush plaque matures, secondary colonization of Prevotella formations. This arrangement is also called as “test tube- intermedia, , Porphyromonas gingivalis brush” formation characterized by large filaments that forms takes place. This ability of bacteria to adhere to different the long axis; and short filaments or gram-negative rods species and genera of microorganisms is known as co- embedded in a amorphous matrix (Fig. 6.10). aggregation (Fig. 6.9). CLINICAL SIGNIFICANCE OF PLAQUE STRUCTURAL AND MICROSCOPIC The microbial aggregations on the tooth surface if prevented PROPERTIES OF PLAQUE from maturing may become compatible with gingival health. Supragingival plaque if allowed to grow and mature, may Supragingival Plaque induce gingivitis and can lead to the formation of a It is usually adherent to the tooth surface. It contains gram- microenvironment that permits the development of positive cocci and gram-negative rods and filaments. The subgingival plaque. Therefore, supragingival plaque 62

pathogenic. According to this, when only small amounts of plaque are present, the products released by this gets neutralized by the host. Similarly, large amounts of plaque would produce large amounts of noxious products, which would overwhelm the host’s defenses. However, several authors have contradicted this concept. First, many patients have considerable amounts of plaque and calculus as well as gingivitis, but only a minority suffer from destructive

periodontal disease even then in only few sites. This paradox PART III might be explained by specific plaque hypothesis, which states that destructive periodontal disease is a result of Fig. 6.10: Mature plaque diagram specific microbial pathogens in plaque. Thus, although the amount of plaque present correlates well with disease strongly influences the growth, accumulation and pathologic severity, it correlates poorly in individual patients. potential of subgingival plaque, especially in the early stages But it is the nonspecific plaque hypothesis, which forms of gingivitis and periodontitis. the basis for virtually all the current modalities for treatment, and prevention, which relies on the principle of reducing Subgingival Plaque

Etiopathogenesis plaque scores to a minimum. Thus, although the nonspecific In association with the presence of supragingival plaque, plaque hypothesis has been discarded in favor of the specific there are inflammatory changes that modify the anatomic plaque hypothesis, much clinical treatment is still based on relationships of the gingival margin and tooth surface. the nonspecific plaque hypothesis. This result in enlarged gingiva, which increases the space for bacterial colonization and also protects bacteria from Specific Plaque Hypothesis normal cleansing mechanisms. They derive nutrients from It states that, not all plaque is pathogenic and its gingival crevicular fluid. Many of these microorganisms pathogenicity depends on the presence of certain specific lack the adherence ability and utilizes supragingival microbial pathogens in plaque. This is based on the fact plaque bacteria as a means of colonization of the that, the specific microorganisms responsible for periodontal subgingival area. diseases release certain damaging factors that mediates the Electron microscopic studies have demonstrated the destruction of the host tissue. This concept was accepted existence of an organic material called cuticle between the easily due to the recognition of Actinobacillus actinomy- root surface and subgingival plaque. It is covered by a dense cetemcomitans as a possible pathogen responsible for layer of microorganisms and is believed to be a remnant or localized juvenile periodontitis. secretory product of the junctional epithelial cells. WHAT MAKES PLAQUE PATHOGENIC? MICROBIAL SPECIFICITY OF PERIODONTAL The following are the possible pathogenic mechanisms by DISEASES which the plaque microorganisms can cause periodontal Walter Loesche proposed the nonspecific and specific disease. plaque hypothesis in 1976. The nonspecific plaque a. Physical nature of plaque. hypothesis states that it is the total bulk of plaque, which b. Invasion of tissues by bacteria. determines the pathogenicity rather than the individual c. Release of toxic and inflammatory substances. species within it. In other words, all plaque is equally d. Role of bacterial specificity. 63

MICROORGANISMS ASSOCIATED WITH Barr virus, human cytomegalovirus and mixed herpes viral PERIODONTAL DISEASES infections. Viral infection can contribute to periodontitis by altering the functions of neutrophils, macrophages and It is well accepted that a plaque bacteria is the primary lymphocytes which in turn promotes the overgrowth of etiologic agent in periodontal disease. Bacteria are seen in periodontopathic organisms in the subgingival flora. The 6 CHAPTER the oral cavity from birth to death. It is estimated that about other possibility is that, the viral infection can destroy the 400 different species are capable of colonizing in the mouth. oral epithelial cells thus disrupting the barrier function of Counts in subgingival sites range from about 103 in healthy the periodontium. sulci to greater than 108 in deep periodontal pockets. It has not been possible to identify and study all the organisms Bacteria Associated with Periodontal present in the bacterial plaque, of nearly 400 species; only Health and Disease

30 of them are considered to be periodontopathic. Koch’s Plaque) (Dental Microbiology Periodontal See Table 6.3. postulates, generally used to identify the periodonto- pathogenecity of a microorganism, are not applicable in Table 6.3: Reclassification of periodontal bacteria periodontal disease, as more than one organism is involved Previous status Current status in periodontal diseases. Hence, Socransky (1977) had Wolinella recta Campylobacter rectus proposed the following criteria for identifying the possible (C. rectus) causative organisms in periodontal diseases: Bacteroides gingivalis Porphyromonas gingivalis (P. gingivalis) 1. The number of etiologic organisms in the diseased site Bacteroides intermedius must be increased and conversely the number of (P. intermedia) organisms must be reduced or absent in healthy sites. Bacteroides melaninogenicus Prevotella melaninogenica (P. melaninogenica) 2. If the etiologic organism is eliminated or suppressed, Bacteroides forsythus Tannerella forsythus the disease should stop. Actinobacillus Aggregatibacter actinomycetemcomitans actinomycetemcomitans 3. Presence of specific antibodies to those microorganisms. 4. Presence of virulence factors associated with certain Health microorganisms (e.g. toxins, enzymes, etc.). • Actinomyces (viscosus and naeslundii) 5. In vitro or animal experiments should be able to • Streptococcus (S. mitis and S. sangius) demonstrate the human disease process. • Veillonella parvula, small amounts of gram-negative There are many speculations regarding the pathogens species are also found. responsible for periodontitis whether they could be exogenous or components of indigenous flora. To explain Chronic Gingivitis this controversy, two theories have been proposed. According to the first theory, periodontopathic organisms Gram-positive (56%), Gram-negative (44%) organisms are a part of indigenous flora and they tend to overgrow are found. Predominant gram-positive species include, during the disease progression. The second proposal is that, S. sangius, S. mitis, S. oralis, A. viscosus, A. naeslundii, they are not components of indigenous oral flora, but are Peptostreptococcus micros. exogenous pathogens derived from outside sources. This Gram-negative Organisms concept hints that the quantity of plaque is not necessary for disease onset. Instead, the site should be contaminated • Fusobacterium nulceatum with specific periodontopathogens. • Prevotella intermedia Recent reports have demonstrated a possibility of viral • Veillonella parvula as well as Haemophilus, etiology in periodontitis and implicated viruses are Epstein Capnocytophaga and Campylobacter species. 64

Pregnancy-associated Gingivitis Refractory Periodontitis • Prevotella intermedia. • Actinobacillus actinomycetemcomitans • Bacteroides forsythus Acute Necrotizing Ulcerative Gingivitis • Porphyromonas gingivalis • Spirochetes • Prevotella intermedia • Prevotella intermedia. • Wolinella recta. Adult Periodontitis Abscesses of the Periodontium • Porphyromonas gingivalis PART III • Bacteroides (Tannerella) forsythus • Fusobacterium nucleatum • Prevotella intermedia • Prevotella intermedia • Campylobacter rectus • Peptostreptococcus micros • Eikenella corrodens • Bacteroides forsythus • Fusobacterium nucleatum • Porphyromonas gingivalis. • Actinobacillus actinomycetemcomitans • Peptostreptococcus micros • Treponema, and 1. Dental plaque is defined as an adherent intercellular

• Eubacterium species. matrix, composed primarily of proliferating micro- Etiopathogenesis organisms, along with a scattering of epithelial cells, Viruses leukocytes and macrophages. • EBV-1 (Ebstein-Barr virus) 2. Structurally dental plaque is now considered to be a biofilm of complex and dynamic microbial community. • HCMV (Human cytomegalovirus). 3. Based on its relationship to the gingival margin, plaque is differentiated into two categories, supragingival and Localized Juvenile Periodontitis subgingival plaque. • Actinobacillus (Aggregatibacter) actinomycetem- 4. Subgingival plaque can be, tooth-associated, epithelium- associated, connective tissue-associated and comitans unattached plaque. • Porphyromonas gingivalis 5. Dental plaque is mainly composed of bacteria and • Eikenella corrodens intercellular matrix. 6. In the formation of dental plaque first step is pellicle • Campylobacter rectus formation followed by bacterial adherence and growth • Fusobacterium nucleatum and accumulation of bacteria. • Bacteroides capillus • Eubacterium brachy • Capnocytophaga • Herpes virus. KNOW MORE ...

Generalized Juvenile Periodontitis Types of Infection • Actinobacillus (Aggregatibacter) actinomycetem- Several types of infections can be distinguished comitans a. Endogenous infections with bacteria that belong to • Porphyromonas gingivalis the resident flora, e.g. skin, nose, oral cavity, intestinal • Prevotella intermedia and urinary tract. • Capnocytophaga Note: Members of the resident flora at one site may • Eikenella corrodens cause life-threatening infections in other organ system. • Neisseria. 65 b. Opportunistic infection in a systemically or locally a. Spread of Streptococcus mutans which was grown compromised host, the opportunistic organisms which on to neighboring teeth. are usually avirulent can become virulent. b. Spread of A. actinomycetemcomitans via periodontal c. Exogenous infection with microorganisms that are probes in patients with localized aggressive perio- usually not members of the resident flora, e.g. among

dontitis. 6 CHAPTER periodontopathogens, in particular some virulent The significance of this transmission or translocation clones of A. actinomycetemcomitans and P. gingivalis of bacteria lies in reinfection of previously treated sites might be considered exogenous pathogens. However, by bacteria from untreated sites or other intraoral niches. it should be noted that bacteria alone cannot induce Hence, to prevent this a new treatment strategy called destructive periodontal disease. one-stage, was introduced by Microbial Shifts from Health to Disease Leuven and group. This strategy consists of combination of following treatment approaches. • Gram-positive to gram-negative microorganisms a. Full mouth scaling and root planing within 24 hours.

• Cocci to rods (and at later stage to spirochetes) Plaque) (Dental Microbiology Periodontal b. Subgingival irrigation of all periodontal pockets with • Nonmotile organisms to motile organisms 1 percent gel. • Facultative anaerobes to obligate anaerobes c. Tongue brushing with antiseptic. • From fermenting to proteolytic species. d. Mouthrinsing with an antiseptic to reduce bacteria in Principles of Intraoral Translocation, Transmission other intraoral niches. or Cross-infection of Bacteria Benefits of one-stage, full mouth disinfection over It has been substantiated that bacterial pathogens are conventional quadrant-wise approach has better results transmissible within family members. This transmission in clinical attachment, pocket depth reduction and micro- differs from contagious disease which refers to the biological shifts. likelihood of a microorganism to cause disease in an uninfected host once transmitted from an infected host. Periodontal Vaccines This is supported by the finding of transmission of Periodontal disease can be considered as one of the most cariogenic microorganisms from mother to child. prevalent of the polymicrobial, chronic inflammatory On the basis of physical and morphological criteria, diseases affecting humans. Despite intensive research oral cavity has been divided into five major ecosystems in its treatment modalities, none have been completely (also called niches): successful in regenerating the lost hard and soft tissues. 1. Intraoral, supragingival hard surfaces (teeth, implants, The advent of advanced molecular diagnostic techniques restorations and prosthesis). and a better understanding of the role of specific 2. Periodontal/peri-implant pocket (with its crevicular pathogens and the contributory role of the host immune fluid, the root cementum or implant surface and pocket response in the initiation and progression of periodontal epithelium). disease have led to the development of periodontal 3. Buccal epithelium, palatal epithelium and epithelium vaccines. However, successful vaccine development that of floor of the mouth. fully utilizes the current level of understanding has not 4. Dorsum of the tongue. yet occurred for human use. 5. Tonsils. Various forms of active and passive immunization It has been seen that intraoral transmission (also methods have been tried. Although, most of the studies called translocation or cross-infection) of bacteria occurs from one intraoral niche to another. It occurs through have yielded encouraging results none of these modalities intraoral fluid and transport media (saliva) or transmitted of immunization have been able to be incorporated as a via dental explorer during examination. sole or complete ‘vaccine’ against periodontal disease Certain examples have been cited to prove the for use in the human population. Thus, the current status transmission of periodontal and cariogenic pathogens of our understanding in the field of vaccines against within the oral cavity. Notable amongst these are: periodontal disease is incomplete. 66 Contd... . α and TNF- and 2 and interleukin- 1.

α PART III cytoskeletal disruption in epithelial cells cytoskeletal proteins, immunoglobulins Degrades sulfur containing substances Degrades sulfur containing Causes agglutination and lysis of erythrocytes • inhibition of host cells-fibroblasts Causes metabolic • loss of cellular volume regulation, Cell detachment, • of basement membrane; serum Degradation • Activation of MMPs • Known to inhibit superoxide production in PMNs. • Also induces release of MMPs. Causes stimulation of production nitric oxide, tumor necrosis factor- Destruction of immunoglobulins, complement factors Causes degradation of type I and IV collagen. Causes degradation of host collagenase inhibitors. Acts on degraded proteins. Causes agglutination and lysis of erythrocytes. Degrades fibrinogen rapidly rendering host in a non clotting condition. Potent stimulator of osteoblasts and monocytes to release IL-1, PGE

ains] Etiopathogenesis Major surface proteins (Msp) like Chymotrypsin proteases (CTLP) Others include: Outer sheath associated peptidases, trypsin like proteases Lipopolysaccharides Cystalysin Hemolysins Proteases [Gingip types- rgpA, rgpB, kgp. Prolyl tripeptidyl peptidase- membrane enzyme Periodontain Hemolysin Lipopolysaccharide Cultivated in broth media enriched with serum, trypticase, various fatty acids and growth factors. Addition of lecithin, ascorbic acid, and ammonium is required for optimum growth. Grows anaero- bically with dark pigmentation on blood agar. Key characteristics of specific periodontal pathogens T. denticola, T. amylovorum T. maltophilum, T. medium, T. T. pectinovorum, socranskii, T. vincentii. T. 6 forms have been identified based on cap- sule types. m in fimbriae μ m in length μ facilitate morphology. Helical shaped, 5-15 and 0.5 diameter. Irregular spirals. with peri-plasmic flagella. Coccal to short rod Possess that adhesion and coaggregation. Bacterialproperties Morphology Species identification Strains/ Culture and factors Virulence Actions Gram-negative anaerobic highly motile microorganisms Porphyromonas gingivalis Bacterialproperties Morphology Species identification Strains/ Culture and factors Virulence Actions Gram-negative, anaerobic, nonmotile. .

κβ 67 Contd... HPE 6 CHAPTER , and also nuclear factor α -glucosaminidase causes undermining of

β Periodontal Microbiology (Dental Plaque) (Dental Microbiology Periodontal The pore forming property of leukotoxin leads to cells. pathologic alterations in cell membrane of target Heat labile toxin causing eukaryotic cell distension, cycle arrest, actin filament rearrangement and apoptosis. blastogenesis, antibody production, cytokine Also effects and synthesis, neutrophil function, chemotaxis phagocytosis. Causes bone resorption, platelet aggregation and necrosis of tissues. production of interleukins and TNF. Stimulates Destruction of collagen. Cleavage of immunoglobulin- IgG. Degrades benzoyl-DL arginine naphthylamide. Also induces apoptotic cell death. Sialidases are known to degrade host glycoproteins and glycolipids. N-acetyl- basement membrane in periodontal pockets. Cell envelope lipoprotein stimulates gingival fibroblasts to produce IL-6 and TNF- - β Leukotoxins Immunosuppressive factors or cytolethal distending toxins LPS Collagenase Protease Trypsin like Trypsin proteases Sialidases N- acetyl- glucosaminidase. Cell envelope lipoprotein 14 atleast Difficult to grow. Difficult Requires days to grow. Requires N- acetylmuramic acid for growth. Grows in serum or blood agar in anaerobic environment. Translucent colonies with star shaped internal morphology. is c T. D-10 is most b '. in LJP 'b' e to and a Various strains Various have been described on the basis of DNA component. Of which forsythus most commonly found in supragingival and subgingival plaque samples. Serotypes based on heat stable surface antigen ' a common, 10%, elevated. ) μ shaped or filament shaped morphology. Highly pleomorphic microorganism. • spindle Exhibits Small, short (.4-1 straight or curved rod morphology. shaped colonies- Star called Actinobacillus Fimbriae- peritrichous. Tannerella forsythus Tannerella Aggregatibacter actinomycetemcomitans Actinobacillus actinomycetemcomitans Also known as Bacterialproperties Morphology Species identification Strains/ Culture and factors Virulence Actions Gram-negative Capnophilic Nonmotile Saccharolyticus in Occur singly, clumps or pairs Bacteroides forsythus Also known as Bacterialproperties Morphology Species identification Strains/ Culture and factors Virulence Actions Gram-negative, anaerobic micro organisms. Contd... 68 sequestering , IL-6, IL-8.

β , IL-1

α PART III proteins. of RBCs Lysis Release of IL-1, IL-6, IL-8 Inhibits complement by degradation of C3 which is common to all pathways. Degradation of hemoglobin. Degradation of immunoglobulins, heme Induces apoptotic cell death. and oxygen Also causes release of cytokines, elastase radicals from macrophages.

Induces release of cytokines- TNF- Etiopathogenesis Toxic metabolites Cell wall Hydrolases Hemolysin LPS A Interpain Cysteine protease Grown on agar enriched with horse or sheep blood. Produces black pigmented colonies on blood agar. Produces dark colonies on blood agar containing trypticase, peptone and serum. VPI 8944 like strains are related to gingivitis. VPI 4197 like strains (which include 25611) ATCC are related to periodontitis 2 morphotypes have been described- rough and smooth. F. fusiforme F. vincentii F. periodonticum F. Short rods with rounded ends. Possess fimbriae. Slender spindle shaped with ends. tapered show Often intracellular granules. Oval to rod shaped morphology. , Gram-positive, anaerobic bacteria. Asaccharolyticus microaerophilic. Fusobacterium nucleatum Bacterialproperties Morphology Species Strains/ identification Culture and factors Virulence Actions Peptostreptococcus micros Bacterialproperties Morphology Species Strains/ identification Culture and factors Virulence Actions Prevotella intermedia Bacterialproperties Morphology Species Strains/ identification Culture and factors Virulence Actions Gram- negative, anaerobic, nonmotile Gram- negative, anaerobic TNF–Tumor necrosis factor, LPS–Lipopolysaccharide, IL–Interleukins, MMP–Matrix Metalloproteinases necrosis factor, TNF–Tumor Contd... 69

REVIEW QUESTIONS 2. Slots Jorgen, Taubman A Martin. Contemporary oral micro- biology and immunology. 1. Define plaque and describe the steps in formation of 3. Newman, Nissengaard. Oral microbiology and immunology, 2nd plaque. edn, WB Saunders and Company. 2. What are the types and composition of dental plaque? 4. Max A, Listgarten. The structure of dental plaque. Periodontol HPE 6 CHAPTER 3. What is specific and non-specific plaque hypothesis? 2000;5:1994. 5. Sigmund S, Socransky, Haffajee Anne D. Dental biofilms: 4. Describe the role of plaque in periodontal disease. difficult therapeutic targets. Periodontol 2000;28:2002. 5. What is the clinical significance of plaque? 6. Sigmund, Socransky, Haffajee Anne D. Evidence of bacterial 6. What are differences between supra and subgingival etiology, a historical perspective. Periodontol 2000;5:1994. plaque? 7. Moore WEC, Moore Lillian VH. The bacteria of periodontal diseases. Periodontol 2000;5:1994. BIBLIOGRAPHY 8. Quirynen M, Bollen CM, Vandekerckhove BN, et al. Full mouth

vs partial mouth disinfection in the treatment of periodontal Plaque) (Dental Microbiology Periodontal 1. Lindhe Jan. Clinical Periodontology and Implant Dentistry. 4th infections. A short term clinical and microbiologic observation. edn 2003, Blackwell Munksgaard Publication. J Dent Res 74:1459;1995. 7 ChapterChapter

Calculus and other Etiological Factors

 CALCULUS • Differences between Supra- and • Definition Subgingival Calculus • Types  OTHER CONTRIBUTING ETIOLOGICAL • Structure FACTORS INCLUDING FOOD IMPACTION • Composition

CALCULUS Subgingival Calculus As the name implies, it is that calcified deposits that is Definition formed on the root surfaces below the free marginal gingiva. Dental calculus is an adherent, calcified or calcifying mass It is believed to be formed from the gingival exudate and that forms on the surfaces of teeth and dental appliances. It hence called serumal calculus (Figs 7.1 and 7.2). is covered on its external surface by vital, tightly adherent, nonmineralized plaque. Structure The deposits of supragingival calculus are usually whitish- Types yellow in color and can get stained by tobacco or food Depending upon the position of calculus in relation to the pigments, consistency is hard and clay-like. Since they marginal gingiva it is classified as: derive the mineral salts from salivary secretions, they are 1. Supragingival calculus most abundant on the lingual surfaces of lower anterior teeth, 2. Subgingival calculus opposite Wharton’s duct and Bartholin’s duct and buccal aspects of maxillary molars opposite the Stenson’s duct Supragingival Calculus (Fig. 7.3). It is the tightly adherent calcified deposit that forms on the Subgingival calculus is usually dark-brown or greenish- clinical crowns of the teeth above the free gingival margin. black in color and the deposits are firmly attached to the Hence, it is clinically visible. It is also called as salivary tooth surface. Since they are hard and firm, it cannot be calculus because it forms from the saliva. removed easily. Unlike supragingival calculus, subgingival CHAPTER 7 Calculus and other Etiological Factors 71 in the interproximal areas Radiograph illustrating subgingival calculus Table 7.1: Inorganic components Table

Fig. 7.4: Trace amounts of zinc, strontium, bromine, copper, amounts Trace ComponentInorganicCalciumPhosphorusCarbonateSodiumMagnesiumFluorideCrystal forms Dry weight (in percent) HydroxyapatiteMagnesium whitlockiteOctacalcium phosphateBrushite 70-90 16-18 27-29 2-3 0.6-0.8 1.5-2.5 0.003-0.04 21 12 58 9 Composition components and organic It consists of inorganic 7.1 and 7.2). (Tables At least, two- seen. manganese, gold and aluminium are also component is crystalline in structure. thirds of inorganic Magnesium The main crystal forms are: Hydroxyapatite, Brushite. whitlockite, Octacalcium phosphate and calculus can be found on any root surface with a periodontal calculus can be found on any root surface forms, it can appear in different pocket. Morphologically, formations crusty, most commonly ring-like or ledge-like it can be seen as spiny or nodular deposits. Less frequently and fern-like formations (Fig. 7.4). finger-like of lower anteriors Subgingival deposits on the root surface on Subgingival deposits of extracted lower anterior tooth

Radiograph illustrating subgingival deposits in lower anterior and posterior teeth Supragingival calculus on the lingual surfaces

Fig. 7.2: Fig. 7.1: Fig. 7.3: Etiopathogenesis PART III 72 calculocementum. appear similarinmorphologyandthushasbeentermedas Closeadaptationofcalculusundersurfacedepressions 4. Penetrationofcalculusbacteriaintocementum. 3. Mechanicalinterlockingintosurfaceirregularitiessuch 2. Attachmentbymeansofanorganic pellicle. 1. been reported. Four typesofattachmentcalculustotoothsurfacehave Attachment totheTooth Surface See Table7.3. Subgingival Calculus Differences betweenSupragingivaland agnmarginsofthegingiva Subgingival Color— margin Location— Supragingival 0.2 5.9-8.2 Lipids Proteins rhamnose, mannose) 1.9-9.1 (consists ofglucose,galactose, microorganisms. Carbohydrate cells, leukocytesandvarious complexes, desquamatedepithelial Mixture ofprotein,polysaccharide Component oimcneti esrSodiumcontentincreases Theyare absent Sodium contentislesser exudate Salivary proteinsarepresent octacalciumphosphate and less magnesiumwhitlockite octacalciumphosphate and Composition— salivary secretions Source— Calculus whenembeddeddeeplyincementummay surface. to thegentlyslopingmoundsofunalteredcementum as resorptionlacunaeandcaries. Table 7.3:Differencesbetweensupra-and white, yellow in color Brown or greenish-black or Brown white, yellowincolor eie rmFormed fromgingival derived from bv h igvlDepositspresentbelowthe gingival the above

PART I Table 7.2:Organiccomponents more brushite subgingival calculus Conversely lessbrushiteand with thedepthofpocket more magnesiumwhitlockite Dry weight(inpercent) Theories ofCalculusFormation referred toasreversalphenomenon. food andfromthelips,cheekstongue. This declineis a declineinitsformation,duetomechanicalwearfrom levels inabout10weeksand6months,afterwhichthereis increase insizeandcoalescetoformasolidmassofcalculus. of theplaque. These fociofmineralizationgradually days. Calcificationstartsinseparatefociontheinnersurface mineralized and60to90percentgetsin12 plaque formation.Intwodayscanbe50percent mineral salts,whichcanstartbetween1stand14thdayof mineralization. Calculusisformedbytheprecipitationof Calculus isnothingbut,dentalplaquethathasundergone Formation ofCalculus .Anotherconceptthathasbeenmost widelyheldis 2. Precipitationofmineralscanoccurfromalocalrisein 1. It canbeexplainedmainlyundertwocategories: Calculus formationcontinuesuntilitreachesmaximum calcification. These focienlarge andcoalescetoform According tothis,seedingagents inducesmallfociof “Epitactic Concept”(heterogenous nucleation). c. b. a. this isexplainedin, the degreeofsaturationcalciumandphosphateions, concentration offreephosphateions. phosphates insaliva,thusincreasingthe calcium phosphatebyhydrolyzingorganic desquamated epithelialcells,orbacteriaprecipitate Phosphatase calcium andphosphoroussalts. colloids settleandresultintheprecipitationof solution. When salivastagnatesintheoral cavity, phosphate ionsthusproducingasupersaturated Colloidal proteins insaliva phosphate saltscanoccurare: could leadtoriseinpH. loss ofcarbondioxideandproductionammonia a localriseinthepHofsaliva.Factorssuchas precipitation ofcalciumphosphatesaltsresultsfrom Booster mechanism: Other waysbywhichtheprecipitationofcalcium liberatedfromdentalplaque, According tothistheory, bindtocalciumand CHAPTER 7 Calculus and other Etiological Factors 73 Over- Subgingival restorations can is defined as the dimension of the soft is defined as the dimension to lower anterior teeth Margins of restoration in relation

Fig. 7.5: plaque. associated one that favors the growth of the disease of the health-associated at the expense organisms, organisms. retentive that subgingival restorations are plaque instruments, areas that are inaccessible to scaling and deeper hence greater chance of severe gingivitis pockets (Fig. 7.5). i. the accumulation of Providing ideal locations for ii. of the gingiva to Changing the ecological balance iii. et al (1978) Waerhaug It was also demonstrated by Biologic width Margins of restorations: Margins contribute to periodontal diseases by, contoured or improperly-contoured restorations tend to contoured or improperly-contoured restorations the self- accumulate plaque and possibly prevent cleansing mechanisms of the adjacent cheek, lips and Contour of restorations/artificial crowns: Contour of restorations/artificial a. of restorations Margins b. restorations overhanging dental Contours and c. Occlusion d. Dental materials e. partial dentures Design of removable f. Restorative procedures themselves. tissue, which is attached to the portion of the tooth coronal to to the portion of the tooth coronal tissue, which is attached commonly The biologic width is bone. the crest of the alveolar which represents the sum of epithelial stated to be 2.04 mm, measurements. Hence, encroachment and connective tissue width frequently leads to gingival of the biologic and bone loss. inflammation, clinical loss of attachment a. b. This theory considers the possibility This theory considers calculus. Hence, more appropriately called as appropriately called Hence, more calculus. calculus seeding agents in nucleation. The heterogenous be, agents could known, but suspected is not clearly of plaque, carbohydrate protein intercellular matrix bacteria. complexes and plaque Inhibition theory: of calcification occurring only at specific sites because, of calcification occurring mechanism at non-calcifying there exists an inhibiting inhibitor is Wherever calcification occurs, the sites. One such inhibiting agents either altered or removed. which prevents the initial could be pyrophosphate by possibly ‘poisoning’ the nucleus from growing, growth centers of the crystal. Hence, there is no doubt that, the mineralized deposits Hence, there is no doubt that, the mineralized supporting structures. hygiene methods. OTHER CONTRIBUTING ETIOLOGICAL INCLUDING FOOD IMPACTION FACTORS 3. Six characteristics of restorations are important from periodontal point of view. Faulty Restorations Faults in the dental restorations and prosthesis referred to as iatrogenic factors are common causes of gingival inflammation and periodontal destruction. Iatrogenic Factors Before 1960s the belief was that calculus was the principle Before 1960s the belief was that calculus current the However, etiologic factor in periodontal diseases. in the margin view is that the initial damage to the gingival of effects periodontal disease is due to the pathogenic get could the effect in plaque. However, microorganisms because it more pronounced by calculus accumulation microorganisms. further provides retention of more plaque can— a. Bring the bacterial deposits more closely to the b. mechanisms. Interfere with the local self-cleansing defense c. And also enable the patients to perform proper oral Pathogenic Potential of Calculus Diseases in Periodontal Etiopathogenesis PART III 74 d. c. interferes withthemetabolism andgrowthofbacteria, attachment ofthebacteria to thepellicleanditalso leaking fromtheglassionomer cementpreventsthe from periodontalpointofview. Fluorideconstantly seems toretainlessplaqueandthusaremoreacceptable to theclinician,glassionomerrestorationsandporcelain Compared toallrestorativematerialsthatareavailable accumulation andcontributestoperiodontaldiseases. It istherough,unpolishedsurfacesthatfavorplaque not bythemselvesinjurioustotheperiodontaltissues. Dental materials: Some oftheexamplesare: injury iscalled“primarytraumafromtheocclusion”. supporting normalperiodontaltissues. This typeoftissue occlusal disharmoniesthatmaybeinjurioustothe Occlusion: (Fig. 7.6). increase thespecificperiodontalpathogensinplaque overhangs notonlyincreaseplaquemassbutalso resembling thefloraseeninchronicperiodontitis.Hence, changes intheassociatedmicrofloratothatofone placement ofthesubgingivaloverhangsresultin posterior teethwithoverhangingrestorations. The demonstrated radiographicbonelossadjacentto periodontal attachmentloss.Manyauthorshave to beacontributingfactorgingivitisandpossible in theseareas. “fluted orbarreledout”toaccommodateoralhygiene than theCEJandthatfurcationareas,shouldbe contours shouldbe‘flat’,notfat,usually<0.5mmwider Kaldahl (1981)opinedthatbuccalandlingualcrown of periodontalprostheticinteractions,Beckerand necessary formaintaininggingivalhealth.Inareview tongue. Propercontoursoftheartificialcrownare i.Thedriftingmovementorextrusion oftheteeth iii. v Theorthodonticmovementofteethinto iv. i Insertionofaprosthesis,replacementthatcreates ii. .Insertionofa“highfilling”. i. Overhanging dentalrestorationshasbeenconsidered functionally unacceptablepositions. into spacescreatedbyunreplacedmissingteethor, excessive forcesonabutmentorantagonisticteeth. PART I Poorly-constructed restorationwillcause Ingeneral,restorativematerialsare f. e. .Creatingexcessiveand/orunfavorable forcesonthe c. Directlyinjuringthegingivaasaresultofoverextended b. Favoringplaqueretention andalsomodifyingthe a. Orthodontic therapymayaffect theperiodontiumby: Orthodontic Therapy Periodontal Problems Associated with degrees ofgingivalinflammation. manner astolaceratethegingiva,resultsinvarying clamps, copperbands,matrixbandsanddisksinsucha destruction ofperiodontium. The useoftherubberdam Restorative procedures themselves acceptable thantheremovableone. periodontal pointofview, fixedprosthesisismore development ofmostpathogenicbacteria.Hence,from but alsoqualitativechangesbypromotingthe dentures notonlyinducesquantitativechangesinplaque, accumulation. The presenceof removablepartial formation. This isduetotheincreasedplaque within gingivalinflammationandperiodontalpocket there isanincreaseinthemobilityofabutmentteeth have shownthataftertheinsertionofpartialdentures, Design ofremovable partialdentures: plaque formationandpermitsitsrapidremovaltoo. whereas highly-polishedsurfacesofporcelaininhibits supporting toothstructures causesnecrosisofthe gingiva fromtoothcausing gingival recession. bands whichmayalsoleadtoforcefuldetachmentof gingival ecosystem. Fig. 7.6:

Radiographic illustrationofoverhanging amalgam restoration can alsocause Severalstudies CHAPTER 7 Calculus and other Etiological Factors 75 Sequelae of unreplaced

missing first molar Figs 7.8A and B: in the involved area. in the involved periodontal ligament, sensitivity to percussion. periodontal ligament, alveolar bone. Destruction of the in the vertical dimension. v. formation. Periodontal abscess ii.in the jaws. radiates deep pain that Vague iv. Gingival recession. vi. involvement of degrees of inflammatory Varying iii. taste and a foul with bleeding Gingival inflammation vii. viii. caries. Root Unreplaced Missing Teeth Unreplaced Missing a series of changes Failure to replace extracted teeth initiates The diseases. that produce various degrees of periodontal failure to replace missing pattern of changes that may follow, In extreme cases, it first molars is characteristic (Fig. 7.8). consists of the following: a. molars tilt, resulting in a decrease The second and third This is one of the most This is one of the In addition to food impaction It can lead to food impaction with orthodontic therapy Periodontal changes associated Periodontal Fig. 7.7: between the teeth. periodontal ligament and adjacent alveolar bone, periodontal ligament and adjacent of apical root excessive forces also increase the risk resorption (Fig. 7.7). According to Hirschfeld food impaction can occur in According to Hirschfeld food impaction Uneven occlusal wear: the proximal areas because deflection of food away from does not occur. contact: Loss of proximal It may be due to, common cause for food impaction. periodontal disease, non-replaced missing teeth, proximal caries and abnormal biting habits. Lateral food impaction: caused by occlusal forces, lateral pressure from the lips, This cheeks, tongue may force food interproximally. usually occurs when the gingival embrasure is enlarged by periodontitis or by recession. The following signs and symptoms may occur in the i. to dig the material from Feeling of pressure and urge the following conditions: a. b. c. Congenital morphologic abnormalities of teeth. d. Improperly-constructed restorations. e. Food Impaction into the periodontium It is the forceful wedging of the food forcibly wedge food by occlusal forces. Cusps that tend to cusps”. interproximally are known as “Plunger association with food impaction: Etiopathogenesis PART III 76 of periodontaldiseasesasfollows: Sorren hasclassifiedhabits of significanceintheetiology Habits f. e. d. c. b. a. 7.9). (Fig. on theetiologyofgingivitisandperiodontaldiseases Depending onitsnature,malocclusionexertsvariedeffect Malocclusion (Figs7.9and7.10AB) Diastemaiscreatedbytheseparation oftheanterior f. Theanteriorteethextrudebecausetheincisalopposition e. Themaxillaryincisorsarepushedlabiallyandlaterally. d. Theanterioroverbiteisincreased. The mandibular c. Thepremolarsmovedistallyandthemandibularincisors b. than 25yearsinthoseyounger25. molars andappearstooccurmoreofteninindividualsolder results inthecreationofverticaldefectsdistaltosecond studies havereportedthattheextractionofthirdmolarsoften periodontal atrophy. Open bite: Deep bite: Occlusal disharmony: Facially-displaced teeth: of proximalcontactcanoccur. Spacing betweenteeth: difficult. Irregular alignmentofteeth: Loss ofproximalcontactrelationshipsleadsto, teeth. has largely disappeared. traumatize thegingiva. incisors strikethemaxillaryneargingivaor tilt ordriftlingually. Extraction ofimpactedthird molars: Followed bybonelossandtoothmobility.

Inflammationofpalatalmucosa. PART I Leadstoaccumulationofplaqueand Gingival inflammation Pocket formation Food impaction Results ininjurytoperiodontium. Same sequelaefollowingloss Canleadtogingivalrecession. ↓ ↓ ↓ Makesplaquecontrol Numerous clinical a. Fig. 7.9: Figs 7.10A andB: biting andocclusalneurosis. mandible, othersincludetongue thrusting,fingernail would leadtoextrafunctional positioningofthe Neurosis: photograph, (B)Postoperativephotograph

Gingival changesassociatedwithmalocclusion Suchaslipbitingandcheek bitingwhich

(A) Canineimpaction: Preoperative CHAPTER 7 Calculus and other Etiological Factors 77 Leukoplakia

with tongue thrusting Fig. 7.13: Anterior overbite, pathologic migration associated tooth structure. (Due to the nicotine and its major (Due to the nicotine tooth structure. on the root cotinine are deposited metabolite, surfaces). (Fig. 7.13). the gingiva may occur mucous glands with characterized by prominent the orifices and a diffuse inflammation of wrinkled, “cobble stone” erythema or by a (Fig 7.14). surface, may occur gingivitis.

1. of deposits and discoloration Brownish, tar-like 2. of Diffuse grayish discoloration and leukoplakia 3. “Smokers palate” (nicotinic stomatitis), 4.to acute necrotizing ulcerative Predisposition 5. Delayed postsurgical healing. 6. Marked increase in gingival crevicular fluid flow. Fig. 7.12: ↓ ↓ Such as holding of nails in the of nails in Such as holding Such as pipe or cigarette smoking, Such as pipe It is the persistent, forceful wedging It is the persistent, forceful Gingivitis is often associated with Gingivitis is often The following oral changes may occur Gingival changes associated with mouth breathing

Tongue thrusting causes excessive lateral pressure, Tongue from Numerous secondary sequelae may develop favors the Also interferes with food excursion and contributing thrusting is an important Tongue which may be traumatic to the periodontium. It also which may be traumatic to the periodontium. teeth. causes spreading and tilting of the anterior They include, change in the direction tongue thrusting. pressure against of the functional forces so that lateral the crowns is increased. margin. accumulation of the food debris at the gingival (Fig. 7.12). factor in the pathologic tooth migration Use of tobacco: Mouth breathing: gingival changes include The mouth breathing. shiny a diffuse and enlargement erythema, edema, exposed areas (Fig. 7.11). appearance on the thrusting: Tongue the teeth. Instead of the dorsum of the tongue against placed against the palate with the of the tongue being swallowing, the tip behind the maxillary teeth during teeth. tongue is thrust forward against the anterior in the smokers: Occupational habits: Occupational mouth, e.g. carpenters, cobblers, etc. carpenters, cobblers, mouth, e.g. habits: Miscellaneous tobacco chewing, incorrect methods of tooth brushing, tobacco chewing, incorrect thumb sucking. mouth breathing and I. II. III. Fig. 7.11: b. c. Etiopathogenesis PART III 78 IV. changes. Toothbrush trauma: .Tooth bristlesforcibly embeddedandretained 5. Diffuse erythemaanddenudationoftheattached 4. Painfulvesicleformationinthetraumatizedareas 3. Punctatelesionsareproducedbythepenetration 2. Sloughingoftheepithelialsurfaceoccursalong 1. Acute changesare: .Oralpolymorphonuclearcellsfromsmokers 8. .Moreseveregingivitisandperiodontitishave 7. gingival abscess. in thegingivaareacommon causeoftheacute brush. commonly occurwhenthepatientusesanew sequelae oftheoverzealousbrushing. gingiva throughoutthemouthmaybestriking is alsoseen. of thegingivabytoothbrushbristles. tissue toformapainfulgingivalbruise. with denudationoftheunderlyingconnective show reducedabilitytophagocytoseparticles. chewing oftobacco. and alveolarbonehasbeenattributedtothe toxica been reportedinsmokers. The acutegingivalchangesnotedcan Special typeofgingivitis,termed PART I Fig. 7.14: characterizedbydestructionofthegingiva

Smoker’s palateSmoker’s Acute orchronicgingival gingivitis aim ofthisapplianceistoprotect thetoothsurfaceandto the mosteffective meansoftreatingBruxism.The main contraindicated. gingival inflammation. has beenshownbetweenbruxismandperiodontitis or movement) sleepmaybethemostdamaging.Noassociation shown thatbruxismoccurringduringREM(rapideye bruxism bythepresenceoffacetpatterns.Sleepstudieshave bruxists. Bruxism/Nonstress bruxistsanddiurnalbruxism/stress restorations, toothwearoruncosmeticmusclehypertrophy. pressure. the individualisnotchewingorswallowing. bruxism andclenching. predisposing todentalcaries. leading toxerostomiaandchangesintheoralflora Radiation alsoincludesatrophyofthesalivaryglands suppuration. The bonealsoundergoes degeneration. including gingiva,whichleadstoulcerations,infectionsand develop erythemaanddesquamationoftheoralmucosa adjacent regionswhoaretreatedwithradiationsinitially to alleviatetoothacheandinjudicioususeofescharoticdrugs. dentifrices ordenturematerials,applicationofaspirintablet ulceration. The substancesinclude,strongmouthwashes, from simpleerythematopainfulvesicleformationand be causedbychemicalirritation. The gingivalchangesrange Maxillary stabilizationappliance Treatment ofbruxism: Clinical features ofbruxism: Two typesofbruxismhavebeenreported—Nocturnal Bruxism mayleadtofractureoftheteethordental Clenching: Bruxism: Occlusal neurosis orparafunctionalhabits: Radiation: Chemical irritation: .Oftenthegingival margin isenlarged andappears 2. Gingivalrecession withdenudationofroot 1. Chronic traumaresults toothbrush in: conformity withthestrokesoftoothbrush. to be“piledup”,asifitweremoldedin surface It istheclenching/grindingofteethwhen Itistheclosureofjawsundervertical Patients withcanceroftheoralcavityand Acute gingivalinflammationmay Clinicallyyoucandiagnose Occlusal adjustmentis is advised,which They are CHAPTER 7 Calculus and other Etiological Factors 79 They occur on the external surface They occur within the tooth substance They develop or originate from within They develop or originate from sources KNOW MORE ... KNOW MORE Discoloration of teeth can occur in three different ways: different Discoloration of teeth can occur in three restorative material. Extrinsic stains: of the tooth and may be removed by procedures like tooth-brushing, scaling and/or polishing. Intrinsic stains: and cannot be removed by scaling and polishing. Exogenous: may be extrinsic outside the tooth. Exogenous stains and stay on the outer surface of tooth or intrinsic and become incorporated within the tooth. Endogenous: the tooth. Endogenous stains are always intrinsic and usually are discolorations of dentin reflected through enamel. food into the periodontium. food into the chewing or swallowing. Clenching is the individual is not under vertical pressure. the closure of the jaws Other Contributing Etiological Factors Stains on tooth surface are called stains. Pigmented deposits • surface. adhering directly to tooth Stains • within the calculus and soft deposits. contained Stains • incorporated within the tooth structure or Stains Classification of Stains Based on location a. b. Based on source a. b. Calculus formation varies from person to The rate of calculus calculus may form faster than others. person. For some, as heavy, Accordingly they have been classified factors Various moderate, mild and non-calculus formers. rate of calculus formation are—oral hygiene the affecting for professional care, diet, age, accessibility habits, medications and frequency of professional scaling, systemic diseases. 11. of the forceful wedging is defined as the Food impaction 12. when grinding of the teeth is the clenching or Bruxism Other Contributing Etiological Factors including Other Contributing Etiological Factors Food Impaction Calculus directly injuring the gingiva due to over extension of bands, favoring the plaque retention and changing gingival ecosystem and creating unfavorable forces on the supporting tooth structures. referred to as iatrogenic factors. restorations are important: a. Margins of restorations. b. restorations. dental Contours and overhanging c. Occlusion. d. Materials. e. dentures. partial Design of removable f. themselves. Restorative procedures that forms on the surface of the teeth and dentalthat forms on the surface of the teeth appliances. calculus is seen. has been reported. mineral salts. a. mechanism. Booster b. or heterogenous nucleation Epitactic c.theory Inhibition that shows calculus and periodontal disease, it is plaque disease. a greater correlation with periodontal 9. 6 characteristics of From the periodontal point of view, 8. restorations and prosthesis are Faults in the dental 1. is an adherent, calcified or calcifying mass calculus Dental 2.calculus, supragingival and subgingival types of Two 3. It is made up of organic and inorganic constituents. 4. of calculus to the tooth surface Four types of attachments 5. of Calculus formation takes place by the precipitation 6.in calculus formation are: Theories that are explained 7. between although a positive correlation exists Finally, 10. the periodontium by, Orthodontic therapy may affect dissipate forces built up in the musculoskeletal system the musculoskeletal forces built up in dissipate to treat nocturnal This is more ideal bruxism. through the habits. It daytime clenching than for correcting bruxism reduction in the masseter and results in an immediate be The appliance should activity levels. temporalis muscle 4 weeks and thereafter over longer readjusted in 2 to should be observed in the follow-up intervals bruxofacets should be burnished with a smooth, visits and the surface rubber wheel. pumice impregnated Etiopathogenesis PART III 80 3. 2. 1. Extrinsic Stains 4. actinomyces species,prevotellamelaninogenicus and individualswithexcellentoralhygiene. removal. Itisseenmorecommoninwomen,children and asdiffuse patchesonproximalsurfaces. and lingualsurfacesofteethalongthegingivalmargin Black stain: pre-existent acquiredcoatings. consumed, butdependstoaconsiderabledegreeon is notnecessarilyproportionaltoamountoftobacco dentin bytobaccoby-products. The degreeofstaining and frompenetrationofpits andfissures,enamel surfaces ofteeth. tooth substance. Itiscommonlyseenonthelingual black depositaccompanied bybrowndiscolorationof Tobacco stain: anterior teeth. maxillary molarsandlingualsurfaceofmandibular dentifrice withinadequatecleansingaction. individuals whodonotbrushadequatelyoruse usually bacteriafree,pigmentedpellicle.Itisseenin Brown stain: more frequentinboys(65%) thangirls(63%). seen ongingivalhalfofmaxillary anteriorteeth.Itis stained remnants ofenamelcuticle.Itiscommonly commonly seeninchildren.Itisconsideredtobe Green stain: Fig. 7.15: It iscausedbychromogenicbacterianamely It isfirmlyattached andtendstorecurafter Staining resultfromcoaltar combustionproducts The browncolorisduetopresenceoftannin. It iscommonlyseenonthebuccalsurfaceof PART I

Tobacco stainsonthelingualsurface It occursasathinblacklineonthefacial of theloweranteriorteeth It isseenasthin,translucent,acquired, Greenorgreenishyellowstain is It isseenastenaciousdarkbrownor . Erythroblastosis fetalis. • Dental fluorosis • Enamel hypoplasia • Developmental anomaliesnamelyamelogenesis • Tetracycline administrationduringvariousstagesof • Example: Endogenous sources Drugs 2. Restorativematerials 1. Exogenous sources Stains thatoccurwithinthetoothcanbecausedby: Intrinsic Stains 7. 6. 5. imperfecta, dentinogenesisimperfecta tooth development Ammonical silvernitrateproducesdarkbrownto – Stannous fluorideproducesbrownstain – Copperamalgamproducesbluish-greencolor. – Silveramalgam imparts grayishhuetothetooth – Precipitation ofanionicdietarychromogens. – Denaturationofproteinsresultingintheformation – Catalysis ofbrowningreactioncarbohydrates – Degradationofchlorhexidineresultinginthe – staining: Following mechanismshavebeensuggestedtocause not dependonconcentrationofchlorhexidinerinse. chlorhexidine mouthrinse.Intensityofstaining does tongue hasbeennotedfollowingtheuseof Chlorhexidine stains: black stains. stain; nickelcausesgreenstain andsilvercauses causes blackstain; mercurycausesgreenishblack stain; irondustcausesbrownstain; manganese workers duetoinhalationofmetal containing dust. products intoacquiredcoatings.Itisseeninindustrial incorporation ofmetals andmetallic salts andtheir Metallic stains: bacteria: surfaces ofanteriorteeth.Itiscausedbychromogenic Orange stain: as penicillinandaspergillus. black stain. of sulphides and aminoacidsbychlorhexidine formation ofparachloraniline Commonly seenarecopperstains seenasgreen It iscausedbyfluorescentbacteriaandfungisuch Nonvital tooth Serratia marcescens Itisseenonbothfacialandlingual Metallic stains arecausedby Brown colorstaining ofteethand and Flavobacterium . CHAPTER 7 Calculus and other Etiological Factors 81 BIBLIOGRAPHY Publication 1990. Publication edn 1988. Publication Data 1995. Library Cataloguing in diseases. Periodontol 2000;2:1993. the etiology and periodontal and bacterial plaque characteristics, veneers on gingival health 1994;21:638-40. Journal of Clinical Periodontol WB Saunders Co, Ninth Edition 2002. Periodontology. interaction. Periodontology 2000;27:2001. America 1985;29:266-78. Clinics of North Company Publications 1990. 1.Mosby Company Periodontics. CV Genco. Contemporary 2. 6th Stern, Listgarten. Periodontics. Mosby Publications, Grant, 3. Outline of Periodontics. 3rd edn. British BM Eley. JD Manson, 4. local factors in S, Kornman, Harold Loe. The role of Kenneth 5. of porcelain laminate Pavis. The effect Walsh, Kourkenta, 6. Carranza. Clinical A Fermin Takei, Newman, Henry 7. Robert G Keim. Esthetics in clinical orthodontic periodontic 8. Robert I Sachs: Restorative dentistry and periodontium. Dental 9. Robert J Genco. Contemporary Periodontics. CV Mosby REVIEW QUESTIONS REVIEW periodontium? of formation of dental calculus. of formation of dental calculus. 2. What are the causes for the food impaction? 3. missing teeth? What is the sequelae following unreplaced 4. of smoking on periodontium? What are the effects 5. What are parafunctional habits? 1. What are the effects of overhanging restorations on Other Contributing Etiological Factors Other Contributing Impaction including Food 2. of dental calculus? What is the composition 3. supragingival and subgingival between Differences Calculus 1. the types and theories Define dental calculus. Describe 8 ChapterChapter

Host Response: Basic Concepts

 ROLE OF SALIVA IN THE HOST DEFENCE  INFLAMMATORY CELL RESPONSE  GINGIVAL EPITHELIUM  IMMUNOLOGICAL MECHANISMS  GINGIVAL CREVICULAR FLUID  IMMUNOLOGY OF PERIODONTAL DISEASE  COMPLEMENT

INTRODUCTION The host responds to the attack of bacteria and its toxins Health is not a static condition. It is a dynamic state in which at various levels. the living and functioning organism or tissue remains in balance with a constantly changing environment. This ROLE OF SALIVA IN THE HOST DEFENCE constant process of readjustment to maintain a functional 1. A vehicle for swallowing bacteria. integrity is known as “Homeostasis”. It is a well known 2. Inhibition of attachment of bacteria. fact that bacteria constitute an important part of environment 3. Bactericidal action by the peroxidase system. and all the external surfaces in nature including living tissues 4. Bactericidal action by lysozyme, lactoferrin and other are covered by bacteria, the skin, the gut and oral mucosa factors. are of no exceptions. When different forms of life exist together there is competition for existence, hence various Salivary Peroxidase System mechanisms have evolved to help one form to protect it SCN– +HO → HOSCN from another called Host defence mechanisms. 2 2 (Thiocyanate (Generated (Peroxidase Hypothio- The tissues of the periodontium are exposed to various from salivary by salivary enzyme) cyanous environmental factors in the oral cavity. Over 300 species glands) glands, bacteria, acid, kills the neutrophils, etc.) bacteria) of bacteria have been isolated in the oral cavity. The periodontal tissues remain in a state of partnership Peroxidase is synthesized by salivary gland acini and (symbiosis) with most of the bacteria and only under certain secreted into the saliva, where it becomes bound to bacteria circumstances do we suffer from their attack because, host and thiocyanate is secreted into saliva by the ductal cells. defence system strikes a balance between the two. Hydrogen peroxide is constantly secreted in low 83

concentration by bacteria, neutrophils and other host cells COMPLEMENT (FIG. 8.1) and is used by peroxidase to oxidize the thiocyanate to The functions of complement are: hypothiocyanous acid, which kills bacteria. a. Chemotaxis cellular activation: Complement products Lactoferrin: It is secreted by serous salivary gland, which released in this reaction attracts phagocytes to the site binds iron, an important growth factor or requirement for 8 CHAPTER of infection, e.g. C3a and C5a. many microorganisms. This action is bacteriostatic rather b. Opsonization: Once they arrive at the site of infection than bactericidal. the complement components coat the bacterial surface Lysozyme: It is an antimicrobial enzyme in the saliva and allow the phagocytes to recognize the bacteria and secreted mainly by mucous salivary glands and it degrades thereby facilitating the bacterial phagocytosis, e.g. C3b. mucopeptides in the cell wall of gram-positive bacteria, c. Cytolysis: Damage to the plasma membranes of the cells weakening the wall and causing lysis.

can lead to lysis of the cell, e.g. C1-C9. Host Response: Basic Concepts Basic Response: Host The complement system comprises of nine major GINGIVAL EPITHELIUM complement proteins which circulate in an inactive form Gingival epithelium has three functions: and which, like the clotting system, are activated in an 1. Epithelial cells are tightly attached to each other. enzyme cascade. 2. Keratinization to resist trauma. C1-C9 causes cytolytic and cytotoxic damage to the cell. 3. Presence of permeability barriers. Classical Pathway GINGIVAL CREVICULAR FLUID The sequence is C1, C4, C2, C3, C5, C6, C7, C8, C9. Gingival crevicular fluid functions are: 1. Washing nonadherent bacteria and their products out of Alternative Pathway the crevice. It is activated by antibodies of immunoglobulins and also 2. Reducing the diffusion of plaque products into the tissues. by endotoxins. They can initiate the third component of the 3. It also carries a steady supply of inflammatory mediators, complement without starting from the beginning of the protease inhibitors and host defence agents such as cascade.

complement and antibody, into the crevice. The sequence is C3, C5, C6, C7, C8, C9.

Fig. 8.1: Complement activation 84

THE INFLAMMATORY CELL RESPONSE •CD11a/CD18 (or) It involves emigration of neutrophils, macrophages and Mac-1/CD11b/CD18 lymphocytes from the blood vessels into the tissues. •CD11c/CD18 Neutrophils and macrophages perform inflammatory functions whereas macrophages and lymphocytes perform These leukocyte B2-integrins act as the molecular immunological functions. mediators of binding to the endothelial cells and their binding affinity can be increased or decreased as the Neutrophils leukocyte traverses the postcapillary venule.

PART III Chemotaxis: It is the directed movement of a cell along They are the initial leukocytes seen in the gingiva. They a chemical gradient. The neutrophils are attracted by exit the circulation and migrate into the junctional chemical signals from multiple sources, e.g. chemotaxins epithelium and gingival crevice, where they provide the first which include compounds such as complement fragments cellular host mechanism to control periodontopathic (C5a). bacteria. LTB4: It is secreted by mast cells, neutrophils macrophages, and also bacterial products including LPS and Functions of Neutrophils factors released by damaged tissues. Emigration and chemotaxis: Leukocytes normally travel Chemotaxis requires phagocyte, which possess specific

Etiopathogenesis along the center of the lumen of the blood vessel, but in chemotaxin receptors, and the most well-studied chemotaxin inflamed tissues the blood flow is slowed by fluid exuda- receptor is the receptor for formylmethionyl peptides, known tion and they adhere more readily to endothelial cells, the as the FPR (Formylmethionyl Peptide Receptor). mechanism is called “rolling” and “margination”. When the neutrophils migrate across the endothelium it is called “dia- Stages in neutrophil chemotaxis (Fig. 8.2) pedesis” and “interendothelial transmigration”. Stage I: Soluble products diffuse forming a concentration Hence, there are two phases of leukocyte endothelium gradient. adherence. Stage II: Resting neutrophils detect chemotaxins using a. The selectin-dependent phase (primarily in rolling and surface receptors. margination). b. The integrin-dependent phase (primarily in diapedesis). The selectin-dependent phase: The various selectins are: 1. L-selectin—expressed on the surface of the leukocyte. 2. P-selectin—stored in the granules of endothelial cells (Weibel-Palade bodies). 3. E-selectin—expressed by endothelial cells. P-selectin and E-selectin: They both strengthen the binding between the leukocyte and the endothelial cell and increase the number of leukocyte “rolling”.

The integrin-dependent phase: (Leukocyte B2- integrins): The three leukocyte integrins are sequestered in the specific granules of leukocytes, • LFA-1—leukocyte function-associated antigen-1 Fig. 8.2: Stages in neutrophil chemotaxis 85

Stage III: Receptors move to front of neutrophils, which becomes polarized. Stage IV: Neutrophils crawl up to the concentration gradient. Stage V: When concentration is constant, directional migration ceases. 8 CHAPTER II Phagocytosis (Fig. 8.3) Once they arrive at the site of inflammation, the phagocytes have to recognize the infectious agent. This can be enhanced

if the organism has been coated by C3b. They may then attach to microorganism via their nonspecific cell surface receptors.

After attachment the phagocytes proceed to engulf the Host Response: Basic Concepts Basic Response: Host microorganism by extending pseudopodia around it. Once inside, lysozymes fuse with the phagosome/phagocytic vacuole to form a phagolysozyme and the infectious agent is killed by a battery of microbiocidal mechanisms. Fig. 8.3: Phagocytosis The main stages of bacterial killing by phagocytes: For efficient phagocytosis, the particle should be coated with one or more host serum proteins. This process is called internalized, lysozymes fuse with the phagosome to form a opsonization (meaning “to prepare for eating”). The two phagolysozyme. Various killing mechanisms are activated, principal types of serum proteins referred to as opsonins they are (Fig. 8.4): A. Nonoxygen-dependent killing mechanisms. are IgG and C3b. There are receptors of these two proteins on the phagocytes. Hence, the opsonization could be either B. Oxygen-dependent killing mechanisms. complement-dependent, antibody-dependent and the Oxidative mechanism: Stimulation of phagocytic cells combination of both. Once the organism has been leads to an increase in cellular consumption of molecular

Fig. 8.4: Neutrophil: Oxidative and nonoxidative mechanisms for controlling microbes 86

oxygen, a process termed as the respiratory burst. This is • Rapidly progressive periodontitis (RPP). associated with the generation of various oxygen metabolites, • Refractory periodontitis (RP). which are injurious to many species of microorganisms. The majority of the oxygen consumed by the phagocyte is Functions of Macrophages in the Gingiva, – converted directly to superoxide anion (O2 ) through the Crevice and Pocket action of a membrane—bound NADPH oxidase. Superoxide Macrophages develop from blood monocytes, which radicals inturn may undergo conversion to hydrogen emigrate into the tissues from the blood and are triggered peroxide (H2O2) either spontaneously or via superoxide to develop into mature macrophages by cytokines, other dismutase and contribute significantly to microbicidal PART III inflammatory mediators, bacterial products such as activity of the phagocytic cells. Additional oxidants, e.g. endotoxins. hypochlorous acid and toxic aldehydes are generated as a Functions of macrophages (Fig. 8.5) includes: consequence of the interaction between hydrogen peroxide 1. Phagocytose and kill bacteria. and azurophil enzyme (MPO). Hence, the oxygen-dependent 2. Remove damaged host tissue during inflammation. bactericidal activity is further divided into: 3. And also trap and present antigens to lymphocytes for • Myeloperoxidase—dependent induction of immune responses. • Myeloperoxidase—independent. Because these functions unite inflammation and Non-oxidative mechanisms: It appears to be based on

the various components of the cell. Neutrophils contain three immunity the macrophages play an important role in all Etiopathogenesis types of granules: bacterial infections. 1. Primary granules/azurophilic granules: Myeloperoxidase, Most of the above mentioned functions are carried out lysozyme, acid phosphatase, and acid hydrolases. through the secretion of inflammatory mediators, including 2. Secondary/specific granules: Lactoferrin, lysozyme, cytokines, prostaglandins, leukotrienes and complement azurocidin. components. Particularly important is the secretion of the 3. Tertiary granules: Alkaline phosphatase, collagenase, cytokines and although other cells such as fibroblasts, and gelatinase.

Neutrophil Disorders Associated with Periodontal Diseases

1. Diabetes mellitus 2. Papillon-Lefevre syndrome 3. Down’s syndrome 4. Chediak-Higashi syndrome 5. Drug-induced agranulocytosis 6. Cyclic neutropenia.

Periodontal Diseases Associated with Neutrophil Disorders • Acute necrotizing ulcerative gingivitis (ANUG). • Localized juvenile periodontitis (LJP). • Prepubertal periodontitis (PPP). Fig. 8.5: Functions of macrophage in periodontal tissues 87

endothelial cells and keratinocytes also secrete cytokines, Different types of T-cells include: macrophages secrete the greatest quantities. The most Helper inducer T-cells (TH-cells) or CD4: They aid in the significant cytokine in inflammation is interlenkin-1 cellular response of the B-cells to differentiate into plasma (IL-1), which is a key mediator both in inflammation and cells and produce antibodies.

immunity-induced by bacteria. Tumor necrosis factor (TNF) Suppressor-cytotoxic T-cells (TS-cells) or CD8: 8 CHAPTER is also produced by macrophages. Both TNF and IL-1 have Stimulates cytotoxic and microbicidal activity of the similar functions. immune cells. Subdivided into TH1 TH2 TH0. They increase inflammation by, releasing histamine from • TH cells release IL-2 and IFN (interferons) mast cells, attracting neutrophils and more macrophages • TS cells release interleukin: IL-4 and IL-5 into the tissues and by causing many other cells to release • In adult periodontitis TH cells increase and TS cells prostaglandins. decrease with increased gingival inflammation.

In summary, macrophages, like neutrophils are required Concepts Basic Response: Host for the effective host response, but can mediate a small amount The humoral response to plaque (Fig. 8.7): Plaque of bystander damage. The damage could be caused by direct bacteria and their soluble products such as enzymes and effect that is by secreting enzymes and toxins (similar to toxins carry out activation of the humoral response. neutrophils) and indirectly by secretion of cytokines. In excess Antigens, which pass into the tissues, are carried to the local amounts IL-1 and TNF can have several damaging effects lymph nodes, probably by macrophages, where they are such as stimulation of bone resorption and tissue fibrosis. presented to lymphocytes, which circulate continually Other cells such as mast cells, fibroblasts, endothelial cells, plasma cells and epithelial cells are also seen in gingival connective tissue during inflammatory response. Lymphocytes (Fig. 8.6): Three types of cells are included, 1. T-lymphocytes or T-cells: Derived from the thymus and play a role in cell-mediated immunity. 2. B-lymphocytes or B-cells: Derived from liver, spleen and bone marrow. They are precursors for plasma cells and play a role in humoral immunity. 3. Natural killer (NK) cells.

Fig. 8.6: Derivation and response of B and T-lymphocytes Fig. 8.7: Systemic humoral immune response 88

through the nodes and tissues. The lymphocytes, which recognize each individual antigen, are activated, undergo clonal expansion and differentiate into plasma cells, which secrete antibody under the control of helper and suppressor T-lymphocytes. Most of the lymphocytes and plasma cells remain in the lymph nodes and secrete antibodies into the bloodstream. The antibody predominantly is IgG, which can opsonize and activate the complement. Small amounts of

IgM is also seen which is more of an activator of the PART III complement and less of an effective opsonin. These antibodies pass into the gingival inflammatory exudates and then out into the gingival crevice in the crevicular fluid. Possible mechanisms of action of antibodies in periodontitis: I. Binding to bacteria, thus: a. Opsonizing for phagocytosis b. Activating neutrophil enzyme secretion c. Coating bacteria and inhibiting attachment

Etiopathogenesis d. Activating complement and thus enhancing opsonization e. Directly inhibiting bacterial metabolism. II. Binding to soluble factors, thus: a. Neutralizing toxins. Fig. 8.8: Local cellular immune response b. Inhibiting enzymes. The cell-mediated response in periodontal diseases: It is so called because it involves contact between cytotoxic T-cells and the target to be destroyed. These reactions are effective against persistent antigens, which are resistant to degradation, and the cells infected with viruses and tumor cells (Fig. 8.8).

IMMUNOLOGICAL MECHANISMS (FIG. 8.9) They are stimulus—specific and differentiate between individual pathogenic species and sometimes-individual strains. Microorganisms and their products are recognized as being different from the host because they contain structures, which are not found in the human body. These so called antigens (antibody-generating) are first recognized by the lymphocytes and each lymphocyte is capable of recognizing only one foreign antigen and when it comes in

contact with that antigen it is triggered to divide several Fig. 8.9: Antibody production by salivary and humoral times and therefore within few days there are many more immune systems and by polyclonal B cell activation 89 cells with the same specificity. This amplification process is known as clonal expansion. This will result in the production of larger pool of cells, which are differentiated to protect the host either by humoral or cell-mediated mechanisms. 8 CHAPTER Humoral responses are carried out by lymphocytes, which differentiate into plasma cells and secrete antibody directed against the original antigen. Cell-mediated responses, in contrast, do not require antibody, but depend on the clonal expansion to provide large number of lymphocytes, which destroy targets directly. This direct effect of an immune reaction against a foreign antigen results Concepts Basic Response: Host in significant tissue damage is referred to as hypersensitivity reaction.

Type I: Anaphylactic Reactions Two variations in the anaphylactic hypersensitivity may occur, depending on the route of the administration of antigen. If injected locally into the skin, the reaction is called cutaneous anaphylaxis. If the antigen is injected intravenously it is called Fig. 8.10: Immunologic mechanism of tissue damage systemic or generalized anaphylaxis. The basic mechanisms of both types are similar (Fig. 8.10). IgG or IgM class. In addition to inducing cell lysis, cytotoxic antibodies may cause tissue damage by increasing the Mechanisms of Anaphylactic Hypersensitivity synthesis and release of lysozymal enzymes by cells Anaphylaxis occurs when two Ig E antibodies that are fixed (PMNs). The tissue in the vicinity of these enzymes will to a mast cell or basophil react with the antigen through the then be damaged. Fab portion of the antibodies. This antibody-antigen reaction Cytotoxic reactions are seen in the autoimmune diseases causes the release of the pharmacologically-active where antibodies react with body’s own tissue components. substances from the sensitized-cells. For example, this occurs in pemphigus where antibodies These mediators released by the human mast cells react with cell membranes and pemphigoid antibodies react include: with the epithelial basement membrane. To date evidence a. Histamine—increased capillary permeability. suggests an important role for the cytotoxic reactions in the b. Alpha 2-macroglobulins—collagenase activation. gingivitis and periodontitis. c. SRS-A—smooth muscle contraction. d. Bradykinin—increased permeability same as SRS-A. Type III: Immune Complex or Arthus Reactions (Slow release substance of anaphylaxis). When high levels of antigen are present and persist without being eliminated antigen-antibody (IgG or IgM) complexes Type II: Cytotoxic Reactions precipitate in and around small blood vessels and with In cytotoxic type, antibodies react directly with antigens subsequent complement activation cause tissue damage at tightly bound to cells. A cytotoxic reaction involving these the site of the local reaction. Inflammation, hemorrhage and cells will result in hemolysis. Cytotoxic antibodies are of necrosis may occur. Tissue damage appears to be due to the 90

release of lysozymal enzymes from various cells such as Contd. neutrophils, mast cells, etc. This reaction is referred to as Disease Immune response

immune complex or Arthus reaction. • Presence of immune complexes in tissues Type IV: Cell-mediated or Delayed • Cell-mediated immunity to gingival Hypersensitivity bacteria Juvenile Periodontitis: Cellular immunity does not include circulating antibodies LJP • Polymorphonuclear leukocytes but is based on the interaction of the antigens with the chemotactic defect and depressed phagocytosis PART III surface of T-lymphocytes. • Elevated antibody levels to Actino- bacillus actinomycetemcomitans

IMMUNOLOGY OF PERIODONTAL DISEASE • Defect in GP110 receptors (FIG. 8.11) GJP • PMN chemotactic defect and depressed phagocytosis Immune responses may be both beneficial and detrimental. • Elevated antibody levels to P. Several components of the immune system are active in gingivalis periodontal disease. These host variables may influence Prepubertal • PMN and monocyte chemotactic bacterial colonization, bacterial invasion, tissue destruction, periodontitis defects healing and fibrosis (Tables 8.1 and 8.2). Rapidly-progressing • Suppressed or enhanced PMN,

periodontitis monocyte chemotaxis Etiopathogenesis • Elevated antibody levels to several Table 8.1: Influence of host responses on Gram-negative bacteria periodontal diseases Refractory • Reduced PMN chemotaxis • Bacterial colonization: Subgingivally, antibody, complement periodontitis in crevicular fluid inhibits adherence and co-aggregation of bacteria and potentially reduces their numbers by lysis. • Bacterial invasion: Antibody-complement-mediated lysis reduces bacterial counts. Neutrophil-mediated lysis also reduces bacterial counts. 1. Host defence is established at different levels. • Tissue destruction: Antibody-mediated hypersensitivity, cell- 2. Saliva acts as a vehicle for swallowing bacteria, inhibits mediated immune responses, activation of tissue factors the attachment of bacteria, and kills the bacteria by the such as collagenase. peroxidase system, lysozyme and lactoferrin. • Healing and fibrosis: Lymphocytes and macrophage 3. Functions of gingival epithelium are structural produced chemotactic factor for fibroblasts, fibroblast- arrangement of epithelial cells, prevents bacterial entry, activating factors. keratinization, resists trauma and also has a permeability barrier. 4. Complement functions are cellular activation, Table 8.2: Significant immune findings opsonization by C and cytolysis (C -C ). in periodontal diseases 3b 1 9 5. The complement activation can be classical pathway with Disease Immune response the sequence of C1, C4, C2, C3, C5, C6, C7, C8, C9, alternative pathway C3, C5, C6, C7, C8, C9. ANUG • PMN chemotactic defects 6. Various killing mechanisms of neutrophils are, non- • Elevated antibody titers to oxygen-dependent mechanisms and oxidative Prevotella intermedia and mechanisms. intermediate-sized spirochetes 7. Macrophages phagocytose and kill bacteria, removes Pregnancy gingivitis • No significant findings reported damaged host tissue during inflammation and also traps Adult periodontitis • Elevated antibody titers to the and presents the antigens to lymphocytes for induction Porphyromonas gingivalis and of immune responses. other pathogens 8. There are three types of lymphocytes, T-lymphocytes, B-lymphocytes and natural killer (NK) cells. Contd. 91

HPE 8 CHAPTER Host Response: Basic Concepts Basic Response: Host

Fig. 8.11: Host defence against local and systemic infections of periodontal origin 92

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Characteristics of inflammatory cells

Cells Features Functions Granulocytes a. Neutrophils • Polymorphonuclear leukocytes • Comprise 40-75% of total number of • Forms first line of defense PART III leukocytes • Diameter ranges from 10-15 μm • Chemotaxis/cell mobilization • It has multilobed nucleus and • Phagocytosis granules containing proteases, • Oxygen/non-oxygen dependent myeloperoxidase, lysozyme, killing of microorganisms. esterase, aryl sulfatase, acid and alkaline phosphatase.

b. Eosinophils • Comprise 1-6% of total number Involved in reactions to foreign of leukocytes proteins, antigen antibody • Measures about 10-12 μm reactions. in diameter

Etiopathogenesis • It has a bilobed nucleus • Consists of eosinophilic granules.

c. Basophils • Comprise 1% of total number Releases histamine and heparin of leukocytes. through mast cells and mediates • Diameter ranges from 10-15 μm inflammatory reactions. • It has bilobed nucleus • Consists coarse basophilic granules. Agranulocytes d. Lymphocytes • Comprise 20-45% of total number Involved in humoral immunity • B- lymphocytes of leukocytes. and cell-mediated immunity • T- lymphocytes • Lymphocytes in the peripheral blood measure about 9-12 μm in diameter. • It possesses a round or slightly indented nucleus with coarsely clumped chromatin network. • It has scanty basophilic cytoplasm. • Comprise 4-10% of total number of leukocytes

e. Monocytes • Largest mature leukocyte measuring Functions through macrophages, 12- 20 μm. same as that of neutrophils-comprise • It possesses a large central, oval, the second line of defense against notched or indented or horse-shoe microorganisms. shaped nucleus. • It has abundant pale blue cytoplasm.

Structure Immunoglobulins or Antibodies It is a “Y” shaped molecule, the tail end of the Y contains These are glycoproteins which represent the components the ends of the heavy chains, “Fc fragment” i.e. of adaptive immune system. These immunoglobulins (Ig) complement binding site. The remainder of the “Y” are produced by plasma cells in response to an antigen. contains light chains, “Fab” antibody binding site. 93

Functions of Immunoglobulins: IgG,A,M,D&E 2. Role of neutrophils in periodontal disease. 3. Describe the complement activation and functions of Types of immunoglobulin Functions antibodies. IgG Only maternal immunoglobulin

BIBLIOGRAPHY 8 CHAPTER Subclasses IgG1 Helps in phagocytosis by binding to IgG4 to microorganisms. Plays a role in 1. Erica Gemmell, Gregory J Seymour. Modulation of immune most of the immunological reactions response to periodontol bacteria. Current Opinion in Periodontol 1994;18-34. IgA Secreted in the body fluids. 2. Genco. Contemporary Periodontics. CV Mosby Company Subclasses IgA1, IgA2 Attaches to the mucosal surfaces Publication 1990. thus providing first line of defense against bacteria by preventing their 3. Manson JD, Meley B. Outline of Periodontics, British Library

penetration. Cataloguing in Publication data, 3rd edn, 1995. Concepts Basic Response: Host 4. Jeffrey L, Ebersole, Martin A Taubman. The protective nature IgM Provides primary immune of host responses in periodontal disease. Periodontol response (synthesized in the 2000; 5:1994. fetus) More effective than IgG in 5. Newman, Takei, Fermin A Carranza, Clinical Periodontology, opsonization and bactericidal 9th edn, WB Saunders Co. 2002. action. 6. Robert J Genco. Host response in periodontal disease: Current concepts. Jr of Periodontol 1992;63(4). IgD Unknown 7. Sigmund S. Socransky, Anne D Haffajee, Bacterial etiology of IgE Causes immediate hypersensitivity destructive periodontal disease: current concepts Jr. of reactions. periodontal April 1992 (Supply Copy), 63(4). 8. Thomas E Van Dyke, Jaywanth Vaikuntan. Neutrophil function REVIEW QUESTIONS and dysfunction in periodontal disease. Current Opinion in periodontol 1994;19-28. 1. What are the function of saliva and gingival crevicular 9. Williams, Francis J Hughey. Pathology of Periodontal Disease. fluids? Oxford Medical Publications 1992. 9 ChapterChapter

Trauma from Occlusion

 PHYSIOLOGICAL ADAPTIVE CAPACITY OF Effect of Insufficient Occlusal Force THE PERIODONTIUM TO OCCLUSAL FORCES Reversibility of Traumatic Lesion  TRAUMA FROM OCCLUSION Effect of Increased Forces on Pulp • Definition and Terminology  ROLE OF THE TRAUMA FROM OCCLUSION IN • Types THE PROGRESSION OF PERIODONTAL • Signs and Symptoms DISEASE • Histologic Changes  PATHOLOGIC TOOTH MIGRATION • Other Properties  OTHER CAUSES

PHYSIOLOGIC ADAPTIVE CAPACITY b. Direction: Changes in the direction causes reorientation OF THE PERIODONTIUM TO of the stresses and strains within the periodontium OCCLUSAL FORCES (lateral or horizontal forces, torque or rotational forces are more likely to injure the periodontium). One must appreciate the dynamics of the periodontium to c. Duration: Constant pressure on the bone is more accommodate the forces exerted on the crown, which is injurious than intermittent forces. called as adaptive capacity. This varies in different persons d. Frequency: The more frequent the application of an and in the same person at different times. This is mainly intermittent force, the more injurious to the periodontium. explained by four factors which mainly influence the effect of occlusal forces on the periodontium. TRAUMA FROM OCCLUSION (TFO) a. Magnitude (the amount): When it is increased the periodontium responds (a) with a thickening of the Definition and Terminology periodontal ligament, (b) an increase in the number and According to Orban and Glickman et al (1968): Trauma width of periodontal ligament fibers and (c) an increase from occlusion is defined as, when occlusal forces exceed in the density of the alveolar bone. the adaptive capacity of periodontal tissues, the tissue injury 95 results. This resultant injury is termed as trauma from In summary, occlusion. 1. The criterion that determines whether an occlusion is WHO in 1978 defined trauma from occlusion as “damage traumatic is whether it produces periodontal injury, not in the periodontium caused by, stress on the teeth produced how the teeth occlude. directly or indirectly by the teeth of the opposing jaw”. 2. Any occlusion that produces periodontal injury is 9 CHAPTER Other terms often used are, traumatizing occlusion, considered traumatic. occlusal trauma, occlusal overload, periodontal traumatism, 3. Malocclusion is not necessary to produce trauma. occlusal disharmony, functional imbalance and occlusal dystrophy. One must note that trauma from occlusion refers Signs and Symptoms to the tissue injury, not the occlusal force. An occlusion 1. Clinical and,

that produces such an injury is called as traumatic occlusion. 2. Radiographic changes Trauma from Occlusion from Trauma Types Clinical Signs and Symptoms i. Depending on the onset and duration. ii. Depending on the cause: a. In acute situations: Excessive tooth pain, tenderness on a. Due to the alterations in the occlusal forces. percussion, increased tooth mobility (hypermobility) is b. Reduced capacity of the periodontium. seen. In severe cases, periodontal abscess formation and iii. Depending on the onset and duration: cemental tears can be seen. Others such as presence of a. Acute trauma from occlusion (TFO). infrabony pockets, furcation involvement, attrition, b. Chronic trauma from occlusion (TFO). pathologic migration may also be present. Acute trauma from occlusion: Results from the abrupt b. Fremitus test is positive. changes in the occlusal forces, such as that produced by c. Radiographic changes biting on a hard object, in addition, could also be due to i. Increase in the width of the periodontal ligament iatrogenic factors (faulty restorations/prosthetic space often with thickening of the lamina dura along appliance). the lateral borders of the root, apical and bifurcation Chronic trauma from occlusion: As a result of the areas. gradual changes produced in the periodontium due to ii. “Vertical” rather than horizontal destruction of the the tooth wear, drifting movement, extrusion of the interdental septum. teeth combined with parafunctional habits such as iii. Radiolucency and condensation of the alveolar bruxism and clenching. bone. iv. Depending on the cause (Table 9.1): iv. Root resorption. Changes produced by primary trauma from occlusion are usually reversible, may be because, the supracrestal Histologic Changes gingival fibers are not affected and thus prevents the The response of tissues to increased occlusal forces is apical migration of junctional epithelium. explained under three stages.

Table 9.1: Types of TFO: Depending on the cause

Primary trauma from occlusion Secondary trauma from occlusion It is a tissue injury, which is elicited around a tooth with normal It is related to situations in which occlusal forces cause height of periodontium. For example: Insertion of high fillings, injury in a periodontium of reduced height. For example: insertion of the prosthetic replacement, orthodontic Periodontitis. movement in functionally-unacceptable positions. 96

• Stage 1: Injury called buttressing bone formation which is an important • Stage 2: Repair feature of reparative process associated with trauma from • Stage 3: Adaptive remodeling of the periodontium. occlusion (also occurs during inflammation or tumors). Buttressing bone formation can occur within the jaw, Stage 1: Injury called central buttressing and on the bone surface, called as When a tooth is exposed to excessive occlusal forces, the peripheral buttressing. It usually occurs on the facial and periodontal tissues are unable to withstand and hence they lingual plates of the alveolar bone, if it produces a shelf- distribute, while maintaining the stability of the tooth. This like thickening of alveolar bone it is referred as lipping.

PART III may lead to certain well-defined reactions in the periodontal ligament and alveolar bone, eventually resulting in Stage 3: Adaptive Remodeling of the Periodontium adaptation of the periodontal structures to altered functional If the repair process cannot keep pace with the destruction demand. When the tooth is subjected to horizontal forces caused by occlusion, the periodontium may get remodelled the tooth rotates or tilts in the direction of force. This tilting in order to maintain the structural relationship. This may results in the pressure and tension zones, within the marginal result in thickened periodontal ligament, angular defects in and apical parts of the periodontium. Depending on the types the bone with no pocket formation, loose teeth and increased of forces there can be many histologic changes (Table 9.2). vascularization. In summary, histometric changes shown during these

Etiopathogenesis Stage 2: Repair three stages are: TFO stimulates increased reparative activity. 1. The injury phase shows an increase in areas of resorption When bone is resorbed by excessive occlusal forces, and a decrease in bone formation. the body attempts to reinforce the thinned-bony trabeculae 2. The repair phase shows increase in areas of bone with new bone. This attempt to compensate for lost bone is formation and decreased resorption.

Table 9.2: Histologic changes in periodontal tissues after injury

a. Slightly-excessive pressure Slightly-excessive tension Changes are as follows: 1. Widening of the periodontal ligament. 1. Elongation of periodontal ligament fibers. 2. Resorption of alveolar bone called as direct bone 2. Apposition of alveolar bone. resorption. 3. The number of blood vessels are increased but 3. Blood vessels are enlarged and less. the size is reduced.

b. Greater pressure Greater/severe tension The changes in the tissues are as follows: 1. Causes widening of the periodontal ligament, 1. Compression of fibers producing areas thrombosis, hemorrhage, tearing of periodontal of the hyalinization. ligament. 2. Injury to the cells like fibroblasts and other connective 2. Resorption of alveolar bone. tissue cells leading to necrosis of areas of the ligament. 3. Changes in the blood vessels-breaking of vessel wall. 4. Increased resorption of alveolar bone. 5. Resorption of tooth surface.

c. Pressure severe enough to force the root against bone causes necrosis of periodontal ligament and bone. The bone is resorbed from viable periodontal ligament adjacent to necrotic areas and from marrow spaces, a process called undermining resorption or indirect bone resorption takes place. The furcation is the most susceptible area to injury due to excessive occlusal forces. 97

3. Remodeling phase shows return of normal resorption in the periodontium as a result of plaque accumulation may and formation. impair the reversibility of traumatic lesions. The animal experiments conducted to study the effect of traumatic occlusion on the periodontium had raised a lot Effect of Increased Occlusal Forces on Pulp of criticism. In these studies, the teeth were subjected to a 9 CHAPTER The effects on the pulp have not been established. unilateral horizontal force and the changes were observed. However, it has been suggested that in humans, the occlusal ROLE OF THE TRAUMA FROM forces act alternatively in one and then in the opposite OCCLUSION IN THE PROGRESSION direction, which is termed as jiggling forces. It is important OF PERIODONTAL DISEASE to note the difference in the forces because, unilateral horizontal force creates pressure and tension zones in the The various studies conducted on animals and humans have coronal and apical parts of the periodontium, whereas with shown changes produced by the pressure and tension sides Occlusion from Trauma jiggling forces pressure and tension zones occur on both of the tooth, with an increase in the width of the periodontal sides of the jiggled tooth. Moreover, in humans the tooth ligament and increased tooth mobility. None of these rotates around a fulcrum which in single rooted teeth is methods have caused gingival inflammation or pocket located at the junction between the apical-third and the formation. This was explained by: middle-third of the root. In multirooted teeth the fulcrum is Glickman’s concept (1965, 1967). He claimed that the located at the furcation area. pathway of the spread of plaque associated gingival lesion In the response to increased occlusal forces, the can be changed if the forces of an abnormal magnitude are periodontal ligament gradually increases in width on both acting on teeth harboring subgingival plaque. He has the sides of the tooth. This is associated with, (a) Inflam- explained that, teeth which are nontraumatized exhibit matory changes in the ligament tissue, (b) Active bone suprabony pockets and horizontal bone loss, whereas teeth resorption. (c) Progressive mobility of the teeth. When the with trauma exhibit angular bony defects and infrabony effect of the forces applied has been compensated by the pockets. increased width of the periodontal ligament space, the According to him, the periodontal structures are divided ligament no longer shows the above mentioned signs, except into two zones: that the tooth remains hypermobile, but the mobility is no 1. The zone of irritation and longer of the progressive type. 2. The zone of co-destruction. The zone of irritation includes the marginal and Other Properties interdental gingiva, which is affected only by microbial plaque. In a plaque associated lesion, at a “nontraumatized” Effect of Insufficient Occlusal Force tooth, the inflammation spreads in an apical direction, first It may also be injurious to periodontal tissues which results involving the alveolar bone and later the periodontal in the thinning of the periodontal, ligament, atrophy of the ligament area. Hence, there is an even (horizontal) bone fibers, osteoporosis of alveolar bone and reduction in loss. alveolar bone height. Hypofunction can result from an open The zone of codestruction includes the periodontal bite relationship, absence of functional antagonists, or ligament, the root cementum and the alveolar bone, which unilateral chewing habits. are coronally demarcated by the transseptal and the dentoalveolar collagen fibers. The tissue in this region Reversibility of Traumatic Lesion becomes the seat of a lesion caused by the trauma from Trauma from occlusion is reversible. When the injurious force occlusion. Here the spread of inflammation is from the zone is removed, the repair occurs. The presence of inflammation of irritation directly down into the periodontal ligament and 98

Waerhaug’s concept: From his similar studies he concluded that angular defects and infrabony pockets occur often at periodontal sites of teeth not affected by trauma from occlusion. In other words, he refuted the hypothesis that trauma from occlusion played a role in the spread of a gingival lesion into the zone of codestruction. The loss of periodontium, according to Waerhaug was as a result of inflammatory lesions associated with subgingival plaque.

He concluded that angular defects occur when the PART III subgingival plaque of one tooth has reached a more apical level than the microbiota on the neighboring tooth, and when the volume of the alveolar bone surrounding the roots is comparatively large. This was also supported by Prichard (1965) and Manson (1976). Fig. 9.1: Zone of irritation and zone of codestruction In conclusion, four possibilities can occur when a tooth with gingival inflammation is exposed to trauma. 1. Trauma from occlusion may alter the pathway of extension hence angular bony defects with infrabony pockets are seen of gingival inflammation to the underlying tissues. Etiopathogenesis (Figs 9.1 and 9.2). Inflammation may proceed to the periodontal ligament The summary of this concept is that trauma from rather than to the alveolar bone and the resulting bone occlusion is a codestructive factor of importance especially loss would be angular with infrabony pockets. in situations where angular defects combined with infrabony 2. It may favor the environment for the formation and pockets are found in one or several teeth. attachment of plaque and calculus and may be responsible for development of deeper lesions. 3. Supragingival plaque can become subgingival if the tooth is tilted orthodontically or migrates into an edentulous area, resulting in the transformation of a suprabony pocket into an infrabony pocket. 4. Increased tooth mobility associated with trauma to the periodontium may have a pumping effect on plaque metabolites increasing their diffusion.

PATHOLOGIC TOOTH MIGRATION Refers to tooth displacement that results when the balance among the factors that maintain physiologic tooth position is disturbed by periodontal disease. Pathologic migration occurs most frequently in the anterior region, but posterior teeth may also be affected. The teeth may move in any direction and the migration is usually accompanied by mobility and rotation. Pathologic migration in occlusal or incisal direction is called as Fig. 9.2: Pathway of inflammatory process “extrusion” (Figs 9.3 and 9.4). 99

Changes in the Forces Exerted on the Teeth Changes in the forces may occur as a result of (a) unreplaced missing teeth, (b) Failure to replace first molars, or (c) other causes. These forces do not have to be abnormal to cause HPE 9 CHAPTER pathologic migration, if the periodontium is sufficiently weakened. a. Unreplaced missing teeth: This leads to drifting of teeth into the spaces created by unreplaced missing teeth. Drifting differs from pathologic migration, in that it does not result from destruction of the periodontal tissues.

However, it usually creates conditions that leads to Trauma from Occlusion from Trauma Fig. 9.3: Pathologic migration periodontal diseases and thus the initial tooth movement is aggrevated by loss of periodontal support. b. Failure to replace first molars: It consists of the following: 1. The second and third molars tilt resulting in decrease in vertical dimension. 2. The premolars move distally and the mandibular incisors tilt or drift lingually. 3. Anterior overbite is increased. 4. The maxillary incisors are pushed labially and laterally. 5. The anterior teeth extrude due to disappearance of incisal apposition. Fig. 9.4: Pathologic migration associated with tongue thrusting 6. Diastema is created by the separation of the anterior teeth. Pathogenesis Two major factors play a role in maintaining the normal OTHER CAUSES position of the teeth. 1. Pressure from the tongue: It may either have a direct 1. The health and normal height of the periodontium. effect, that is, it may cause drifting of teeth in the absence 2. The forces exerted on the teeth. of periodontal disease or may contribute to pathologic migration of the teeth with reduced periodontal support. The Health and Normal Height of the Periodontium 2. Pressure from the granulation tissue of periodontal A tooth with weakened periodontal support is unable to pocket: It has also been listed as a contributing factor to withstand the forces and moves away from the opposing pathologic migration. Usually tooth may return to their force. It is important to understand that the abnormality in original position after pockets are treated, but if the pathologic migration rests with the weakened periodontium. destruction of the periodontium is more severe on one The force itself need not be abnormal. Forces that are side of a tooth rather than the other, the healing tissue acceptable to an intact periodontium become injurious when may pull the tooth in the direction of lesser destruction. periodontal support is reduced. Pathologic migration may 3. To summarize, trauma from occulsion does not have any: continue even after a tooth no longer contacts its antagonist. a. Effect on the supracrestal gingival tissue. 100

b. Human and animal studies have shown neither b. Continuous forces/very low forces (e.g. orthodontic unilateral nor jiggling force can result in pocket forces). formation. c. Impact forces-which are mainly high forces but of short c. Bone resorption and increased mobility in the duration, if it is beyond the adaptive capacity, may result in tooth fracture. absence of the pockets can be associated with trauma d. Jiggling forces are considered to be most traumatic, from occlusion. e.g. high fillings, premature contacts on crowns and d. In cases of teeth affected by periodontal disease, fillings. trauma from occlusion may aggravate the rate of Clinical Indicators for Trauma from Occlusion progression of the disease and can also act as a co- a. Mobility. PART III factor in tissue destruction. b. Fremitus test being positive. c. Malocclusion. d. Wear facets. e. Tooth migration. f. Fractured tooth/teeth. 1. When occlusal forces exceed the adaptive capacity of the periodontal tissues, tissue injury results. This resultant g. Thermal sensitivity. injury is termed as “trauma from occlusion”. h. Muscle hypertonicity. 2. Depending on the onset of duration trauma from the occlusion (TFO) may be divided into, acute trauma from occlusion, chronic trauma from occlusion. Depending on REVIEW QUESTIONS the cause, primary trauma from occlusion, secondary

Etiopathogenesis trauma from occlusion. 3. Primary trauma from occlusion is a tissue injury, which is 1. Define trauma from the occlusion. Describe the clinical elicited around a tooth with a normal height of and radiographic changes associated with trauma from periodontium whereas secondary trauma from occlusion occlusion. is related to situations in which occlusal forces cause injury in a periodontium of reduced height. 2. What is the role of trauma from occlusion in the 4. Role of trauma from occlusion in the progression of progression of periodontal diseases? periodontal disease is explained by two concepts, (a) Glickman’s concept supports trauma from occlusion that 3. What are the causes for pathologic tooth migration? is a co-destructive factor of importance, especially in 4. Differences between primary trauma from occlusion and situations where angular defects combined with infrabony pockets are found in one or several teeth where as secondary trauma from occlusion. Waerhaug’s concept refutes this hypothesis and proposes that, angular defects and infrabony pockets occur often at sites not affected by trauma from occlusion. He BIBLIOGRAPHY proceeds to explain, that, angular defects occur, when the subgingival plaque of one tooth reaches a more apical 1. Burgett FG. Trauma from occlusion, periodontal concerns. level than the plaque on the neighboring tooth and also Dental Clinics of North America 1995;39(2):301. when the volume of the alveolar bone surrounding the 2. Elizabeth A Pawlak, Philip M Hoag. Essentials of Periodontics. roots is comparatively large. 5. Pathologic tooth migration refers to tooth displacement Mosby, Jaypee Brothers Medical Publishers. that results when the balance among the factors that 3. Gher ME. Changing concepts. The effect of occlusion on maintain physiologic tooth position is disturbed by periodontics. Dental Clinics of North America 1998; 42(2): periodontal diseases. 285. 4. Jan lindhe. Clinical periodontology and Implant dentistry, 4th edn. BlackWell Munksgaurd Publication 2003. KNOW MORE ... 5. JD Manson, BM Eley. Outline of periodontics, 3rd edn, KM Varghese Company. Various Types of Occlusal Forces 6. Newman, Takei, Fermin A Carranza. Clinical periodontology, a. Normal or physiological occlusal forces which rarely 9th edn, WB Saunders Co., 2002. exceeds 5N which is required to provide positive 7. Robert J Genco, Henry M Goldman, D Walter Cohen. stimulus to maintain the periodontium. Contemporary periodontics, CV Mosby Company, 1990. 10 ChapterChapter

Role of Systemic Diseases in the Etiology of Periodontal Diseases

 DIETARY AND NUTRITIONAL ASPECTS OF  CARDIOVASCULAR DISEASES PERIODONTAL DISEASE  ANTIBODY DEFICIENCY DISORDERS  EFFECTS OF HEMATOLOGICAL DISORDERS  OTHER SYSTEMIC DISEASES ON PERIODONTIUM  PSYCHOSOMATIC DISORDERS  METABOLIC AND ENDOCRINE DISORDERS

INTRODUCTION of the dentogingival junction and the underlying connective tissues are the most dynamic tissues. It is a well established fact that the primary etiological agent The majority of opinions and research findings point to in periodontal disease is bacterial plaque. The toxins and the following: enzymes produced by the bacterial plaque elicit 1. Nutritional deficiencies produce changes in the oral inflammatory and immunologic changes in the periodontal cavity. tissues at both cellular and molecular levels. These responses 2. There are no nutritional deficiencies that by themselves can be affected by a variety of systemic factors that can cause gingivitis or periodontal pockets. alter the response of the tissue to plaque. Further more, certain systemic disorders can have a direct effect on the The Consistency of Diet periodontal tissues and these represent the periodontal From the viewpoint of promoting and maintaining gingival manifestations of systemic diseases. In general, these and periodontal health, it is often stated that a firm and diseases do not initiate chronic destructive periodontitis but fibrous diet is more beneficial than an intake of soft and may accelerate its progression and increase tissue more loosely-textured food. Softer diets tend to produce destruction. greater deposits of plaque and an increase in plaque can be noticed, when the soft diet especially contains high DIETARY AND NUTRITIONAL ASPECTS OF proportion of sucrose. Diets that are predominantly fibrous PERIODONTAL DISEASE are considered advantageous as they possess the ability to The vitality of periodontal tissues, in both health and disease impart a natural cleansing action to the teeth and the depends strongly on the essential nutrients. The epithelium periodontium. 102

A coarse diet, requires vigorous mastication and the Possible Etiologic Relationships between plaque that forms approximately tends to be towards the Ascorbic Acid and Periodontal Disease cleansable buccal and lingual surfaces of the teeth. However, 1. Low levels of Ascorbic acid influences the metabolism coarse and granular diets can predispose to a direct traumatic of collagen within the periodontium, thereby affecting injury to the supporting tissues. the ability of the tissue to regenerate and repair by itself. 2. It interferes with bone formation leading to the loss of Protein Deficiency and Periodontal Disease the alveolar bone. PART III Proteins are constituents of the organic matrices of all the 3. Increases the permeability of oral mucosa to tritiated dental tissues including the alveolar bone. The integrity of endotoxin and inulin. the periodontal ligament is also dependent upon proteins 4. Increased levels of Ascorbic acid enhances both the (amino acid). Studies have indicated that on deprivation of chemotactic and migratory action of leukocytes without proteins, extreme pathologic changes occur and there is influencing phagocytic activity. marked degeneration of periodontal support. 5. Optimal level of Ascorbic acid is required to maintain the integrity of the periodontal microvasculature as well Vitamins and Periodontal Disease as the vascular response to bacterial irritation and wound

Vitamins are essential, biologically-active constituents of a healing. Etiopathogenesis diet which cannot be replaced by other dietary components. 6. Depletion of vitamin C may interfere with the ecologic equilibrium of bacteria in plaque and increases its Vitamin C pathogenicity.

Its deficiency in humans results in scurvy, a disease Periodontal Features of Scurvy characterized by hemorrhagic diathesis and retardation of The oral symptoms are that of chronic gingivitis which can wound healing. involve the free gingiva, attached gingiva and alveolar mucosa. In severe cases, the gingiva becomes brilliant-red, Clinical Manifestations tender and grossly swollen. The spongy tissues are extremely 1. Increased susceptibility to infections. hyperemic and bleed spontaneously. In long standing cases, 2. Impaired wound healing. the tissues attain a dark blue or purple hue. Alveolar bone 3. Bleeding and swollen gums. resorption with increased tooth mobility has also been 4. Mobile teeth. reported.

Histopathological Features Vitamin D Deficiency

1. Defective formation and maintenance of collagen. Vitamin D is essential for the absorption of calcium from 2. Retardation or cessation of osteoid formation and the gastrointestinal tract and the maintenance of calcium- impaired osteoblastic function. phosphorus balance. 3. Increased capillary permeability. Radiographically, there is a generalized partial to 4. Susceptibility to traumatic hemorrhage. complete disappearance of the lamina dura and reduced 5. Hyporeactivity of contractile elements of the peripheral density of supporting bone, loss of trabeculae, increased blood vessels. radiolucency of the trabecular interstices and increased 6. Sluggishness of blood flow. prominence of the remaining trabeculae. CHAPTER 10 Role of Systemic Diseases in the Etiology of Periodontal Diseases 103 is a bright-red, hyper- include oral ulceration, include hyperplastic gingivitis Plaque control and use of antimicrobial Plaque control, supportive measures like Plaque control, supportive measures Appropriate antimicrobial agent should be Appropriate antimicrobial The main periodontal feature The main periodontal feature Treatment: Periodontal manifestations Periodontal manifestations Treatment: Treatment: Chronic Idiopathic Neutropenia There is a persistent neutropenia from birth and is not cyclical. Clinical symptoms include persistent recurrent life. infections throughout the patient’s Chronic Benign Neutropenia of Childhood months of age and in The onset is usually between 6 to 20 most patients, the condition is self-limiting. Benign Familial Neutropenia The It is transmitted as an autosomal dominant trait. periodontal manifestations There is exhibiting edematous and bright-red appearance. The gingival marked bone loss around the first molars. tissues bleed profusely on probing. Cyclic Neutropenia a cyclic depression of the PMN count It is characterized by The cyclic intervals are usually between in peripheral blood. problems include pyrexia, oral 19 and 21 days. Clinical infections. ulceration and skin d. familial neutropenia. Severe e. neutropenia. Chronic idiopathic plastic, edematous gingiva confined to the width of attached plastic, edematous gingiva confined to exhibit bleeding on probing The gingival tissues gingiva. degrees of gingival and show areas of desquamation, varying recession and pocketing are seen. mouth washes. inflamed gingiva, rapid periodontal breakdown, and alveolar inflamed gingiva, rapid is most obvious around the lower bone loss. Bone loss incisors and first permanent molars. prescribed. antiseptic mouth wash, antimicrobial therapy has been antiseptic mouth wash, antimicrobial proposed. The possible role is based upon its ability to interfere The possible role EFFECTS OF HEMATOLOGICAL DISORDERS EFFECTS OF HEMATOLOGICAL ON PERIODONTIUM a. neutropenia. Cyclic b. of childhood. Chronic benign neutropenia c. Benign familial neutropenia. Neutropenias The WBC’s disorders that affect the periodontium can be the periodontium disorders that affect WBC’s The categorized as either a disorder of numbers or defect in function. White Blood Cell Disorders Disorders of the blood and blood forming tissue can have a Disorders of the blood and blood forming tissues and their response on the periodontal profound effect the most WBC disorders have The to bacterial plaque. periodontal tissues. Disorders of on the pronounced effect to the underlying hemostasis can be classified according There can be a defect in the vascular constriction, defect. platelet adhesion and aggregation, coagulation and fibrinolysis. Vitamin B-Complex Vitamin in just one Oral disease is rarely due to a deficiency changes common component of the B-complex group. Oral deficiencies are gingivitis, glossitis, B-complex to—Vitamin of the entire glossodynia, angular cheilitis and inflammation oral mucosa. Vitamin A Vitamin functions of the retina, for growth, It is essential for normal tissues and for and maintenance of epithelial differentiation development. bone growth and embryonic with the production of prostaglandins. with the production Vitamin E Vitamin and E acts as a antioxidant suggests that vitamin Evidence of cell the stability role in maintaining plays an important blood cells against hemolysis. membranes and protecting 104

Periodontal manifestations include persistent severe susceptibility of the periodontium to fungal, viral or gingivitis. The gingiva is cherry-red edematous and bacterial infections. hypertrophic with occasional desquamation. Treatment: Strict oral hygiene program, scaling and Treatment Plan for Leukemic Patients regular prophylaxis. Antiseptic irrigation and antibiotic 1. Refer the patient for medical evaluation and treatment. prophylaxis are advisable before tissue manipulation. 2. Prior to chemotherapy, a complete periodontal plan Leukemia should be developed. PART III It is a malignant disease caused by proliferation of WBC a. Monitor hematologic laboratory values. forming tissue, especially those in bone marrow. Acute b. Administer suitable antibiotics before any periodon- leukemia is more frequent in people under 20 years of age. tal treatment. Chronic leukemia’s occur in people over 40 years of age. c. Periodontal treatment consists of scaling and root planing, twice daily rinsing with 0.12 percent Periodontal Manifestations chlorhexidine gluconate is recommended. If there is The major manifestations being gingival enlargement, irregular bleeding time, careful debridement with gingival bleeding and periodontal infections. The incidence cotton pellets soaked in 3 percent hydrogen peroxide and severity of these problems varies according to the type is performed.

Etiopathogenesis and nature of leukemia (Fig. 10.1). 3. During the acute phases of leukemia: a. Cleanse the area with 3 percent hydrogen peroxide

(H2O2) or 0.12 percent chlorhexidine. b. Carefully explore the area and remove any etiologic local factors.

c. Re-cleanse the area with 3 percent H2O2. d. Place a cotton pellet soaked in thrombin against the bleeding point. e. Cover with gauze and apply pressure for 15 to 20 minutes. f. Acute gingival or periodontal abscesses are treated by systemic antibiotics, gentle incision and drainage

or by treating with 3 percent H2O2/0.12 percent Fig. 10.1: Gingival changes associated with leukemia chlorhexidine gluconate. g. Oral ulcerations should be treated with antibiotics a. Gingival enlargement is primarily due to a massive and bland mouth rinses. leukemic cell infiltration into the gingival connective 4. In patients with chronic leukemia, scaling and root tissue. The enlarged gingiva will hinder mechanical planing can be performed but periodontal surgery should plaque removal; hence there will be an inflammatory be avoided. Plaque control and frequent recall visits component enhancing this enlargement. should receive particular attention. b. Gingival bleeding is a common oral manifestation of acute leukemia. The bleeding is secondary to Thrombocytopenic Purpura thrombocytopenia that accompanies leukemia. c. Infections of the periodontal tissues secondary to It is characterized by a low platelet count, a prolonged clot leukemia can be of two types, either an exacerbation of retraction and bleeding time, and a normal or slightly- an existing periodontal disease or an increased prolonged clotting time. CHAPTER 10 Role of Systemic Diseases in the Etiology of Periodontal Diseases 105 include marked, diffuse, Pernicious anemia Fig. 10.3: Periodontal manifestations Severe gingival inflammation appears to be a common appears to be a inflammation Severe gingival Red Blood Cell Disorders disorders but only a There are many types of red blood cell on the periodontal tissues. few appear to have any effect Aplastic Anemia by a reduction in It is a bone marrow disorder characterized replaced with fat, and hematopoietic tissue, bone marrow is Lazy Leukocyte Syndrome Lazy Leukocyte syndrome is a defect in leukocyte The feature of the has also Marked gingivitis mobility. chemotaxis and random been described. Chronic Granulomatous Disease characterized by the A genetically-transmitted disorder certain infecting inability of phagocytic cells to destroy microorganisms. of buccal gingivitis with an accompanying ulceration mucosa. degranulation and diminished intracellular bactericidal intracellular and diminished degranulation capacity. The nature of the syndrome. finding in Chédiak-Higashi may be plaque induced, secondary inflammatory changes defect. to the underlying PMNL’s to infection or related . 3 include spontaneous bleeding Thrombocytopenic purpura with petechiae and Thrombocytopenic purpura with petechiae hemorrhagic vesicles in the lining mucosa Clinical manifestations low platelet levels. is indicated, it should be as atraumatic as If surgery count is at least 80,000 cells/mm Fig. 10.2: into skin or from mucous membranes. Petechiae and into skin or from mucous membranes. is Gingiva cavity. hemorrhagic vesicles occur in the oral spontaneously swollen, soft and friable. Bleeding occurs (Fig. 10.2). 5. may be carefully performed at Scaling and root planing possible, stents or thrombin-soaked cotton pellets placed gentle hydrogen peroxide mouth washes interproximally, follow-up is recommended. and close postsurgical It is a rare familial and often fatal disease which is from transmitted as an autosomal recessive trait. PMNL’s patients with this syndrome show defective migration, defective chemotaxis, failure of postphagocytic Chédiak-Higashi Syndrome Disorders of WBC Function 1. referral for a definitive diagnosis. Physician 2. Oral hygiene instructions. 3. Prophylactic treatment of potential abscesses. 4. surgical No are indicated unless platelet procedures Treatment 106

pancytopenia. Bleeding from the gingival margins appears to be a feature in these cases.

Fanconi’s Anemia This is a rare type of aplastic anemia characterized by a familial bone marrow hypoplasia that becomes manifested in the first decade of life. The periodontal manifestations

PART III being loss of several teeth, severe bone loss with pocketing greater than 10 mm. The gingiva will be bluish-red, bleed on probing, and shows suppuration on gentle pressure.

Sickle Cell Anemia Fig. 10.4: Diabetic patient—multiple periodontal abscess In this condition, the red blood cells undergoes sickling when subjected to hypoxia. Hence patients with sickle cell Pathogenesis anemia are susceptible to infections. In some patients with sickle cell anemia, periodontal disease may provide a There are several underlying factors that accompany diabetes mellitus which may account for the apparent Etiopathogenesis sufficient inflammatory response to precipitate a sickling crisis. increased prevalence of periodontal disease in this condition. These factors can be considered under the following Acatalasia headings. It is caused by a lack of the enzyme catalase in many cells, 1. Vascular changes: Changes include thickening and especially the red blood cells and leukocytes. It causes hyalinization of vascular walls, PAS-positive, diastase- hypoxia and necrosis of the gingival tissues. Severe resistant thickening of capillary basement membranes, periodontal destruction and gingival necrosis are seen. swelling and occasional proliferation of the endothelial cells, and splitting of capillary basement membrane. METABOLIC AND ENDOCRINE DISORDERS Diabetic-induced changes in the capillary basement membrane may have an inhibitory effect on the transport The endocrine glands produce hormones that control of oxygen, white blood cells, immune factors and waste metabolism and maintain hemostasis. Diabetes mellitus is products, all of which could affect tissue repair and the main endocrine disorder that affects the periodontium. regeneration. The sex hormone can alter the response of periodontal 2. PMNL’s function: Impairment of PMN function is a tissues to plaque. Disorders of the pituitary, thyroid and feature of diabetes mellitus. Disorders include reduced adrenal glands have little direct effect on the periodontal phagocytosis and intracellular killing, impaired structures or in altering the host response to bacterial plaque. adherence and impaired chemotactic response. Suggested causes include inhibition of the glycolytic Diabetes Mellitus and Periodontal Disease pathway with the PMNL’s, abnormal cyclic nucleotide Studies suggested that diabetic patient is more susceptible metabolism, which disrupts the organization of to periodontal breakdown, which is characterized by microtubules and microfilaments, or a reduction in extensive bone loss, increased tooth mobility, widening of leukocyte membrane receptors. periodontal ligament space, suppuration and abscess 3. Biochemistry of crevicular fluid: Alterations in the formation (Fig. 10.4). constituents and flow rate of crevicular fluid have been CHAPTER 10 Role of Systemic Diseases in the Etiology of Periodontal Diseases 107 Routine periodontal therapy must be Hypopituitarism leads to crowding and malposition of Hypopituitarism leads to crowding and Treatment: medical management should not receive periodontal medical management therapy until the condition is stabilized. caution. pressor amines should be given with their diminished sedatives and narcotics because of ability to tolerate drugs. should be stressed. should be There are several types of gingival diseases in which modification of the sex hormones is considered to be either an initiating or complicating factor; gingival alterations are associated with physiologic hormonal changes with a predominant marked hemorrhagic tendency. Pituitary Gland Pituitary localized areas of Hyperpituitarism causes enlarged lips; folds. It is also hyperpigmentation are seen along nasolabial is seen. associated with food impaction and hypercementosis teeth. Parathyroid Glands generalized Parathyroid hypersecretion produces changes include demineralization of the skeleton. Oral radiographic evidence of malocclusion and tooth mobility, alveolar osteoporosis, widening of the periodontal space and absence of lamina dura. Gonads Thyroid Gland leads to cretinism in children and Hypothyroidism There are no notable periodontal myxedema in adults. changes. Treatment 1. and those with inadequate Patients with thyrotoxicosis 2. Medications such as epinephrine, atropine and other 3. careful administration of Hypothyroid patients require 6. care fastidious home oral appointments and Recall instituted but the dental practitioner must be attuned to the oral and dental changes that occur. Studies have indicated Studies prandial blood glucose, glycated hemoglobin, prandial blood glucose, glycated glucose. glucose tolerance test (GTT), urinary should be immediate care, prophylactic antibiotics given. Glucose levels should be health is a necessity. treatment continuously monitored and periodontal is in a well- should be performed when the disease should be controlled state. Prophylactic antibiotics Penicillin is the drug started 2 days preoperatively, of first choice. shown to be associated with diabetes. Cyclic AMP levels AMP Cyclic be associated with diabetes. shown to when diabetes group be reduced in the seems to with control. compared microflora: Changes in plaque that proteolytic activity has not been altered but that proteolytic activity is lower in plaque from diabetes. hyaluronidase activity should be altered. minimally (less than 2 hours) as possible. For anxious patients, if preoperative sedation is required, epinephrine concentration should not be greater than 1:1,00,000. therapy. has been taken, followed by a meal. Morning appoint- ments are ideal, after breakfast, because of optimal insulin levels. should be performed: 1. physician. Consult the patient’s 2. laboratory tests, fasting blood glucose, post- Analyze 3. requires If there is periodontal condition that 4. diabetic, optimal periodontal If patient is a ‘brittle’ diabetes is contraindicated. 4. 3. should be handled as atraumatically and as Tissues 4. should be made. Diet recommendation 5. Antibiotic prophylaxis is recommended for extensive 2. procedures, postoperative insulin dose surgical After any 1. Clinician should make certain that the prescribed insulin Guidelines b.diabetic, following procedures If suspected to be a Treatment a. uncontrolled- Periodontal treatment in patient with 108

3. Marginal and interdental gingiva is edematous, pits on pressure and sometime presents raspberry-like appearance. 4. It has been suggested that during pregnancy there is depression of maternal T-lymphocyte response. 5. Aggravation of gingivitis has been attributed principally to increased levels of progesterone which produces

PART III dilatation and tortuosity of the gingival microvascu- lature, circulatory stasis and increased susceptibility to mechanical irritation. 6. Increased crevicular fluid flow, pocket depth and Fig. 10.5: Gingivitis in puberty with edema, discoloration mobility are also seen. and gingival enlargement Treatment: Requires elimination of all local irritants that are responsible for precipitating gingival changes. Marginal and interdental gingival inflammation and Gingivitis in Puberty (Fig. 10.5) enlargement are treated with scaling and root planing.

Treatment of tumor-like gingival enlargements consists Etiopathogenesis Pronounced inflammation, bluish-red discoloration, edema of surgical excision, scaling and planing of tooth surfaces. and enlarged gingiva may be seen. In pregnancy emphasis should be on: Treatment: It is treated by scaling and curettage, removal • Preventing gingival disease before it occurs. of all sources of irritation and plaque control. In severe cases, • Treating existing gingival disease before it becomes surgical removal of enlarged tissue may be required. worse.

Gingival Changes Associated with Menopausal Gingivostomatitis Menstrual Cycle It occurs during menopause or in the postmenopausal period. There is increased prevalence of gingivitis, bleeding gingiva. Clinical manifestations include dry, shiny oral mucosa, dry Exudation from inflamed gingiva is also increased, but the burning sensation of oral mucosa, abnormal taste sensation crevicular fluid flow is not affected. The salivary bacterial described as salty, peppery or sour. count is increased. No active treatment is required.

Gingival Diseases in Pregnancy (Fig. 10.6)

Pregnancy accentuates the gingival response to plaque. The severity of gingivitis is increased during pregnancy, beginning in the second or third month. It becomes more severe by the eighth month and decreases during ninth month.

Clinical Features

1. Pronounced base of bleeding. Fig. 10.6: Gingiva in pregnancy showing edema, 2. Gingiva is bright-red to bluish-red. discoloration and enlargement CHAPTER 10 Role of Systemic Diseases in the Etiology of Periodontal Diseases 109 gingival enlargement Gingiva in pregnancy with localized Fig. 10.7: irrigation with chlorhexidine. irrigation for patients with moderate cillin should be prescribed destruction. Use of prophylactic to severe tissue should be considered. antifungal medication ulcerative treatment for necrotizing In summary, ulcerative periodontitis for necrotizing Treatment OTHER SYSTEMIC DISEASES Ingestion of metals such as mercury, lead, bismuth may lead, Ingestion of metals such as mercury, their intoxication or result in oral manifestations owing to absorption without evidence of toxicity. Bismuth Intoxication characterized by Chronic bismuth intoxication is and jaundice gastrointestinal disturbances, nausea, vomiting b. subgingival areas and perform and polish affected Scale c. rinse. Prescribe chlorhexidine gluconate mouth d. visits. Reevaluation and frequent recall e. amoxi- antibiotics such as metronidazole or Systemic as prescription of an antibiotic such stomatitis includes and use of an antimicrobial metronidazole or amoxicillin mouth rinse. and root planing, includes local debridement, scaling establishment of irrigation with Betadine solution and home use of meticulous oral hygiene, including antibiotic therapy antimicrobial rinses. In severe NUP, daily for 5 to 7 days). is a must (metronidazole 400 mg thrice NUP (Necrotizing ulcerative (Necrotizing NUP

Recommended management for linear In HIV gingivitis persistent, linear, easily persistent, linear, gingivitis In HIV is characterized by soft tissue necrosis and Treatment: ANTIBODY DEFICIENCY DISORDERS CARDIOVASCULAR DISEASES CARDIOVASCULAR periodontitis) rapid periodontal destruction that results in marked inter- proximal bone loss. It is severely painful at onset. gingival erythema is as follows: a. Instruct the patient to perform meticulous oral hygiene. Clinical Manifestations gingivitis: HIV periodontitis: HIV bleeding, erythematous gingivitis has been described. Linear bleeding, erythematous gingivitis has been gingivitis lesions may be localized or generalized in nature. The erythematous gingivitis may be limited to marginal tissue, or extend into attached gingiva in a punctuate or a severely A erythema or extend into alveolar mucosa. diffuse destructive, acutely painful necrotizing ulcerative stomatitis has been reported. It is caused by a persistent HIV virus and is characterized It is caused by a persistent HIV virus the patient by destruction of lymphocytes, rendering including destructive susceptible to opportunistic infections periodontal lesions. Acquired Immunodeficiency Syndrome In cases of tetralogy of fallot, oral changes include a of fallot, oral changes include In cases of tetralogy and gingiva and purplish-red discoloration of the lips gingivitis and periodontal sometimes severe marginal appears coated, fissured and The tongue destruction. of the fungiform edematous and there is extreme reddening and filliform papillae. Congenital Heart Disease Congenital In aged individuals, arteriosclerotic changes in the arteriosclerotic changes in In aged individuals, initial thickening, characterized by, blood vessels are thickening of media, and hyalinization narrowing of lumen, are with or without calcification of media and adventitia, common. Arteriosclerosis 110

as well as by an ulcerative gingivostomatitis. Generally may be derived from neurotic habits, which are potentially pigmentation is accompanied by a metallic taste and a injurious to the periodontium. burning sensation of the oral mucosa. The tongue may be sore and inflamed. Urticaria, exanthematous eruptions of different types, bullous and purpuric lesions are among the KNOW MORE ... dermatologic lesions that are attributed to bismuth intoxication. Diabetes and Periodontium

PART III It usually appears as a narrow, bluish-black discoloration Various other factors contributing to the development of the gingival margin in areas of pre-existent gingival of periodontal diseases: inflammation. The hyperglycemic state can result in: • Reduced polymorphonuclear leukocyte (PMNL) Lead Intoxication function. • Altered collagen metabolism which is associated with Lead is slowly absorbed and toxic symptoms are not increased collagenase activity and decreased collagen particularly definitive when they do occur. Among the oral synthesis. signs are increased salivation, coated-tongue, peculiar • Excessive levels of advanced glycation end products (AGEs). sweetish taste, gingival pigmentation and ulceration. The • Colonization of pathogenic subgingival flora.

Etiopathogenesis pigmentation of gingiva is linear (Burtonian line), steel gray and associated with local irritation. REVIEW QUESTIONS

Mercury Intoxication 1. Describe the influence of systemic diseases on Gingival pigmentation in linear form results from the periodontium. deposits of mercuric sulfide. The chemical also acts as an 2. Explain the role of diabetes in periodontal disease. irritant which accentuates the pre-existing inflammation and commonly leads to notable ulceration of the gingiva and BIBLIOGRAPHY adjacent mucosa and destruction of underlying bone. 1. Garcia RI, Henshaw MM, Krall EA. Relationship between periodontal disease and systemic health. Periodontol Other Chemicals 2000;25:2001. Phosphorus, arsenic, chromium, may cause necrosis 2. Genco RJ, Loe H. The role of systemic conditions and disorders of the alveolar bone with loosening and exfoliation of teeth. in periodontal disease. Periodontol 2000;2:1993. 3. Mendieta C, Recve CM. Periodontal manifestations of systemic PSYCHOSOMATIC DISORDERS disease and management of patients with systemic disease, Current Opinion. Periodontol 1993;111-28. There are two ways by which psychosomatic disorders may 4. Newman, Takaê, Fermin A Carranza’s Clinical Periodontology, be induced in the oral cavity, through the development of 9th edn, WB Saunders Co., 2002. habits injurious to the periodontium and by the direct effect 5. Salmon A, Kang MC. Influence of hormonal variations on the of the autonomous nervous system on the physiologic tissue periodontium on woman. Periodontol 2000; 6:1994. 6. Seymour RA, Heasman PA, Macgregor I DM. Drugs, Diseases balance. and the Periodontium. Oxford University Press Publication, However, under the conditions of mental and emotional 1992. stress, the mouth may subconsciously become an outlet for 7. Yalda B, Offenbacher S, Collins JG. Diabetes as a modifier of the gratification of basic drives in the adult. Gratification periodontal disease expression. Periodontol 2000;6:1994. 11 ChapterChapter

Oral Malodor

Srinivas K

 INTRODUCTION  Clinical Examination  CLASSIFICATION OF HALITOSIS  Intraoral  ETIOLOGY   Causes for Physiologic Halitosis  Measurement of Oral Malodor  Causes for Pathologic Halitosis  TREATMENT AND MANAGEMENT OF ORAL  DIAGNOSIS OF HALITOSIS MALODOR  History  SUMMARY

INTRODUCTION cheese), smoking and alcohol consumption. Because the mouth is dry and inactive during the night, the odor is usually Halitosis is a term used to describe noticeably unpleasant worse upon awakening (morning breath). Bad breath may odor exhaled in breathing. It is a general term used to also be persistent (chronic bad breath) which is a more describe the unpleasant breath regardless of its sources, oral serious condition, affecting at least 25% of population in or non-oral. Whereas, oral malodor is the term especially varying degrees. used to describe the odor emanating from the oral cavity. Halitosis which is in synonym with breath malodor, foul breath and fetor oris or simply bad breath, affects a large CLASSIFICATION OF HALITOSIS proportion of population which may cause a significant Genuine Halitosis social or psychological handicap to those suffering from it. This common disease has been ignored for too long by  Physiologic halitosis periodontologists even though the most common cause is  Pathologic halitosis related to the microbiota of the subgingival areas and the  Oral related tongue coating. The intensity of the bad breath differs  Extraoral during the day, (which may be due to the stress or fasting), Is an obvious malodor, with intensity beyond socially eating certain foods (such as garlic, onions, meat, fish and acceptable level is perceived. 112

Pseudohalitosis f. Oral pathologic lesions like oral cancers, candidiasis. Obvious malodor is not perceived by others, although the g. Parotitis, cleft palate. patient stubbornly complains of its existence, condition can h. Aphthous ulcers, dental abscesses. be improved by counseling and simple oral hygiene measures. Systemic and Extraoral Factors a. Nasal infections like rhinitis, sinusitis, tumors and Halitophobia foreign bodies. After treatment for genuine halitosis or pseudo-halitosis, b. Diseases of gastrointestinal tract (GIT) like hiatus hernia, PART III the patient persists in believing that he/she has halitosis. carcinomas, Gastroesophageal Reflux Disorder (GERD). c. Pulmonary infections like bronchitis, pneumonia, ETIOLOGY tuberculosis, and carcinomas. d. Certain hormonal changes that occur during ovulation, At least 90% of all malodor originates from the oral cavity, menstruation, pregnancy and menopause. whereas, the remaining 10% has systemic or local causes. Oral malodor is commonly the result of microbial e. Systemic diseases like diabetes mellitus, hepatic failure, putrefaction of food debris, cells, saliva and blood within renal failure, uremia, blood dyscrasias, rheumatologic the oral cavity. In particular, proteolysis of proteins to diseases, dehydration and fever, cirrhosis of liver.

Etiopathogenesis peptides and amino acids takes place. The resultant substrates with free thiol groups such as cystein and reduced DIAGNOSIS OF HALITOSIS glutathionine, rises to volatile sulfur compounds (VSCs), a. Review of Medical, Dental and Personal History. which are malodour substances. The most common b. Clinical examination: physiological and pathological causes of halitosis are i. Intraoral examination: discussed below: 1. Tongue coating. 2. Evidence of mouthbreathing. Causes for Physiologic Halitosis 3. Xerostomia: Dry mucosa. a. Mouthbreathing. 4. Other oral causes. b. Medications. ii. Complete periodontal examination: c. Aging and poor dental hygiene. 1. General personal care, state of oral hygiene. d. Fasting/starvation. 2. Probing for attachment levels, probing e. Tobacco. depths (Periodontal status). f. Foods (onion, garlic, etc.) and alcohol. 3. Evidence of neglect; past history of dental hygiene care. Causes for Pathologic Halitosis c. Measurement of oral malodor: Patients should be instructed not to eat, chew, rinse or smoke for at least Oral and other contributing factors such as: two hours before examination. Patients who are on a. Periodontal infection: Odor from subgingival dental antibiotics should be seen 2 weeks after discontinuation biofilm. Specific diseases like acute necrotizing of medicines. The tests used to detect halitosis are as ulcerative gingivitis and pericoronitis. follows: b. Tongue coating harbors microorganisms. i. Subjective organoleptic method: This has been used c. Stomatitis, xerostomia. as a bench mark for oral malodor measurement. d. Faulty restorations retaining food and bacteria. ii. Gas chromatography: In order to assess oral e. Unclean dentures. malodor objectively, a portable industrial monitor CHAPTER 11 Oral Malodor 113 Halimeters Figs 11.2A and B: Figs 11.2A the mercury compound and the resultant reaction This test is highly sensitive as causes fluorescence. it can measure even the low levels of sulfur compounds in the sample, which is in contradiction to testing with a halimeter. TREATMENT AND MANAGEMENT OF TREATMENT ORAL MALODOR Treatment of oral malodor is a step-by-step problem solving Treatment procedure. Before commencing the treatment a clinician P. gingivalis, T. gingivalis, P. . It is accurate in produce waste products hydrogen sulfide, methyl hydrogen This test involves mixing a Gas chromatograph B. forsythus These machines measure the level of These machines measure and Some of the bacteria like Fig. 11.1: Fig. 11.1:

: denticola sample containing sulfur compound (VSCs) with that are quite odiferous and as a result contribute in that are quite odiferous and as a result question have causing bad breath. These bacteria in produce an the characteristic of being able to enzyme that degrades the compound N-benzoyl-dL- of When a sample arginine-2naphthylamide. saliva that contains these bacteria is placed patient’s they cause it within the BANA testing compound As a result of this degradation the to breakdown. test compound changes its color indicating a positive reaction. Chemiluminescence: mide) has been developed. These machines are specifically These machines has been developed. of molecular levels to digitally measure designed (VSCs) Sulfur Compounds Volatile the three major air ( in a sample of mouth mercaptan and dimethyl sulfide) mercaptan and dimethyl components of the breath and measuring the sulfur in graph form via computer produces visual results interface (Fig. 11.1). Halimeters: in a persons breath. But it has sulfide gas found in clinical applications, some of certain drawbacks are not the common sulfides such as mercaptan in test easily recorded and can be misrepresented The Halimeter is also very sensitive to results. alcohol or alcohol, so one should avoid drinking for at least using alcohol containing mouth-washes and B). 12 hours prior to being tested (Figs 11.2A . (N-benzoyl-dL-arginine-2-naphthyla- Test BANA v. iv iii. 114

must determine the source of malodor. The simplest way important diseases, if it can be analyzed accurately. VSC to distinguish oral from non-oral origin is to compare the in periodontal pockets might be used as a predictor of smell from mouth and nose. If the origin is nasal or due periodontal diseases and also to monitor therapy sites. to any other medical etiology they must be referred to a However, current available tools/tests are not applicable for concerned specialist. The odor generating from the mouth achieving these goals due to lack of accuracy and objectivity. often requires dental treatment. There are no standard and The dental research community has long since ignored accepted protocols for the treatment of oral malodor, the subject of oral malodor. Recently, along with the growing however, the possible protocols contains the basic elements public and media interest in oral malodor, dental

including standard dental and periodontal treatment. professionals are becoming more aware of this problem. PART III Let us hope that future research will overcome the problems For genuine halitosis with oral causes, the treatment is as related to diagnosing and treating oral malodor effectively. follows: a. Reduction of anaerobic load by improving oral hygiene and periodontal health through basic dental care and if 1. Halitosis is a term used to describe noticeably unpleasant necessary incorporate advanced hygiene methods odor exhaled in breathing. including oral irrigation and sonic or ultrasonic tooth 2. Halitosis is classified into genuine halitosis, pseudo- brushes. halitosis and halitophobia. 3. Most commonly halitosis is as a result of problems b. If oral malodor persists in spite of adequate conventional originating from the oral cavity (90%). The remaining Etiopathogenesis oral hygiene, tongue brushing should be advised. 10% is from systemic and non-oral origin. 4. Measurement of oral malodor is done by various c. Chemical reduction of oral microbial load includes methods like, organoleptic method, gas chromatography, rinsing or gargling with an effective . One Halimeters and BANA tests. way to treat oral malodor associated with periodontitis 5. Treatment of oral malodor is a step-by-step problem solving procedure. It involves a complete recording of is to combine regular periodontal treatment and a history, periodontal examination, and oral hygiene chlorhexidine mouth rinse. However, their long-term maintenance. 6. If oral malodor persists, chemical reduction of oral effect remains to be determined. microbial load should be incorporated. d. Another treatment strategy for oral malodor is conversion of volatile sulfur compounds by using ++ various metal ions. Zinc (Zn ) is an ion which bonds KNOW MORE ... to the twice negatively charged sulfur radicals to reduce the expression of VSCs. Halita™ is a new solution Specific character of breath odor can be related to a containing 0.05% chlorhexidine, 0.05% cetyl pyridium particular systemic malfunction chloride (CPC) and 0.14% zinc lactate with no alcohol • A “rotten eggs” smell indicative of volatile sulfur compounds (VSCs). has been more efficient than 0.2% chlorhexidine • A sweet odor could be associated with liver formulation in reducing the VSC levels. The special insufficiency (accumulation of aliphatic acids). effect of Halita™ may result from the VSC conversion • The smell of “rotten apples” associated with ability of zinc, besides its antimicrobial action. uncontrolled diabetes (accumulation of ketones). • A “fish odor” associated with kidney insufficiency (accumulation of di- and trimethylamine). SUMMARY

Halitosis affects a large proportion of population and may REVIEW QUESTIONS cause a significant social or psychological handicap to those 1. Describe the causes for oral malodor. who are suffering from it. Oral malodor can also reveal 2. Enumerate various methods of treating oral malodor. CHAPTER 11 Oral Malodor 115 and its association with age and sex in a general population in sex in a general population with age and and its association Diseases 2007;13:105-09. Brazil. Oral Assoc 2000;66:257- J Can Dent of halitosis; clinical perspectives. 61. 3.A. Oral Malodor Ponce de Leon Carvalho LBM, P, Nadanovsky 4. Examination, Classification, and treatment K, Coil JM. Yaegaki BIBLIOGRAPHY Oral Diseases 2007;13:63-70. Oral Diseases Journal of Am An Interdisciplinary approach. Halitosis: Otolaryngology 1998;19:8-11. 2.Laufer Don. Hannah, Horowitz Gershon, Nir Dan, Ben-Aryeh 1.halitosis. of subjects with AC. Clinical examination Donaldson 12 ChapterChapter

Pathogenesis of Periodontal Diseases

 ROLE OF BACTERIAL INVASION  EVASION OF HOST RESPONSES  ROLE OF EXOTOXINS  THE HOST DERIVED BONE RESORBING  ROLE OF CELL CONSTITUENTS AGENTS  ROLE OF ENZYMES  ROLE OF CYTOKINES

INTRODUCTION Junctional epithelium: It is the tissue most directly challenged by the pathogenic plaque bacteria. The microbial Gingivitis and periodontitis are caused by bacteria that mass releases large quantities of metabolites like butyric colonize the gingival crevice and attach to the tooth surface. acid and propionic acids which are toxic to periodontal The pathogenic potential of the bacteria within the plaque tissues. The keratinocytes respond to these bacterial products varies from gingiva site to site. Small amounts of plaque by releasing cytokines and proinflammatory mediators. can be tolerated without causing periodontal disease, may Interleukin (IL) and prostaglandin E2 (PGE2) and matrix be because of the host defence. metalloproteinases are released from the junctional epithelial When bacteria and its products in the plaque increase cells. Neutrophils are present in the junctional epithelium beyond the threshold level of the host, then the balance shifts as a part of host defence system. Activation of complement from health to disease. The mechanisms by which plays an important role in the earliest host response in the subgingival bacteria contribute to the pathogenesis of the gingival crevice. periodontal disease are different. The pathogenesis of periodontal disease can be caused by subgingival bacteria ROLE OF BACTERIAL INVASION alone or indirectly by evasion of immunologic host response. The properties that enable the bacterium to cause a disease Direct effect can be by bacterial invasion, production of are termed virulence factors, hence entry of bacterium itself exotoxins, role of cell constituents, and production of (invasion) or of bacterial products into the periodontal various enzymes. The direct exposure or effect can be on tissues may be essential in the disease process. the fibroblasts, epithelial cells, endothelial cells and The gingival sulcus and periodontal pockets are bathed inflammatory cells. in gingival crevicular fluid. Bacterial species that colonize 117 this region must attach to the available surfaces to avoid XII, activate the complement (C) system by the alternative the displacement by the fluid flow. The surfaces available pathway, lead to localized Schwartzman phenomena, with for attachment include the tooth or the root, the tissues and tissue necrosis occurring after two or more exposure to the HPE 12 CHAPTER pre-existing plaque mass. endotoxin, may also have cytotoxic effects on the cells such Bacteria that initially colonize the periodontal as fibroblasts and induce bone resorption. These endotoxins environment most likely attach to the pellicle or saliva- can penetrate gingival epithelium. Bacteria can also produce coated tooth surface, e.g. adherence of A. viscosus through fatty and organic acids such as butyric acid and propionic fimbriae on the bacterial surface to a proline-rich protein acids, amines, volatile sulphur compounds, indole, ammonia found on the saliva-coated tooth surfaces. and glycans. Bacterial attachment to the pre-existing plaque is studied Peptidoglycan: A cell wall component may affect a variety by examining the adherence between different bacterial of host responses including complement activation, Diseases Periodontal of Pathogenesis strains (coaggregation), e.g. A. viscosus with S. sanguis. immunosuppressive activity and stimulation of the These are important in the colonization of the periodontal reticuloendothelial system. It helps in the bone resorption environment. The presence of bacteria in patients with and in stimulating macrophages to produce prostaglandin ANUG was studied by Listgarten (1965). Microorganisms and collagenases. were recognized in the gingival connective tissue and in proximity to alveolar bone. Bacteria may also enter through ROLE OF ENZYMES ulceration in the pocket epithelium. In the Localized The bacterial enzymes that are capable of contributing to Juvenile Periodontitis (LJP), A. actinomycetemcomitans the disease process include collagenases, hyaluronidase, have been observed in gingival connective tissue. The gelatinase, aminopeptidase, phospholipases and alkaline and presence of this organism within the tissues appears to make acid phosphatases. the disease more resistant to treatment and requires the use Destruction of periodontal tissues is by degradation of of antibiotics. collagen. P. gingivalis and some strains of A. actinomy- cetemcomitans have been found to produce collagenase. ROLE OF EXOTOXINS Bacterial hyaluronidase is capable of altering gingival permeability by allowing the apical proliferation of the A. actinomycetemcomitans produces an exotoxin referred junctional epithelium along the root surfaces. Hyaluronidase to as leukotoxin because of its toxic effect on the human is found in high concentrations in periodontal pocket. polymorphonuclear neutrophils (PMNs). The production of leucotoxin may enable A. actinomycetemcomitans to evade the host defence. EVASION OF HOST RESPONSES (TABLES 12.1 TO 12.5)

ROLE OF CELL CONSTITUENTS Bacterial factors can also indirectly compromise the host tissues. These factors influence both the cellular and humoral Cell constituents of both gram-positive and gram-negative immune responses. bacteria include endotoxins, bacterial surface components For example, and capsular components. Endotoxin or lipooligosaccharide (LOS) previously 1. Inhibition of PMNs by leukotoxin chemotactic termed as lipopolysaccharide (LPS) is found in the outer inhibitors, decreased phagocytosis. membrane of all gram-negative bacteria. They are toxic 2. Immunoglobulins are inactivated by proteases. substances affecting the tissues directly and through 3. Lymphocyte alterations activation of the host responses. Its role in periodontal 4. Endotoxicity disease is, their ability to produce leukopenia, activate factor 5. Catalase reaction. 118

Table 12.1: Influence of host response on Table 12.3: Mechanism which results in periodontal disease changes in epithelium

Aspect of Host factors Mechanism Effects disease 1. Bacterial toxins, e.g. • Cytotoxic to keratinocytes 1. Bacterial Subgingivally, antibody, complement in endotoxins • Disruption of normal colonization crevicular fluids inhibits adherence and epithelial turnover and coaggregation of bacteria and potentially differentiation reduces their numbers by lysis.

PART III 2. Bacterial Antibody-complement 2. Bacterial enzymes • Damage to keratinocytes invasion 1. Mediated lysis reduces bacterial counts. 2. Neutrophils as a consequence of chemo- 3. Release of enzymes • Damage of keratinocytes taxis, phagocytosis and lysis reduces from neutrophils bacterial counts 4. Complement activation • Cell damage 3. Tissue By antibody-mediated hypersensitivity, destruction cell-mediated immune responses. Activation 5. Production of TNF • Decreased → keratinocyte of tissue destruction factors such as colla- and interferon G by proliferation genase. activated T-lymphocytes 4. Healing and Lymphocytes and macrophages produce fibrosis chemotactic factors for fibroblasts, fibroblast 6. Production of IL-1 by • Increased → keratinocyte

Etiopathogenesis activating factors. macrophages proliferation

Table 12.2: Impact of microorganisms Table 12.4: Mechanisms which result in on inflammation and immunity changes in connective tissue

Microbes and products Effects Mechanisms Effects

1. Microorganisms • Activate complement Bacterial toxins, e.g. • Toxic to fibroblasts • Activate neutrophils and endotoxins • Decrease in collagen macrophages. production • Are antigenic. Bacterial enzymes, e.g. • Degradation of extracellular collagenase, hyaluronidase matrix components. 2. Most peptides and • Chemotactic for neutrophils Release of enzymes from • Damage to extracellular proteins secreted by and macrophages. neutrophils matrix components. microorganisms • Are antigenic. Complement activation • Damage to fibroblasts • Decrease in collagen 3. Enzymes • Damage host cells. production • Degrade connective tissue Production of IL-1 and • Increased secretion of colla- matrix. TNF genase and proliferations • Activate and degrade by fibroblasts complement. Production of TGF and • Stimulation of fibroblast • Degrade antibody. Platelet derived chemotoxin proliferation, • Are antigenic. growth factors (PDGF) matrix synthesis and attempts at repair. 4. Lipopolysaccharide • Activate complement. Products of tissue damage • Stimulation of fibroblast cells • Damage host cells and alveolar bone resorption. • Is antigenic. THE HOST DERIVED BONE RESORBING AGENTS 5. Polysaccharide plaque • Polyclonal B-cell activator. matrix and bacterial • Are antigenic. Cytokines capsule 6. Other toxins, acids, • Damage host cells. • IL-1 reducing agents • Are antigenic. • TNF 119

Table 12.5: Pathogenic immune reactions Important Cytokines Associated with Periodontal Disease Types Description Definition Examples HPE 12 CHAPTER Type-I Anaphylactic Antigen reacts with Urticaria, hay 1. IL-1: It is produced predominantly by macrophages and cells sensitized by fever, asthma, lymphocytes. Fibroblasts, platelets and keratinocytes and IgE antibodies and food allergies. release mediators. endothelial cells also release IL-1. It upregulates adhesion molecules on endothelial cells, lymphocytes, Type-II Cytotoxic Antibody reacts Transfusion neutrophils and monocytes. It activates T and B with cell-associated reaction auto- α antigen usually, immune hemo- lymphocytes and promotes antibody production. IL-1 but not always, lytic anemia and IL-1β are potent stimulators of connective tissue

kills cells with help destructions. It triggers the release of large quantities of Diseases Periodontal of Pathogenesis of complement or phagocytic cells. prostaglandins E2 from fibroblasts and monocytes and stimulates secretion of matrix metalloproteinases. Type-III Arthus Antibody reacts Serum 2. IL-2: Monocytes and T lymphocytes produce IL-2. It reaction with antigen in sickness, tissue spaces or Arthus reaction stimulates T cells and enhances clonal expansion of beta blood stream to cells into plasma cells. cause vasculitis, requires 3. IL-4, IL-5 and IL-10: They are produced by TH2 cells complement. and help in the activation of beta cells into plasma cells and down regulate monocytic response. Type-IV Delayed Lymphocyte reacts Tuberculin hyper- with antigen. This reaction, con- 4. IL-6: It is released by lymphocytes, fibroblasts and sensitivity reaction is medi- act dermatitis, monocytes. Lipopolysaccharide, IL-1 and tumor necrosis ated by lympho- allograft rejec- factor alpha upregulates the secretion of the IL-6. It is cytes, macrophages tion. or their products. believed to be responsible for conversion of blood monocytes into osteoclasts. • TGF-β 5. IL-8: It is secreted by monocytes, keratinocytes and • IL-6 fibroblasts. It is a strong chemoattractant of PMNLs at low concentrations. Other Inflammatory Mediators 6. TNF: Tumor necrosis factor are produced by macro- phages and release lymphotoxins. They stimulate the • Prostaglandins proliferation of osteoclast precursor cells and also • Leukotrienes activate the mature osteoclasts to resorb bone. It augments leukocyte chemotaxis, degranulation, adherence to ROLE OF CYTOKINES endothelial cells and its ability to kill bacteria. Meaning “cell protein” is used for molecules which transmit 7. Prostaglandin E2: Sources are macrophages and information or signals from one cell to another. Interleukins, fibroblasts. IL-1 induces its production. It is a potent growth factors, chemokines and interferon belong to the mediator of osteoclastic resorption. family of cytokines. They act on fibroblasts, macrophages, 8. Matrix metalloproteinases (MMPs): These are a family keratinocytes and PMNLs to release matrix metallo- of enzymes capable of degrading connective tissue proteinases (MMPs) that degrade connective tissue matrix. matrix. These enzymes are secreted in the latent form However, most findings show that tissue destruction that by fibroblasts, macrophages, keratinocytes and PMNLs, occurs in periodontal disease is mainly due to host response e.g. collagenase, gelatinase, stromalysin, matrilysin. to the bacteria and their products. IL-1 play an important role in upregulation of MMPs. 120

The leukotrienes, prostaglandins and related molecules REVIEW QUESTIONS are short range hormones that are produced by many cells; they exert their effect locally and are destroyed 1. Describe the role of plaque bacteria in the pathogenesis rapidly and spontaneously. of periodontal disease. Prostaglandins and leukotrienes have been detected in 2. What are endotoxins? biologically-active concentrations in the inflammatory 3. What are cytokines? exudates, leukotrienes C4, D4, and E4 known as slow

PART III reacting substances of anaphylaxis (SRS-A) are released BIBLIOGRAPHY from mast cells and basophils. 1. Denis F Kinane. Causation and pathogenesis of periodontal disease. Periodontol 2000;25:2001. KNOW MORE ... 2. Genco. Contemporary Periodontics. CV Mosby Company Publication, 1990. Various bacterial enzymes capable of 3. Jan Lindhe. Clinical Periodontology and Implant Dentistry 4th degrading host tissue edn, Blackwell Munksgaard Publication, 2003. They are collagenase, trypsin-like enzyme, phospho- 4. Michael S Reddy, Harjoice K Jeffcoat. Periodontal disease lipase A, arylsulfatase, and neuraminidase. progression. Current Opinion in Periodontology 1993; 111: 128.

Etiopathogenesis In addition to immune cells, cells of the periodontium 5. Saul Schluger. Periodontal diseases basic phenomena, clinical express toll-like receptors (TLR). Signaling of these management and occlusal and restorative inter-relationships. 2nd receptors results in innate immune responses including edn, Lea and Iebiger publication. the release of various antibacterial peptides. Matrix metalloproteinases (MMP) are a group of 6. William B Clark Harald Loe. Mechanisms of initiation proteolytic enzymes found in neutrophils, macrophages, and progression of periodontal disease. Periodontol 2000;2: fibroblasts, epithelial cells and osteoblasts. They degrade 1993. extracellular matrix molecules such as collagen, gelatin and elastin. 13 ChapterChapter

Periodontal Medicine

 ERA OF FOCAL INFECTION  PERIODONTAL DISEASE AND CHRONIC  PERIODONTAL DISEASES AND CORONARY OBSTRUCTIVE PULMONARY DISEASE HEART DISEASE/ATHEROSCLEROSIS  PERIODONTAL DISEASE AND ACUTE  EFFECT OF PERIODONTAL INFECTION RESPIRATORY INFECTION  PERIODONTAL DISEASE AND DIABETES  PERIODONTAL MEDICINE IN CLINICAL MELLITUS PRACTICE  ROLE OF PERIODONTITIS IN PREGNANCY OUTCOME

INTRODUCTION premature low-birth infants and pulmonary diseases). Thus, the emerging evidence has shed light on the converse Advances in science and technology over the last century relationship between systemic health and oral health, i.e. have greatly expanded our knowledge of the pathogenesis the potential effects of periodontal disease on a wide range of periodontal diseases. It is clear that certain systemic of organ systems. Thus, this chapter examines the emerging conditions may affect the initiation and progression of new evidence collected since the early 1990s implicating gingivitis and periodontitis. periodontal infection as a risk factor for several systemic The oral cavity is continuously challenged by conditions. opportunistic infections on one hand and the oral complications of systemic diseases and disorders occur on ERA OF FOCAL INFECTION the other hand, thus an association between oral infections and systemic diseases has been suspected for centuries. At the beginning of the twentieth century, medicine and The effect of oral health on the rest of the human body was dentistry were searching for reasons to explain why people proposed by the Assyrian’s in the seventh century BC. In became afflicted with a wide range of systemic diseases. the 18th century a Pennsylvanian physician name Benjamin Medicine at that time had very little insight into what caused Rush quoted that arthritis could be treated in some people diseases such as arthritis, pneumonia and pancreatitis, to after they had extracted the infected teeth. But, over the name a few. Then, through the writings and lectures of past decade, growing scientific evidence suggests an principally two individuals, WD Miller and William Hunter, exquisite association between oral infection (e.g. viruses, the concept that oral bacteria and infection were the likely bacteria, yeasts) and systemic diseases (e.g. atherosclerosis, cause of most of a person’s systemic illness suddenly became cardiovascular diseases, cerebrovascular diseases, very popular. For the next 40 years infections, especially 122

those originating in the mouth caused most of the man’s However, it was not until the last decade of the twentieth suffering and illness. This era, which came to be known as century that dentistry and medicine again began to examine the ‘era of focal infection’ can be attributed primarily to a the relationship of oral infections as a risk for systemic microbiologist in Philadelphia, Willoughby D. Miller and a disease and now there is a careful new look at periodontitis London Physician, William Hunter. as a possible risk for systemic disease using discrete ‘Focal infection’ implied that there was a nidus of scientific levels of evidence. infection somewhere in the body, such as periodontitis, which via the bloodstream could affect distant sites and organs. PERIODONTAL DISEASE AND CORONARY HEART DISEASE/ATHEROSCLEROSIS PART III PART Throughout the 1920s and 1930s, dentists and physicians believed that bacteria on the teeth and the resultant infectious CHD and CHD-related events are a major cause of death. diseases such as caries, gingivitis and periodontitis that Myocardial infarction has been associated with acute followed were a ‘focus of infection’ that led to a wide variety systemic bacterial and viral infections and infarction is of systemic problems. It became popular during this period sometimes preceded by influenza like symptoms. to extract teeth as a means of ridding the body of oral Is it possible that oral infections is similarly related to bacteria and preventing and/or treating diseases affecting myocardial infarction? the joints as well as diseases of the heart, liver, kidneys and Traditional risk factors such as smoking, dislipidemia, pancreas. hypertension and diabetes mellitus do not explain the

Etiopathogenesis Hunter believed that teeth were liable to septic infection presence of coronary atherosclerosis in a large number of primarily due to their structure and their relationship to the patients. Localized infection resulting in a chronic alveolar bone. He stated that ‘the degree of systemic effect inflammatory reaction has been suggested as a mechanism produced by oral sepsis depended on the virulence of the underlying coronary heart disease in these individuals. oral infection and degree of resistance of the individual’. He In cross-sectional studies of patients with acute also felt that oral organisms has specific actions on different myocardial infarction or confirmed CHD compared with tissues and that these organisms acted by producing toxins, age and gender matched control patients, myocardial resulting in low grade ‘subinfections’, which produced infarction patients had significantly worse dental health than systemic effect over prolonged periods. did controls. This association between poor dental health However, by 1940, medicine and dentistry were realizing and myocardial infarction was independent of known that there was much more to explain a patient’s general risk factors for heart disease such as age, cholesterol systemic condition than bacteria in his or her mouth. Dentists level, hypertension, diabetes and smoking, because and physicians realized that: (1) extracting a person’s teeth artherosclerosis is a major determinant of CHD-related did not necessarily make the person better or make their events, dental health has also been related to coronary disease go away, (2) people with very healthy mouths and atheromatosus. no obvious oral infection developed systemic diseases, and Mattila and colleagues performed oral radiographic (3) people who had no teeth and thus no apparent oral examinations and diagnostic coronary angiography infection still developed systemic diseases. examinations on men with CHD. There was a significant By 1950, medicine was making great strides in correlation between the severity of dental disease and degree discovering the true etiologies and dentistry was making of coronary atheromatosus. This relationship remained great strides in the prevention as well as the treatment of significant after accounting for other known risk factors caries and periodontal disease and so the era of ‘focal for coronary artery disease. Cross-sectional studies, thus infection’ as a primary cause of systemic diseases finally suggest a link between oral health and coronary heart came to an end. disease. 123

However, such studies cannot determine causality in this relationship. Rather, dental diseases may be indicators of general health practices for example, periodontal disease and CHD are both related to lifestyle and share numerous CHAPTER 13 risk factors such as smoking, diabetes and low socioeconomic status. Bacterial infections have significant effects on endothelial cells, blood coagulation, lipid metabolism and monocyte macrophages. The research of Mattila and colleagues showed that dental infections were the only factors, other than classic and well-recognized coronary risk factors, that were associated independently with the severity of coronary arteriosclerosis. Medicine Periodontal This study and others in which periodontal condition is known to have preceded the CHD-related events, support the concept that periodontal disease is a risk factor for CHD, independent of other classic risk factors.

EFFECT OF PERIODONTAL INFECTION Periodontal infection may affect the onset or progression of atherosclerosis and coronary heart disease through certain mechanisms. Periodontitis and atherosclerosis both have complex etiologic factors, combining genetic and environmental influences. The diseases share many risk factors and have distinct similarities in basic pathogenic Fig. 13.1: Factors affecting blood viscosity in health mechanisms. involved in coronary thrombogenesis since platelets Ischemic Heart Diseases selectively bind some strains of Streptococcus sangius, a Ischemic heart disease is associated with the process of common component of supragingival plaque and atherogenesis and thrombogenesis. Increased viscosity of Porphyromonas gingivalis, a pathogen closely associated blood may promote major ischemic heart disease and stroke with periodontitis. by increasing the thrombus formation. Daily activity: Routine daily activity such as mastication Increased plasma fibrinogen is a recognized risk factor and oral hygiene procedures results in frequent bacteremia for cardiovascular events and peripheral vascular disease. with oral organisms. The exposure time to bacteremias from Also elevated white blood cell count and coagulation factor routine daily chewing and tooth brushing is much greater VIII has been associated with risk of ischemic heart disease than from dental procedures. Periodontal disease may (Fig. 13.1). predispose the patient to an increased incidence of bacteremias. Thrombogenesis It has been estimated that about 8 percent of all cases Platelet aggregation plays a major role in thrombogenesis, of infective endocarditis are associated with periodontal and most cases of acute myocardial infarction are or dental diseases without any preceding dental precipitated by thromboembolisms. Oral organisms may be procedure. 124

Atherosclerosis (Fig. 13.2) PERIODONTAL DISEASE AND DIABETES MELLITUS

An understanding of effects of other infections is useful in determining the mechanisms by which the periodontal infection influences glycemia. Acute bacterial and viral infections have shown to increase insulin resistance and aggravate glycemic control. This occurs in individuals with and without diabetes. Systemic infection increases tissue

PART III PART resistance to insulin, preventing glucose from entering target cells causing elevated blood glucose level and requiring increased pancreatic insulin production to maintain normoglycemia. It is possible that chronic Gram-negative periodontal infection may also result in increased insulin resistance and Fig. 13.2: Atherosclerosis poor glycemic control. In patients with periodontitis, persistent systemic Periodontal Infection and Stroke challenge with periodontopathic bacteria and their products Etiopathogenesis may act in a way similar to well-recognized systemic Ischemic cerebral infarction or stroke is often preceded by infection. This mechanism would explain the worsening of systemic bacterial or viral infections. In one study patients glycemic control associated with severe periodontitis. with cerebral ischemia were five times more likely to have Periodontal treatment designed to decrease the bacterial insult had a systemic infection within 1 week before the ischemic and reduce inflammation might restore insulin sensitivity event than were non-ischemic control subjects. Recent overtime, resulting in improved metabolic control. The infection was a significant risk factor for cerebral ischemia improved glycemic control seen in several studies of and was independent of other known risk factors such as periodontal therapy would support such a hypothesis. hypertension, history of a previous stroke, diabetes, smoking and coronary heart disease. ROLE OF PERIODONTITIS IN In case-control studies, poor dental health was a PREGNANCY OUTCOME significant risk factor for cerebrovascular ischemia. In Periodontitis is a remote Gram-negative infection that may one study bleeding on probing, suppuration, subgingival play a role in preterm low birth weight (Fig. 13.3) and pre- calculus and number of periodontal and periapical lesions eclampsia. were significantly greater in male stroke patients than in Periodontopathic organisms and their products may controls. have wide range effects, most likely mediated through Overall 25 percent of all stroke patients had significant stimulation of host cytokine production in target tissues. dental infections compared with only 2.5 percent of Animal studies suggest that remote reservoirs of Gram- controls. This study supports an association between poor negative organisms and their products may have a negative oral health and stroke in men under age 50. In another impact on pregnancy. Porphyromonas gingivalis implanted study men and women’s of age 50 and older who had a in subcutaneous chambers during gestation caused stroke had significantly more severe periodontitis and more significant increase in fetal death and a decrease in fetal periapical lesions as compared to the non-stroke control birth weight for those that remained viable, when subjects. compared with control animals that were not innoculated. 125

CHAPTER 13 Periodontal Medicine Periodontal

Fig. 13.3: Periodontitis and preterm birth/intrauterine growth retardation

α There was a significant increase in TNF- and PGE2 levels. Chronic obstructive pulmonary disease shares similar There was a significant correlation between TNF-α and pathogenic mechanism with periodontal disease. In both

PGE2 levels, as well as fetal death and growth retardation. diseases, a host inflammatory response is mounted in These data suggest that a remote, non-disseminated response to chronic challenge by bacteria in periodontal infection with Porphyromonas gingivalis may result in disease and by factors such as cigarette smoke in chronic abnormal pregnancy outcome in this model. obstructive pulmonary disease. The resulting neutrophil influx leads to release of oxidative and hydrolytic enzymes PERIODONTAL DISEASE AND CHRONIC that cause tissue destruction directly. OBSTRUCTIVE PULMONARY DISEASE In analyzing data from a longitudinal study of more than Chronic obstructive pulmonary disease is a disease state 1100 men alveolar bone loss was associated with the risk characterized by airflow obstruction due to chronic of chronic obstructive pulmonary disease. The increase in bronchitis or emphysema. Bronchial mucous glands enlarge the risk was independent of age, smoking status and other and an inflammatory process occurs in which neutrophils known risk factors for chronic obstructive pulmonary and mononuclear inflammatory cells accumulate within the disease. Individuals with poor oral hygiene have also been lung tissue. found to be at an increased risk for chronic respiratory 126

diseases such as bronchitis and emphysema. These organisms from periodontal pockets may serve as the associations remain to be confirmed by further research. primary innoculum for suppurative respiratory disease such as pulmonary abscesses that have significant morbidity and PERIODONTAL DISEASE AND ACUTE mortality. Although considerable circumstantial evidence RESPIRATORY INFECTION suggests that periodontal pathogens may cause acute Pneumonia is an infection of lungs caused by bacteria virus, nosocomial pulmonary infection, currently no published fungi or mycoplasma and is broadly categorized as either studies specifically demonstrate an increased risk of such • Community acquired, or infections in patients with periodontal disease.

PART III PART • Hospital acquired Community acquired bacterial pneumonia is caused PERIODONTAL MEDICINE IN primarily by inhalation of infectious aerosols or by CLINICAL PRACTICE aspiration of oropharyngeal organisms. S. pneumonia and The concept of periodontal diseases as localized entities Haemophilus influenzae are most common, although affecting only the teeth and supporting apparatus is over- numerous other species may occur, including anaerobic simplified and needs to be revised. Rather than being bacteria. To date, no associations have been found between confined to periodontium, periodontal diseases may have oral hygiene or periodontal disease and the risk for acute wide-ranging systemic effects. In most persons these effects respiratory conditions such as pneumonia in community may be relatively inconsequential or at least not clinically

Etiopathogenesis dwelling individuals. evident. However in susceptible individuals, periodontal Hospital acquired (nosocomial) bacterial pneumonia has infection may act as an independent risk factor for systemic very high morbidity and mortality rate. The incidence of disease and may be involved in the basic pathogenic nosocomial pneumonia is highest in severely ill patients such mechanism of these conditions. Furthermore, periodontal as those in intensive care units or on ventilatory support. infection may exacerbate existing systemic disorders. Hospital acquired pneumonia is usually caused by Proper use of knowledge of relationship between aspiration of oropharyngeal contents. Oropharyngeal periodontal disease and systemic health requires the dental colonization with potential respiratory pathogens (PRPs) professional to expand his or her horizons, to step back increase during hospitalizations and the longer the hospital from the technically demanding aspects of dental art, and stay the greater the prevalence of PRPs. PRPs are found to recognize the oral cavity as one of the many interrelated predominantly in the gastrointestinal tract and may be passed organ systems. Patient education in this regard is also very through esophageal reflux into the oropharynx where they important. colonize. Subsequent aspirations may lead to pneumonia. The PRPs may also originate in the oral cavity, with dental plaque serving as a reservoir of these organisms. 1. Periodontal infection may affect the onset or progression of atherosclerosis and coronary heart Poor oral hygiene is common in the hospital and nursing disease through certain mechanisms. home settings, especially in severely ill patients. PRPs are 2. Altered microbiota associated with deep periodontal commonly isolated from supragingival plaque and buccal pockets → bacterial translocations/or systemic inflammation → endothelial and altered vascular mucosa of patients in intensive care units than in outpatient response → cytokines and acute phase proteins setting. Thus, organisms that are not routinely found in atherosclerotic changes → coronary artery disease dental plaque become plaque colonizers after prolonged (MI). 3. Studies conducted by Offenbacher has shown that hospitalizations. Subgingival plaque may also harbor PRPs women with severe periodontitis are 7.5 times more and putative periodontal pathogens have been associated likely than women without periodontal disease to have with nosocomial pneumonia. Furthermore anaerobic an infant with preterm low-birth weight. 127

BIBLIOGRAPHY

KNOW MORE ... 1. Carrazas Clinical Periodontology. 9th edn, Newman, Takie, Fermin A Carranza, WB Saunders Co., 2002.

In periodontal medicine, evaluation of evidence 2. Frank A. Scanntrapillo. Relationships between periodontal CHAPTER 13 could be derived from various types of studies disease and respiratory diseases. Periodontal Medicine, BC a. Case reports — provides relatively weak, anecdotal Decker, 2000. evidence. 3. George W. Taylor, Brian A. Burt, Mark P. Becker, Robert J b. Cross-sectional study — compares groups of Genco. Severe periodontitis and risk for poor glycemic control subjects at a single point in time. in patients with non-insulin diabetes mellitus. c. Longitudinal study — stronger than cross sectional study, follows groups of subjects over a period of 4. James Beck, Raul Garcia, Gerardottei. Periodontal disease time. and cardiovascular disease. J Periodontol No 67, Oct

d. Interventional trial — strongest form of evidence 1996. Medicine Periodontal examines effects of some interventions. 5. Offenbacher S, Katz V, Fertik G, Collins J. Periodontal infection as a possible risk factor for preterm low birth weight. J Periodontol 1996; 67: 1103-13. REVIEW QUESTION 6. Thoden Van Velzen, Abraham Inpigin, Moorer. Plaque and 1. Describe the role of periodontal disease as a risk factor systemic disease: A reappraisal of the focal infection concept. J for systemic diseases (Periodontal Medicine). Clin Periodontol 1984; 11: 209-20. 14 ChapterChapter

Smoking and Periodontal Diseases

 EFFECT OF SMOKING ON THE PREVALENCE • Microbiology AND SEVERITY OF PERIODONTAL DISEASE • Immunology • Gingivitis • Physiology • Periodontitis  EFFECT OF SMOKING ON THE RESPONSE TO  EFFECT OF SMOKING ON THE ETIOLOGY AND PERIODONTAL THERAPY PATHOGENESIS OF PERIODONTAL DISEASE  EFFECT OF SMOKING CESSATION

EFFECT OF SMOKING ON THE PREVALENCE Table 14.1: Impact of smoking on periodontal diseases

AND SEVERITY OF PERIODONTAL DISEASE Periodontal disease Impact of smoking

See Table 14.1. Gingivitis • Decreased gingival inflammation and bleeding on probing. EFFECT OF SMOKING ON THE ETIOLOGY AND Periodontitis • Increased prevalence and severity of periodontal destruction. PATHOGENESIS OF PERIODONTAL DISEASE • Increased pocket depth, attachment loss and bone loss. Microbiology • Increased rate of periodontal • Smokers had higher level of Bacteroides forsythus. destruction. • Increased prevalence of severe • Smokers do not respond to mechanical therapy and this periodontitis. is associated with increased level of B.forsythus, • Increased tooth loss. A. actinomycetemcomitans and P. gingivalis remaining • Increased prevalence with increased in the pocket after therapy when compared to number of cigarettes smoked per day. nonsmokers. • Decreased prevalence and severity with smoking cessation. • Eikenella nodatum, Fusobacterium nucleatum, S. vincentii, P. gingivalis, P. intermedia, Peptostrepto- significantly more prevalent in current smokers than in coccus micros, Prevotella nigrescens, B. forsythus were nonsmokers and former smokers. 129

Immunology • Altered neutrophil chemotaxis, phagocytosis and oxidative burst. • Increased TNF-α, and PGE in GCF. 2 CHAPTER 14

• Increased production of PGE2 by monocyte in response to lipopolysaccharides (LPS).

• IgG2 level is reduced suggesting reduced protection against periodontal infection. • Nicotine, a major component of tobacco adversely affect fibroblast function.

• Nicotine suppresses osteoblast proliferation while Smoking and Periodontal Diseases Periodontal and Smoking stimulating alkaline phosphatase activity. Fig. 14.1: Decreased signs of inflammation in smokers • Tobacco products alter normal reparative and regeneration potential of periodontium. • Decreased subgingival temperature. • Increased time needed to recover from local anesthesia. Physiology

• Clinical signs of inflammation are less pronounced, due EFFECT OF SMOKING ON THE RESPONSE TO to alteration in the inflammatory response in smokers PERIODONTAL THERAPY or due to alteration in vascular response of gingival tissues (Fig. 14.1). See Table 14.2. • Decreased gingival blood vessels with increased EFFECT OF SMOKING CESSATION inflammation. • Decreased GCF flow and bleeding on probing with • Gingiva of treated current smokers exhibit minimal increased inflammation. redness and bleeding while brushing presumably

Table 14.2: Effect of smoking on periodontal therapies

Therapy Effect of smoking Non-surgical • Decreased clinical response to scaling and root planing • Decreased reduction in pocket depth • Decreased gain in clinical attachment level. • Decreased negative impact of smoking with increased level of plaque control. Surgery and implants • Decreased pocket depth reduction post surgery. • Increased deterioration of furcation postsurgery. • Decreased gain in clinical attachment level, decreased bone fill, increased recession and increased membrane exposure following guided tissue regeneration (GTR). • Decreased pocket depth reduction after DFDBA allograft. • Decreased pocket depth reduction and gain in clinical attachment level after . • Conflicting data on the impact of smoking on implant success. • Smoking cessation should be recommended prior to implant. Maintenance • Increased pocket depth during maintenance. • Decreased gain in clinical attachment level. Recurrent (refractory) • Increased recurrent/refractory disease in smokers. disease • Increased need for retreatment in smokers. • Increased need for antibiotics in smokers to control the negative effect of periodontal infection on surgical outcome. • Increased tooth loss in smokers after surgical therapy. 130

because of immunosuppression or vascular effect of c. Products of nicotine forms a layer on root surface smoking. which can alter fibroblast attachment and hence • Several weeks following smoking cessation, gingival decreased collagen production. inflammation and bleeding on brushing occurs because – In an attempt to tobacco cessation, various nicotine replacement therapies have been of smoking cessation, gingiva loses its thick fibrotic introduced. Currently, FDA (The US Food and appearance and assumes normal anatomy. Drug Administration) approves nicotine chewing Therefore, smoking status should be considered in gum, nicotine lozenges, nicotine patches, nasal diagnosis, prognosis and treatment planning of periodontitis sprays and nicotine inhaler.

patients. PART III PART REVIEW QUESTION

1. What are the effects of smoking on periodontal disease? 1. In smokers there is decreased gingival inflammation and bleeding on probing. But, increased prevalence and severity of periodontal destruction. BIBLIOGRAPHY 2. There is increased levels of periodontopathic organisms namely, B. forsythus, P. gingivalis, A. actinomycete- 1. Ah MBK, Johnson GK, Kaldahl WB, et al. The effect of smoking mcomitans and others. on the response to periodontol therapy. Journal of Clinical 3. Increased production of inflammatory mediators. Periodontol 1994;21:91. 4. Fibroblast function is diminished. It also alters normal Etiopathogenesis 2. Bergstrom J, Eliassons, Dock J. A 10-year prospective study of reparative and regeneration potential of periodontium. tobacco smoking and periodontol health. Journal of Periodontol 5. In general, there is increased need for retreatment in smokers. 2000;71:1338. 3. Haber J, Wattler J, Crowley H, et al. Evidence of cigarette smoking as a major risk factor for periodontitis. Journal of Periodontol 1993;64:16. KNOW MORE ... 4. Newman, Takei, Fermin. A Carranza. Clinical Periodontology by WB Saunders Co. Local effects of nicotine 5. Robin A Seymour, Peter A. Heasman. Drugs, Diseases and a. Nicotine levels in GCF can be up to nearly 300 times Periodontium. Oxford University Press Publication 1992. that of nicotine plasma concentrations in smokers. 6. Tonneti MS. Cigarette smoking and periodontal diseases, b. Impairs gingival blood flow which in turn affects the etiology and management of disease. Annals of Periodontol wound healing. 1998;3:88. 15 ChapterChapter

Host Modulation in Periodontal Therapy

 INTRODUCTION  PRODUCTION OF ARACHIDONIC ACID  REGULATION OF IMMUNE AND METABOLITES INFLAMMATORY RESPONSES  REGULATION OF BONE METABOLISM  EXCESSIVE PRODUCTION OF MATRIX METALLOPROTEINASES (MMPs)

INTRODUCTION doxycycline marketed as Periostat™ by collagens pharmaceuticals. Specific Aspects of Disease Pathogenesis as Potential Targets for Host Modulation REGULATION OF IMMUNE AND Considering the fact that periodontal disease is, as a result INFLAMMATORY RESPONSES of host interaction between the plaque biofilm and host Currently, it is believed that, small groups of perio- responses, the area of research is mainly directed at altering dontopathic microorganisms within the plaque biofilm are an individual’s reaction to the bacterial challenge. Hence, often associated with disease initiation and progression. various host modulatory therapies (HMT) have been Some of the strongly implicated organisms include developed or proposed to block the pathways responsible Porphyromonas gingivalis, Actinobacillus actinomycete- for periodontal tissue breakdown. In context to this, specific mcomitans (Aggregatibacter actinomycetemcomitans) and aspects of disease pathogenesis that have been investigated Bacteroides forsythus. The disease initiation occurs by for modulation include, microbial challenge consisting of antigens, lipopoly- a. Regulation of immune and inflammatory responses. saccharides (LPS) and other virulence factors, stimulates b. Excessive production of matrix metalloproteinases. host responses thereby resulting in disease either limited to c. Arachidonic acid metabolism. gingiva (gingivitis) or progresses to periodontitis. d. Bone metabolism. Activation of host has both protective and destructive Currently, one systemically administered agent is aspects. Protective aspects of host response include recruit- available for modulation of host, i.e. subantimicrobial dose ment of neutrophils, production of protective antibodies and 132

possibly the release of various anti-inflammatory cytokines produce MMPs including collagenase. It is however, including TGF-β (transforming growth factor-β and believed that endogenous MMPs are not the bacterial interleukins (IL-4, IL-10 and IL-12). On the other hand proteinases primarily responsible for tissue destruction. This perpetuation of the host response due to persistent bacterial further emphasizes the role of host modulatory approaches onslaught may disrupt the homeostatic mechanism and result in periodontal therapy (Fig. 15.1). in release of mediators including proinflammatory Several synthetic MMP inhibitors are being studied in cytokines, (e.g. IL-1, IL-6, TNF-α), matrix metallo- clinical trials. One such most extensively studied inhibitor

proteinases (proteases) and prostaglandin E2 (PGE2), which are the family of tetracycline antibiotics, which can inhibit

can promote extracellular matrix destruction in the gingiva host derived MMPs by mechanisms independent of their PART III to stimulate bone resorption. However, there are other set antimicrobial properties. The development of host of cytokines, which can suppress the action of pro- modulating therapy (HMT), utilizing tetracyclines primarily inflammatory cytokines, they include IL-4, IL-10, IL-11 and involves the use of a reduced dose of doxycycline TGF-β. When administered for therapeutic purposes, these (Periostat™ 20 mg bid). These doses reportedly do not antagonists can reduce inflammation. However, there are exhibit antimicrobial effects, but can effectively lower MMP certain unresolved issues regarding the cytokine modulation levels. This reduced dose has been referred to as therapy like identifying an ideal method to maintain or subantimicrobial dose doxycycline (SDD). inhibit cytokines for long periods and also understanding In addition to use of SDD in host modulating therapy,

of the systemic implications associated with altering 10 different chemically modified tetracyclines (CMTs) have Etiopathogenesis cytokine levels on tissue homeostasis. been developed, 9 of which inhibits MMPs and do not Therefore, additional animal and human studies are possess antimicrobial properties. In animal models CMTs required to apply it routinely in the treatment of have been reported to reduce the progression of periodontitis. experimentally induced periodontitis, however inhibition of human periodontitis is still not established. EXCESSIVE PRODUCTION OF MATRIX METALLOPROTEINASES (MMPs) PRODUCTION OF ARACHIDONIC MMPs are a family of zinc and calcium dependent ACID METABOLITES endopeptidases secreted or released by a variety of Another destructive pathway in the pathogenesis of infiltrating cells like neutrophils, macrophages and resident periodontal disease is synthesis and release of prostaglandins cells like fibroblasts, epithelial cells, osteoblasts and and other arachidonic acid metabolites within periodontal osteoclasts found in the periodontium. tissues. Whenever, there is tissue damage due to bacterial The major functions of MMPs are to degrade the and host factors the phospholipids in the plasma membrane constituents of the extracellular matrix like laminin, of cells becomes available to phospholipase A2, thereby collagen, fibronectin, etc. results in production of free arachidonic acid. Arachidonic acid can be metabolized via the cyclooxygenase or lipoxy- Role of MMPs in Human Periodontal Diseases genase pathway. The final products of the cyclooxygenase One hypothesis regarding periodontal disease pathogenesis pathway include prostaglandins, prostacycline and is that host cells stimulated directly or indirectly by thromboxane, whereas the end result of the lipoxygenase components of the plaque biofilm secrete MMPs, which pathway include leukotrienes and other hydroxyeico-

are associated with altered connective tissue remodeling satetraenoic acids. Elevated levels of PGE2 and other and alveolar bone resorption. Although, several periodontal arachidonic acid metabolites have been reported in pathogens (e.g. P. gingivalis and A.actinomycetem comitans) crevicular fluid in patients with gingivitis and periodontitis. 133

HPE 15 CHAPTER Host Modulation in Periodontal Therapy Periodontal in Modulation Host

Fig. 15.1: Pathological events of periodontal diseases with various host modulatory approaches

Hence, one proposed approach to modulate host response these lipoxins at a metabolically stable state blocked the is inhibition of enzymes responsible for the release of these neutrophil infiltration induced by P. gingivalis and also destructive products. reduced PGE2 levels. However, additional studies are Various in vitro studies have been conducted to assess required to demonstrate the role of lipoxins in the patho- the non-steroidal anti-inflammatory drugs (NSAIDs) as genesis of periodontitis. Recently, a compound that has inhibitors of bone resorption. Multiple NSAIDs including received interest as both antibacterial and anti-inflammatory indomethacin, flurbiprofen, ibuprofen, naproxen, agent is . Dentifrice containing sodium fluoride, meclofenamic acid and piroxicam have demonstrated their triclosan and a copolymer has been tested. However, ability to reduce gingivitis and progression of periodontitis additional studies are required to examine the effect of this in animal models. Ketoprofen, an NSAID which can inhibit combination of drugs on periodontitis. both cyclooxygenase and lipoxygenase pathways, has recently received a lot of attention. In humans, most of these REGULATION OF BONE METABOLISM NSAIDs have shown significant reduction in bone loss, however disease progression returned upon the withdrawal Various drugs have been tried to inhibit the activity of of the agent. Hence, topical administration of NSAIDs has osteoclasts. A new class of drugs used to manage been considered as an alternative method to deliver these osteoporosis, which may also have beneficial effects on the agents. Various drugs that have been evaluated for topical periodontium, are the bisphosphonates. These compounds administration include, ketorolac tromethamine rinse and through the mechanism of chelation of cations seem to S-ketaprofen dentifrice. However, further studies are inhibit MMP activity thereby inhibiting osteoclastic activity. required to determine the efficacy of these agents to provide One of these drugs, alendronate has been evaluated in clinically significant improvements, when used as adjuncts ligature induced periodontitis models. Although it inhibited to scaling and root planing. Other agents that have been loss of bone density in animal models, the human trials have tried for topical use are lipoxins, which are a series of shown minimal effects on clinical parameters. Further oxygenated arachidonic acid derivatives functioning as studies are required to evaluate the effectiveness of these endogenous inflammatory mediators. In animal models, drugs in the treatment of periodontal diseases. 134

Mechanism of action involves direct inhibition of MMPs which indirectly reduces osteoclast activity and bone 1. The current paradigm, for the etiology and pathogenesis resorption. of periodontitis includes the involvement of periodontal Future host modulation agents could be Lipoxins, pathogens and destructive host responses. Resolvins and Probiotics (Lactobacilli and Bifidobacteria). 2. To prevent the disease initiation and progression, mechanical and antimicrobial pharmaceutical agents have been used successfully. 3. For the long-term clinical management of periodontitis REVIEW QUESTION a novel adjunctive therapies such as host modulation

has been introduced. 1. Enumerate various host modulating agents in periodontal PART III 4. The use of HMT (Host Modulation Therapy) as an adjunct therapy. may be particularly useful in susceptible, high risk patients (e.g. smoking, diabetes, genetic predisposition) FDA has recently approved subantimicrobial dose BIBLIOGRAPHY doxycycline (Periostat™) for systemic administration as an adjunct to scaling and root planing in the treatment 1. Genco RJ. Host responses in periodontal diseases: Current of chronic periodontitis. 5. The future holds much hope for application of HMT not Concepts, J Periodontol 1992;63:338. only for managing the periodontitis patients, but also for 2. Golub LM, Suomalainen K, Sorsa T. Host modulation with the practice of periodontal medicine. tetracyclines and their chemically modified analogues, Curr Opin Dent 1992;2:80.

Etiopathogenesis 3. Offenbacher S. Periodontal diseases: pathogenesis, Ann Periodontol 1996;1:821. KNOW MORE ... 4. Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000;1997;14:9. Host Modulators 5. Salvi GE, Lawrence HP, Offenbacher S, Beck JD. Influence of Subantimicrobial dose doxycycline (Periostat®) is risk factors on the pathogenesis of periodontitis, Periodontol available at 20 mg dose which acts as a host modulator. 2000;1997;14:173.

SECTION 1: Gingival Diseases

16 ChapterChapter

Defence Mechanisms of the Gingiva

 DEFENCE MECHANISMS • Significance of Gingival Vasculature and • Nonspecific Protective Mechanisms Crevicular Fluid • Specific Protective Mechanisms • Permeability of Sulcular and Junctional Epithelia  SULCULAR FLUID • Methods of Collection • Anatomy of Gingival Crevice or Sulcus • Composition • Significance of Gingival Sulcus and Fluid • Clinical Significance

DEFENCE MECHANISMS Surface Integrity A number of mechanisms operate to protect the body from The surface integrity of skin and mucous membrane barrier, attack by foreign bodies and toxins, including infections including the gingiva, is maintained by the persistent by bacteria. These mechanisms can be classified as: renewal of the epithelium from its base and desquamation 1. Nonspecific mechanisms. of the surface layers. These two activities are balanced and 2. Mechanisms specific to invading foreign proteins called this helps in maintaining a constant thickness of the antigens which stimulate the immune system. epithelium. The efficiency of the surface barrier is enhanced by keratinization and parakeratinization. The junctional epithelium, although semipermeable, has a very high rate Nonspecific Protective Mechanisms of cell turnover. Bacterial Balance Surface Fluid and Enzymes The mouth as a whole and various zones in the mouth, including what has been called the ‘crevicular domain’ can All vital surfaces are washed by fluids, which are capable be viewed as an ecosystem in which a balance exists between of attacking foreign materials, e.g. gastric acid, lysozyme, different species of microorganisms, their flora and their saliva. Saliva bathes the oral mucosa and contains tissues. antibacterial substances. The gingival fluid exudates flow 138

through the junctional epithelium into the gingival crevice are termed as C3a, C4a and C5a, these take part in the defence and this fluid contains phagocytic leukocytes and enzymes mechanism, in the tissue fluids and are referred to as (Table 16.1). anaphylotoxins, since they can induce smooth muscle contraction, increase permeability of blood vessels and cause Phagocytosis the release of histamine from mast cells and basophils.

Certain cells in the blood stream and in the tissues are C5a, in addition, is chemotactic for neutrophils and capable of engulfing and digesting foreign materials. The monocytes. It augments cell adherence and causes most important phagocytic cells are polymorphonuclear degranulation of these cells, it also enhances arachidonic

neutrophils and the macrophages. metabolism and stimulates production of toxic metabolites. PART IV Macrophages are basically monocytes, which when moved into the tissues, mature and become macrophages, The Inflammatory Reaction unlike polymorphonuclear neutrophils which have The inflammatory reaction is stimulated by tissue injury the capacity to undergo several divisions within the and infection and leads to changes in the local tissues, which progressively increase in number. While microcirculation, which produces hyperemia, increased polymorphonuclear neutrophils are the main line of defence vascular permeability and the formation of a fluid and in acute infections, monocytes are more important in long- cellular exudate. term chronic infections. Phagocytosis is aided by a battery of nine related proteins Specific Protective Mechanism known as complement which are activated by two systems, Animals (vertebrae) have a developed surveillance and namely classical and alternative pathway. In the process of Periodontal Pathology Periodontal attack system called the immune system. This can protect activation of the complement system, fragments are the body from bacteria, viruses and even cancer cells. generated by cleavage of C , C and C . These fragments 3 4 5 The system has three characteristics: 1. It can distinguish between itself and the enemy; thereby it does not attack parts that it recognizes as self. Table 16.1: Functions of saliva Sometimes it may go wrong and thereby results in certain Functions Salivary Probable mechanism diseases known as the autoimmune diseases. components 2. The defences contain elements specific against any given Lubrication Glycoproteins Coating similar to antigen. mucoids gastric mucin 3. The system has a memory. The specific immune Physical Glycoproteins Coating similar to protection mucoids gastric mucin mechanism has two basic components: Cleansing Physical flow Clearance of debris a. Humoral immunity and bacteria b. Cell-mediated immunity Buffering Bicarbonate and Antacids Both arise from stem cells in the bone marrow. phosphate Tooth integrity Minerals glyco- Maturation, reminer- maintenance protein pellicle alization, mechanical SULCULAR FLUID protection IgA Control of bacterial Anatomy of Gingival Crevice or Sulcus colonization Antibacterial Lysozyme Breaks bacterial cell The gingival sulcus is the shallow crevice or space around action walls the tooth, bounded by the surface of the tooth on one side Lactoperoxidase Oxidation of suscep- and the epithelium lining the free margin of the gingiva, on tible bacteria the other. CHAPTER 16 Defence Mechanisms of the Gingiva 139 The generation of crevicular fluid

Fig. 16.1: The significance of such an arrangement in the The significance of such an arrangement Permeability of Sulcular and Junctional Epithelium The main pathway for the transport of substances across the junctional and sulcular epithelia seems to be the intercellular spaces which form, 18 percent of the total volume of the junctional epithelium and 12 percent of that of the outer sulcular epithelium. Barriers to the passage of substances through junctional and sulcular epithelium are represented by the intercellular junctions and especially by the basement membrane. looping of the vessels underlying sulcular and junctional looping of the vessels underlying sulcular below the sulcular The vessels immediately epithelium. are damaged in a flat epithelium and junctional epithelium Since these epithelia do not possess ridges projecting layer. network is into the connective tissue, their vasculature located in a very superficial position. fluid was clearly mechanism of the production of gingival who has demonstrated that the demonstrated by Egelberg, production of crevicular fluid is primarily related to an increase in the permeability of the vessels underlying junctional and sulcular epithelium. Normally, the depth of the gingival sulcus is zero, Normally, Sections of the marginal region of clinically healthy of clinically region of the marginal Sections gingiva will show the presence of three types of epithelia, gingiva will show epithelium covering the gingival the oral or keratinized in continuation with the oral sulcular connective tissue, is not keratinized. It forms the soft tissue epithelium, which is sulcus and the junctional epithelium wall of the gingival the oral sulcular epithelium. It is formed in continuation with a cells, with a long flat basal layer and by a few strata of the surface that forms the base of very small desquamating gingival sulcus. probing depth of the however 1.5 to 3.0 mm of the so called When the normal. gingival sulcus may be considered mm, a new type of probing depth exceeds more than 3 appears. It is epithelium called the “pocket epithelium” discontinuous characterized by irregular ridges, ulceration, the tooth. Below this basal layer and it is not attached to is present; epithelium, a typical junctional epithelium the designation of forming a short epithelial attachment, in the presence of gingival pocket can be used. Finally, 3 to 5 mm is seen, periodontitis, pocket depth greater than colonies are active bone resorption takes place, bacterial surface. found situated very deep along the cementum The blood supply to marginal gingiva is by the vessels of gingiva is The blood supply to marginal both the periodontal ligament and oral mucosa, each consisting of arterioles and venules. In the presence of inflammation, the width and length of capillary and post- capillary venules increases, this results in twisting and Significance of Gingival Vasculature and Significance of Gingival Vasculature Crevicular Fluid (Fig. 16.1) Brill and Krasse have clearly demonstrated that parenterally Brill and Krasse have clearly demonstrated removed from the administered tracer material could be gingival sulcus by using 4 mm wide filter paper strips Brill reported various types of tissue intracrevicularly. damage using the same technique. Now new methods of collecting crevicular fluid are available which do not cause any irritation, for example extracrevicular technique and a simple procedure of drying a chronically inflamed gingiva by a blast of air. Significance of Gingival Sulcus and Fluid Significance of Gingival Sulcus 140

In the presence of inflammation, enlargement of stained with an alcoholic solution of ninhydrin at intercellular space of both junctional epithelium and sulcular concentration of 0.2 percent (gives blue or purple color). epithelium along with partial destruction of the basal The stained area can then be measured with a transparent membrane results in the inward passage of foreign scale, calipers or calibrated magnifying glass. substances. b. By weighing the strip: The strip is weighed before Variety of enzymes such as hyaluronidase and collection of the sample within a sealed micro- collagenase has the ability to alter the permeability centrifugation plastic tube and is also weighed properties of the junctional epithelium and the sulcular immediately after the collection of the sample.

epithelium. They have the ability to penetrate even the intact c. Use of Periotron® (Fig. 16.2): This is the latest and PART IV junctional and sulcular epithelia. Nutritional deficiencies standard method for measuring gingival fluid absorbed such as Ascorbic acid might also alter sulcular permeability on paper strips. It was developed by Harco Electronics. and allow the passage of substances from the gingival sulcus HAR 600 is an electronic device whose functioning units into gingival connective tissue, like histamine, leucine, are a pair of upper and lower counter parts which can thymidine, phenytoin, peroxidase, albumin, dextran, carbon be opened and closed in order to insert or remove the particles, endotoxins and others. strip of filter paper. A moistened strip of paper when One can conclude that the epithelia covering the gingival inserted between the two jaws will give a reading on sulcus, represents a relative barrier to the penetration of the screen. HAR-6000 is the latest technique which was foreign material from the sulcus into the connective tissue. found to be sensitive in detecting small volumes of fluids It is conceivable that plaque components, even of relatively as compared to the former two models. high molecular weight could pass within the gingival

Periodontal Pathology Periodontal Advantages connective tissue, when allowed, to accumulate in the sulcus. • It is a simple procedure. It can be viewed directly. • Quantitative assessment of the fluid can be obtained. Methods of Collection • It seems to be compatible with subsequent chemical It is usually collected from the anterior teeth (least analysis. contamination). A few techniques are available: • By using periotron, evaporation is kept to a minimum. a. Absorbing paper strips b. Sampling by means of micropipettes Disadvantages c. Gingival washings • Contamination can occur. In case of evaporation of d. Other methods. sample, it has to be repeated many times. It is not very reliable (Ninhydrin technique). Absorbing Paper Strips Two techniques are followed: • Intracrevicular: The end of the paper strip is gently inserted into the pocket until minimum resistance is felt. • Extracrevicular: The strip is placed at the entrance of the gingival crevice. This technique has subsequently never been used.

Evaluation of Amount of Fluid Collected a. Appreciation by direct viewing and staining, was proposed by Egelberg and Attstrom. The strip was Fig. 16.2: Periotron CHAPTER 16 Defence Mechanisms of the Gingiva 141 l. In μ l/tooth. (GCF) μ Crevicular Fluid : The volume is calculated by using : This was proposed by Skapski and Lehner. This was proposed l of fluid/day. μ Challa Combe calculated an amount of 0.5 to The strips are placed along the long axis of the tooth or The strips are placed along the long axis Cellular elements 1. Epithelial cells 2. Leukocytes 3. Bacteria Electrolytes 1. Sodium the integrity of the marginal tissue. marginal the integrity of the normal gingiva. area. of cells and bacteria from the crevicular anterior teeth, the volume was between 0.24 to 0.43 2.4 Other Methods • Plastic strips • loops Platinum is applied. inserted into the sulcus and pressure of gingival fluid Volume fluid volume The mean gingival an isotope dilution method. in spaces from molar teeth ranged from 0.43 to 1.56 Composition of Gingival 16.2) (Table A. B. • disturbing gingival fluid without collection of It permits • by this technique. Contamination is least Disadvantages • procedure. It is a complex • of crevicular fluid. It represents a dilution Second method: a the ejection and re-aspiration of The procedure involves the solution into a given interdental known amount of crevice. Advantages • It has an advantage of being useful for cases of clinically • It is useful for studying the number and functional state • counts can be obtained. leukocyte and differential Total Disadvantage quantitative The technique does not permit absolute be determined. assessments, as the dilution factor cannot is used, daily check on the reading is used, daily ® Collection of GCF by micropipettes

This was proposed by Tokamoli and Tokamoli This was proposed by Fig. 16.3: accuracy should be performed; care should be taken to accuracy should be into the machine in a standardized insert the paper strips reading. position for correct cells at the marginal area could be followed by this cells at the marginal technique (polymorphonuclear leukocytes and epithelial cells). demanding. of the fluid makes aspiration through a pipette very of the fluid makes aspiration through difficult. integrity of the marginal tissues. integrity of the marginal Gingival Washings for the study of There are two techniques that are available gingival fluid components. First method: Advantages • Useful for longitudinal studies. • of various enzymes and the number of Concentrations Oppenheim; is based on the individual acrylic appliances. Oppenheim; is based on the individual •the recovery of the sample can also be very Finally Disadvantages • The collection of fluid is difficult because the viscosity Sampling by Means of Micropipettes (Fig. 16.3) Sampling by Means capillary tubing. were the first to utilize Krasse and Egelberg This by capillarity. micropipette permits absorption diameter are placed Capillary tubes of standardized length and and analyzed.in the pockets, their content is centrifuged • When Periotron • the strip, thereby disturbing of the paper Dislocation 142

Table 16.2: Composition of gingival crevicular fluid

Source Action Correlation with disease activity A. Cellular elements 1. Epithelial cells Junctional and sulcular Positive correlation is found. epithelium. 2. Leukocytes Dentogingival vessels Phagocytosis and killing Positive correlation only in some of micro-organisms. instances. 3. Bacteria Oral cavity Poor correlation between bacterial count in gingival fluid and perio- dontal parameters. B. Electrolyte PART IV 1. Sodium Plasma and extracellular • Genesis of plaque Shows positive correlation significantly. fluid. • Precipitation of proteins Increases in the presence of inflammation. 2. Potassium Plasma and extracellular • Precipitation of mucoprotein Positive correlation between fluid. along enamel surface. potassium concentration and the 3. Calcium Plasma and extracellular fluid average pocket depth. Positive correlation. C. Organic compounds 1. Carbohydrates Extracellular fluid Glucose concentration is increased in (glucose, hexo- inflamed tissues, hexosamine and samine and hexuronic acid has no correlation with hexuronic acid) variation in gingival inflammation. 2. Proteins a. Immunoglobulins Plasma or synthesized locally Immune function Positive correlation. b. Complement Blood 1. Control of inflammatory reaction 2. Elimination of antigen 3. Activation of cells Periodontal Pathology Periodontal 4. Preparation of microbes and foreign particles for phago- cytosis. 5. Play a role in immune response. 3. Lipids Serum D. Metabolic and bacterial products 1. Lactic acid Breakdown product of tissue Positive correlation to both the clinical degree of inflammation and intensity of gingival fluid flow. 2. Hydroxyproline Breakdown product of collagen In presence of inflammation, the correlation tends to increase one month after surgery and return to baseline level postoperatively. 3. Prostaglandins • Synthesized by most mam- • Vasodilation It is positively correlated with disease malian cells. • Bone resorption activity. • Are component of inflam- • Inhibition of collagen matory reaction. synthesis 4. Urea Break down products of Elevates the pH of supragin- Urea concentration in gingival fluid bacteria. gival plaque in presence of decreases when gingival inflammation gingivitis and periodontitis increases. due to production of ammonia by microorganisms. 5. Endotoxins These are lipopolysaccharides Highly toxic to gingival tissue Positively correlated with the presence of cell wall of Gram-negative of varying degree of periodontal bacteria. inflammation. 6. Cytotoxic sub- Bacteria Highly toxic metabolite Positively correlated with gingival

stances (like H2S) (cytotoxic effect). inflammation. 7. Antibacterial Saliva Prevents growth of bacteria factors Contd... CHAPTER 16 Defence Mechanisms of the Gingiva 143 -glucuronidase and β gingival fluid and any of the clinical parameters. inflamed gingiva. lactate. the components of bacterialcell wall. gingival fluid and the percentage of of bone loss. effectalso some detrimental upon epithelial cells. destruction. periodontal tissue, thereby contributing to formation of pocket. in the junctionalspaces epithelium. inflammation. glycans, hemoglobin, fibrino-gen and collagen. progression. intercellular spaces, partial destruction of basal mem- brane and loss of collagen. Hydrolyzes hemoglobin,and proteoglycans. Positive correlation. • acid, one of teichoic Attacks of acid phosphatase and both the flow • of connective effect Lytic • of epithelial Widening Plaqueazurophilic granules ofPMNLs.endothelial cells. Plays a role in calculus formation Positive correlation. concentration of fluid and depth the flow of gingival PMNLs. depth. erine endopeptidase contained • Sourceepithelial cells. Action• tissue catabolism. Bacteria • Bacterial plaque• between the intercellular concentration fibroblast, Macrophages, with disease activity Correlation leukocytes.mononuclear human epithelium and connective tissue destruction lated with periodontal pocket. of periodontal in azurophil granules of PMNs fibrinogen, casein, collagen antitrypsin) 1 α macroglobulin 2 α and -glucuronidase • found in It is a hydrolase Used as lysosomal marker between the Positive correlation genase reduction of pyruvate to activity of lactic dehydrogenase in

phataseβ in proteases Cathepsin-Da. b. Elastase enzyme seen in Lysosomal various components of Attacks Azurophil granules of PMNLs corre- concentration is positively Its • Active upon elastin, proteo-c. Cathepsin-G Positively correlated with disease S d. Plasminogen acti- Blood vator (Streptoki- nase, urokinase)e. Collagenasef. Bacterial proteases Bacteria of PMN’s granules Specific g. Serum proteinase Plasma inhibitor ( •activity Collagenolytic • Fibrinolysis Higher concentration in chronically- • • • Plays a role in inflammationdamage Tissue Essential for wound healing • periodontitis increases. Modulates the activity of Concentration increases as severity of Positive correlation. correlation. Positive proteases in the tissue. 8.dehydro- Lactic Bacteria •reversiblethe Catalyzes No significant correlation between total 2. phos- Alkaline 3. Pyrophosphatase In gingival sulcus it is found4. • Plays a role in calcification Positively correlated with pocket 5. Lysozyme PMNLs6. Hyaluronidase7. Serum Mammalian • Bactericidal properties and Positively correlated with the severe • Widening of intercellular Significantly increases in presence of Enzyme and enzyme inhibitors 1. Acid phosphatase PMNLs and desquamating • Associated with connective Negative correlation was found Contd... E. 144

2. Potassium B. Gingival fluid in diabetic patients: The gingiva of 3. Calcium diabetic patients significantly showed higher incidence C. Organic compounds of vascular modifications, which could be an increase 1. Carbohydrates in the width of the basal membrane of capillaries, small 2. Proteins arteries and venules, resulting in higher production of • Immunoglobulins gingival fluid. The exudates collected from the diabetic • Complement components patients showed significantly more levels of glucose than 3. Lipids that collected from healthy individuals.

D. Metabolic and bacterial products PART IV 1. Lactic acid Drugs in Gingival Fluid 2. Hydroxyproline Since the gingival fluid seems to be a characteristic feature 3. Prostaglandins of gingival inflammation, one could reasonably expect that 4. Urea when suitable drugs are given to a patient, it can be carried 5. Endotoxins from the general circulation to the gingival sulcus or pocket 6. Cytotoxic substances by flow of the fluid. 7. Antibacterial factors Bader and Goldhaber (1966) were able to show that E. Enzyme and enzyme inhibitors intravenous administered tetracycline in dogs rapidly 1. Acid phosphatase emerges within the sulcus. It seems likely that a major 2. Alkaline phosphatase pathway of entrance into oral cavity of systemically 3. Pyrophosphatase

Periodontal Pathology Periodontal administered tetracycline is in the gingival sulcus. The β 4. -glucuronidase concentration of drug seems to be five times higher in 5. Lysozyme samples of gingival fluid as compared to the concentrations 6. Hyaluronidase in serum; other drugs that have been detected in human 7. Proteolytic enzymes gingival crevicular fluid are minocycline, erythromycin, • Mammalian proteinases clindamycin and metronidazole. • Bacterial proteinases • Serum proteinase inhibitors Influence of Mechanical Stimuli 8. Lactic dehydrogenase Mechanical stimulation of the marginal gingiva, such as Clinical Significance massage by means of a round instrument, causes a significant increase in the permeability of the blood vessels located General Health and Gingival Fluid below the junctional and sulcular epithelia. The sensitivity A. Gingival fluid flow and sex hormones: Three groups of of gingival vasculature has led several investigators to find females are studied. out whether certain usual powerful mechanical stimuli such First group–during menstruation: There is increase in as chewing or occlusal overload could influence the rate of the gingival fluid flow because the sex hormones gingival fluid production. (estrogen and progesterone) cause increase in the The effect of chewing was investigated by Brill (1959) gingival vascular permeability. in a group of 15 nurses aged 18 to 22 years, showing Second group–females on birth control pills: There is clinically healthy gingival margins. Each subject chewed a significant increase in the amount of exudate recorded. piece of paraffin for 10 minutes and samples of gingival Third group–females during pregnancy: The gingival fluid were recovered by the Brill technique. The amount of exudates reached maximum values during the last gingival fluid was shown to increase significantly under trimester and decreased to minimum after delivery. the influence of chewing. Even the minor stimulus in the CHAPTER 16 Defence Mechanisms of the Gingiva 145 can form the first α KNOW MORE ... leukocytes increases with the intensity of the leukocytes increases More than 90 percent of the inflammatory process. neutrophils and most leukocytes are polymorphonuclear of phagocytosis. capacity of them possess the ratio of the fluid The sodium-potassium demonstrated. correlated with the severity was proved to be positively The general organic destruction. of periodontal fluid seems to be similar to that composition of gingival and complement immunoglobulins of serum. Various demonstrated. Furthermore, the components were also not which are normally metabolic products fluid contains concentrations. found in serum or found only in minute The fluid contains a variety of to be around 7.54 to 7.89. the host or by enzymes, produced both by the cells of the bacteria. periodontitis, seems to increase in case of gingivitis and in the indicating a possible role of the enzymes of the lesions. It was also proved that, pathogenesis as tetracycline systemic administration of antibiotics such gingival fluid is found in a higher concentration in human to serum. as compared fluid are now and the clinical significance of gingival helped known with more precision and have significantly of the pathogenesis of periodontal in the understanding disease. In normal individuals, 30,000 neutrophils per minute line of defense against microbial invasion into the tissues. The internal and external basal lamina can also act as a barrier against infective agents. enter the oral cavity via gingival sulcus across the This flow of neutrophils is important junctional epithelium. health. These viable normal periodontal to maintain neutrophils present in the saliva are known as The oral leukocyte migratory rate index orogranulocytes. (OMRI) allows an objective assessment of periodontal health. Role of Junctional Epithelium in Antimicrobial Defense produced by the junctional The antimicrobial substances epithelium such as defensins, lysosomal enzymes, TNF- interleukins (IL-1, IL-6, IL-8) and 4. absolute number of It has been shown, that the 5. of ions in the gingival fluid were concentrations Various 6. fluid was found In preliminary investigations, the pH of 7. the fluid The concentration of lysosomal enzymes in 8. In conclusion, one can say that the origin, the composition : One week after gingivectomy there : It causes a decrease in the fluid flow, one : It causes a decrease in the fluid flow, : Smoking produces an immediate but transient : Smoking produces are now known with more precision. In a perfectly sound are now known with more precision. In a histologically normal gingiva, a few polymorphonuclear the junctional neutrophils can be seen migrating through fluid can be epithelium while very little or no gingival collected. connective tissue can be seen and a very little fluid can In the beginning, be collected in the absence of irritation. a low concentration of proteins the fluid seems to contain and could represent interstitial liquid generated locally by an osmotic gradient as a result of an increased permeability of gingival venules; it may progress to a higher classical inflammatory exudate, containing of total protein. amounts methods have been proposed Two variety of substances. for the collection of material from the gingival sulcus, capillaries, gingival washings and strips, absorbent paper are used. The first plastic strips or platinum loops are most utilized, even method, absorbant paper strips investigations on the composition of for the quantitative Approximate amount of fluid projected into gingival fluid. the oral cavity is 0.5 to 2.4 ml/day. 1. marginal area The structure and function of the gingival 2. In a clinically healthy gingiva, a small area of infiltrated 3. The junctional and sulcular epithelia are permeable to a After surgical procedure After surgical week after oral prophylaxis and then slowly returned to pre- week after oral prophylaxis and then slowly treatment values. fluid flow due to the was a striking increase in the gingival from the sulci. increased inflammatory cells in the smear of the inflammatory This increase was probably the result the restoration of reaction from the gingival trauma with a gradual drop in fluid flow occurred and gingival integrity, reached to minimum the scores for the gingival fluid flow values, five weeks after gingivectomy. Oral prophylaxis Measurements of gingival fluid flow have been performed Measurements of gingival types of periodontal therapy. before and after different Periodontal Therapy and Gingival Fluid Therapy and Gingival Periodontal Smoking crevicular fluid flow. increase in gingival form of intrasulcular placement of paper strips increases of paper strips placement form of intrasulcular the production of fluid. 146

REVIEW QUESTIONS BIBLIOGRAPHY

1. Describe the functions and significance of gingival 1. Cimasoni G. Monographs in oral science crevicular fluid, crevicular fluid. updated 1992. 2. Describe the methods of collection of gingival crevicular 2. Lamster IB, Celenti R, Ebersole J. The relationship of serum IgG antibody titers to periodontal pathogens to indicators of the fluid. host response in gingival crevicular fluid. J Clin Periodontol 3. What is the composition of gingival crevicular fluid? 1990;17: 419. 4. Describe the various defence mechanisms of gingiva. 3. McLaughlin WS, Lovat FM, Macgregor IDM, et al. The immediate effects of smoking on gingival fluid flow. J Clin PART IV Periodontol 1993;20:448. 4. Newman, Takei, Carranza. Clinical Periodontology. 9th edn, WB

Saunders 2003. Periodontal Pathology Periodontal 17 ChapterChapter

Gingival Inflammation

 STAGE I GINGIVITIS: THE INITIAL LESION  STAGE III GINGIVITIS: THE ESTABLISHED LESION  STAGE II GINGIVITIS: THE EARLY LESION  STAGE IV GINGIVITIS: THE ADVANCED LESION

INTRODUCTION Inflammation of gingiva is termed as gingivitis. The plaque microorganisms can exert its effect on periodontium by releasing certain products (e.g. collagenase, hyaluronidase, protease, chondroitin sulfatase) which can cause damage to the epithelial and connective tissue constituents. The intercellular spaces between the junctional epithelial cells are destroyed and may permit the bacterial products or bacteria themselves to gain access into the connective tissue (Fig. 17.1). The sequence of events during the development of gingivitis can occur in four different stages (Table 17.1).

STAGE I GINGIVITIS: THE INITIAL LESION (FIG. 17.2) Clinically, no visible changes are seen except presence of exudation of fluid from the gingival sulcus, hence this condition is called subclinical gingivitis. Fig. 17.1: Normal marginal gingiva The following features are observed in stage I gingivitis: 2. Exudation of fluid from gingival sulcus. 1. Classic vasculitis of vessels subjacent to the junctional 3. Changes in the coronal most portion of the junctional epithelium. epithelium.

148 PART IV

Fig. 17.2: Initial lesion Fig. 17.3: Early lesion

4. Increased migration of the leukocytes into the junctional STAGE III GINGIVITIS: Periodontal Pathology Periodontal epithelium and gingival sulcus. THE ESTABLISHED LESION 5. Presence of serum proteins. Clinical changes include: 6. Loss of perivascular collagen. a. A bluish hue on the reddened gingiva due to impaired venous return. STAGE II GINGIVITIS: b. The gingiva appears to be moderately to severely THE EARLY LESION (FIG. 17.3) inflammed. Clinically, erythematous gingiva and bleeding on probing may be evident. Microscopic features of the early lesion Microscopically include: 1. Predominant inflammatory cell types are plasma cells, 1. All the changes seen in the initial lesion continue to which invades epithelium and also deep into the intensify. connective tissue, around the blood vessels and between 2. The junctional epithelium may begin to show the the bundles of collagen fibres. development of rete pegs or ridges. 2. Proliferation, apical migration and lateral extension of 3. Accumulation of lymphocytes (majority of them are T the junctional epithelium is seen. Early pocket formation cells) beneath the junctional epithelium. may or may not be present. 4. Further loss of collagen fiber network supporting the 3. Further collagen destruction and continuing loss of marginal gingiva. connective tissue substance seen in the early lesion. 5. Fibroblasts show cytotoxic alteration with a decreased 4. The following enzyme levels are said to be elevated in capacity for collagen production. chronically inflammed gingiva, acid and alkaline CHAPTER 17 Gingival Inflammation 149 Health Early lesion Initial lesion Advanced lesion → → → → Formation of periodontal pocket and ↓↓ ↓↓ ↓↓ glucuronidase β Clinically Histologically Early gingivitis Pristine condition Clinically healthy Chronic periodontitis Progression from Health to Periodontitis 4. Formation of periodontal pockets. 5. Conversion of bone marrow into fibrous tissue. 6. types of inflammatory cells. Presence of almost all the Extension of inflammation into deeper structures including alveolar bone and periodontal ligament. Presence of all types of inflammatory cells. Conversion of bone marrow into fibrous tissue. presence of serum proteins. most Changes in the coronal epithelium. portion of junctional Subclinical gingivitis. of collagen, cells), loss (mostly T alteration. fibroblasts show cytoplasmic Plasma cells are predominantFurther loss of collagen. Increased enzyme levels like acid and alkaline phosphatase, gingiva. and others. Table 17.1: Stages of gingivitis of 17.1: Stages Table -glucuronidase, aminopeptidase and β lesion lesions. established lesions. associated changes. its phosphatase, others. (2-4 days)(2-4 the junctional epithelium. and Loss of perivascular collagen (4-7 days) sulcus lesiondays)(14-21 blood stasis. epithelium, presence of lymphocytes on probing. extension of junctional epithelium and surface texture. consistency Atropic areas Bluish hue around the reddened The following clinical and microscopic features are seen: lesion. periodontal ligament leading to significant amount of bone loss. STAGE IV GINGIVITIS: STAGE LESION THE ADVANCED 1. Initial lesion Classic vasculitis subjacent to Presence of leukocytes (PMNs). Exudation of fluid from the gingival 2.lesion Early proliferation Vascular 3. Rete pegs formation in the junctional Established Same as early lesion, with Erythematous, gingival bleeding Proliferation,apical migration and lateral Changes are seen in color 4. Advanced Same as early and established Persistence of features seen in Stage changes Vascular Microscopic changes Clinical changes 1. described in the established Persistence of features 2. alveolar bone and Extension of the lesion into the 3. Continued loss of collagen. The advanced lesion is also known as phase of advanced periodontal breakdown. 150

BIBLIOGRAPHY

KNOW MORE ... 1. Brecx MC. Histophysiology and histopathology of the gingiva. J West Soc Periodontal 1991;39:33. The American Academy of Periodontology (AAP) defines 2. Brecx MC, Lehman B, Siegmart CM, et al. Observations of the gingivitis as an inflammation confined to the tissues of initial stages of healing following human experimental gingivitis. the marginal gingiva. A clinical and morphological study. J Clin Periodontal Pristine Gingiva 1988;15:123. It is a state of superhealth where normal gingiva is free 3. Saul Schluger. Periodontal diseases, basic phenomena, chemical from significant accumulation of inflammatory cells. Hence management and occlusal and restorative interrelationships, 2nd

PART IV histologically it may be described as pristine gingiva. edn, Lea and Febiger, 1990. Periodontal Pathology Periodontal 18 ChapterChapter

Clinical Features of Gingivitis

 TYPES OF GINGIVITIS • Color Changes in the Gingiva • Depending on Course and Duration • Changes in Consistency and Size of Gingiva • Depending on the Distribution • Surface Texture  CLINICAL FINDINGS • Changes in the Position of Gingiva • Gingival Bleeding on Probing • Changes in Gingival Contour

TYPES OF GINGIVITIS According to distribution, gingivitis could be marginal, papillary or diffuse. If the inflammation is limited to the • Depending on course and duration marginal gingiva, the condition is termed as marginal • Depending on distribution. gingivitis. In papillary gingivitis, the inflammation is limited to the interdental papilla. When the inflammation Depending on the Course and Duration spreads to attached gingiva also, it is termed as diffuse • Acute gingivitis is of sudden onset and short duration gingivitis, i.e. involving marginal, papilla and attached and can be painful gingiva. Papillary, marginal and diffuse gingivitis can • Subacute is a less severe phase of acute condition occur as localized or generalized conditions (Figs 18.1 • Recurrent gingivitis reappears either after treatment or to 18.4). disappears spontaneously • Chronic gingivitis is slow in onset, of long duration, CLINICAL FINDINGS usually painless and the most commonly occurring While examining the gingiva clinically, one must adapt a gingival condition. systematic approach. Close attention should be given to any tissue alterations, because they contribute to diagnosis. The Depending on the Distribution gingiva is examined for the following characteristics, color, If the condition is involving a single tooth or group of teeth, contour, consistency, size, position, severity of bleeding, it is called localized gingivitis, while generalized gingivitis surface texture (Summary of these features are discussed in involves entire mouth. detail in Table 18.1).

152 PART IV

Fig. 18.1: Chronic gingivitis. The marginal and interdental Fig. 18.3: Gingivitis—inflammatory type

gingiva are smooth edematous and discolored Periodontal Pathology Periodontal

Fig. 18.2: Papillary gingivitis Fig. 18.4: Gingivitis—fibrotic type

Gingival Bleeding on Probing (Fig. 18.5) 1. Significance of gingival bleeding. 2. Etiological factors responsible for gingival bleeding. 3. Associated microscopic changes.

Significance of Gingival Bleeding on Probing a. It is one of the earliest visual signs of inflammation. b. It can appear earlier than color changes or any other visual signs of inflammation. c. It also provides an additional advantage, by being a more objective sign that requires less subjective estimation Fig. 18.5: Bleeding on probing by the examiner. CHAPTER 18 Clinical Features of Gingivitis 153 ”. The red. The coral pink Dilation and engorgement of Dilation and engorgement Thinning and microulcerations of the and microulcerations Thinning Changes in the color may start from the interdental In the epithelium: In the epithelium: sulcular epithelium is seen. Thinning of the epithelium Thinning is seen. sulcular epithelium plaque released by to the toxic substances could be due the intercellular junctions. Micro- bacteria which destroys result of bacteria trying to gain entry ulcerations are as a tissue by breaking through the into the connective to inflammation, the neutrophils epithelium or in response tissue cross the epithelial barrier to from the connective infection, in doing so they cause reach the site of or combination of both. ulceration in the epithelium In the connective tissue: place. Since the capillaries are the capillaries takes engorged to the surface which is already and closer are otherwise thinned and less protective, stimuli that capillaries which innocuous can cause rupture of the may result in gingival bleeding. Changes in the Consistency of Gingiva Normal gingiva exhibits a firm and resilient consistency. Factors that are responsible are cellular and fluid content Color Changes in the Gingiva Colorimportant clinical sign of gingival of the gingiva is an be “ diseases. Normally gingiva appears to factors that are responsible for this are tissue vascularity, factors that are responsible for this are of the epithelium. degree of keratinization and thickness to red, to bluish- Generally color of the gingiva may change red, to pale-pink. When there is increased vascularity or reduced moreepithelial keratinization, the gingiva becomes color becomes pale when vascularization is reduced or color becomes pale when vascularization stasis gives a bluish Venous epithelial keratinization increases. of the changes in hue to the gingiva. Detailed description 18.1. Table color in health and disease is discussed in and attached gingiva. papilla and later spread to marginal Systemically absorbed heavy metals may also cause gingival and silver. lead pigmentation, e.g. bismuth, arsenic, mercury, Abnormal melanin pigmentation of the gingiva may be disease, Peutz-Jeghers Addison’s observed in conditions like syndrome and von Recklinghausen’s Albright’s syndrome, disease. a. b. The most common causes are:

include various systemic diseases such as:

is caused due to:

bleeding. gingivitis (ANUG). • Those in acute bleeding factors that result • chronic or recurrent Those factors that cause calculus. or food impaction. whether the lesion is in an active or inactive state. In active or inactive lesion is in an whether the on little or no bleeding there will be inactive lesion, lesions bleed more readily on probing, whereas active probing. the intensity of the inflammation. provoked indicates vitamin K deficiency, platelet disorders such as platelet disorders such vitamin K deficiency, thrombocytopenic purpura, other coagulation defects such as hemophilia, leukemia and others. administration of drugs such as salicylates and anticoagulants such as dicumarol and heparin. In plaque-induced gingival inflammation, the following histological changes are seen: Microscopic Changes Associated with Gingival Microscopic Changes Bleeding on Probing Chronic bleeding: Chronic b. Systemic factors Acute bleeding 1. brush trauma. Tooth 2. Impactation of sharp pieces of hard food. 3. Gingival burns from hot foods or chemicals. 4. In conditions such as acute necrotizing ulcerative 2. Mechanical trauma, e.g. from tooth brushing, tooth picks 3. apples. Biting into solid foods such as Systemic factors: These are divided into: These are divided a. Local factors: 1. Chronic inflammation due to the presence of plaque and Etiological Factors Responsible for Gingival Etiological Factors Bleeding on Probing e. which bleeding can be The severity and ease with d. us to determine probing also helps bleeding on Gingival 2. of excessive Bleeding could also be as a result 1. Hemorrhagic diseases including, vitamin C deficiency, 154

Table 18.1: Gingiva in health and disease

Gingival In health Factors In disease Factors features responsible responsible Clinical changes Disease conditions

1. Color Coral pink • Vascular Color change may be Chronic • Vascular supply • Marginal gingivitis proliferation • Thickness • Diffuse (Erythematous) and degree of • Diffuse or patch like. • Reduction of keratinization keratinization of epithelium Varying shades of red, Chronic gingivitis owing to epithelium • Presence of reddish blue, deep blue. compression by

pigment con- Color changes from Acute gingivitis inflamed tissues PART IV taining cells bright red erythema to • ANUG/HIV (Erythematous) • Shiny slate gray gingivitis • Venous stasis • Dull whitish gray. • Herpetic (Bluish red) gingivostomatitis • Tissue necrosis • Chemical irritation. (Bluish red). Black line following the Bismuth, arsenic and Perivascular precipita- contour of margin. mercury pigmentation tion of metallic sulfides in subepithelial connec- Bluish red or deep blue Lead tive tissue, only in areas linear pigmentation pigmentation of inflammation due to (Burtonian line) increased permeability irritated blood vessel. Violet marginal line. Silver pigmentation Systemic diseases causing pigmentation

2. Contour Marginal gin- • Shape of the tooth Marginal gingiva becomes Chronic gingivitis Inflammatory changes Periodontal Pathology Periodontal giva: Scalloped and thus alignment rolled or rounded. Interden- and knife edged in the arch tal papilla becomes blunt and flat Interdental • Location and size of Punched out and crater ANUG papilla: proximal contact like depressions at the Anterior: • Dimensions of facial crest of interdental pyramidal and lingual gingival papilla extending to the Posterior: embrasures marginal gingiva tent shaped Irregularly-shaped Chronic desquamative denuded appearance gingivitis Exaggerated scalloping Ginginval recession Apostrophe-shaped Stillman’s cleft Described by Stillman as indentations extending a result of trauma from from and into the gingival occlusion and by Box as margins for varying dis- a pathological pocket. tances on the facial Enlargement of inter- surface dental papilla with no Life saver like enlargement Mc Call’s festoon enlargement of marginal of the marginal gingiva gingiva (Pseudocleft) (Canine and premolar facial region) 3. Cons- Firm and Collagenous nature of • Soggy puffiness that • Chronic gingivitis • Infiltration by fluids istency resilient lamina propria and its pits on pressure and cells of inflam- (except free contiguity with the matory exudate margins) mucoperiosteum of • Marked softness and • Exudative • Degeneration of alveolar bone. Cellular friability connective tissue and fluid content of and epithelium tissue. • Firm leathery • Fibrotic • Fibrosis and epithe- lium proliferation Contd... CHAPTER 18 Clinical Features of Gingivitis 155 origin formation intracellular edema. ment tissue. Increase in fibers and decrease in fibers – • malposition Tooth • from soft Friction gingivitis nodular • Fibrotic chronic Surface Texture Under normal conditions, gingiva appears to be stippled (orange peel appearance) due to attachment of gingival enlargement. The factors responsible for this are increase enlargement. in fibers and decrease in cells as in non-inflammatory type. Whereas in inflammatory type there will be increase in cells and decrease in fibers. softeninglike particle of debrisgingivitis Acute membrane pseudo acute inflammatory spontaneous bleedingor bleeding on slight •provocation. ANUGdiseases Systemic sulcular epithelium or ulceration of thinning responsible• puffiness and Diffuse • Sloughing: grayish flake Clinical changes• formation. Vesicle conditions Disease Increased • edema of Diffuse • Necrosis with Gingival • and Intercellular gingival fibers to •shinyand Smooth • Exudative chronic gingival fibres as a alternate roundedprotuberance anddepressions in thegingival surface. •texture Leathery •(Papillary layer of nodular Minutely connective tissue projects into the surface.elevations). • Hyperkeratosis • Non-inflammatory vature of tooth gingival hyperplasia. gingivitis mative surface. • High frenum attach- of cellular and inter-and cellular elements supplyvascular their Inflammatory type. •by Microscopically enlargement • Peeling of surface • decrease in cells – Non- desqua- Chronic type. inflammatory in cells and Increase (viewed bydrying) the underlying bone. • Firm and gingivitis result of inflammation the cemento-enameljunction the arch • Root bone angle • Mesiodistal cur- •placed. Coronally Pseudopockets • Gingival inflamma- tion texture present the onprobing capillaries lium and normal •recurrent, Chronic •gingivitis Chronic ment of capillaries and 4. Size Normal5. Surface of the bulk Sum total is Stippling • of Due to attachment Loss of stippling Gingivitis6. Position 1 mm above Due to destruction of • Position of tooth in •placed Apically 7. Bleedingrecession Gingival • brush trauma Tooth sulcular epithe- Intact Present and engorge- Dilation Gingivalfeatures In health Factors responsible In disease Factors Normal size depends on the sum of the bulk of cellular and In disease intercellular elements and their vascular supply. the size is increased which can be termed as gingival Changes in the Size of the Gingiva and collagenous nature of lamina propria. In disease conditions, it can be soggy and edematous or firm and leathery in consistency. Contd... 156

fibers to the underlying bone. Microscopically, alternate rounded protuberance and depressions in the gingival layer may give rise to stippled appearance. Stippling is absent in disease conditions, hence the gingiva may appear smooth and shiny.

Changes in the Position of Gingiva Normally the gingiva is attached to the tooth at the cemento-

enamel junction. In disease, the position can be shifted either PART IV coronally (pseudopocket) or apical to the cementoenamel junction (gingival recession).

Definition Gingival recession is defined as the exposure of the root surface by an apical shift in the position of the gingiva.

Fig. 18.6: Apparent and actual positions of gingiva Types bone or soft tissue in the interdental area. This can be narrow There are two types of recession, i.e. visible, which is or wide.

clinically observable and hidden, which is covered by Periodontal Pathology Periodontal gingiva and can only be measured with probe. Gingival Class III: Marginal tissue recession that extends to or beyond recession may also be localized or generalized. the mucogingival junction. In addition, there is loss of bone Position of the gingiva can be actual or apparent and/or soft tissue in the interdental area or there is (Fig. 18.6). Actual position is the level of epithelial malpositioning of the tooth. attachment on the tooth, i.e. from the cementoenamel Class IV: Marginal tissue recession that extends to or beyond junction to the probable depth of the pocket, whereas the mucogingival junction with severe loss of bone and soft apparent position is the level of crest of the gingival margin, tissue interdentally and/or severe malpositioning of the i.e. from the cementoenamel junction to the gingival margin. tooth. • Prognosis of class I and II is good to excellent Classification of Gingival Recession • Class III–only partial coverage can be expected Two classification systems are available: • Class IV–Poor prognosis. I. According to Sullivan and Atkins—Shallow-narrow, Etiology of Gingival Recession shallow-wide, deep-narrow and deep-wide. (Figs 18.7 to 18.11) II. According to PD Miller’s—Class I, Class II, Class III and Class IV. Plaque-induced gingival inflammation is the primary etiological factor responsible for gingival recession; next Class I: Marginal tissue recession that does not extend to most common cause is faulty tooth brushing. Other the mucogingival junction. There is no loss of bone or soft secondary/contributing factors of gingival recession are tissue in the interdental area. This can be narrow or wide. broadly categorized (for convenience) as: Class II: Marginal tissue recession that extends to or a. Anatomic factors beyond the mucogingival junction. There is no loss of b. Habits CHAPTER 18 Clinical Features of Gingivitis 157 faulty tooth brushing Stillman’s cleft in the lower gingiva Stillman’s Gingival recession associated with Fig. 18.11: Fig. 18.11: Fig. 18.10: When a tooth is labially placed, the periodontium When on the labial aspect will be invariably thin. this is exposed to any kind of trauma or frictional forces, gingival recession results. etc. tooth surface. In rotated and facially-displaced teeth, Anatomic factors include: 1. of the tooth in the arch. malposition or position Tooth 2. and fenestrations. Presence of dehiscence 3. Gingival ablation from soft tissues like cheek, lips, 4. Root-bone angle and mesiodistal curvature of the c. Iatrogenic factors d. Physiologic factors a. malpositioning Gingival recession due to inflammation Gingival recession associated with tooth

Gingival recession associated with periodontitis Fig. 18.7: Fig. 18.9: Fig. 18.8: 158

bony plates are either thinned or shortened and 3. Gingiva can be examined for its color, contour, recession results from repeated trauma to the thin consistency, size, position, surface texture and gingival periodontal tissues. bleeding on probing. 4. Causes for gingival bleeding on probing could be local b. Habits: Faulty tooth brushing or brushing with hard factors and systemic factors. bristles may lead to gingival recession. Recently it has 5. Normal color of gingiva is “coral pink”. In disease it can been noted that there may be a positive relationship change to red, bluish-red or pale-pink. 6. Normally, consistency of gingiva is firm and resilient. In between smoking and recession. But the exact diseased conditions, it can exhibit soft and edematous mechanism is not reported. or firm and leathery consistency. c. Iatrogenic factors: Primary trauma from occlusion has 7. Contour is scalloped and knife edged, interdental papilla

PART IV in the anterior region is pyramidal and posteriorly tent- been reported to cause gingival recession. Orthodontic shaped. In disease, it can become rounded or rolled, movement in a labial direction and improper restorations whereas interdental papilla can become blunt and flat. can lead to gingival recession. 8. Normal stippled gingiva may appear smooth and shiny. In diseased conditions, destruction of gingival fibers is d. Physiologic factors: Gingival recession was thought to responsible for loss of stippling. be a physiologic process related to aging. However, this 9. Position of the gingiva can be actual or apparent. When idea was discarded because there was no convincing position is shifted apically exposing the root surface, it is called as gingival recession. evidence for a physiologic shift of the gingival attachment.

Clinical Significance of Gingival Recession 1. The exposed root surface may be extremely sensitive. KNOW MORE ...

2. Hyperemia of the pulp may result due to gingival Periodontal Pathology Periodontal recession. Metallic Pigmentation 3. Interproximal recession creates oral hygiene problems Heavy metals like bismuth, arsenic mercury, lead and silver absorbed systemically either from therapeutic use thereby resulting in plaque accumulation. or occupational hazard may discolor the gingiva. Gingival 4. Finally, it is aesthetically unacceptable. pigmentation from systemically absorbed metals results from perivascular precipitation of metallic sulfides in the Changes in Gingival Contour connective tissue and not as a result of systemic toxicity. It occurs only in the areas of inflammation and can be Normally, marginal gingiva is scalloped and knife edged, eliminated by treating the inflammatory changes without whereas interdental papilla in the anterior region is necessarily discontinuing medication. pyramidal and posteriorly tent-shaped. The factors that maintain normal contour are, shape of the teeth and its REVIEW QUESTIONS alignment in the arch, location and size of the proximal contact and dimensions of facial and lingual gingival 1. Describe in detail gingiva in health and disease. embrasures. In diseased conditions, the marginal gingiva 2. What are the causes of gingival bleeding of probing? may become rounded or rolled whereas interdental papilla 3. Write about definition, types and etiology of gingival can become blunt and flat. The various diseased conditions recession. related to gingival contour is given in Table 18.1. BIBLIOGRAPHY

1. David M. Williams, Francis J. Hugley. Pathology of Periodontal 1. Inflammation of the gingiva is termed as gingivitis. Diseases. Oxford Medical Publishers 1992. 2. Gingivitis can be classified depending on its course and 2. Newman, Takei, Fermin A Carranza. Clinical Periodontology. duration and its distribution. 9th edn; WB Saunders Co, 2002. 19 ChapterChapter

Gingival Enlargement

 CLASSIFICATION OF GINGIVAL • Enlargement in Puberty ENLARGEMENTS • Vitamin C Deficiency  INFLAMMATORY ENLARGEMENT • Plasma Cell Gingivitis • Acute Inflammatory Enlargement • Nonspecific Conditioned Enlargement • Chronic Inflammatory Enlargement (Granuloma Pyogenicum)  NONINFLAMMATORY GINGIVAL • Systemic Disease Causing Gingival Enlargement ENLARGEMENT • Granulomatous Diseases • Phenytoin-induced Gingival Hyperplasia  NEOPLASTIC ENLARGEMENT (GINGIVAL • Idiopathic Gingival Fibromatosis TUMOR) • Combined Enlargement • Benign Tumors  ENLARGEMENT ASSOCIATED WITH SYSTEMIC • Malignant Tumors DISEASE OR CONDITIONS  FALSE ENLARGEMENT • Conditioned Enlargement • Underlying Osseous Lesions • Enlargement in Pregnancy • Underlying Dental Tissues

INTRODUCTION (ii) Puberty (iii) Vitamin C deficiency Current clinical descriptive terminology used to describe (iv) Plasma cell gingivitis increase in size of the gingiva is gingival enlargement and (v) Nonspecific conditioned enlargement gingival overgrowth. (Granuloma pyogenicum) b. Systemic diseases causing gingival enlargements CLASSIFICATION (i) Leukemia A. According to etiologic factors and pathologic changes, (ii) Granulomatous diseases gingival enlargements could be listed out as: IV. Neoplastic enlargement (Gingival tumors) I. Inflammatory enlargement a. Benign tumors a. Chronic b. Malignant tumors b. Acute V. False enlargement II. Drug-induced enlargement B. According to location and distribution, gingival III. Enlargements associated with systemic diseases enlargement can be classified as follows: a. Conditioned enlargement Localized : Gingival enlargement limited to one or (i) Pregnancy more (group of) teeth. 160

Generalized : Entire mouth, the gingiva is enlarged Signs and Symptoms Marginal : Limited to the marginal gingiva a. It is a rapidly expanding lesion, which is usually limited Papillary : Confined to the interdental papilla to marginal gingiva or interdental papilla. Diffuse : Involves all the parts of the gingiva, i.e. b. It appears as a red swelling with smooth shiny surface marginal, attached and interdental which is painful and the associated teeth are sensitive to gingiva percussion. Discrete : Isolated sessile or pedunculated tumor-like c. The lesion becomes fluctuant and pointed with a surface enlargement orifice from which purulent exudate may be expressed.

PART IV If it is allowed to progress, the lesion may rupture According to the Degree of Gingival Enlargement spontaneously. Grade 0 : No sign of gingival enlargement Grade I : Enlargement confined to the interdental Etiology papilla It occurs as a result of bacteria, being carried deep into the Grade II : Enlargement involves papilla and marginal tissues when foreign substances such as toothbrush bristle gingiva or fragments of food substance are forcefully embedded into Grade III : Enlargement covers three quarters or more the gingiva. of the crown Histopathology INFLAMMATORY ENLARGEMENT (TABLE 19.1) It consists of a purulent focus surrounded by a diffuse Periodontal Pathology Periodontal It can be of two types: infiltration of polymorphonuclear leukocytes, edematous a. Acute inflammatory enlargement tissue and vascular engorgement. The surface epithelium is b. Chronic inflammatory enlargement ulcerated and shows varying degrees of intra and extracellular edema, invaded by leukocytes. Acute Inflammatory Enlargement (Table 19.2) Periodontal (lateral abscess) also produce enlargement Gingival abscess is a localized, painful, rapidly expanding of the gingiva, but they also involve the supporting lesion, that is usually sudden in onset. periodontal tissues.

Table 19.1: Inflammatory enlargement Chronic inflammatory enlargement Acute inflammatory enlargement

Etiology Prolonged exposure to plaque and the From bacteria carried deep into the tissues. factors that favor plaque retention. When a foreign object like a tooth brush or a lobster shell fragment is forcefully embedded into the gingiva. Location and Distribution Generally papillary or marginal gingiva. Localized: Marginal or papillary, e.g. gingival/ May be localized or generalized. periodontal abscess. Clinical Features Life preserver like bulge around the Painful, rapidly-expanding lesion of sudden onset. involved tooth. Occasionally, occurs as Within 24 to 48 hours, it becomes fluctuant and a discrete mass which is sessile or pointed with a surface orifice through which pedunculated. Sometimes painful purulent exudate comes out. ulceration in the fluid between marginal and adjacent gingiva. Histopathology Preponderance of inflammatory cells Gingival abscess consists of a purulent focus in the and fluid with vascular engorgement, connective tissue surrounded by a diffuse capillary formation and degenerative infiltration of polymorphonuclear neutrophils, changes. edematous tissue and vascular engorgement. 161

Table 19.2: Acute inflammatory enlargement Gingival abscess Periodontal abscess Periapical abscess Pericoronal abscess Location Localized swelling Usually affects the Usually seen near the Seen near the incompletely affecting the deeper periodontal root apex, i.e. in the erupted teeth marginal and structures including mucogingival junction 19 CHAPTER interdental gingiva deep pockets, and alveolar mucosa furcations and vertical osseous defects and located beyond the mucogingival junction Etiology Impactation of Periodontal pocket Due to dental caries Plaque induced inflammation foreign objects in related to destruction involving the pulp and its of the pericoronal flap, i.e. previously healthy by periodontitis extension into the pericoronitis sites periapical area Enlargement Gingival Associated Gingiva appears to • Associated with a • Mostly deep carious • Gingiva overlying the clinical be red, swollen and periodontal pocket involvement of tooth partially erupted or findings extremely painful which may be either which is non-vital. unerupted tooth. and sometimes suprabony or • Pocket may or may • Appears to be red, impacted foreign infrabony. not be present. erythematous, swollen object may still be • Tooth elevation and Mobility is absent. and extremely painful. embedded into the mobility may be seen. • Tooth is tender on • Swelling may interfere gingiva • Tooth is tender on percussion. with occlusion. lateral percussion. • Pain cannot be • Flap can be separated • Pain is localized and localized. from the tooth with patient can identify • May be associated severe food impaction. the offending tooth. with sinus tract. • Affected tooth may be vital or sometimes non-vital. • May be associated with a fistula. Radiographic No bone loss is Bone loss is seen. Radio- No bone loss. Impacted tooth features evident lucency along the lateral Periapical radiolucency aspect of the root. seen.

Treatment of Gingival Abscess Chronic Inflammatory Enlargement (Fig. 19.1)

• If the cause of the abscess is still present it should be Types are: removed. • Localized • Drainage can be established by warm salt water • Generalized mouthwashes used every 2 hours. • Discrete/Tumor-like. • If the lesion persists it can be curetted under local Localized/Generalized anesthesia or incised, if it is pointing. • If it is persistent and severe systemic, antibiotic may be • It originates as a slight ballooning of the interdental prescribed. papilla or marginal gingiva. • Any residual pocketing can be removed by subgingival • In the early stages, it produces a lifesaver-like bulge curettage or localized gingivectomy. around the involved tooth and this bulge increases until it covers part of the crown. 162

or saddle areas of removable prosthesis, nasal obstructions, habits such as mouth breathing and tongue thrusting.

In mouth breathers: • Gingivitis and gingival enlargement are often seen. • The gingiva appears to be red and edematous with a diffuse shiny surface at the exposed area. • Maxillary anterior region is the common site and their

effects are generally attributed to irritation from surface PART IV dehydration.

Treatment Fig. 19.1: Chronic inflammatory gingival enlargement localized to the lower anterior region a. Scaling and curettage: If the size of the enlargement does not interfere with the complete removal of deposits, the enlargement caused due to inflammation is treated by • It progresses slowly and painlessly unless it is scaling and curettage. complicated by acute infection or trauma. b. Surgical removal: It is indicated for two reasons: i. In enlargement with significant fibrotic component Discrete/Tumor-like that does not undergo shrinkage following scaling

Periodontal Pathology Periodontal Occasionally, they may occur as a discrete sessile or and curettage. pedunculated mass resembling a tumor. It may occur in the ii. If the size of the enlargement interferes with the interproximal/marginal/attached gingiva. access to the root surface deposits. Surgical techniques include: Histopathology a. Gingivectomy technique: The incision should be at least • Microscopically it can exhibit either exudative/ 1 to 2 mm coronal to the mucogingival line. proliferative features depending on the clinical lesion. b. Flap operation. • The lesions are clinically deep red or bluish-red, are soft and friable with a smooth-shiny surface and bleed easily. NONINFLAMMATORY GINGIVAL • They will have preponderance of inflammatory cells and ENLARGEMENT (FIBROTIC GINGIVAL ENLARGEMENT) (TABLE 19.3) fluid with vascular engorgement, new capillary formation and associated degenerative changes. • This is produced by factors other than local irritation. • Lesions that are relatively firm, resilient and pink will • This condition is uncommon and most of the cases occur have a greater fibrotic component with an abundance of due to drugs such as phenytoin, cyclosporine, nifedipine. fibroblasts and collagen fibers. • In few cases, diltiazem, verapamil and sodium valproate can also result in fibrotic enlargement. Etiology Phenytoin-induced Gingival Hyperplasia It is caused by prolonged local irritation. Following are the (Fig. 19.2) typical etiological factors; poor oral hygiene, abnormal relationships of adjacent teeth and opposing teeth, lack of Phenytoin is an anticonvulsant drug widely used in the tooth function, cervical cavities, overhanging margins of control of epilepsy and other convulsive disorders. It is also dental restorations, food impaction, irritation from clasps used in trigeminal and glossopharyngeal neuralgias. 163

Table 19.3: Noninflammatory gingival enlargement Drug-induced fibrotic enlargement Idiopathic gingival enlargement (Phenytoin, cyclosporine, nifedipine) Etiology Long-term therapy of the respective drug Unknown, possible etiology may be hereditary HPE 19 CHAPTER Location Marginal and papillary, generalized Diffuse enlargement and generalized Clinical features • Bead-like enlargement of facial and lingual • Facial and lingual surface of maxillary and gingival margins. mandibular teeth are affected but involvement • Massive tissue folds covering the crowns limited to either jaw. of teeth interfering with occlusion. • Enlarged gingiva is pink in color, firm and leathery • Appears to project from beneath the in consistency and has a characteristic pebbled gingival margin. surface. • Does not occur in edentulous spaces. • Enlargement projects into the oral vestibule • More severe in maxillary and mandibular and jaw appears distorted.

anterior region. Enlargement Gingival • It may occur in mouths with little or no plaque and may be absent in mouths with abundant deposits. Histopathology • Hyperplasia of connective tissue and Increase in the amount of connective tissue and epithelium. consists of densely-arranged collagen bundles and • Abundance of amorphous ground substance. numerous fibroblasts. • Fibroblast to collagen ratio is equal to that of normal gingiva. • The connective tissue appears highly vascularized in cyclosporine-induced enlargement.

• As the condition progresses, the marginal and papillary enlargement unite and develop into a massive tissue fold covering a considerable portion of the crown and may interfere with the occlusion. • When uncomplicated by inflammation, the lesion is mulberry-shaped, firm, pale-pink and resilient with a minutely lobulated surface and no tendency to bleed. • The enlargement characteristically appears to project from beneath the gingival margin, from which it is separated by a linear groove. • The hyperplasia is usually generalized throughout the mouth, but is more severe in maxillary and mandibular Fig. 19.2: Phenytoin-induced gingival enlargement anterior region. • It occurs in areas in which teeth are present, but hyperplasia of the mucosa in the edentulous mouth has Clinical Features been reported, but is rare. • The overgrowth of the gingiva usually becomes apparent • The presence of the enlargement will result in a in the first three months after phenytoin dosage and is secondary inflammatory process that complicates most rapid in the first year. gingival hyperplasia caused by the drug. • Clinically, it starts as a painless, bead-like enlargement • Secondary inflammatory changes produce red or bluish- of facial and lingual gingival margins and interdental red discoloration and result in an increased tendency papillae. towards bleeding. 164

Histopathology Several changes have been observed in both epithelium and connective tissue. • The epithelium shows varying degree of acanthosis, with elongated, thin rete pegs/ridges that tend to divide at their ends. • This can give rise to increased incidence of epithelial pearls. • The degree of inflammation will determine the presence

PART IV and extent of polymorphonuclear neutrophils in the gingival epithelium. • The main change in the lamina propria is proliferation of fibroblasts and increase in the collagen production. Fig. 19.3: Gingival enlargement associated with cyclosporine therapy Pathogenesis There are many theories as to why phenytoin causes gingival • It also reduces hypertension by dilating the peripheral overgrowth. The most convincing at present is the direct vasculature. effect of drug or metabolites on the gingival tissue. • Gingival overgrowth occurs in about 20 percent of cases. Major metabolite of phenytoin is 5-parahydroxy phenyl or 5-phenylhydantoin (5-P-HPPH). Treatment of Drug-associated Gingival Enlargement Periodontal Pathology Periodontal It is suggested that there are different subpopulation of fibroblasts in gingival tissue, some of which synthesize large Three different types of drugs are associated with gingival amount of protein and collagen (high activity fibroblasts) enlargement, namely anti-convulsants, calcium channel and others which are only capable of low protein synthesis blockers and the immunosuppressants like cyclosporine. (low activity fibroblasts). Treatment options are: Hassell suggested that high activity fibroblasts become sensitive to phenytoin, with subsequent increase in collagen First Step production. • Oral hygiene reinforcement, chlorhexidine gluconate Cyclosporine (Fig. 19.3) rinses, scaling and root planing. • It is a fairly potent immunosuppressive agent used to • Possible drug substitution. When it is attempted it is prevent organ transplant rejection and to treat several necessary to allow at least a period of 6 to 12 months diseases of autoimmune origin. between the discontinuation of the offending drug and • It appears to be selectively and reversibly inhibit T helper the possible resolution of gingival enlargement. cells, which play a role in cellular and humoral immune • Professional recalls. responses. • In 30 percent of the cases, gingival growth was recorded. Second Step • Clinically and microscopically the gingival hyperplasia If enlargement persists even after following the above induced by cyclosporine is similar to that, induced by mentioned approaches, surgical therapy is indicated. There phenytoin. are two surgical options available based on the features it Nifedipine presents: • It is a calcium channel blocker that induces direct • Small areas of enlargement with no attachment loss or dilatation of coronary arteries and arterioles, improving bone loss and has good keratinized tissue, gingivectomy oxygen supply to heart muscle. is the technique of choice. 165

• Large areas of enlargement with presence of osseous arranged collagen fiber bundles and numerous defects and limited keratinized gingiva, periodontal flap fibroblasts. surgery may be indicated. Etiology Idiopathic Gingival Fibromatosis (Fig. 19.4) 19 CHAPTER It is unknown. Some cases have hereditary basis. But the Other designated terms include, gingival mitosis, exact mechanism is not well-understood. elephantiasis gingivae, diffuse fibroma, idiopathic Gingival hyperplasia has been described in "tuberous fibromatosis, hereditary gingival hyperplasia and congenital sclerosis", which is an inherited condition characterized by familial fibromatosis. a triad of epilepsy, mental deficiency and cutaneous angiofibromas.

Clinical Features Gingival Enlargement Gingival • The enlargement affects the attached gingiva as well as Combined Enlargement gingival margins and interdental papillae (diffuse). It results when gingival hyperplasia is complicated by • The gingiva is firm, pink and leathery in consistency secondary inflammatory changes. These changes occur and has a characteristic pebbled surface. when gingival hyperplasia produces conditions favorable • In severe cases, the teeth are almost completely covered for the accumulation of plaque and interferes with effective and the gingival enlargement projects into the oral oral hygiene measures. vestibule. It consists of two components: • The jaws appear distorted because of bulbous a. Primary or basic hyperplasia of connective tissue and enlargement of the gingiva. Secondary inflammatory epithelium, the origin of which is unrelated to in- changes are common at the gingival margin. flammation. b. Secondary complicating inflammatory component. Histopathology • The surface epithelium is thickened and acanthotic with Treatment elongated rete pegs. Gingivectomy/ is indicated. • There is an increase in the amount of connective tissue, which is relatively avascular and consists of densely- ENLARGEMENT ASSOCIATED WITH SYSTEMIC DISEASES OR CONDITIONS (TABLE 19.4)

The systemic diseases/condition can affect the periodontium by two different mechanisms: a. Magnification of an existing inflammation initiated by dental plaque. These groups of diseases include some of the hormonal conditions (e.g. pregnancy and puberty), nutritional diseases such as vitamin C deficiency. Both belong to conditioned enlargement and some cases in which systemic influence is not identified—Conditioned enlargement. b. Manifestation of systemic disease, independently of the Fig. 19.4: Idiopathic hyperplastic gingival enlargement inflammatory status of gingiva. This includes systemic 166 ane- meshwork Gingival monocytic 18.7% cytes and connective tissue infiltrated Isolated areas of polymorphonuclear leukocytes, bacteria alignant neoplasms Incidence: • Acute myelocytic Bluish-red, sponge- • or marginal Diffuse • Localized or generalized Leukemia ously. ously.

spherical, PART IV base membrane endothelial a flattened, tion or spont proliferation Surface ulceration with immature Surface ulceration and purulent exudation gement having apseudo- and necrosis chronic inflam- mature leuko- Nonspecific condi- pyogenicum) origin Trauma M dietary irritants to of leukocyte

attached broad nized matory infiltrate turally shows • oral aspect Connectiveshowsdense infil-trate ofplasma cells inflammation with of fibrin, necrotic nous cells, epithelial thelium isparakerati- lation tissue with mmation with gingiva 66.7% dentifrices or various components (Atypicalgingivitis) (Granuloma • Ultrastruc- and • Red, friable, • Discrete shiny granular with a peduncu-persistently bleeds C Plasma cell hyper- easily to aneously involved attached • Acute monocytic

amin C possibly Periodontal Pathology Periodontal Marginal gingiva Marginal and Localized, discrete deficiency gingivitis tioned enlargement leaking blood • red, soft, friable soft, red, sometimes tumor like massfriable, and like undergoes • Surface necrosis of are similar spont is enlarged gingiva is enlarged, isTissue surface. bleeds and attachment lated on slight provoca- interproximal disease membrane purple and can Prominent bulbousProminent Gingiva is bluish- local factorslocal chewing gums, precursors Table 19.4: Enlargement—associated with systemic disease/conditions Table interproximal associated degenerative changes shows spongiosis Pregnancy tumor1.8-5% (afterand Marginal facial interdental is Labial aspect of flattened, spacered or magenta, has smooth, shiny surface with numerous deep-red pin point markings, consis- painless, tency varies from and friable soft to semifirm formation be friable or firm. Discrete, • anterior teeth • Generally dusky- withferation with prominent edema MarginalPregnancy tumor Puberty Vitamin response to local 10-70%Generalized. pregnancy) third month of gingiva More • (increased estrogen andprogesterone) with disturbance vit the interproximally prominent epithelium,which is and inflammation and may show thickened withatrophy. severe prominent rete Connective tissue pegs. Connectivepegs. tissue showsnewlynumerous poorly- shows fibers and manycollagen formed signs ofand spinous damage to and exudation are commonprolifera- and leukocytes ting • formed andengorged and thin-walled layer basal necrotizing acute in color, soft in color, and friable spherical massgingiva lingual spongy, bright-red ormagenta mushroom-like, spherical massfacial papillae, has smooth, has a smoothbleedto spontaneouslyorsessile with or unaltered. is margin gingival gingival matory emic and bleedsandKeratinized stratified •on Located proli- Endothelial pseudo- with enlar- keloid-like inflammation Chronic gingiva Epithelium •or Bright-red • formation is seen. Oral epi- • Mass of granu- •infla- Chronic Gingiva is • It has a tendencyfromprotrude that to chronic inflam- shiny surface.base pedunculated • Features capillarieswith edema and leukocyte infiltration vessels tissue pseudomembra- squamous capillary formation and associated thinning and • Pregnancy accentuates • Marginal• Incidence— • Pregnancy • Altered tissue metabolismendocrine Altered of Deficiency Allergic in Location and distribution features Histopathology Clinical Etiology 167

disease causing gingival enlargement and neoplastic • Color—dusky red or magenta with smooth glistening enlargement. surface that frequently exhibits numerous deep red, pin- point markings. Conditioned Enlargement • Consistency—semifirm, but may have varying degrees HPE 19 CHAPTER • Hormonal (Pregnancy, puberty) of softness and friability. • Nutritional (Vitamin C deficiency) • It is usually painless, unless complicated by either accumu- • Allergic lation of debris under its margin or interference with Local irritation is necessary for the initiation of this type occlusion—in which case, painful ulceration may occur. of enlargement. Conditioned enlargement occurs when the Histopathology systemic condition of the patient exaggerates the usual

gingival response to dental plaque. • Both marginal, tumor-like enlargement consists of a Gingival Enlargement Gingival central mass of connective tissue, the periphery of which Enlargement in Pregnancy is outlined with stratified squamous epithelium. • The connective tissue consists of numerous, engorged Marginal Enlargement capillaries and between the capillary network is a fibrous • Results from the aggravation of previous inflammation stroma with varying degrees of edema and leukocyte and does not occur without the clinical evidence of local infiltration. irritation. • The epithelium is thickened with varying degree of extra • Pregnancy does not cause the condition. The altered and intracellular edema. The epithelium also exhibits tissue metabolism in pregnancy accentuates the response prominent rete pegs. to local irritation. • Gingival enlargement in pregnancy is also termed as angiogranuloma in order to avoid implication of Clinical features neoplasm. (Implicated in terms such as pregnancy tumors • The enlargement is usually generalized and tends to be or fibrohemangioma). more prominent interproximally than on the facial and lingual surface. Treatment • The enlarged gingiva is bright-red or magenta, soft and friable and has a smooth, shiny surface. • The aim of the periodontal therapy for pregnant patient • Bleeding occurs spontaneously or on slight provocation. is to minimize the potential exaggerated inflammatory response related to hormonal alteration. Tumor-like Gingival Enlargement or Pregnancy • Meticulous plaque control, scaling and root planing, Tumor polishing should be the only non-emergent periodontal procedures performed. It is not a neoplasm but an inflammatory response to local • The second trimester is the safest time in which treatment irritation and is modified by the patient's condition. It usually may be performed. However, long stressful appointment appears after the first trimester but may also occur earlier. and periodontal surgical procedures should be postponed Clinical features until postpartum. • The lesion appears as a discrete mushroom-like flattened • One must be aware of a condition, 'supine hypotensive spherical mass that protrude from the interdental papilla syndrome' that occurs during the third trimester which or the gingival margin and is attached by a sessile or is characterized by a decreased blood pressure, syncope pedunculated base. and loss of consciousness. In view of this, the • It tends to expand laterally and pressure from the tongue appointments should be kept short and the patient should and cheek increases its flattened appearance. be allowed to change the position frequently. 168

• Fully reclining position should be avoided as far as • Eleven to seventeen years of age showed a high possible. prevalence of gingival enlargement. The gingival • Medication and radiographs should not be prescribed. microbiology of children between the ages of 11 to 14 • In case of marginal and interdental enlargement, scaling and their association with clinical parameters has and curettage can be performed. implicated Capnocytophaga species in the initiation of • In case of a tumor-like enlargement, surgical excision is pubertal gingivitis. required which, if possible, should be postponed until Histopathology postpartum. During pregnancy the lesion should be

removed surgically only when it interferes with Same as chronic inflammatory enlargement. PART IV mastication and causes severe disfigurement and if the Treatment patient willingly wants to get it removed. Scaling, curettage and oral hygiene instructions. Surgical Enlargement in Puberty (Fig. 19.5) removal may be performed in severe cases. Clinical Features Vitamin C Deficiency The enlargement is seen in both marginal and interdental Acute vitamin C deficiency does not itself cause gingival papilla and is characterized by prominent bulbous inflammation but it causes hemorrhage, collagen interproximal papilla. degeneration and edema of gingival connective tissue. These • Frequently only the facial gingiva is affected, because changes modify the response of the gingiva to plaque. mechanical action of the tongue prevents accumulation Periodontal Pathology Periodontal of food on the lingual surfaces. Clinical Features • Gingival enlargement during puberty has all the clinical features associated with chronic inflammatory gingival Gingival enlargement is marginal and is bluish-red, soft, disease. It is the degree of enlargement and tendency to friable and has smooth, shiny surface. Hemorrhage occurring develop massive recurrence in the presence of relatively either spontaneously or on slight provocation and surface little local irritation that distinguishes pubertal gingival necrosis with pseudomembrane formation are common enlargement from uncomplicated chronic inflammatory features. gingival enlargement. Histopathology Areas of hemorrhage with engorged capillaries and marked diffuse edema, collagen degeneration and scarcity of collagen fibers and fibroblasts are striking features.

Plasma Cell Gingivitis • It is also referred to as atypical and plasma cell gingivostomatitis and frequently consists of a mild- marginal gingival enlargement that extends to attached gingiva. • Clinically, gingiva appears red, friable and bleeds easily. An associated cheilitis and glossitis have been reported. • It is thought to be allergic in origin, possibly related to Fig. 19.5: Conditioned gingival enlargement in puberty the components of chewing gum or dentrifices. 169

• Microscopically the connective tissue contains a dense • It is a bright-red or purple and either friable or firm, infiltrate of plasma cells, that also extends to oral depending on its duration. In majority of the cases it epithelium. presents with surface ulceration and purulent exudation. • The lesion tends to involute spontaneously to become a HPE 19 CHAPTER Nonspecific Conditioned Enlargement fibroepithelial papilloma or persists relatively unchanged (Granuloma Pyogenicum) (Figs 19.6 and 19.7) for years. It is a tumor-like gingival enlargement that is considered to be an exaggerated conditioned response to minor trauma. Histopathology The exact nature of the systemic conditioning factor has It appears as a mass of granulation tissue with chronic not yet been identified. inflammatory cellular infiltration. Surface ulceration and

exudation are common features. Enlargement Gingival Clinical Features

• The lesion varies from a discrete, spherical tumor-like Treatment mass with a pedunculated attachment to a flattened, Consists of removal of the lesion along with the elimination keloid-like enlargement with a broad base. of local irritating factors.

Systemic Disease Causing Gingival Enlargement

Leukemia • The enlargement may be diffuse or marginal, localized or generalized. It may appear as an oversized extension of the marginal gingiva or a discrete tumor-like interproximal mass. • The gingiva appears as bluish-red with a shiny surface. • The consistency is moderately firm but there is a tendency towards friability and hemorrhage occurring Fig. 19.6: Pyogenic granuloma in a young woman either spontaneously or on slight provocation. • ANUG may sometimes be seen. • True leukemic enlargement occurs commonly in acute leukemia but may also be seen in subacute leukemia. It seldom occurs in chronic leukemia (Fig. 19.8). Histopathology It shows varying degrees of chronic inflammation with mature leukocytes and areas of connective tissue infiltrated with a dense mass of immature and proliferating leukocytes the specific nature of which varies with type of leukemia. Isolated surface areas of acute necrotizing inflammation with a pseudomembranous meshwork of fibrin, necrotic epithelial cells, polymorphonuclear neutrophils and bacteria Fig. 19.7: Pyogenic granuloma (Courtesy: Dr Deepak Daryani) are frequently seen. 170

c. Extract all hopeless, non-maintainable or potentially infectious teeth, at least 10 days prior to initiation of chemotherapy. d. Thorough periodontal debridement (scaling and root planing) is done and oral hygiene instructions are given. If there is an irregular bleeding time, careful debridement with cotton pellets soaked in hydrogen peroxide may be performed around the neck of the teeth.

PART IV During acute phases of leukemia, patients should receive only emergency periodontal care.

A. If there is a persistent gingival bleeding: It should be Fig. 19.8: Leukemic gingival enlargement treated as follows: i. Cleanse the area with 3 percent hydrogen peroxide. Treatment ii. Carefully explore the area and remove any etiologic • After the acute symptoms subside, attention is directed local factors making sure to avoid gingival injury. to correct the gingival enlargement. The rationale of iii. Recleanse the area with 3 percent hydrogen treatment is to remove the local deposits and to control peroxide. inflammatory component of the enlargement. iv. Place a cotton pellet soaked in thrombin against

• The enlargement is treated by scaling and curettage the bleeding point. Periodontal Pathology Periodontal which is carried out in stages under topical anesthesia. v. Cover with a gauze and apply pressure for 15 to 20 Oral hygiene procedures are extremely important in these minutes. cases. vi. If oozing persists after the removal of the gauze • Antibiotics are administered systemically the evening and pressure, replace the cotton pellet saturated with

before and for 24 hours after each treatment to reduce 3 percent H2O2 firmly, then place a periodontal the risk of infection. dressing over the area for 24 hours. B. NUG: Follow routine treatment for NUG. In leukemic patients the following instructions should be followed (in general): C. Acute gingival or periodontal abscess: They are usually (i) Refer the patient to the physician for medical evaluation associated with regional lymphadenopathy and systemic and treatment. For this, close cooperation with the complications. physician is required. Treatment: It is as follows: (ii) Prior to chemotherapy, a complete periodontal treatment i. Systemic antibiotics. plan should be prepared with the physician, because once ii. Gentle incision and drainage. the chemotherapy is started the patient will become iii. Cleanse the area with cotton pellets saturated with 3 immunosuppressed, thus increasing the risk of secondary percent hydrogen peroxide. infection. iv. Apply topical pressure with gauze for 15 to 20 minutes. The treatment plan for these patients is: D. Oral ulceration: It is treated with antibiotics and bland a. Monitor hematological lab values daily (bleeding time, mouth rinses-topical rinses such as viscous xylocaine clotting time, partial thromboplastin time and platelet or promethazine hydrochloride syrup may be prescribed. count). Topical protective ointments and sharp irritational areas b. Administer antibiotics prior to any periodontal therapy. or appliances should be removed. 171

Oral moniliasis is common in leukemic patient and can • At one time the usual outcome was death from kidney be treated with nystatin suspensions. failure but more recently the use of immunosuppressive drugs has produced prolonged remission. In Chronic Leukemia HPE 19 CHAPTER Scaling and root planing can be performed without Sarcoidosis complication, but an effort should be made to avoid periodontal surgery. It is a granulomatous disease of unknown etiology. It starts Before every procedure: Bleeding time should be measured. in individuals in their twenties and thirties and can involve If any changes are seen, postpone the appointment and refer almost any organ, including the gingiva, where a red, smooth the patient to physician. enlargement may occur. Plaque control and frequent recall intervals should be given attention particularly. NEOPLASTIC ENLARGEMENT Enlargement Gingival (GINGIVAL TUMOR) Granulomatous Diseases (Table 19.5) Benign Tumors of the Gingiva (Table 19.6) Wegener's Granulomatosis • It is a rare disease characterized by a granulomatous • Fibroma necrotizing lesion of the respiratory tract, including nasal • Papilloma and oral defects. • Peripheral giant cell granuloma • The initial manifestation of Wegener's granulomatosis • Central giant cell granuloma may involve the orofacial region and include oral • Leukoplakia mucosal ulceration, gingival enlargement, abnormal • Gingival cyst. tooth mobility, exfoliation of teeth and delayed healing response. Malignant Tumors of the Gingiva (Table 19.7) • Clinically the enlargement appears reddish-purple in color and bleeds easily on stimulation. The etiology of • Carcinoma Wegener's ganulomatosis is unknown, but the condition • Malignant melanoma is considered as an immunologically mediated tissue • Sarcoma most commonly Kaposi's sarcoma injury. • Metastasis.

Table 19.5: Granulomatous disease

Wegener’s Granulomatosis Sarcoidosis (Multisystem Granuloma) Etiology Immunologically-mediated tissue injury Unknown, but may be impaired cell-mediated immunity Location and Distribution Papillary enlargement Nonspecific Clinical features Shows oral mucosal ulceration, reddish Red, smooth enlargement purple gingival enlargements, bleeds on stimulation, abnormal tooth mobility, exfoliation of teeth, and delayed healing response Histopathology Chronic inflammation with giant cells Sarcoid granuloma consists of whorls of epithelioid and micro-abscesses covered by thin cells and multinucleated Langerhans giant cells with acanthotic epithelium peripheral mono-nuclear cells. Caseation and necrosis do not occur 172 incisor area Mandibular bicuspid, membrane of implantation epithelium

• Traumatic • of Remnants PART IV irregularly- bular canine or underlying commissures, cuspid connective tissues. deficiency, hor-deficiency, mones, candidiasis periodontal epithelial islands of show of e Buccal mucosa, ain flattened scaly lesion • Occurs in mandi- the jaw from Varies • Involves marginal s of loose Thickening of epi- Cyst cavity lined appearance. jaw due plaque. • Painless and causes plate is seen.expansion. with of injury chronic Tobacco, slight discomfort. to a thick lated blood and osteoid are seen. andible is mor commonly involved anterior segmentand does notuncommonly crossmidline and soft palate, and gingiva and produces floor of the mouth grayish-white, gingiva or attached • Collagen fibers

Central giant Leukoplakia Gingival cyst Periodontal Pathology Periodontal the connective tissue. capillaries. mmatory infiltrate articles and chronic many proliferating and some degree of without localized Frequently on labialsurface. than maxilla. alveolar mucosa, More common in tongue, lips, hard irregularly-shaped cavitation. No p lated, painless. Firmor spongy and color varies from pink to cortical deep red or purplish blue. Ulcerations are sometimes seen. occasionally seen.Overlying epitheliumis hyperplastic with • whorled Multinucleated giant cells are prominent. cell granuloma cell granuloma Table 19.6: Benign tumors of gingiva Table of many It has numerous foci • It consist stratified Bone formation is Some unknown syphilis, vitamin enamel organ, and discrete and discreteSlowly growing gingival margin. Hard, wart-like Smooth, regularly Arise within spherical mass thattends to be firm protuberance from outlined masses to gingival surface and nodular, butand nodular, may be soft and Usuallyvascular. pedunculated multilobulated protuberance with surface indentation. Sessile or peduncu- Slight to moderate bulging of but covered by stratified to expansion of squamous epithelium shaped keratinous premolar area. erosion of bone Consists of bundlesConsists It consists The surface isAreas of calcification up of are also seen. thin central connec- tive tissue core. ulceration at the base. Foci of extra vascu- of interlacing collagenfibers interspersed long thin, finger-with varying number like projections andof fibroblasts extending above of multinuclear giantsmall blood vessels. mucosa, each made the surface of p cells and hemosiderin in squamous epithelium. fibrillar connective a and containing tissue stroma with inflammatory infiltrate thelium with hyper- keratosis, acanthosis fibroblasts by thin flattened and small epithelium with or dyskeratosis, infla- areas of thickening. Localized, diffuse Localized, diffuse Interdental or from M or chronic irritation virus papilloma alcohol, irritation, dental lamina, Reaction to trauma Mostly due to Local injury History Fibroma Papilloma Peripheral giant distribution Clinical features Histopathology Location and Etiology 173

Table 19.7: Malignant tumors of the gingiva

Squamous cell carcinoma Malignant melanoma Etiology Chronic irritation, tobacco, alcohol, syphilis, Neoplasms of epidermal melanocytes. nutritional deficiency. Sunlight exposure is possible etiological

factor in cutaneous melanoma. 19 CHAPTER Location and distribution Mandibular gingiva is more commonly Palate, maxillary gingiva and alveolar ridge. involved than the maxillary gingiva. Attached gingiva is more frequently involved than free gingiva. Clinical features • Exophytic or ulcerative which appears Deeply-pigmented area at times ulcerated as flat, erosive lesion. and hemorrhagic which increases in size. • Locally invasive to underlying bone or adjacent mucosa.

• It may or may not be painful. Gingival Enlargement Gingival • Attached gingiva is more frequently involved than free gingiva. • Metastasis is common. Histopathology Well-differentiated lesion which consists • Radial growth phase of superficial of sheets and nests of cells with origin spreading melanoma is characterized from squamous epithelium. Nuclei of by presence of large, epitheloid neoplastic cells are hyperchromatic. melanocytes distributed in pagetoid Mitotic figures are atypical. Individual manner. Vertical growth phase is cell keratinization or epithelial pearls characterized by proliferation of are present. Shows rapidly dividing malignant epitheloid melanocytes malignant cells. Resembles less to cells into connective tissue. Macrophages of origin. and melanophages are present. Melanin pigment is scanty.

FALSE ENLARGEMENT (FIG. 19.9) crown. This enlargement has been termed as developmental enlargement. These are not true enlargements of gingival tissues but may In strict sense, this type of enlargement is physiologic. appear as a result of increase in size of the underlying However, it may be complicated by marginal inflammation osseous or dental tissues. in which case alleviation of the marginal inflammation is sufficient rather than resection of the enlargement. Underlying Osseous Lesions Enlargement of the gingiva due to enlargement of underling bone occurs most commonly in tori and exostosis but it can also occur in Paget's disease, fibrous dysplasia, cherubism, central giant cell granuloma, osteoma, osteosarcoma. The gingiva usually presents with no abnormal clinical features except the massive increase in size in the specific area.

Underlying Dental Tissues During the various stages of eruption of primary dentition, the gingiva may show bulbous, marginal distortion caused by the superimposition of the bulk of the gingiva on the Fig. 19.9: False enlargement in the normal prominence of the enamel in the gingival half of the right upper posterior region 174

1. Gingival enlargements can be classified according to, KNOW MORE ... etiologic factors and pathologic changes, location and distribution and the degree of gingival enlargement. Various Groups of Drugs Associated 2. Inflammatory enlargement can be of two types— acute with Gingival Enlargement type, e.g. gingival abscess and chronic type of • Anticonvulsants such as Phenytoin, Valproic acid, enlargements. Succinimides, Phenobarbitone and Ethosuximide 3. Three categories of drugs have been identified to be • Immunosuppressants like Cyclosporine and associated with gingival enlargements, anticonvulsants, Tacrolimus calcium channel blockers and immunosuppressants.

PART IV • Calcium channel blockers like Nifidipine, Nitrendipine, 4. The drug-induced enlargements are differentiated from Amlodipine, Felodipine, etc. idiopathic enlargement, in the latter the enlargement • Other agents include Dilitiazem and Verapamil. involves all parts of the gingiva, hence called diffuse enlargement. Syndromes Associated with Gingival Fibromatosis 5. Treatment options for drug induced enlargements are— • Gingival fibromatosis with Hypertrichosis drug substitution and surgical therapy including • Zimmerman-Laband syndrome gingivectomy or flap surgery. • Cross syndrome 6. Enlargements associated with systemic diseases can • Murray-Puretic-Drescher syndrome be: • Rutherford’s syndrome a. Magnification of an existing inflammation caused by • Tuberous sclerosis dental plaque discussed as "conditioned • Ramon’s syndrome enlargement" which includes some hormonal • Sturge-Weber’s syndrome conditions (e.g. pregnancy and puberty), nutritional diseases such as vitamin C deficiency and some Periodontal Pathology Periodontal REVIEW QUESTIONS cases in which the systemic influence is not identified (nonspecific conditioned enlargement). 1. Classify gingival enlargement. Discuss in detail clinical b. Second category includes, manifestation of the features, pathogenesis and treatment of drug-induced systemic disease not dependent on the inflammatory status of the gingiva discussed as “systemic diseases gingival enlargement. causing gingival diseases” and “neoplastic 2. What are the differences between gingival and enlargement (Gingival tumors)”. periodontal abscess? 3. What is granuloma pyogenicum?

BIBLIOGRAPHY

1. Newman Takei, Fermin A Carranza. Clinical Periodontology, 9th edn, WB Saunders, 2002. 2. Robin A Seymeur, Peter A Heasman. Drugs, Diseases and the Periodontium. Oxford University Press Publication 1992. 3. Thomas M Hassell, A Paul Burtner, Donald McNeal. Oral problems and genetic aspects of individuals with epilepsy. Periodontal 2000;6:1994. 20 ChapterChapter

Acute Gingival Infections

 CLASSIFICATION OF VARIOUS ACUTE • History GINGIVAL LESIONS • Histopathology  NECROTIZING ULCERATIVE GINGIVITIS • Diagnosis • Terminology • Differential Diagnosis • Clinical Features • Treatment • Intraoral/Extraoral Signs and Symptoms  PERICORONITIS • Clinical Course • Definition • Etiology • Types • Histopathology, Diagnosis and Treatment • Clinical Features  ACUTE HERPETIC GINGIVOSTOMATITIS • Complications • Clinical Features • Treatment • Etiology

CLASSIFICATION OF VARIOUS ACUTE • Herpes varicella/zoster virus infections GINGIVAL LESIONS • Glandular fever c. Bacterial infections: According to Manson • Necrotizing ulcerative gingivitis a. Traumatic lesions of gingiva: • Tuberculosis • Physical injury • Syphilis • Chemical injury d. Fungal diseases: b. Viral infections: • Candidiasis • Acute herpetic gingivostomatitis e. Gingival abscess • Herpangina f. Aphthous ulceration • Hand, foot and mouth diseases g. Erythema multiforme • Measles h. Drug allergy and contact hypersensitivity 176

NECROTIZING ULCERATIVE GINGIVITIS (NUG)

Terminology

Necrotizing ulcerative gingivitis (NUG) is an inflammatory, destructive disease of the gingiva, which presents charac- teristic signs and symptoms (Fig. 20.1). Other terms used to describe this condition are: • Vincent’s infection

PART IV • Trench mouth • Acute ulceromembranous gingivitis and others. NUG (necrotizing ulcerative gingivitis) can cause Fig. 20.1: ANUG (Punched out interdental papilla destruction of the supporting structures. When it involves between two central incisors) the bone it causes bone loss, the condition is referred as necrotizing ulcerative periodontitis (NUP). Necrotizing Lateral ulceration, which is (less common) involving ulcerative gingivitis can occur in acute, subacute and primarily the buccal wall of the papillae, margins and recurrent forms. possibly the attached gingiva, occurs in the distribution of the lateral blood supply. Deep ulceration involves Clinical Features (Fig. 20.1) necrosis of the tissues of the embrasure giving rise to typical truncated papillae, occurs in the distribution of Necrotizing ulcerative gingivitis is characterized by sudden

Periodontal Pathology Periodontal the intra-alveolar vessels (more common). onset, sometimes may be followed by an episode of d. Other signs include gingival hemorrhage or pronounced debilitating diseases or acute respiratory tract infections. bleeding on the slightest stimulation. Long hours of working without adequate rest and e. Fetid odor and increased salivation. psychologic stress are also frequent features in the history of necrotizing ulcerative gingivitis. Oral Symptoms

Intraoral Signs and Symptoms 1. The lesions are extremely sensitive to touch. 2. Complains of a constant radiating, gnawing pain that is a. Oral signs: Lesions are characterized by punched out, intensified by eating spicy or hot foods and chewing. crater-like depressions at the crest of the interdental 3. There is a metallic foul taste, and the patient is conscious papillae, subsequently involving marginal gingiva and of an excessive amount of “pasty saliva”. rarely attached gingiva. b. These craters are covered by grayish pseudomembranous Extraoral Signs and Symptoms slough, which is demarcated from the remaining of the mucosa by a pronounced linear erythema. In mild to moderate stages of the disease local lymphadeno- c. The ulcerations of necrotizing ulcerative gingivitis could pathy and a slight elevation in temperature are common be of two types—lateral ulceration and necrosis, deep features. In severe, cases marked systemic complications ulceration and necrosis. This is related to the fact that such as high fever, increased pulse rate, leukocytosis, loss the gingival tissues are supplied by two main sources of of appetite and general lassitude are common. Systemic blood supply. Supraperiosteal vessels supplying the reactions could be more severe in children. In rare cases, attached gingiva, lateral margins and lateral parts of the severe sequelae such as the following may occur, noma or papillae, while intra-alveolar vessels supplying to the gangrenous stomatitis, fusospirochetal meningitis, col and central portions of the papillae. peritonitis, toxemia, and fatal brain abscess. CHAPTER 20 Acute Gingival Infections 177 A poor diet has been reported as a poor diet has been A or necrotizing ulcerative periodontitis Deep periodontal pockets, pericoronal flaps are Deep periodontal traumatized by opposing teeth in Areas of the gingiva correlation Many investigators have reported a positive substances. reflections of stress. i. Pre-existing gingivitis ii. Injury to the gingiva iii. Smoking Systemic Predisposing Factors Nutritional deficiency: deficiencies such Nutritional predisposing factor in NUG. the response of as vitamin B and vitamin C accentuate gingival tissues produced by increased pathogenic flora. Several researchers have found an increase in the fusospiro- chetal flora in patients with nutritionally-deficient diets. Local Predisposing Factors Local Predisposing factors are: predisposing Most important particularly vulnerable areas for the occurrence of the areas for the occurrence of particularly vulnerable a favorable environment for the offer disease because they are fusospirochetes and hence, they proliferation of the zones. called as incubation surface behind the malocclusion, such as the palatal surface of the maxillary incisors and the labial gingival sites of necrotizing mandibular incisors are frequent ulcerative gingivitis. ulcerative gingivitis. between smoking and acute necrotizing The possible reasons are: • on the gingiva. Direct toxic effect of tobacco • or other changes induced by nicotine or other Vascular • ulcerative gingivitis are both Smoking and necrotizing Table 20.1: Stages in the progression of NUG 20.1: Stages Table Prevotella intermedia Prevotella . The variable flora consists The variable . Bacteroides intermedius Bacteroides Constant flora is composed of fusospirochetal organisms Constant flora is composed of fusospirochetal Horning and Cohen have described the following stages Horning and Cohen 3.4.5. the gingival margin Necrosis extending to 6. also to the attached gingiva Necrosis extending 7. into buccal or labial mucosa Necrosis extending exposing alveolar bone Necrosis Necrosis perforating skin of cheek 1 21 6 Necrotizing ulcerative periodontitis Necrotizing ulcerative periodontitis Necrotizing stomatitis 1 0 Necrotizing stomatitis Noma 1.2. of the tip of the interdental papilla Necrosis Necrosis of the entire papilla 93 NUG Necrotizing ulcerative gingivitis 19 NUG or NUP Necrotizing ulcerative gingivitis Stages Involvement of the lesion of cases % Clinical conditions of a heterogeneous array of bacterial types. These bacterio- of a heterogeneous array of bacterial types. immunologic data, logic findings have been supported by titers to spirochetes increased IgG and IgM antibody (intermediate sized up to 90%) and studies have has been demonstrated. Electron microscopic small, intermediate demonstrated three types of spirochetes, spirochetes. and large sized (maximum number up to 90%) gingivitis has The specific cause of necrotizing ulcerative The common opinion is that it is not been established. but requires produced by a complex of bacterial organisms underlying tissue changes to facilitate the pathogenic activity of the bacteria. Plaut and Vincent introduced the concept that necrotizing Vincent Plaut and bacteria namely, ulcerative gingivitis is caused by a specific More organisms. a fusiform bacillus and a spirochetal a constant and a recently Loesche and colleagues described ANUG. variable flora associated with and also Role of Bacteria Etiology in the progression of necrotizing ulcerative gingivitis (NUG) in the progression of 20.1). (Table Clinical Course Clinical destruction it may lead to if left untreated, It is indefinite, (necrotizing of roots and denudation of the periodontium, combined with severe toxic ulcerative periodontitis), systemic complications. 178

Debilitating diseases: May predispose to the development 3. Zone III—Necrotic zone: Consists of a dead tissue cells, of acute necrotizing ulcerative gingivitis. Such systemic remnants of connective tissue fragments, and numerous disturbances are metallic intoxication, severe gastrointesti- spirochetes. nal disorders, blood dyscrasias such as anemia, leukemia 4. Zone IV—Zone of spirochetal infiltration: Consists and acquired immunodeficiency syndrome. of a well preserved tissue infiltrated with spirochetes of intermediate and large-sized without other organisms. Psychosomatic factors: Appears to be important in the etiology of acute necrotizing ulcerative gingivitis. The Diagnosis mechanisms whereby psychological factors create or

PART IV predispose to gingival damage have not been established, Diagnosis is based on clinical findings. A bacterial smear but an alteration in digital and gingival capillary responses may be used to corroborate the clinical diagnosis, but it is suggestive of increased autonomous nervous activity has not necessary nor definitive because the bacterial picture is been demonstrated. Cohen and coworkers have suggested not appreciably different from the other conditions. that a psychiatric disturbance may lead to activation of the Differential diagnosis includes: hypothalamic pituitary adrenal axis. This results in elevation a. Gonococcal stomatitis of serum and urine cortisol levels, which is associated with b. Agranulocytosis a depression of lymphocyte and polymorphonuclear c. Vincent’s angina leukocytes function that may predispose to necrotizing d. Desquamative gingivitis ulcerative gingivitis. e. Necrotizing ulcerative gingivitis in leukemia f. Necrotizing ulcerative gingivitis in AIDS

Periodontal Pathology Periodontal Histopathology g. Streptococcal gingivostomatitis. Microscopically, the lesions involve both epithelium and Treatment underlying connective tissue. The surface epithelium is destroyed and is replaced by a pseudomembranous mesh 1. Non-ambulatory patient: With symptoms of generalized work of fibrin, necrotic epithelial cells, polymorphonuclear systemic complications. neutrophils and various types of microorganisms. This is 2. Ambulatory patient: With no serious systemic compli- the zone that appears clinically as the surface pseudo- cations. membrane. The underlying connective tissue is markedly hyperemic, with numerous engorged capillaries and dense Treatment for Non-ambulatory Patients infiltration of polymorphonuclear neutrophils. This acutely- Day 1: inflamed hyperemic zone appears clinically as the surface a. Local treatment limited to gently removing the necrotic pseudomembrane. pseudomembrane with a pellet of cotton saturated with

hydrogen peroxide (H2O2). Relationship of Bacteria to the Characteristic Lesions b. Advised bed rest and rinse the mouth every 2 hours with Listgarten and colleagues described four zones namely: a diluted 3 percent hydrogen peroxide (H2O2). 1. Zone I—Bacterial zone: It is the most superficial zone, c. Systemic antibiotics like penicillin or metronidazole can consists of varied bacteria, including a few spirochetes be prescribed. of the small, medium-sized and large types. Day 2: If condition is improved, proceed to the treatment 2. Zone II—Neutrophil-rich zone: Contains numerous described for ambulatory patients. If there is no leukocytes predominantly neutrophils with bacteria improvement at the end of the 24 hours, a bedside visit including spirochetes of various types. should be made. The treatment again includes gently swab CHAPTER 20 Acute Gingival Infections 179 gingivostomatitis Vesicles on the tongue in primary herpetic Vesicles Fig. 20.2: of the gingiva and the adjacent oral mucosa with varying of the gingiva and the adjacent oral mucosa degrees of edema and gingival bleeding. labial areas, e.g. clusters of vesicles dispersed in different and tongue. and buccal mucosa, hard palate, pharynx hydrogen peroxide, sodium perborate). hydrogen peroxide, systemic complications. of analgesics and adequate bed tion and administration rest. ACUTE HERPETIC GINGIVOSTOMATITIS AND 20.3) (AHG) (FIGS 20.2 Clinical Features Primary Gingivostomatitis Oral Signs 1. shiny erythematous, involvement It appears as a diffuse, 2. discrete, spherical, In its initial stage it may appear as Further Treatment Considerations Further Treatment 1. Gingivoplasty. 2.(escharotic drugs and silver nitrate, Role of drugs 3. toxic antibiotics—only in patients with Systemic 4.systemic treatment—copious fluid consump- Supportive 5. supplements—vitamin B/C supplements. Nutritional membrane caused It is a viral infection of the oral mucous It occurs most by HSV I and II (Herpes simplex virus). than 6 years of frequently in infants and children younger age but is also seen in adults. calers and curettes are added to the instru- calers and curettes are added to the Oral hygiene instructions are reinforced and Scaling and root planing are repeated, plaque A topical anesthetic is applied and after 2 or 3 topical anesthetic A Appointments are fixed for treatment of chronic Most cases, the condition will be improved, start will be improved, the condition Most cases, for every two hours. aids and with a bland dentifrice, use of interdental chlorhexidine mouth rinse are recommended. Subgingival scaling and curettage are contraindicated Subgingival scaling and curettage are Fifth visit: Third visit: Third Fourth visit: thorough scaling and root planing are performed. gingivitis, periodontal pockets and pericoronal flaps, and for the elimination of all local irritants. Patient is placed on maintenance program. mentarium. Shrinkage of the gingiva may expose previously covered calculus which is gently removed. Same instructions are reinforced. control instructions are given. Hydrogen peroxide rinses are discontinued. Second visit:S 3. Confine toothbrushing to the removal of surface debris Instructions to the patient 1. smoking and alcohol. Avoid 2. 3 percent hydrogen peroxide and warm water Rinse with at this time because of possibility of extending the infection at this time because of possibility of extending to deeper tissues. the treatment for ambulatory patients. the treatment for ambulatory Patients Ambulatory for Treatment First visit: to gently swabbed with a cotton pellet minutes the areas are and non-attached surface debris. remove pseudomembrane with warm water the superficial After the area is cleansed with ultrasonic scalers. Patients with calculus is removed gingivitis and moderate or severe necrotizing ulcerative regime of are placed on antibiotic local lymphadenopathy, for penicillin-sensitive Amoxicillin 500 mg thrice daily, Azithromycin 500 mg once a day for three days or patients daily for seven days. Metronidazole 200 mg or 400 mg twice Day 3: the area with hydrogen peroxide, instructions of the previous instructions of hydrogen peroxide, the area with day are repeated. 180

Etiology Acute herpetic gingivostomatitis is caused by HSV (Herpes simplex virus) with a size of approximately 100 to 200 μm. When fully formed, it consists of a core containing genetic material (DNA) surrounded by a capsid. The capsid is made up of a hexagonal particle called capsomers. The capsid in turn is surrounded by a membrane or envelope. The fully grown virion penetrates the cell membrane, once inside,

PART IV the virion loses, its coating and later it gains entrance into the nucleus. In the nucleus the DNA of the virus converts the host nucleus and codes the host DNA for the production of material necessary for viral replication. Herpes viruses that cause orofacial diseases in humans Fig. 20.3: Primary herpetic gingivostomatitis in a 10-year-old are: patient with diffuse erythematous involvement of the gingiva 1. Herpes virus type 1—(Infections above the waist) (Courtesy: Dr Deepak Daryani) oropharyngeal lesions responsible for acute herpetic gingivostomatitis (HGS) and cold sores. After approximately 24 hours the vesicles rupture and 2. Herpes virus type 2—(Infections below the waist)– Also form painful shallow ulcers with scalloped borders and affects the mouth with changing sexual practices surrounding erythema. Periodontal Pathology Periodontal 3. Cytomegalovirus—Severe Oral Ulcerations 3. Diffuse, edematous, erythematous enlargement of the 4. Varicella zoster virus—responsible for chickenpox and gingiva with a tendency towards bleeding is seen. herpes zoster (shingles) 4. The course of the disease is 7 to 10 days. 5. Epstein-Barr virus—responsible for infectious mono- nucleosis and Hairy Leukoplakia Oral Symptoms 6. Human herpes virus 8—Kaposi’s sarcoma. 1. Generalized soreness of the oral cavity which interferes with eating and drinking. Histopathology 2. The ruptured vesicles are sensitive to touch, thermal Vesicles rupture to form a discrete ulceration, which appears changes and food. to have a central portion of acute inflammation characterized

Extraoral and Systemic Signs and Symptoms

There is a 1-3 day prodrome of fever, loss of appetite and myalgia. Cervical lymphadenopathy is present.

Recrudescent Oral HSV Infection After the primary infection the virus remains latent in the nerve tissue. If reactivation occurs it causes Herpes labialis (cold sore). It is associated with prodrome of tingling and itching on the corners of lip followed by vesicle formation and ulceration (Fig. 20.4). Fig. 20.4: Herpetic vesicles (Herpes labialis) CHAPTER 20 Acute Gingival Infections 181 spherical ulcer. Diffuse involvement of gingiva, may include Diffuse involvement of gingiva, may spherical ulcer. Herpes labialis can be managed with topical antiviral Herpes labialis can be managed with the The lesions may occur anywhere in the oral cavity, Treatment topical lignocaine Primary Gingivostomatitis is treated with Acyclovir at 15 mg/kg five times a day for for pain relief. halts the progression 5-7 days reduces the duration of fever, of lesions and reduces infectivity. or 3% Penciclovir medications such as 5% acyclovir cream at the first sign of cream applied three to five times a day the lesion. Recurrent Aphthous Stomatitis (RAS) Recurrent aphthous stomatitis (RAS; aphthae; canker sores) is a common condition which is characterized by multiple recurrent small, round or ovoid ulcers with circumscribed erythematous halo, and yellow or gray floors margins, typically presenting first in childhood or adolescence. a painful buccal and labial mucosae are common sites. It’s lesion and may occur as a single lesion or as lesions scattered of each lesion is 7 to The duration throughout the mouth. 10 days. Differential Diagnosis 20.2) 1. Necrotizing ulcerative gingivitis (Table 2. Erythema multiforme 3. syndrome Stevens-Johnson 4. (Canker sores). Aphthous stomatitis seudomembranous slough, seudomembranous The material is obtained from the base Host bacterial interaction, mostly fusospirochetes Host bacterial interaction, viral etiology Specific Table 20.2: Distinction between necrotizing ulcerative gingivitis and primary herpetic gingivostomatitis gingivitis and necrotizing ulcerative between 20.2: Distinction Table scraping oral lesions Tzanck smear: The finding of of the lesion and smeared and stained. multinucleated cells with swelling, ballooning and degeneration is adequate for diagnosis. The microscopic picture of the vesicle is characterized The microscopic picture of the vesicle Necrotizing condition marginal gingiva. lesions affecting Punched out crater-like with p The lesions are covered leaving slightly depressed oval and rupture Vesicles Diffuse erythema and vesicular eruptions Necrotizing ulcerative gingivitis (NUG) ulcerative gingivitis Necrotizing Etiology: Primary herpetic gingivostomatitis (PHG) other oral tissues are rarely affected.other oral tissues are Uncommon in childrenNo definite durationNot contagious buccal mucosa and lips Occurs more frequently in children Duration of 7 to 10 days Contagious Diagnosis It is usually established from the patients’ history and the tests the material clinical findings. For confirmatory, may be obtained from the lesion and submitted to the laboratory. 1. cell culture is the gold standard HSV isolation by 2. by Polymerase Chain Reaction from swabs obtained 3. by extra- and intracellular edema and degeneration of by extra- and intracellular edema The cell cytoplasm appears to be the epithelial cells. Later the nucleus also degenerates. The liquefied and clear. of the vesicle formation results from fragmentation round degenerated epithelial cells. Occasionally, in the nuclei of eosinophilic inclusion bodies are found of These inclusion bodies may be a colony epithelial cells. remnants of the virus particles, degenerated protoplasmic cell, or a combination of both, called Lipschutz’s affected by plasma cells. bodies. Connective tissue is infiltrated Tzanks smear and the stain used is Smear obtained is stain. Giemsa’s by ulceration and varying degrees of purulent exudate, by ulceration and varying degrees blood vessels. surrounded by a zone rich in engorged 182

Aphthous stomatitis may occur in the following forms: Minor aphthae: Is the most common affecting about 80% of patients with RAS: ulcers are round or oval usually <5 mm in diameter with a gray-white pseudomembrane and an erythematous halo. The ulcers heal within 10-14 days without scarring.

Major aphthae: Is a rare severe form of Aphthous ulcer. Ulcers are oval and may exceed 1 cm in diameter. Ulcers PART IV persist for up to 6 weeks and often heal with scarring.

Herpetiform aphthae: Is the least common variety and is Fig. 20.5: Pericoronitis–third molar partially-covered by characterized by multiple recurrent crops of widespread infected flap small, painful ulcers. As many as 100 ulcers may be present at a given time, each measuring 2-3 mm in diameter. Types Acute, subacute or chronic. Etiology Clinical Features It is unknown. Major factors linked to RAS are genetic predisposition, Hematinic deficiencies, immunologic Signs and Symptoms abnormalities, stress, food allergy and gastrointestinal Include markedly red, edematous suppurating lesion that is

Periodontal Pathology Periodontal disorders. Predisposing factors include hormonal distur- extremely tender with radiating pain to the ear, throat and bances, trauma, cessation of smoking and menstruation. floor of the mouth. The patient is extremely uncomfortable because of the Treatment foul taste and inability to close the jaws. In addition to the Various medications have been used in the treatment of this pain, swelling of the cheek in the region of the angle of the condition including: jaw is seen. a. Local applications: Using topical lignocaine and benzocaine in mild cases. Topical steroids like Acute Pericoronitis Triamcinolone and Clobetasol application in severe It is identified by varying degrees of involvement of cases shortens healing time. pericoronal flap as well as with systemic complications. An b. Systemic therapy: Drugs like Colchicines, Pentoxi- influx of inflammatory fluid and cellular exudates results fylline, Dapsone, short bursts of systemic steroids and in an increase in bulk of the flap which interferes with Thalidomide have been used to reduce the number of complete closure of the jaws. The flap is traumatized by ulcers and recurrences. contact with the opposing jaw and inflammatory involve- ment is aggravated. PERICORONITIS (FIG. 20.5) Lymphadenitis is a common finding; the patient may also have toxic systemic complications such as fever, Definition leukocytosis and malaise. It is an acute infection which refers to inflammation of gingiva and surrounding soft tissues of an incompletely Complications erupted tooth. It occurs most frequently in the mandibular • The involvement may become localized, in the form of third molar area. pericoronal abscess. CHAPTER 20 Acute Gingival Infections 183 superficial debris and exudate followed by application debris and exudate superficial agent. of topical anesthetic the area is flushed with warm water. is also removed and of salt in a glass of warm water, solution of a teaspoonful and administration of systemic rest, copious fluid intake symptoms are present. antibiotics, if toxic is made with a posterior incision to establish drainage by insertion of No. 15 bard parker blade, followed 1/4th inch gauze wick. as to whether In the next visit, determination is made First Visit 1.to remove with warm water is gently flushed The area 2.the underlying debris The flap is reflected with a scaler and 3. a patient include hourly rinses with Instructions to the 4. an antero- If the gingival flap is swollen and fluctuant This decision is the tooth is to be retained or extracted. eruption into a good governed by the likelihood of further functional position. Treatment of pericoronitis. (A, B) Pericoronal flap covering partially erupted lower IIIrd molar, (C, D) With the of pericoronitis. (A, B) Pericoronal flap covering partially erupted lower IIIrd molar, Treatment

rise to cyst formation. rise to cyst the base of the tongue, making it area and medially into for the patient to swallow. difficult and retropharyn- cervical, deep cervical submaxillary, geal lymph node. but nevertheless potential sequelae angina are infrequent of acute pericoronitis. help of a scalor flap is reflected to cleanse the underlying debris, (E) A wedge-shaped incision is made to section the tissue wedge-shaped incision A help of a scalor flap is reflected to cleanse the underlying debris, (E) Figs 20.6A to E: Treatment (Figs 20.6A to E) (Figs 20.6A Treatment on: The treatment of pericoronitis depends • Severity of the inflammation. • complications, and The systemic • tooth. The advisability of retaining the involved • into the oropharyngeal It may spread posteriorly • there is involvement of the Depending on the severity • and Ludwig’s Peritonsillar abscess formation, cellulitis • vital tooth it may give a partly-erupted If it occurs in 184

If it is decided to retain the tooth, the necessary surgical procedures are performed using a periodontal knife or electrosurgery. Under anesthesia, a wedge-shaped incision KNOW MORE ... is made to section a tissue that includes the gingival flap The term transmissible denotes a capacity for the with the tissue distal to the involved tooth as well. maintenance of an infectious agent in successive After the tissue is removed, a periodontal pack is placed. passages through a susceptible animal host. Whereas the term communicable signifies a capacity for the maintenance of infection by natural modes of spread, such as direct contact through drinking water, food and eating

1. Acute gingival lesions are classified as acute necrotizing utensils. Hence, a disease that is communicable is PART IV ulcerative gingivitis (ANUG), primary herpetic gingivo- described as contagious. stomatitis, and pericoronitis. 2. ANUG is an inflammatory, destructive disease of the gingiva, which presents with characteristic signs and REVIEW QUESTIONS symptoms. 3. Oral lesions are characterized by punched-out, crater- 1. Classify acute gingival lesions; discuss the etiology, like depressions at the crest of the interdental papillae, clinical features and treatment for acute necrotizing subsequently involving marginal gingiva and rarely ulcerative gingivitis. attached gingiva. 4. These craters are covered by grayish pseudomembra- 2. Differentiate between acute necrotizing ulcerative nous slough. gingivitis and acute herpetic gingivostomatitis. 5. Patients with ANUG complain of a constant radiating, 3. Pericoronitis—definition, clinical features and treatment. gnawing pain and metallic taste with excessive amount of pasty saliva.

Periodontal Pathology Periodontal 6. Etiological factors responsible for ANUG are divided into: BIBLIOGRAPHY • Role of bacteria (fusospirochetal complex) • Local predisposing factors like preexisting gingivitis, 1. Arduino PG, Porter SR. Oral and perioral herpes simplex virus injury to the gingiva and smoking. type 1 (HSV-1) infection: review of its management. Oral • Systemic predisposing factors like nutritional Diseases 2006;12:254-70. deficiency, debilitating diseases and psychosomatic 2. Carranza, Newman. Clinical Periodontology. 8th edition, WB factors Saunders. 7. Primary herpetic gingivostomatitis is a viral infection 3. Greenberg MS, Glick M, Ship JA. Burkets Oral Medicine, 11th characterized by diffuse erythema and vesicular eruptions. Edition. BC Decker 2008. 8. Pericoronitis is an acute infection, which refers to 4. JD Manson, Bmeley. Outline of Periodontitis. 3rd edn, British inflammation of the gingiva and the surrounding soft Library Cataloging in Publication Data, 1995. tissues of an incompletely erupted tooth (Mostly in 5. Jurge S, Kuffer R, Scully C, Porter SR. Recurrent aphthous mandibular III molar area). Stomatitis: Oral Diseases 2006;12:1-21. 6. Loesche WJ, Syed SA, Langhorn BE. The bacteriology of acute necrotizing ulcerative gingivitis. J Periodontol 1982;53:223. 7. Yoji Murayama, Hidemi Kurihara, Thomas E. Van Dyke. Acute necrotizing ulcerative gingivitis, risk factors involving host defense mechanisms. Periodontol 2000;6:1994. 21 ChapterChapter

Periodontal Diseases in Children and Young Adolescents

 ANATOMIC CONSIDERATIONS IN CHILDREN  CLASSIFICATION OF PERIODONTAL • Changes in Gingiva, Cementum, Periodontal DISEASES IN CHILDREN Ligament, and Alveolar Bone • Gingival Lesions  HISTOPATHOLOGY OF GINGIVITIS IN CHILDREN • Types of Periodontitis  MICROBIOLOGY OF PERIODONTAL DISEASES  PERIODONTITIS ASSOCIATED WITH IN CHILDREN SYSTEMIC DISEASE

INTRODUCTION ANATOMIC CONSIDERATIONS IN CHILDREN

Periodontal disease consists of a group of infections Changes in Gingiva affecting the gingiva and the supporting structures: cementum, periodontal ligament and alveolar bone. Gingival 1. The gingival tissues are more reddish due to a thinner and periodontal changes in children could be due to the epithelium, a lesser degree of cornification, and a greater plaque and certain systemic diseases, which have a direct vascularity. effect on the periodontium. 2. The gingiva lacks the stippling, due to shorter and flatter While the periodontal diseases are generally considered papillae from the lamina propria. Normally, stippling to affect the adults, children and adolescents can also appears at about 3 years of age and occurs in 35% of manifest certain periodontal disorders, for example, children between ages of 5 and 15 years. prepubertal and juvenile periodontitis. This group of patients 3. The gingival margins appear to be rounded, rolled due will benefit from an early periodontal evaluation and any to hyperemia and edema that follows eruption. necessary treatment. 4. Greater sulcular depth, due to relative ease of gingival The gingiva and periodontium of children differ in some retraction. respects from those of adults. Hence, periodontal diseases 5. The gingiva appears to be flabbier due to the in children can be studied from anatomical, microbiological lower density of the connective tissue in the lamina and cellular aspects. propria. 186

Cementum Table 21.1: Microbial species in children’s and adult plaques Changes in the cementum include: Species in greater numbers Species in adult plaques The cementum in the children is thinner and less dense in children’s plaque and shows a tendency to hyperplasia of cementum apical to • Leptotrichia species • Fusobacterium the epithelial attachments. • Capnocytophaga • Eubacterium • Selenomonas species • Bacteroides species Periodontal Ligament

Changes in the periodontal ligament include: • Necrotizing-ulcerative gingivitis PART IV The periodontal ligament in children is wider, has fewer • Candidiasis and less dense fibers per unit area. It also has increased 2. Chronic marginal gingivitis hydration with a greater blood and lymph supplies than in • Plaque induced adults. • Puberty gingivitis 3. Factitious gingivitis Alveolar Bone 4. Localized gingival recession

Changes in the alveolar bone include: Periodontal Lesions 1. In children, the lamina dura is thinner, fewer trabeculae and larger marrow spaces. There is also a smaller amount Early Onset Periodontitis of calcification, greater blood and lymph supply and the • Prepubertal

Periodontal Pathology Periodontal crest of the alveolar bone appears flatter. – Localized 2. The contact points between the deciduous teeth – Generalized are not as tight as those between the permanent dentition. • Juvenile – Localized HISTOPATHOLOGY OF GINGIVITIS – Generalized IN CHILDREN

1. Adult tissues show a greater density of plasma cells PERIODONTITIS ASSOCIATED WITH whereas in children, there were seen seven times as many SYSTEMIC DISEASE lymphocytes as plasma cells. • Papillon-Lefévre syndrome 2. Increased vascularity is seen. • Ehler-Danlos syndrome • Hypophosphatasia MICROBIOLOGY OF PERIODONTAL • Chediak-Higashi syndrome DISEASES IN CHILDREN • Leukocyte adhesion deficiency Experimental gingivitis in children and the adults has shown • Neutropenia in Table 21.1. • Down’s syndrome.

CLASSIFICATION OF PERIODONTAL Gingival Lesions DISEASES IN CHILDREN Acute Herpetic Gingivostomatitis Gingival Lesions It is a viral infection of the oral mucosa caused by herpes 1. Acute gingivitis simplex virus. It occurs most frequently in infants and • Herpetic gingivostomatitis children younger than 6 years of age. 187

Clinical Features 2. In the initial stage, it appears to be discrete, spherical grey vesicles involving labial and buccal mucosa, soft I. Intraoral signs and symptoms palate, pharynx and tongue, approximately after 24 hours II. Extraoral signs and symptoms the vesicles rupture leaving painful ulcers. HPE 21 CHAPTER Intraoral signs (Figs 21.1 and 21.2) 3. The ulcers appear to be red, elevated with halo-like 1. Gingiva appears to be diffuse red, erythematous, with margins and a depressed yellowish or grayish-white varying degree of edema and gingival bleeding. central portion. 4. The course of the disease is 7 to 10 days.

Oral symptoms 1. Generalized soreness of the oral cavity, which interferes

with the eating and drinking. Periodontal Diseases in Children and Young Adolescents Young and Children in Diseases Periodontal 2. The ruptured vesicles are sensitive to touch, thermal changes and food.

Extraoral and systemic signs and symptoms 1. Involvement of the lips and face (Herpes labialis, cold sore) 2. Cervical adenitis, fever is as high as 101 to 105ºF and generalized malaise are common.

Treatment a. Local application—using Talbot’s iodine, zinc chloride 80 percent, riboflavin, thiamine, have been used. Fig. 21.1: Herpetic vesicles— late stage showing crusted Chlortetracycline (Aureomycin) has been used lesions (Courtesy: Dr Deepak Daryani) successfully. b. Palliative treatment—food debris and superficial debris is removed, relief of pain is obtained with 0.5 percent dyclonine hydrochloride mouthwash which has a topical anesthetic effect. c. Supportive treatment—copious fluid intake, for relief of pain systemically administered aspirin is usually sufficient.

Acute Necrotizing Ulcerative Gingivitis (NUG) Affects both children and adults, and is characterized by sudden onset. Sometimes following an episode of debilitating disease of acute respiratory tract infections.

Clinical features

Fig. 21.2: Herpetic gingivostomatitis involving gingiva and • Intraoral signs and symptoms palate (Courtesy: Dr Deepak Daryani) • Extraoral signs and symptoms. 188

Oral signs Local predisposing factors include: 1. Two types of ulcerations are seen, lateral ulceration, deep • Pre-existing gingivitis, e.g. incubation zones. ulceration and necrosis. It has been suggested that these • Injury to the gingiva, e.g. malocclusion patterns of necrosis are related to the fact that major • Smoking. blood supply to the two areas of gingiva is different. a. Direct toxic effect of tobacco The gingival tissues gets blood supply from two main b. Vascular or other changes induced by nicotine or sources, i.e. supraperiosteal and intra-alveolar vessels. other substances 2. Lateral ulceration is characterized by involvement of c. As a reflection of stress.

buccal wall of the papillae, margins and possibly the PART IV attached gingiva occurs in the distribution of lateral Systemic predisposing factors include: blood supply (less common). Deep ulceration involving • Nutritional deficiency. primarily necrosis of the tissues of the embrasure, giving • Debilitating diseases. rise to the typical truncated papillae occurs in the • Psychosomatic factors. distribution of the intra-alveolar vessels (comparatively Treatment Should follow an orderly sequence. more common). First visit: Treatment is confined to the acutely involved 3. These craters are caused by gray pseudomembranous areas, after applying topical anesthesia. The areas are gently slough demarcated from the remainder of the gingival swabbed to remove the pseudomembrane. Superficial mucosa by a pronounced linear erythema. calculus is removed with ultrasonic scaler. The patient is 4. Other signs include—gingival hemorrhage or instructed to rinse the mouth every 2 hours with a glassful pronounced bleeding on slightest provocation. Periodontal Pathology Periodontal of an equal mixture of warm water and 3 percent hydrogen Oral symptoms peroxide (chlorhexidine rinses are also recommended). In 1. The lesions are extremely sensitive to touch. the presence of systemic symptoms penicillin or 2. Constant radiating, gnawing pain that is intensified by erythromycin or metronidazole is prescribed. eating spicy or hot food and chewing. Second visit: Scaling is performed (After 1 to 2 days). 3. Metallic foul taste and the patient is conscious of an Third visit: After 1 to 2 days of second visit. Scaling and excessive amount of “pasty saliva”. root planing are repeated with plaque control instructions, Extraoral and systemic signs and symptoms: hydrogen peroxide rinses are discontinued, but In mild to moderate stages—local lymphadenopathy and chlorhexidine rinses can be maintained for 2 to 3 weeks. slight elevation in temperature is seen. In severe cases—high fever, increased pulse rate, Candidiasis: Acute Candidiasis leukocytosis, loss of appetite is seen. (Moniliasis, Thrush) In very rare cases, severe sequelae may follow: It is the most common mycotic infection of the oral mucosa • Noma or gangrenous stomatitis. caused by Candida albicans. It is seen in three types of • Fusospirochetal meningitis. individuals; debilitated or immunosuppressed adults, infants • Toxemia and fatal brain abscess. and adults who have been on antibiotic therapy for sometime. Etiology a. Bacteriology consists of constant flora composed of Oral lesions are described as four clinical types: fusospirochetal organisms, variable flora consists of a. Pseudomembranous type—white curd-like plaques. spirochetes of varying sizes and Bacteroides intermedius. b. Atrophic type—usually seen on the dorsum of the tongue b. Predisposing factors—local and systemic. with erythema and papillary atrophy. 189 c. Hyperplastic type—hyperkeratosis of the epithelium become more severe. These inflammatory lesions are usually with white plaques. nondestructive and do not progress to attachment loss. The d. Epidermal and perioral type—scaling patches at the treatment is plaque control instruction and debridement. The corner of the lips. accumulation of plaque in children is probably more rapid HPE 21 CHAPTER than in adults, but the host response is generally not as Treatment Current treatment is the use of the antimycotic intense. Calculus, in contrast, is found less frequently in agent like cotrimoxazole in the form of oral troches every 3 children than in adults, but gradually increases as the child hours (for a total of 6 per day) for 7 to 10 days. enters the teenage years. Chronic Candidiasis Factitious Gingivitis (Gingivitis Artefacta) It is a rare type of C. albicans infections resulting in a It is of two types: granulomatous lesion that begins in infancy or early Adolescents Young and Children in Diseases Periodontal • Major form. childhood and may persist for several years. • Minor form. Minor form results from the rubbing or picking the Chronic Marginal Gingivitis gingiva with finger nail (habitual). Major form is more It is the most common type of gingival disease in childhood. severe and involves deeper peridontal tissues (psychological Gingival color changes and swelling appear to be more causes). common expressions of gingivitis in children than a bleeding and increased pocket depth. Localized Gingival Recession It may be seen around individual teeth or groups of teeth. Etiology The recession may be seen in the presence or absence of Plaque and calculus are most common causes. In children inflamed gingiva depending on the local irritants. In children certain conditions predispose the gingivitis they include: the position of the tooth in the arch is the most important a. Gingivitis associated with tooth eruption is called as cause, e.g. labially-positioned, tilted or rotated teeth and eruption gingivitis. anterior open bite, the recession may be transitional phase b. Partially-exfoliated, loose deciduous teeth frequently in tooth eruption and may correct itself or it may be cause gingivitis. necessary to realign the tooth orthodontically. c. Gingivitis occurs more frequently around malposed Types of Periodontitis teeth. d. Gingivitis is increased in children with excessive Prepubertal Periodontitis overbite and overjet, mouth breathing and nasal Prepubertal periodontitis occurs in localized and generalized obstruction. forms. e. A higher prevalence and severity of gingivitis and gingival enlargement is found in the circum pubertal Localized Prepubertal Periodontitis period. This form of gingivitis has been termed as Clinical features pubertal gingivitis. There may be a gingival enlargement • The age of onset is approximately 4 years. as a result of hormonal changes that magnify tissue • Plaque levels are usually low. response to the local irritants. • Alveolar bone loss is rapid. These inflammatory changes may persist during the time • Defect in neutrophil or monocyte functions has been the primary tooth is in the mouth and with exfoliation may reported. 190

Generalized Prepubertal Periodontitis 1. Production of opsonizing antibodies against Aa (Actinobacillus actinomycetem comitans). • Entire width of attached gingiva appears to be fiery- 2. Bacteria antagonistic to Aa may develop thereby red. decreasing the number of colonization sites. • Gingival hyperplasia, cleft formation and recession. 3. Aa may lose its leukotoxin producing ability for • Rapid destruction of the alveolar bone. unknown reasons. • Systemic involvement like recurrent bacterial infections. Localization of the lesions could also be due to the defect • Defects in polymorphonuclear leukocytes and in cementum formation [hypoplastic/aplastic cementum]. monocytes.

PART IV Pathogenesis of LJP is related to the interplay of several Juvenile Periodontitis factors. These include the specific microbiology of Definition was given by Baer, who described it, “as a disease subgingival plaque, defects in cementum, hereditary factors, of the periodontium occurring in an otherwise healthy impaired PMN functions and disorders of the immune adolescents, which is characterized by a rapid loss of system. alveolar bone around more than one tooth of the permanent Microbiology of LJP: Two types of bacteria are considered dentition”. It exists in two forms: to be pathogenic in LJP. a. Localized • Actinobacillus actinomycetem comitans b. Generalized. • Capnocytophaga

Clinical features of localized juvenile periodontitis Virulence factors produced by A. actinomycetemcomitans

Periodontal Pathology Periodontal (LJP) are as follows: 1. Age and sex distribution—between 11 and 15 years some a. Leukotoxin—destroys polymorphonuclear leukocytes studies show predilection for female patients. (PMNs) and macrophages. 2. Distribution of lesions—three types of involvement is b. Endotoxin—activates host cells to secrete inflammatory seen: mediators (PG’s, IL1b, TNFa). a. First molar and/or incisors. c. Bacteriocin—may inhibit the growth of beneficial b. First molar and/or incisors with additional teeth (not species. exceeding 14 teeth). d. Immunosuppressive factors—may inhibit IgG and IgM c. Generalized involvement. production. 3. The most striking feature is lack of clinical e. Collagenase—causes degradation of collagen. inflammation, despite the presence of deep periodontal f. Chemotactic inhibition factors—may inhibit neutrophil pockets. chemotaxis. 4. Small amounts of plaque is seen which rarely mineralizes Radiographic findings: to become calculus corrected. 1. Vertical/angular bone loss around, the first molars and 5. Most common initial symptoms are mobility, migration incisors in an otherwise healthy teenagers is a diagnostic of the incisors and first molars. Classically, a distolabial sign of classic Juvenile periodontitis (J.P.) “Arc-shaped” migration of the maxillary incisors with diastema loss of alveolar bone extending from the distal surface formation occurs. of the 2nd premolar to the mesial surface of the 2nd For LJP, classic distribution is the involvement of first molar is seen. molars and incisors with least distribution in the cuspid, 2. Bilateral symmetrical patterns of bone loss is seen premolar area. The reasons could be: [mirror-image pattern]. 191

Immunologic findings: A large proportion of patients (70%) Ehlers-Danlos Syndrome with LJP have a defect in PMN chemotaxis, which is cell- It is an inherited disorder affecting the connective tissues, associated and depressed PMN phagocytosis, which is the defect is in collagen molecular biology, but the nature serum-associated. PMN show reduced cell surface receptors of the defect is unknown. The syndrome is named after two 21 CHAPTER to the synthetic polypeptide chemotactic factors. N- clinicians, who described excessive joint mobility, skin formylmethionyl phenylalanine (FMLP) and the hyperextensibility, easy bruising and peculiar scarring, complement factor C5a, also have reduced amounts of which occur after skin wounds. surface glycoproteins GP-110 which is important for chemotactic response. Oral and periodontal manifestations: The oral mucosa, gingival tissues, teeth and temporomandibular joints can Clinical features of GJP: The age of diagnosis is between all be affected by Ehlers-Danlos syndrome.

20 and 30 years. Severe generalized bone loss is the Adolescents Young and Children in Diseases Periodontal characteristic feature. This may be restricted to upper or Oral mucosa lower arch. Patients of GJP often show good plaque control • It is often fragile and susceptible to bruising. and the extent of bone loss does not commensurate with the • Post-extraction hemorrhage can be a problem, due to level of oral hygiene. fragility of blood vessels and defects in the supporting connective tissues. Treatment: In the past, the prognosis for juvenile Gingival tissues: These are often fragile and bleed readily on periodontitis was considered to be poor. toothbrushing. Some forms of Ehler-Danlos syndrome (type Current therapy: Systemic tetracycline hydrochloride 250 VII) are reported to have advanced periodontal destruction. mg q.i.d. for at least 1 week should be given in conjunction Teeth: Teeth in Ehler-Danlos syndrome are fragile and with the local mechanical therapy. Several reports have fracture easily. shown excellent bone fill in cases of LJP treated with tetracycline, flap surgery and placement of grafts. TMJ: Subluxation of temporomandibular joints have been In refractory cases, tetracycline resistant Aa has been reported. suspected. In such cases a combination of amoxicillin and Treatment metronidazole has been suggested. 1. A thorough preventive program should be followed. 2. Due to the fragility of oral mucosa and gingiva, the Periodontitis Associated with Syndromes periodontal therapy in Ehlers-Danlos syndrome should be as atraumatic as possible. Papillon-Lefévre Syndrome a. It is characterized by hyperkeratotic skin lesions and Down’s Syndrome (Mongolism, trisomy 21) severe destruction of the periodontium. It is a congenital disease caused by a chromosomal b. These changes may appear before the age of 4 years. abnormality and characterized by mental deficiency and c. Characteristic skin lesions are hyperkeratosis of growth retardation. localized areas on palms and soles, knees and elbows. The oral findings include presence of plaque, calculus, d. Periodontal involvement includes, early inflammatory other local irritants, e.g. diastema, crowding of teeth, high changes that lead to bone loss and exfoliation of teeth. frenum attachment and malocclusion. Primary teeth are lost by 5 or 6 years of age. The permanent dentition erupts normally but within few Periodontal disease in Down’s syndrome: include the years the permanent teeth are also lost. formation of deep periodontal pockets associated with 192

plaque accumulation and moderate gingivitis, usually 2. Most common lesions in children are gingival lesions generalized but more severe in the lower anterior region including acute gingivitis, chronic marginal gingivitis facititious gingivitis and localized gingival recession. (may be due to high frenal attachment). Acute necrotizing 3. Periodontal lesions include, early onset periodontitis, lesions are also common. prepubertal and juvenile periodontitis, periodontitis Two factors have been proposed to explain high associated with systemic diseases. 4. Most of the signs of periodontitis are seen during prevalence and increased severity of periodontal destruction adolescence, with primary prevention one may help to in Down’s syndrome. reduce the tooth loss. 5. Further investigations should be carried out whenever 1. Reduced resistance to infections because of poor there is bleeding after gentle probing in the presence of

circulation (especially peripheral). relatively healthy gingiva, so that early onset periodontal PART IV 2. Defect in T-cell maturation and polymorphonuclear lesions and prepubertal conditions can be ruled out. leukocyte chemotaxis. Neutropenias: Destructive generalized periodontal lesions have been described in children with neutropenia. KNOW MORE ... Chédiak-Higashi syndrome (C-H syndrome): This is a rare Classification of Gingival Diseases in syndrome characterized by recurrent bacterial infections. It Childhood and Adolescents exhibits oral ulcerations and rapidly destructive periodontitis. 1. Eruption gingivitis 2. Plaque induced gingivitis Hypophosphatasia: This is a rare familial skeletal disease 3. Acute lesions: characterized by rickets, poor cranial formation, premature – HSV infection

loss of primary dentition—particularly incisors. Patients – Aphthous ulcers (recurrent in nature) Periodontal Pathology Periodontal have low levels of serum alkaline phosphatase. Teeth are – NUG – Acute candidiasis lost with no clinical evidences of gingival inflammation and 4. Gingival enlargement associated with: show reduced cementum formation. – Puberty – Idiopathic Acute and subacute leukemia (Malignant Neoplasias of – Drug induced and WBC Precursors): Accomplished by severe periodontal – Vitamin deficiency destruction. Leukocyte adhesion deficiency: These cases are rare and BIBLIOGRAPHY begin during, or immediately after eruption of the primary teeth. Extreme acute inflammation and proliferation of 1. Baer PN. The case for the periodontitis as a clinical entity. J of gingival tissues with rapid bone loss are found. Profound Periodontol 1971; 42:516-19. defects in peripheral blood neutrophils and monocytes are 2. Boer PN, Benjamin SD. Periodontal disease in children and adolescents. Philadelphia;JB, 1974. seen, hence they are absent in gingival tissues. 3. Bradely RE. Periodontal lesions in children: their recognition Patients with leukocyte adhesion disease also have frequent and treatment. Dent Clin North Am 1961; 5:671-85. respiratory tract infection and sometimes otitis media. 4. Carranza. Newman Clinical Periodontology, 8th edition. 5. Cohen B. Morphological factors in the pathogenesis of periodontal disease. Br Dent J 1959;107:31-9. 1. Various anatomic variations in the gingiva, periodontal 6. Davies RM, Smith RG, Porter SR. Destructive forms of ligament, cementum and alveolar bone may predispose periodontal disease in adolescent and young adults. Br Dent J to the disease of the periodontium. 1985;158:429-36. 193

7. Longhurst P, Johnson NW, Hopps RM. Differences in 11. Page RC, Schroeder HE. Periodontitis in man and other animals. lymphocytes and plasma cell densities in inflamed gingiva from A comparative review. Karger, Basle, 1982. adults and young children. J Periodontol 1977;48:707-10. 12. Ruber MP, Frankel SNM, Wallace S. The histopathology 8. Machtei EE, Zubery Y, Bimstein E, Becker A. Anterior open of periodontal disease in children. J Periodontol 1971;42:

bite and gingival recession in children and adolescents. Int Dent 473-84. 21 CHAPTER J 1990;40:369. 13. Schwartz, Lamster, Fine. Clinical Guide to Periodontics, WB 9. More WEC, et al. Bacteriology of experimental gingivitis in Saunders Company, 1995. children. Infection and Immunity 1984;46:1-6. 14. Waite IM, Furniss JS. Periodontal disease in children, a review. 10. Page RC, et al. Rapidly progressive periodontitis, a distinct Journal of Paediatric Dentistry 1987;3:59-67.

clinical condition. J Periodontol 1983;54:197-209. 15. Zapplers. Periodontal Disease in Children 1948;27:333-40. Periodontal Diseases in Children and Young Adolescents Young and Children in Diseases Periodontal 22 ChapterChapter

Desquamative Gingivitis

Srinivas K

 INTRODUCTION  DISEASES CLINICALLY PRESENTING AS  CLASSIFICATION DESQUAMATIVE GINGIVITIS  CLINICAL FEATURES • Lichen Planus • Cicatricial Pemphigoid  DIAGNOSIS • Bullous Pemphigoid  HISTOPATHOLOGY • Linear IgA Disease  THERAPY • Dermatitis Herpetiformis • Pemphigus Vulgaris • Drug Reaction or Eruptions

INTRODUCTION CLASSIFICATION

The term chronic desquamative gingivitis was coined by A. Dermatoses Prinz in 1932 to describe a peculiar condition characterized • Oral lichen planus by intense erythema, desquamation and ulceration of the • Mucous membrane pemphigoid free and attached gingiva. In 1960, Mc Carthy and • Pemphigus vulgaris colleagues suggested that desquamative gingivitis was not • Bullous pemphigoid a specific disease entity, but a gingival response associated • Erythema multiforme with a variety of conditions. Desquamative gingivitis is a • Linear IgA disease generic term that may represent a variety of specific disease • Lupus erythematosus processes, but the clinical picture is indisputable. There may • Epidermolysis bullosa aquisita be threads or tags of loose necrotic epithelium, as the name • Dermatitis herpetiformis suggests. Desquamative gingivitis involves not only marginal gingiva, as do most cases of gingivitis, but it also B. Local hypersensitivity reactions to peels the attached gingiva often in a band-like fashion. The Sodium lauryl sulphate, mouthwashes, dental materials, clinical description of desquamative gingivitis represents drugs, cosmetics, chewing gum and cinnamon, etc. gingival manifestations of a variety of diseases. 195

HPE 22 CHAPTER Desquamative Gingivitis Desquamative

Fig. 22.1: A case of pemphigus vulgaris presenting as Fig. 22.2: Nikolsky’s sign in a case of bullous pemphigoid desquamative gingivitis

C. Miscellaneous • Chronic ulcerative stomatitis • Orofacial granulomatosis • Plasma cell gingivitis

CLINICAL FEATURES

• Females are more frequently affected. • Buccal aspect of anterior gingiva most commonly affected. • The gingiva is fiery red, friable and desquamates easily (Fig. 22.1). • Patients complain of soreness, especially when eating spicy or acidic food, and of bleeding and discomfort Fig. 22.3: A case of lichen planus—note the presence of with toothbrushing. white striae along with desquamation • Lesions get aggravated by local plaque accumulation. • A positive Nikolsky’s sign where the surface epithelium inflammatory cells in the underlying connective tissue in “floats away” when lateral pressure is applied to the most of the cases. In most of the bullous diseases mucosa, may indicate vesiculobullous disorders (Fig. histopathology may not confirm the diagnosis and direct 22.2). immunofluorescence will be required to arrive at a accurate • The presence of white plaques or white striae indicate diagnosis. lichen planus (Fig. 22.3). DIAGNOSIS HISTOPATHOLOGY The success of any given therapeutic approach resides on Microscopically, there will be a thin atrophic epithelium the establishment of an accurate final diagnosis. The with little or no keratin at the surface. Acantholysis will be following approach helps us to elucidate the disease seen in bullous lesions and diffuse infiltration of chronic triggering desquamative gingivitis. 196

THERAPY 4. Atropic lesions: Atrophy of the gingival tissues results in erythema confined to gingiva. • Removal of underlying cause if known allergen or irritant is present Histopathology • Improvement of oral hygiene • Treatment of underlying disease (Table 22.1) Microscopic criteria include hyperkeratosis, saw-toothed • Local or systemic steroid or immunosuppressive appearance to the rete pegs, liquefaction degeneration of treatment. basal cell layer, an eosinophilic band may be seen just benath the basement membrane and a dense subepithelial band

PART IV DISEASES CLINICALLY PRESENTING AS shaped infiltrate of lymphocytes and macrophages is DESQUAMATIVE GINGIVITIS characteristic of the disease. Direct immunofluorescence demonstrates the presence of fibrinogen in the basement LICHEN PLANUS membrane.

It is a relatively common, chronic dermatosis characterized Differential Diagnosis by the presence of cutaneous violaceous papules that may • Lichenoid drug reaction • Hyperplastic candidiasis coalesce to form plaques. Majority of the patients with oral • Lupus erythematosis • Contact hypersensitivity lichen planus are middle aged. • Cheek biting • Speckled leukoplakia Clinical Features Treatment (Fig. 22.4) and Prognosis

Periodontal Pathology Periodontal Oral Lesions Corticosteroids are the single most effective group of drugs. Oral LP almost invariably occurs as a bilateral disease and Topical application and local injection of steroids have also it involves the posterior buccal mucosa. Clinically, oral LP been successful. appears as radiating white or gray-velvety thread like lesion, Addition of antifungal therapy typically enhances clini- which consists of papules in linear, annular or retiform cal results. The erosive, bullous and ulcerative lesions are arrangement. A tiny white elevated dot is present at the treated with high potency topical steroid such as 0.05 percent intersection of the white lines knows as ‘Wickham’s striae’ or ‘Honiton Lace’ (Fig. 22.3).

Gingival Lesions Oral LP is the main disorder associated desquamative gingivitis with up to 10 percent of patients having lesions restricted to the gingival tissue. 1. Keratotic lesions: Raised white lesions may present as groups of individual plaques, linear or reticular lesions. 2. Erosive lesions: These extensive erythematous areas with a patchy distribution may present as focal or diffuse hemorrhagic areas. 3. Vesicular or bullous lesions: These raised fluid-filled

lesions are short lived on gingiva resulting in an Fig. 22.4: Case of lichen planus shown in Figure 22.3 treated ulceration. with topical steroid 197

Fluocinolone acetonide. Intralesional injection of custom made flexible mouthguard may be used. Rinsing triamcinolone acetonide (10 to 20 mg) has also been used with chlorhexidine is often a useful adjunct. Tetracycline successfully. Other treatment modalities are retinoids, and doxycycline are helpful in treating steroid resistant hydroxychloroquine, cyclosporine and free gingival grafts. cases. In severe cases, immunosuppressive agents HPE 22 CHAPTER (azathioprine, cyclophosphamide, cyclosporine) may be CICATRICIAL PEMPHIGOID occasionally added to the prednisolone regimen, but it often It is a chronic autoimmune subepithelial disease primarily provides disappointing results. Very high dose may be affecting the mucous membranes of patients over the age required to achieve any significant results. of 50. It is characterized by mucosal blister formation with BULLOUS PEMPHIGOID subsequent scarring, while the oral and ocular mucosa are

most often involved, other mucosal surfaces may also be It is the most common blistering autoimmune disorder Desquamative Gingivitis Desquamative affected. caused by binding of autoantibodies to specific antigens found in lamina lucida region of the basement membrane. Clinical Features It is often seen in elderly individuals. It usually presents It tends to affect women more than men. The oral mucosal with pruritis and bullous lesions. presentation ranges from erosion or desquamation of Clinical Features attached gingival tissues to large areas of vesiculobullous eruptions. Bullae are rarely seen because the blisters are It is seen primarily in the elders, with the peak evidence in fragile and short lived. Lesions are chronic and may heal the seventh and eighth decades. The gingival lesions may with scarring. Gingival lesions appear as patchy red zones. be the only site of oral involvement that consists of Concomitant ulcers may be seen on marginal and attached generalized edema, inflammation and desquamation with gingiva. With chronicity, pain typically diminishes in localized areas of discrete vesicle formation. intensity. Nikolsky’s sign may also be seen. Histopathology Histopathology Bullae are subepithelial in bullous pemphigoid and appear It is a subepithelial or sub-basal clefting disorder. There is similar to those in cicatricial pemphigoid. Ultrastructurally no evidence of acantholysis. Lamina propria is infiltrated the basement membrane is cleaved at the level of lamina by lymphocytes. lucida.

Differential Diagnosis Treatment

• Pemphigus vulgaris Systemic corticosteroids are generally used to control this • Atrophic lichen planus disease. Nonsteroidal immunosuppressive agents may also • Discoid lupus erythematosus effectively control the disease process as well as reduce the side effects. A combination of tetracycline or doxycycline Treatment and Prognosis with niacinamide has provided some clinical success. Topical or systemic corticosteroids are typically used. LINEAR IgA DISEASE Prednisolone is used for moderate to severe disease because of its side effects which may outweigh benefits, highly It is an uncommon subepithelial mucocutaneous disorder potent topical steroids such as clobetasol, betamethasone with predilection in women. It is characterized by deposition dipropionate, fluocinoxide are used for gingival diseases, a of IgA rather than IgG in the basement membrane. Clinically, 198

it represents as a pruritic papules and blisters at the site of Histopathology trauma. Collections of neutrophils, eosinophils and fibrin are seen at the papillary tips of dermis. Subsequent exudation at this Oral Lesions location contributes to epidermal separation. A It consists of vesicles, painful ulcerations or erosions. The lymphophagocytic infiltrate is seen in perivascular spaces. hard and soft palates are commonly affected. Rarely oral lesions may be the only manifestation before the Treatment presentation of cutaneous lesions. It is generally treated with dapsone, sulfoxone and PART IV sulfapyridine. Because patients often have an associated Histopathology enteropathy, a gluten-free diet may also be a part of the Separation at the basement membrane is seen. Direct therapeutic regimen. immunofluorescence demonstrates deposition of IgA. PEMPHIGUS VULGARIS Differential Diagnosis It is an autoimmune mucocutaneous disease characterized • Erosive lichen planus by autoantibodies to glycoprotein adhesion molecule • Chronic ulcerative stomatitis desmoglien-3 resulting in intraepithelial blister formation. • Pemphigus vulgaris • Bullous pemphigoid Clinical Features • Lupus erythematosus. Periodontal Pathology Periodontal Skin lesions present as ulcers preceeded by bullae. Presentation of the lesions may initially be as fluid-filled Treatment bullae. Bullae rapidly rupture leaving a collapsed roof. This The primary treatment comprises combination of grayish membrane is easily removed with a guaze sponge, Sulfapyridine and Niacinamide. Small amounts of leaving a red, painful ulcerated base. Nikolsky’s sign is seen. prednisone (10 to 30 mg) can be added. The incidence is equal in both sexes.

DERMATITIS HERPETIFORMIS Histopathology

It is a skin eruption. The cause is unknown, but most patients It represents the prototypical suprabasal or intraepithelial have an associated gluten-sensitive enteropathy. clefting morphology. It is the acantholytic lesion that features squamous epithelial cells lying free within the bulla or Clinical Features vesicle cavity. Tzanck cells are seen, characterized by It is a chronic disease typically seen in young and middle nuclear enlargement and hyperchromatosis subsequent to aged adults. Periods of exacerbation and remission formation of the suprabasal cleft. The intact basal layer characterize the disease. Lesions are usually symmetrical remains attached to lamina propria. in their distribution, aggregated but are often individually disposed. In the oral cavity vesicles and bullae are Differential Diagnosis evanescent. Subsequent to rupture, superficial nonspecific • Bullous and cicatricial pemphigoid ulcers have a fibrinous base with erythematous margins. • Erythema multiforme Lesions may involve both keratinized and nonkeratinized • Bullous lichen planus mucosae. • Dermatitis herpetiformis. 199

Treatment

Disease control may be achieved with intermediate dose of 1. Chronic desquamative gingivitis is characterized by steroid. For more severely affected patients, high dose of intense redness and desquamation of the surface epithelium of marginal and attached gingiva. corticosteroid is used followed by a combined drug approach 2. Chronic desquamative gingivitis is the clinical 22 CHAPTER that includes alternate day prednisolone plus manifestation of several different disorders, the clinical immunosuppressive agent such as azathioprine, features are variable and diagnosis of the underlying condition is necessary for optimum management. methotrexate or cyclophosphamide. 3. Removal of plaque is an important part of treatment. Mild cases can be managed with topical steroids and DRUG REACTION OR ERUPTIONS severe cases need systemic immunsuppression. Periodic recall and careful follow-up is the most important Drugs can act as an allergen either alone or in combination, part of management. sensitizing the tissues and then resulting in allergic reaction Gingivitis Desquamative of skin and oral cavity. Stomatitis medicamentosa is characterized by eruptions in the oral cavity resulting from KNOW MORE ... sensitivity to drugs that have been taken by mouth or parenterally. The local use of medicaments in the mouth is Treatment of Desquamative Gingivitis referred to as stomatitis venenata or contact stomatitis, • Most symptomatic cases of desquamative gingivitis can be managed by topical steroids (Triamcinolone examples are, aspirin burn or stomatitis due to topical acetonide/clobetasol proprionate/fluocinolone penicillin. Clinically, drug eruption in the oral cavity could acetonide with orabase) be: Lower the strength of the preparation as soon as • Vesicular or bullous—most commonly seen the lesions heal and become asymptomatic should be lowered. • Pigmented or nonpigmented macular lesions • A splint with spacer for applying topical steroids can Erosions, followed by deep ulceration with purpuric be used for resistant cases. lesions, may also occur in different parts of oral cavity with • A combination of topical and systemic steroids is gingival being most commonly affected. Some of the preferred for severe cases. • Prednisolone is the most preferred systemic steroid compounds that may cause contact allergy in the gingiva and a dosage of 20-40 mg/day. are, mercurial compounds (e.g. amalgam) tartar control The dose should be reduced by 5–10 mg/day toothpastes (e.g. pyrophosphates) and cinnamon compounds gradually over a 2–4 week period (to prevent can result in intense erythema of gingival tissue (plasma Hypothalamopituitary axis (HPA) suppression. • Important—Always a topical antifungal like clotrimazole cell gingivitis). Elimination of the offending agent usually should be combined with steroid therapy to prevent leads to resolution of the lesions within a week. secondary candidiasis.

DISEASES CLINICALLY PRESENTING AS REVIEW QUESTION DESQUAMATIVE GINGIVITIS 1. Classify desquamative lesions. Discuss in detail clinical It is listed in Table 22.1. features and treatment of desquamative gingivitis. 200 s Contd... steroids tis transformation

• Surveillance for malignant for extraoral involvement

PART IV Periodontal Pathology Periodontal desquamation with localized areas of discrete vesicle formation sign positive • Nikolsky’s tetracycline and nicotinamide • Lesions confined only gingiva (8-10%) may be entirely to erythematous with no reticular or elements papular • Desquamative gingivitis may of be the only manifestation the disease Thin layer of epithelium peels • away in an irregular pattern leaving a denuded base sign positive • Nikolsky’s plaque like, bullous and ulcerative patterns DIF— Fibrin, fibrinogen at BMZunresponsive for chloroquine cases. 4 Integrin, which spread slowly DIF— C3, IgG at BMZreferral Appropriate phamide. β 6 α BP 180 and BP 230BP and 180 BP found in lamina seen in buccal mucosalucida region onthe hemidesmosomes inflammation and • Gingival lesions consist of generalized edema, (Lamina lucida);inflammatoryrich Eosinophil infiltrate DIF—IgG at BMZ like azathioprine, cyclophos- • Immunosuppressive drugs of • Dapsone/Combination phamide adhesion complex(BP180, appear as nonspecific erosions basal laminaglycoproteinadhesion moleculespresent on shallow irregular ulcers seenDesmosomesDesmoglien 3 and 1 which rapidly breaks to leave keratinocytes (Tzank cells) like azathioprine, cyclophos- and gingiva on buccal mucosa palate basilar bullae; acantholytic like azathioprine, cyclophos- IgA, IgM, Complement DIF— IgG, • Immunosuppressive drugs phamide intercellularepithelial the within • Surveillance for relapses spaces (Unidentifiedepithelial antigen) papular, of reticular, can be a part erythematous or erosive areasinfiltrateinflammatory lymphocyte sporine or systemic hydroxy degeneration; subepithelial or cyclo- tacrolimus Topical • Laminin 5 and 6) Table 22.1 Etiology, clinical features, investigations and treatment of diseases clinically presenting as desquamative gingivi 22.1 Etiology, Table Mucous membranepemphigoid Autoantibodies to vesicles of gingival or other • Intact HP— Subepithelial vesicle basement membrane mucosal surfaces but frequently formation; vacuolation in thePemphigus vulgarissteroid systemic and Topical • Autoantibodies to • Immunosuppressive drugs • Bullae on noninflamed basesupra-Acantholysis; HP— Bullous pemphigoidsteroids systemic and Topical • Autoantibodies to • Bullae which breaks into ulcers HP— Subepithelial bullae formationsystemic and Topical • DiseaseOral lichen planus Cell mediated Etiology lesions and red • White papular HP— Hyperkeratosis; basal cell Clinical featuressteroids systemic and Topical • Investigations Treatment 201

HPE 22 CHAPTER Desquamative Gingivitis Desquamative DIF— IgM, IgG and C3 at BMZ vacuolization and vesicle formation in a perivascular distribution DIF— Fibrin C3 and cytoid bodies at BMZ • Nikolsky’s sign positive • Nikolsky’s desquamative gingivitis mucosa tongue and palateinfiltrateperivascular lymphocytic involvement anchoring fibrils ofbasement membrane and laryngeal lesions. genital lesions, eye lesions (Thick linear pattern) sensitivegluten with enteropathy areas of superficial ulceration microabscesses form and at any intraoral site progress to subepidermal involving immunecomplexes erythematous lesions seen on gingiva, buccal deposits, thickening of PAS+ cases. vascular basement membrane, • Surveillance for extraoral inciting factors areHSV and drugs • Severe crusting and bleeding of the lipskeratinocytes; Necrotic multiformae erythema infiltrate inflammatory Mixed EpidermolysisBullosaAquisita Autoantibodies to • Bullae which break into ulcers type VII collagen –Dermatitis component ofHerpetiformis HP— Subepithelial Blister seen in oral mucosa accompanied Formation by widespread skin lesions, disease associated Immune mediatedsteroids systemic and Topical • rupture rapidly to leave and bullae which Vesicles At BMZ DIF— C3 and IgG HP—Neutrophil accumulation papillary in dermal papillae; • Immunosuppressive drugs gluten Sulfapyridine, Dapsone, free diet Linear IgAdiseaseLupus Autoantibodies (IgA) toerythematosus Blisters and ulcers of oral basement membraneby accompanied mucosa autoimmune diseasewith interspersed Prototype of HP— Subepithelial blister formationsteroids systemic and Topical • at BMZ (Linear pattern) DIF— IgA in severe cases • Dapsone White radiating striae lamina propria edema, subepithelial • Hydroxy chloroquine for mild HP—Keratinocyte vacuolization, and systemic steroids Topical • Contd... DiseaseErythemamultiforme Etiology Hypersensitivity reaction – Common which are large and confluent • Erosions and ulcerations Clinical features epithelial vesiculation; HP— Subepithelial or intra-associated HSV for Acyclovir • steroids systemic and Topical • Investigations Treatment Antinuclear antibodies ANA- DIF- Direct immunofluorescence, C3- Complement 3, BMZ- Basement membrane zone, HP- Histopathology, 202

BIBLIOGRAPHY 4. Lucio Lo Russo, et al. Diagnostic Pathways and Clinical Significance of Desquamative Gingivitis. Journal of 1. Greenberg Glick. Ship: Burket’s Oral Medicine. 11th edn, BC Periodontology 2008;79(1):4-24. Decker Inc, 2008. 5. NA Robinson, D Wray. Desquamative Gingivitis: A sign of 2. JC Leao, et al. Desquamative Gingivitis: Retrospective Analysis mucocutaneous disorders — a review. Australian Dental Journal of Disease Associations of a Large Cohort: Oral Diseases 2003;48(4):206-11. 2008;14(6):556-60. 6. Richards Andrea. Desquamative Gingivitis: Investigation, 3. Lucio Lo Russo, et al. Epidemiology of Desquamative Diagnosis and Therapeutic Management in Practice, PERIO Gingivitis: Evaluation of 125 Patients and Review of the Periodontal Practice Today 2005;2(3):183-90.

Literature. International Journal of Dermatology, 2009;48(10): PART IV

1049-52. Periodontal Pathology Periodontal SECTION 2: Periodontal Diseases

23 ChapterChapter

The Periodontal Pocket

 DEFINITION AND CLASSIFICATION • Changes in Root Surface Wall CLINICAL FEATURES • Periodontal Disease Activity • Signs and Symptoms  RELATION OF LOSS OF ATTACHMENT AND PATHOGENESIS BONE LOSS TO POCKET DEPTH HISTOPATHOLOGY  DIFFERENCES BETWEEN SUPRABONY AND • Changes in the Soft Tissue Wall INFRABONY POCKETS • Microtopography of the Gingival Wall  PERIODONTAL CYST • Periodontal Pocket as Healing Lesions  DETERMINATION OF POCKET DEPTH • Pocket Contents  TREATMENT OF PERIODONTAL POCKETS

INTRODUCTION DEFINITION “Pocket can be defined as deepening of the gingival sulcus.” A sulcus depth up to 3 mm is considered to be normal, If this happens due to coronal migration of the marginal provided the patient can maintain oral hygiene. If it is gingiva it is called as gingival or pseudo-pocket. Deepening increased beyond 3 mm it is called as a pocket. The cause due to apical migration of the junctional epithelium is for this is mainly extension of inflammation leading to referred to as “true pocket”. pathologic deepening of the gingival sulcus, and this marks the transition from gingivitis to periodontitis. Periodontitis CLASSIFICATION (FIG. 23.1) is always preceded by gingivitis, but not all gingivitis 1. Depending upon its morphology progresses to periodontitis. a. Gingival/false/relative pocket. 204

CLINICAL FEATURES Signs

1. Enlarged, bluish-red marginal gingiva with a ‘rolled’ edge separated from the tooth surface. 2. A bluish-red vertical zone extending from the gingival margin to the alveolar mucosa. 3. A break in the faciolingual continuity of the interdental gingiva. PART IV 4. Shiny, discolored and puffy gingiva associated with exposed root surfaces. 5. Gingival bleeding, purulent exudate from the gingival margin. 6. Mobility, extrusion and migration of teeth. 7. The development of diastema where none had existed previously.

Symptoms a. Localized pain or a sensation of pressure in the gingiva after eating, which gradually diminishes. Periodontal Pathology Periodontal Fig. 23.1: Types of pockets b. A foul taste in localized areas. c. A tendency to suck material from the interproximal b. Periodontal/absolute/true pocket. spaces. c. Combined pocket. d. Radiating pain “deep in the bone”. 2. Depending upon its relationship to crestal bone e. A “gnawing’ feeling or feeling of itching in the gums. periodontal pockets are further classified as: f. The urge to dig a pointed instrument into the gums and a. Suprabony/supracrestal/supra-alveolar pocket. b. Infrabony/intrabony/subcrestal/intra-alveolar relief is obtained from the resultant bleeding. pocket. g. Patient complains that food “sticks between the teeth” 3. Depending upon the number of surfaces involved: or that the teeth “feel loose” or a preference to “eat on a. Simple pocket—involving one tooth surface. the other side.” b. Compound pocket—involving two or more tooth h. Sensitivity to heat and cold; toothache in the absence of surfaces. caries. c. Complex pocket—where the base of the pocket is not in direct communication with the gingival PATHOGENESIS (Figs 23.2A to G) margin. It is also known as spiral pocket. The first event in pocket formation is the laying down of a 4. Depending upon the nature of the soft tissue wall of the lawn of gram-positive bacteria on the supragingival tooth pocket surface and its extension into the gingival sulcus. a. Edematous pocket. The periodontal pockets are caused by micro-organisms b. Fibrotic pocket. and their products, which produce pathologic changes that 5. Depending upon the disease activity lead to the deepening of the gingival sulcus. a. Active pocket. As a result of inflammation, the following changes are b. Inactive pocket. seen in the junctional epithelium. 205

HPE 23 CHAPTER The Periodontal Pocket Periodontal The

Fig. 23.2A: Schematic illustration of normal gingiva Fig. 23.2C: Extension of supragingival plaque into the gingival sulcus

Fig. 23.2B: Accumulation of supragingival plaque Fig. 23.2D: Detachment and apical migration of junctional epithelium

1. The junctional epithelium proliferates along the root in b. Physical force exerted by rapidly growing bacteria the form of finger-like projections. c. Bacteria may also interfere with growth and synthetic 2. The coronal portion of the junctional epithelium activities of junctional epithelial cells and also with detaches from the root as the apical portion migrates. the normal maintenance of the attachment lamina. The epithelial cell detachment can take place due to: d. Exudate associated with the advancing bacteria may a. Enzymes released by bacteria also be important.

206 PART IV

Fig. 23.2F: Ulceration of pocket epithelium

Fig. 23.2E: Phagocytic action of neutrophils

gingival sulcus and oral cavity. Most bacteria produce

substances that chemotactically attract neutrophils. Periodontal Pathology Periodontal A chemical gradient of chemotactic agents seems to exist across normal, intact junctional epithelium and connective tissue. Neutrophils leaving the blood vessels are guided by this gradient towards the gingival margin and into the gingival sulcus. Under normal conditions, the transmigrating cells leave no trace of their passage and cause no damage. These neutrophils are the primary and first line of defence around the teeth; the epithelial barrier is the second. 4. Extension of plaque subgingivally causes an increase in the number of transmigrating neutrophils, which may be due to the increased concentration of chemotactic factors and other inflammation induced substances derived from the bacteria. These substances cause Fig. 23.2G: Periodontal pocket is established vasculitis. Neutrophils adhere to the endothelial lining and migrate into the connective tissue, but they still do Thus the sulcus base shifts apically and this will be not accumulate there. Instead they rapidly pass through replaced by pocket epithelium. the junctional or pocket epithelium to form a thick layer 3. Under normal conditions a constant stream of that covers the surface of the subgingival plaque. Upon neutrophils emigrate from the vessels of the gingival arrival at the plaque surface, the neutrophils are viable plexus through the junctional epithelium into the partly, but not completely functional. Their role is to 207

limit further extension and spread of bacteria by Summary of Pathogenesis phagocytosis and killing. This may be inhibited by First Event lipopolysaccharides and leukotoxin. A constant battle occurs at the neutrophil plaque interface. Usually the HPE 23 CHAPTER normal neutrophil activities are sufficient to limit the extension of plaque, however increasing growth rate of bacteria, swamps the neutrophil system and permits tissue destruction to occur. 5. Assuming the pocket formation proceeds either because of aggressive growth and action of bacteria or because

of ever increasing number of neutrophils that Pocket Periodontal The transmigrate in constant streams through the junctional epithelium and pocket epithelium causes open Colonization of Gram-positive bacteria supragingivally and communication between the pocket and connective its extension into the gingival sulcus and conversion of tissue (by disrupting the epithelial barrier). Gram-positive aerobes to Gram-negative anaerobes. Ulceration of this sort is the second major event in pocket formation. Once the epithelial barrier is breached, Second Event the gradient of chemotactic agents released by the pocket bacteria may be disrupted. As a result the neutrophils no longer have a guidance systems, to direct them from the vessels through tissues and into the pocket; they remain in the connective tissue moving randomly. Also because of the rupture of the epithelial barrier, the connective tissue become flooded with the bacterial substances, and bacteria may enter the connective tissue. 6. The neutrophils now encounter these substances within the connective tissue rather than outside in the pocket. The neutrophils become activated and undertake phagocytosis with resultant release of lysosomal

enzymes, collagenases and other substances (PGE2) that cause extensive tissue damage. HISTOPATHOLOGY As soon as the bacterial substances have entered the During the initial stages of pocket formation the changes connective tissue many systems other than the that takes place are described in stages I, II, III gingivitis. neutrophils are activated like macrophages lymphocytes Once the pocket is formed the following microscopic and complement system. features are present. 7. When the epithelial barrier is re-established the chemotactic gradient is formed again and the destructive Changes in the Soft Tissue Wall process subsides. If this barrier is not re-established, • The blood vessels are engorged and dilated. tissue destruction continues and alveolar bone is • The connective tissue is edematous and densely resorbed. A periodontal pocket is now established. infiltrated with plasma cells (80%), lymphocytes and 208

a scattering of polymorphonuclear leukocytes Bacteria accumulate in the previously quiescent areas, (PMNLs). triggering the emergence of leukocytes and the leukocyte- • Special note should be made of the fact that extension bacterial interaction. This leads to intense epithelial of the junctional epithelium along the root requires desquamation and finally to ulceration and hemorrhage. the presence of healthy epithelial cells, because of this it is reasonable to assume that the degenerative Periodontal Pocket as a Healing Lesion changes occur along the lateral walls of the pocket. It is characterized by interplay of destructive and The changes are as follows: constructive tissue changes.

PART IV 1. The epithelium along the lateral wall of the pocket The destructive changes are characterized by fluid and presents striking proliferative and degenerative changes. cellular inflammatory exudates and by the associated 2. The epithelial projection extends deep into the degenerative changes initiated by the plaque bacteria. connective tissue and also extends further apically than The constructive changes consist of the formation of the junctional epithelium. blood vessels in an effort to repair the tissue damage caused 3. The epithelium is infiltrated with leukocytes and other by inflammation. The balance between destructive and inflammatory cells. constructive changes determines clinical features such as 4. Degeneration and necrosis of the epithelium leading to color, consistency and surface texture of the pocket wall. ulceration of the epithelium and exposure of the underlying connective tissue. Pocket Contents 5. Bacterial invasion along the lateral and apical areas of

Periodontal Pathology Periodontal It consists of debris principally containing micro-organisms the pocket. Some bacteria traverse the basement lamina and their products, (like enzymes, endotoxins and other and invade the subepithelial connective tissue. metabolic products) dental plaque, gingival fluid, food The following morphotypes of bacteria have been remnants, salivary mucin, desquamated epithelial cells and identified, filamentous rods and coccoid organisms with leukocytes. If purulent exudate is present, it consists of predominant Gram-negative bacteria. Increased numbers of living, degenerated and necrotic leukocytes (PMNLs), living Langerhans’ cells were found in the epithelium. and dead bacteria, serum and a scanty amount of fibrin. Pus formation is a common feature in periodontal disease but it Microtopography of the Gingival Wall is only a secondary sign. of the Pocket Changes in the Root Surface Wall Under scanning electron microscope the following areas have been noted: 1. Structural changes: 1. Areas of relative quiescence. a. Presence of pathologic granules 2. Areas of bacterial accumulation—mainly cocci, rods, b. Areas of increased mineralization filamentous rods with a few spirochetes. c. Areas of demineralization/root caries 3. Area of emergence of leukocytes. 2. Chemical changes: The mineral content of exposed 4. Area of leukocyte—bacterial interaction. cementum is increased. The following minerals are 5. Areas of intense epithelial desquamation. increased in diseased root surfaces: calcium, magnesium, 6. Areas of ulceration with exposed connective tissue. phosphate, fluoride and others. Hence, a highly increased 7. Areas of hemorrhage with numerous erythrocytes. resistant calcified layer to decay is formed. This can also The transition could be postulated as follows: be harmful if the adsorbed products are toxic. 209

3. Cytotoxic changes: Bacterial penetration into the Relation of Loss of Attachment and Bone Loss to cementum can be found as deep as cementodentinal Pocket Depth (Fig. 23.4) junction. In addition, bacterial products such as Pocket of same depth may be associated with different endotoxins have also been detected. degree of attachment loss. Pocket of different depth may be 23 CHAPTER The following zones can be found in the base of a associated with same amount of attachment loss. periodontal pocket (Fig. 23.3): 1. Cementum covered by calculus where all the changes Area between the base of the pocket and the alveolar described earlier takes place. bone is always constant. The radius of action of the plaque 2. Attached plaque which covers calculus (100 to 500 u) bacteria is 0.5 to 2.7 mm. 3. The zone of unattached plaque. 4. The zone where the junctional epithelium is attached to PERIODONTAL CYST

the tooth. This zone, which is normally more than 500 μ Pocket Periodontal The is usually reduced to less than 100 μ in periodontal • It is an uncommon lesion that produces localized pocket. destruction of the periodontal tissues along the lateral 5. Apical to the junctional epithelium there may be a zone root surface. of semidestroyed connective tissue fibers. • Most common in the mandibular canine—premolar area. The following possible etiologies have been suggested: • Odontogenic cyst caused by proliferation of the epithelial rests of Malassez. • Lateral dentigerous cyst (retained in the jaw after tooth eruption). • Primordial cyst of supernumerary tooth germ. • Stimulation of epithelial rests of the periodontal ligament by infection from a periodontal abscess or from the pulp through an accessory canal. Usually asymptomatic but may present as a localized tender swelling. Radiographically seen at the site of the root as a radiolucent area bordered by a radiopaque line (can not be differentiated radiographically from periodontal abscess).

Fig. 23.3: Zones in the base of the periodontal pocket Determination of Pocket Depth

Periodontal Disease Activity • Probing depth measurement (Fig. 23.5). • Clinical detection of attachment loss. • Clinical detection of suprabony and infrabony pockets. Clinically, probing depth measurement is recorded from the crest of the marginal gingiva to the probable depth of the pocket. Whereas attachment level is measured from cementoenamel junction to the probable depth of the pocket. To differentiate between pseudo and true pocket, attachment level measurement should be considered.

210

PART IV Periodontal Pathology Periodontal

Fig. 23.4: Relation of loss of attachment

Clinical detection of attachment level is done by first identifying the cementoenamel junction (CEJ) with the probe tip (since junctional epithelium is attached at the CEJ), if the probe passes beyond the point of CEJ then it is considered to be a true pocket. While probing, soft tissue resistance on lateral pressure indicates suprabony pocket and hard tissue resistance indicates infrabony pocket.

TREATMENT OF PERIODONTAL POCKET

Fig. 23.5: Probing of a pocket I. Treatment of pocket depends on the type of pocket 211 HPE 23 CHAPTER

Fig. 23.6: Differences between suprabony and infrabony pockets Pocket Periodontal The

3. Apical displacement of pocket wall by apically II. Treatment of suprabony and infrabony pockets displaced flap. c. Removal of the tooth side of the pocket, by tooth extraction or partial tooth extraction such as hemisection or root resection.

Table 23.1: Differences between suprabony and infrabony pocket (Fig. 23.6) Suprabony pockets Infrabony pockets

a. The base of the pocket a. The base of the pocket is is coronal to the crest apical to the crest of the of alveolar bone. alveolar bone. b. The pattern of bone b. The pattern of bone des- destruction is horizontal truction is vertical/angular c. Interproximally, the c. Interproximally, the tran- transeptal fibers are septal fibers are arranged arranged horizontally. in an oblique pattern, ex- d. On the facial and lingual tending from cementum surfaces, the periodontal below the pocket over to III. Treatment of pockets can also be classified under three ligament fibers follow the cementum of the main headings. normal horizontal-oblique adjacent tooth. a. New attachment techniques: It offers ideal result by course between the tooth d. On facial and lingual sur- and bone. faces the periodontal reuniting the gingiva to the tooth at a position coronal ligament fibers follow the to the base of pre-existing pocket. Here all the structures angular pattern of the of lost periodontium are restored. Following are the adjacent bone. techniques for new attachment: • Non-graft associated new attachment procedures. • Graft associated new attachment procedures. 1. Pockets are defined as the pathologic deepening of the • Combined techniques. gingival sulcus. b. Removal of pocket wall by, 2. They can be pseudo or true pockets; simple, compound or complex pockets; suprabony or infrabony pockets. 1. Retraction or shrinkage, e.g. scaling and root planing. 3. Microscopically, in a periodontal pocket certain changes 2. Surgical removal by gingivectomy or by means of are observed in both the soft tissue wall and the root an undisplaced flap. surface. 212

4. Clinically, true pocket can be identified by recording the periodontal abscess may form in the sealed-off portion attachment level (which is measured from the of the pocket. cementoenamel junction to the probable depth of the 5. Treatment with systemic antibiotics along with root pocket). planing in advanced periodontal patients may result 5. Pockets can be treated by: (a) new attachment in abscess formation. Other factors that may cause techniques, (b) removal of the pocket wall; (c) removal periodontal abscess include: of the tooth side of the pocket. a. Impactation of foreign bodies especially related 6. Only infrabony pockets can be treated successfully by various regenerative procedures. to oral hygiene aids (toothbrush bristle, piece of dental floss) have been termed as “oral hygiene abscess”

b. Perforation of the lateral wall of root in endodontic PART IV therapy. (Differences between gingival abscess, KNOW MORE ... periodontal abscess and periapical abscess is dis- cussed in detail in Chapter ‘Gingival enlargement’). Significance of Pus Formation Treatment options for periodontal abscess are: a. Drainage through pocket retraction or incision. Pus is a common feature of periodontal diseases but it is b. Non-surgical therapy including scaling root planing only a secondary sign. It merely reflects the nature of the and antimicrobial therapy. inflammatory changes in the pocket. c. Periodontal surgery. A periodontal abscess is a localized purulent infection d. Extraction of the offending tooth. of the periodontal tissues which may lead to destruction Antibiotic options for acute, periodontal abscess are: of periodontal ligament and alveolar bone. It is also • Amoxicillin 500 mg three times a day for 3 days. referred to as a lateral or parietal abscess. Periodontal • Clindamycin – 600 mg loading dose subsequently 300 abscess can be classified. mg four times a day for 3 days. a. According to location

Periodontal Pathology Periodontal • Azithromycin, 500 mg four times a day for 3 days. – Abscess along the lateral aspect of the root – Abscess in the soft tissue wall of the deep periodontal pocket REVIEW QUESTIONS b. According to onset and course – Acute periodontal abscess 1. Define, classify periodontal pockets, and describe the – Chronic periodontal abscess pathogenesis and treatment of a periodontal pocket. c. Depending on number 2. Describe the various pocket elimination procedures. – Single and multiple periodontal abscess 3. Describe the histopathology of a periodontal pocket. 4. What are the root surface changes associated with a Causes of Periodontal Abscess periodontal pocket? Mainly divided into: 5. Differentiate between suprabony and infrabony pockets. I. Abscess related to periodontal diseases. II. Periodontal abscess caused by other factors (Non- BIBLIOGRAPHY periodontitis related abscess). Periodontal abscess may occur in the following ways: 1. Bonakdar MPS, Barber PM, Newman HN. The vasculature in 1. Deep extension of infection from a periodontal pocket chronic adult periodontitis: A qualitative and quantitative study. into the supporting tissues and localization of J Periodontol 1997; 68:50. suppurative inflammatory process along the lateral 2. Boshardt DP, Selvig KA. Dental cementum: the dynamic tissue aspect of the root. 2. Lateral extension of inflammation from inner surface covering the root. Periodontol 2000;1997; 13: 41. of a pocket into the connective tissue of the pocket. 3. Krayer JW, Rees TD. Histologic observation on the topography 3. The existence of tortuous pockets, with cul-de-sac of human periodontal pocket viewed in transverse step serial that eventually becomes isolated and may favour sections. J Periodontol 1993; 64: 585. abscess formation. 4. Newman, Takei, Carranza. Clinical Periodontology, 9th edn, WB 4. Incomplete removal of calculus during treatment of a Saunders, 2002. 5. Takada T, Donath K. The mechanism of pocket formation. A periodontal pocket may lead to occlusion of the pocket light microscopic study of undecalcified human transverse step orifice due to shrinkage of gingival wall and a serial sections. J Periodontol 1988; 59: 215. 24 ChapterChapter

Bone Loss and Patterns of Bone Destruction

 NORMAL ANATOMY OF ALVEOLAR BONE  BONE DESTRUCTION PATTERNS IN  MECHANISM OF BONE FORMATION AND PERIODONTAL DISEASE BONE DESTRUCTION • Local Factors  PREVALENCE AND DISTRIBUTION OF BONE • Systemic Factors DEFECTS IN MODERATE ADULT  FACTORS DETERMINING BONE MORPHOLOGY PERIODONTITIS IN PERIODONTAL DISEASE

INTRODUCTION

Osseous defects are those defects, which are formed as a result of destruction of alveolar bone due to periodontal disease. The normal height of alveolar bone is at cemento- enamel junction and this height is maintained by physiologic equilibrium between bone formation by osteoblasts and bone loss by osteoclasts, which in turn are regulated by local and systemic influences.

NORMAL ANATOMY OF ALVEOLAR BONE (FIG. 24.1)

Alveolar bone is that part of jaw bone that surrounds and Fig. 24.1: Normal anatomy of alveolar bone supports the teeth. It has facial and lingual cortical plate or compact bone between which cancellous bone is It is partially tooth-dependent and hence it is resorbed sandwiched. once the tooth is extracted. The shape, size, thickness varies 214

in different regions of the same mouth. The margins of the b. From the gingiva alveolar crest run parallel to the cementoenamel junction at ↓ (Less common; seen in trauma from occlusion) a remarkably constant distance of 1 to 2 mm. Periodontal ligament Facially and lingually: MECHANISM OF BONE FORMATION a. From the gingiva along the outer periosteum AND BONE DESTRUCTION ↓ Osteoblasts are the primary cells responsible for the Into the bone synthesis of the bone matrix, which subsequently undergoes b. From the gingiva calcification. Initially, uncalcified matrix, called osteoid, is

PART IV ↓ formed and this is mineralized as a result of deposition of Into the periodontal ligament crystals of hydroxyapatite. Bone destruction in periodontal disease is caused by When the inflammation reaches the bone by extension local factors and systemic factors. from the gingiva, it spreads into marrow spaces and it Bone destruction in periodontal disease is not a process replaces it with a leukocytic and fluid exudate, new blood of bone necrosis. It involves the activity of the live cells vessels and proliferating fibroblasts. Multinuclear osteo- along the viable bone. Tissue necrosis and pus if present clasts and mononuclear phagocytes are increased in number are seen in the soft tissue walls of the periodontal pocket and bone surfaces are lined with cone-like resorption but not along the resorbing margins of the underlying bone. lacunae. In the marrow spaces, resorption proceeds within, causing first thinning of the surrounding bony trabeculae

Local Factors and enlargement of marrow spaces, followed by destruction Periodontal Pathology Periodontal Local factors could be: of bone and reduction in bone height. Around the resorption a. Chronic gingival inflammation areas, normally fatty bone marrow is partially or totally b. Trauma from occlusion replaced by a fibrous type of marrow. c. Combination of both In summary, the changes in the bone could be as follows:

Role of Chronic Gingival Inflammation Gingival inflammation ↓ It is the most common cause for bone destruction in Marrow spaces periodontal disease. It is believed that inflammation spreads ↓ from the gingiva into the deeper tissues along two pathways Replaced by leukocytes and fluid exudates, (This marks the transition from gingivitis to periodontitis). new blood vessels and proliferating fibroblasts The transition from gingivitis to periodontitis is ↓ associated with changes in the composition of bacterial Increase in osteoclasts and mononuclear cells plaque or resistance of the host. The lesion presents with ↓ most pathogenic bacteria, inflammatory cell infiltrate, the Thinning of bone trabeculae and enlargement lesion becoming more progressive and destructive with the of the marrow spaces conversion of T-lymphocyte to B-lymphocytic lesion. ↓ Destruction of the bone and reduction in bone height Pathway of spread of inflammation could be, ↓ Interproximally: Replacement of fatty bone marrow with the fibrous type a. From the gingiva ↓ (around the resorption areas) Bone The following are the possible pathways by which bone ↓ destruction is caused by extension of gingival inflammation Periodontal ligament (by Hausmann): 215

1. Direct action of plaque products on bone progenitor cells (e.g. hyperparathyroidism, leukemia, etc.) by mechanism to release osteoclasts. that may not be related to the usual periodontal bone 2. Plaque products act directly on bone, destroying it destruction. through a non-cellular mechanism. HPE 24 CHAPTER 3. Plaque products stimulate gingival cells, to release Pharmacological Agents and Bone Resorption mediators which in turn induces progenitor cells to These include prostaglandins and their precursors and differentiate into osteoclasts. osteoclast activating factors, all of which are present in 4. Stimulates gingival cells to release agents that destroy inflamed gingiva. Complement can also induce bone bone by direct chemical action without osteoclasts. resorption by enhancing the synthesis of prostaglandins. 5. Plaque products act as co-factors in bone resorption. Prostaglandins are synthesized by fatty acid precursors such

It has been hypothesized that two cell types are respon- as arachidonic acid and is controlled by cyclo-oxygenase Bone Loss and Patterns of Bone Destruction Bone of Patterns and Loss Bone sible for bone resorption: pathway. Flurbiprofen (NSAID) is a potent inhibitor of 1. Osteoclast: Removes the mineral portion of bone. cyclo-oxygenase pathway of arachidonic acid metabolism 2. Mononuclear cells: Plays a role in organic matrix which retards the rate of bone loss. degradation. Both are found near the resorbing bone. Radius of Action Some of the authors suggested that, locally produced bone Bone Destruction Caused by Trauma resorption factors may have to be present in the proximity from Occlusion Alone of the bone surface to be able to exert their action. On the Trauma from occlusion in the absence of inflammation can basis of Waerhaug’s measurements, it was postulated that cause the following changes: there is a range of effectiveness of about 1.5 to 2.5 mm • Increased compression and tension of periodontal within which bacterial plaque can induce bone loss, beyond ligament. 2.5 mm there is no effect. Interproximal angular defects • Increased osteoclasis of alveolar bone and necrosis of can appear only in spaces wider than 2.5 mm because periodontal ligament. narrower spaces are destroyed completely, Large defects These changes are reversible, if offending forces are far exceeding 2.5 mm can be seen in certain conditions, removed. However, persistent trauma from occlusion results like localized juvenile periodontitis and Papillon-Lefevre in funnel-shaped bony defects. syndrome, may be caused by the presence of bacteria within the tissues. Systemic Factors Rate of Bone Loss Local and systemic factors regulate the physiologic equilibrium of bone. When there is generalized tendency Loe and associates found the rate of bone loss on an average towards bone resorption, bone loss is initiated by a local to be about 0.2 mm a year for facial surfaces and about inflammatory process that may be magnified. This systemic 0.3 mm a year for proximal surfaces, when periodontal influence on the response of alveolar bone has been termed disease is allowed to progress untreated. as the bone factor concept in periodontal diseases. In recent years, a lot of studies focussed on the possible relationship Periods of Destruction between periodontal bone loss and osteoporosis. Periodontal destruction occurs in an episodic, intermittent Osteoporosis is a physiologic condition of postmenopausal pattern characterized by periods of activity and exacerbation women, resulting in loss of bone mineral content and followed by periods of remission and quiescence. The microstructural bone changes. Periodontal bone loss destruction results in loss of collagen and alveolar bone may also occur in generalized skeletal disturbances and deepening of periodontal pocket. 216

The reasons for the onset of destructive patterns are not • Increased thickness of alveolar bone margins to totally understood but the following theories have been accommodate functional demands offered: • The alignment of the teeth, root trunk anatomy. 1. Bursts of activity is associated with subgingival For example, angular bone defects cannot form ulceration and an acute inflammatory reaction resulting in thin facial and lingual alveolar plates, which have in loss of alveolar bone. little or no cancellous bone between the outer and 2. Bursts of activity coincides with a predominantly inner cortical layers. In such an instance the entire crest of T-lymphocyte lesion to one with predominance of the bone is destroyed and the height of bone is reduced.

B-lymphocyte plasma cell infiltrate. PART IV 3. Periods of exacerbation is associated with an increase BONE DESTRUCTION PATTERNS IN in loose, unattached motile, gram-negative, anaerobic PERIODONTAL DISEASE pocket flora and period of remission coincides with the Horizontal Bone Loss formation of a dense, unattached, non-motile, gram- positive flora. It is the most common pattern of bone loss in periodontal 4. Presence of antibodies. disease. The bone is reduced in height but the bone margins remain roughly perpendicular to the tooth surface FACTORS DETERMINING BONE (Fig. 24.2). MORPHOLOGY IN PERIODONTAL DISEASE Vertical or Angular Defects (Figs 24.3 and 24.4) Normal Variation in Alveolar Bone

Periodontal Pathology Periodontal They are those that occur in an oblique direction, leaving a It can affect the osseous contours produced by periodontal hollowed out trough in the bone alongside the root, the base disease. The anatomic features that substantially affect the of the defect is located apical to the surrounding bone. In bone destructive pattern in periodontal disease include the most situations angular defects are accompanied by following: infrabony pockets. • Thickness, width and crestal angulation of the interdental Angular defects are classified on the basis of number of septa walls present as: • Thickness of facial and lingual alveolar plates • One-walled or hemiseptal defect—One wall is present • The presence of fenestrations and dehiscences • Two-walled defect—Two walls are present

Fig. 24.2: Radiographic illustration of horizontal bone loss Fig. 24.3: Vertical bone defect in relation to lower first molar 217

HPE 24 CHAPTER Bone Loss and Patterns of Bone Destruction Bone of Patterns and Loss Bone

Fig. 24.4: Types of angular defects

• Three-walled or intrabony defect—Three walls are present (more common on mesial surfaces of upper and lower molars) • Combined osseous defect—The number of walls in the apical portion of the defect are greater than that in its occlusal portion. Radiographs may help upto some extent to locate vertical defects, but the best would be surgical exposure of the defect.

Osseous Craters (Fig. 24.5) They are concavities in the crest of the interdental bone confined within the facial and lingual walls. It is found to make up two-thirds of all mandibular defects, can be Fig. 24.5: Diagrammatic representation of an osseous crater diagnosed by transgingival probing. in a faciolingual section between two lower molars The following reasons have been suggested for the high frequency of interdental craters. • Interdental areas are more prone to the accumulation of plaque and are more difficult to clean • The normal flat or even concave faciolingual shape of the interdental septum in lower molars may favor crater formation • Vascular patterns from the gingiva to center of the crest may provide a pathway for inflammation.

Bulbous Bony Contours (Fig. 24.6) They are bony enlargements caused by exostoses, adaptation to function or buttressing bone formation. They are found more frequently in the maxilla than mandible. Fig. 24.6: Bony exostosis in the buccal aspect 218

Reversed Architecture These defects are produced by loss of interdental bone, including the facial and lingual plates without concomitant loss of radicular bone, thereby reversing the normal architecture (more common in maxilla).

Ledges They are plateau-like bone margins caused by resorption of

PART IV thickened bony plates.

Furcation Involvements (Fig. 24.7) It refers to the invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease. The mandibular Fig. 24.7: Furcation involvement in relation to mandibular first first molars are most common sites and least common are and second molar (Grade-II) maxillary premolars. The role of trauma from occlusion in the etiology of 5. Inconsistent margins and ledges (plateau-like bony furcation involvement is controversial; others include margins) presence of enamel projections into the furcation, presence 6. Reversed architecture. of accessory pulpal canals. Diagnosis is made by careful III. Prichard (1967) expanded this classification and Periodontal Pathology Periodontal probing with Naber’s probe and radiograph of this area is included furcation involvement, anatomic aberrations of the helpful, but can be obscured by various factors like, angula- alveolar process, i.e. thick marginal ledges, exostoses and tion of the beam and radiopacity of adjacent structures. tori, dehiscence and fenestrations. There is a high prevalence of bony defects in posterior PREVALENCE AND DISTRIBUTION OF segments (due to thicker bone). Thin bone leads to horizontal BONE DEFECTS IN MODERATE ADULT defects. In the posterior segments, percentage of osseous PERIODONTITIS defects are more in the mandible. Interdental crater is the Different classifications of bone defects have been proposed: most common defect in the molars and hemisepta presents I. Goldman and Cohen (1958) lower proportion. According to morphology of bone defects, can be classified as: • One-walled defect 1. Osseous defects are those defects which are formed as • Two-walled defect a result of destruction of alveolar bone due to periodontal • Three-walled defect disease. 2. Osteoblasts are the primary cells responsible for the • Combined defect synthesis of bone matrix, which later on undergoes calcification. II. Glickman (1964) classified bony defects as: 3. Bone destruction in periodontal disease is caused by 1. Osseous/interdental craters osteoclasts and mononuclear cells and is mediated by 2. Hemiseptal defects local and systemic factors. 4. Local factors, that are responsible for bone destruction 3. Infrabony defects are: 4. Bulbous bone contours (more seen in maxillae and a. Chronic gingival inflammation are enlargement of bone due to exostoses, buttressing b. Trauma from occlusion bone formations). c. Combination of both. 219

5. Bone destruction patterns in periodontal disease are: REVIEW QUESTIONS a. Horizontal bone loss. 1. Describe the mechanism of bone destruction in b. Vertical or angular defects. periodontal disease. c. Osseous craters.

2. Describe the various patterns of bone loss in periodontal 24 CHAPTER d. Bulbous bony contours. e. Reversed architecture. disease. f. Ledges. g. Furcation involvement. BIBLIOGRAPHY 1. Elizabeth A. Pawlak Philip M. Hoag. Essentials of Periodontics, 3rd edn; Mosby, Jaypee Brothers Medical Publishers. 2. Jeffcoat MT, Lewis CE, Reddy MS, et al. Post-menopausal bone loss and its relationship to oral bone loss. Periodontol 2000,

KNOW MORE ... 2000;23:94. Bone Loss and Patterns of Bone Destruction Bone of Patterns and Loss Bone 3. Manson JD. Bone morphology and bone loss in periodontal Bone Destruction in Periodontal Disease disease. J Clin Periodontol 1976;3:14. • Bacteria mediated — LPS, lipoteichoic acid, 4. Manson JD, Eley BM. Outline of periodontics, 3rd edn, KM lipoproteins and others. Varghese Company. • Host mediated — prostaglandins, leukotrienes, 5. Moskow BS, Polson AM. Histological studies on the extension cytokines and others. of the inflammatory infiltrate in human periodontitis. J Clin Periodontol 1991;18:534. • Combination of both. 6. Newman, Takei, Caranza. Clinical periodontology, 9th edn; WB Diagnosis of Osseous Defects Saunders. a. Clinical examination — transgingival probing. 7. Papapanou PN, Tonetti MS. Diagnosis and epidemiology of b. Radiographs — not very reliable, cannot reveal the periodontal osseous lesions. WB Saunders: Periodontol 2000; extent of involvement and presence/absence of bony 2000;22:8. walls. 8. Schroeder HE. Discussion: Pathogenesis of periodontitis. J Clin c. Surgical exposure — during flap operations, it is the Periodontol 1980;13:426. only reliable method for determining the true archi- 9. Schwartz Z, Goultschin J, Dean DD, et al. Mechanisms of tecture of a bony defect. alveolar bone destruction in periodontitis. Periodontol 2000, 1997;14:158. 25 ChapterChapter

Chronic Periodontitis

 DEFINITION  TYPES BASED ON DISEASE DISTRIBUTION AND  DIAGNOSTIC CRITERIA SEVERITY • Clinical Features  NATURE OF DISEASE PROGRESSION • Microbiological Features  RISK FACTORS FOR DISEASE • Radiographic Features  GENERAL CONCEPT FOR ETIOLOGY

INTRODUCTION 3. No consistent pattern of distribution of lesion is seen, except that they are usually not isolated to one or two Chronic periodontitis was previously known as adult sites. periodontitis or slowly progressive periodontitis. 4. Highly acute inflammatory sites are not seen, mostly gingiva appear to be slight to moderately swollen and DEFINITION color may range from pale-red to magenta. Chronic periodontitis occurs as a result of extension of inflammation from the gingiva into the deeper periodontal tissues. It has recently been defined as “an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss and bone loss”.

DIAGNOSTIC CRITERIA FOR CHRONIC PERIODONTITIS (FIGS 25.1 AND 25.2)

Clinical Features 1. Age of onset is usually 30 to 35 years. 2. The disease is usually generalized, although some areas are more deeply involved than the other areas. Fig. 25.1: Chronic periodontitis in a 45-year-old male CHAPTER 25 Chronic Periodontitis 221 : It is considered generalized when : Periodontitis is considered localized Radiograph showing generalized bone loss Radiograph showing generalized bone

Fig. 25.3: when there is not more than 1 to 2 mm of clinical loss of attachment. TYPES more than 30 percent of the sites assessed in the oral cavity demonstrate attachment loss and bone loss. Slight (Mild) Periodontitis 1. is generally considered slight Periodontal destruction 2. Usually generalized involvement. Types are based on the following: Types Disease Distribution Localized periodontitis when less than 30 percent of the sites assessed in the oral cavity demonstrate attachment loss and bone loss. Generalized periodontitis Disease Severity loss on one tooth surface is greater than that on an adjacent loss on one tooth surface is greater than loss and is usually surface is referred to as vertical bone infrabony pockets. associated with angular bony defects and at a uniform rate When attachment loss and bone loss occur horizontal bone on majority of tooth surfaces it is called suprabony pockets. loss and is generally associated with A case of chronic periodontitis A Fig. 25.2: flattened or cratered papillae may be seen. flattened or cratered papillae may be found. exudate from the pockets may also be formation. infrabony pockets can be found. restorative open interdental contacts, defective and malposed teeth may be frequently seen. margins severity of the disease. Porphyromonas gingivalis (P. gingivalis) gingivalis (P. Porphyromonas intermedia) intermedia (P. Prevotella Capnocytophaga A.actinomycetemcomitans (A.a) (E. corrodens) Eikenella corrodens (C. rectus) Campylobacter rectus 6. inflammation related Spontaneous bleeding and 7. the pocket occludes it may result in abscess When 8. Pocket depths are variable and both suprabony and 9. Conditions that enhance plaque accumulation like 5. and Loss of stippling, blunt or rolled gingival margins 11. cases. mobility is seen in advanced Tooth 10. of microbial deposits are consistent with The amount 12. are seen. No serum neutrophil/monocyte abnormalities Radiographic Features (Fig. 25.3) Pattern of bone loss observed in chronic periodontitis may When attachment loss and bone be vertical or horizontal. Causative organisms of chronic periodontitis are: of chronic Causative organisms • • • • • • Microbiological Features 222

3. Minimal furcation invasions with little or no mobility In Asynchronous Multiple Burst Model, the tissue are observed. destruction occurs at a definite period of time in one’s life, 4. Bone loss is minimal (less than 20% of total attachment). then it passes into a state of remission as in juvenile periodontitis. Moderate Periodontitis RISK FACTORS FOR DISEASE It is considered moderate when there is: 1. 3 to 4 mm of clinical attachment loss. a. Local factors: These include plaque and plaque retentive 2. Early to moderate furcation involvement with slight to factors. Plaque attached to the tooth and gingival

PART IV moderate tooth mobility. surfaces at the dentogingival junction is considered to 3. Bone loss up to 40 percent of the total periodontal be the primary etiologic factor in chronic periodontitis. attachment on the tooth. P. gingivals, B. forythus and Treponema denticola are frequently associated with chronic periodontitis. Plaque Severe Periodontitis retentive factors are those that facilitate plaque 1. When attachment loss is 7 mm or more, the condition is accumulation or prevent the removal of plaque by routine severe. oral hygiene procedures. They play an important role in 2. Furcation involvement up to grade III. the development of chronic periodontitis because they 3. Excessive tooth mobility. allow plaque microorganisms to be in close proximity 4. Bone loss more than 40 percent—both horizontal and to periodontal tissues. Some of these factors include, angular bony defects are observed. calculus, subgingival and/or overhanging margins of

Periodontal Pathology Periodontal restorations, deep carious lesions that extend NATURE OF DISEASE PROGRESSION subgingivally, crowded or malaligned teeth and root surface irregularities (Fig. 25.4). The rate of disease progression in chronic periodontitis is slow, but sometimes may be modified by systemic or other underlying factors. Though onset can occur at anytime, because of its slow progression it usually becomes clinically significant in the mid 30s or later. Several models have been proposed to describe the rate of disease progression. 1. Continuous paradigm. 2. Random burst theory. 3. Asynchronous multiple burst hypothesis. Continuous paradigm implies slow, continuous and progressive destruction of periodontium. This type of progression has been reported in longitudinal studies, not responsive to treatment. The Random Burst Theory proposes that the progression of disease occurs at short periods of active destruction, which are followed by periods of remission that randomly occur with respect to time and site in an individual. An example for this is chronic adult periodontitis. Fig. 25.4: Local factors in chronic periodontitis CHAPTER 25 Chronic Periodontitis 223 KNOW MORE ... periodontal therapy control records accumulation, e.g. correction of ill-fitting appliances, overcontoured crowns, overhanging restorations, etc. membranes. disease resulting in inflammation within the supporting in inflammation disease resulting is characterized by progressive tissues of the teeth, which bone loss.” attachment loss and i.e. less than 30 percent of the localized periodontitis, loss and bone loss. It is sites showing attachment more than 30 percent of sites generalized when loss and bone loss. demonstrate attachment severe forms. as mild, moderate and of disease progression: a. Continuous Paradigm, b.Theory, Burst Random c. Multiple Burst Hypothesis. Asynchronous a. and plaque retentive factors. Local factors like plaque b. Systemic factors—systemic diseases like diabetes. c. factors like smoking. Environmental d. Genetic factors—no clear determinants. Surgical therapy Non-surgical therapy Various Treatment Considerations in Considerations Treatment Various Chronic Periodontitis I. • root planing) Initial therapy (scaling and • Antimicrobial therapy—as an adjunct to routine • Instructions, reinforcement, evaluation of plaque • Removal of all the factors contributing to plaque II. A variety of surgical procedures could be implemented: 1. Periodontal flap surgery 2. procedures Pocket elimination 3. and barrier bone grafts Regenerative therapy including 1. as an “infectious is recently defined Chronic periodontitis 2. it is classified as, Depending on the disease distribution 3. it can be described Depending on the disease severity 4. rate Three models have been proposed to describe the 5. are: periodontitits risk factors for chronic Various periodontitis : Smoking is one chronic etiology of : The role of systemic factors in role of systemic The : : Genetic basis for periodontal disease Role of host status and defence mechanisms in Role of host status influencing the progression of peridontal diseases such factor that presently is receiving a lot of attention. such factor that presently that when combined with plaque it It has been shown It can result in greater attachment induces periodontitis. involvement and deeper loss, bone loss, furcation that There is abundant evidence suggesting pockets. the extent and emotional stress may also influence severity of chronic periodontitis. Genetic factors Systemic factors Systemic and the host response diseases can influence periodontal disease. of periodontal rate of progression increase the II, a non-insulin dependent diabetes Diabetes mostly type to be one of the most important mellitus is considered that can increase the extent and systemic condition disease (Fig. 25.5). severity of periodontal or behavioral factors Environmental demonstrated is based on the recent studies that have members and periodontal destruction among the family Although no clear generations within a family. different for chronic determinants have been described may be observed periodontitis, a genetic predisposition in response to in aggressive periodontal breakdown accumulation of plaque and calculus. Fig. 25.5: GENERAL CONCEPT FOR ETIOLOGY OF CHRONIC PERIODONTITIS are enumerated here: The key points regarding the d. b. c. 224

REVIEW QUESTIONS 2. Kornman KS, di Giouine FS. Genetic variations on cytokine expression: A risk factor for severity of adult periodontitis. Ann 1. Describe the types, etiology and clinical features of periodontol 1998;3:327. 3. Newman, Takei, Carranza. Clinical periodontology, 9th edn, WB chronic periodontitis. Saunders, 2002. 2. What are risk factors for chronic periodontitis? 4. Saul schluger. Periodontol diseases, 2nd edn, Lea and Febiger, 1999. 5. Socransky SS, Haffajee AD, Goodson JM, et al. New concepts BIBLIOGRAPHY of destructive periodontal disease. J Clin Periodontol 1984;11:21. 6. William B Clark, Harold Loe. Mechanisms of initiation and

1. Fleming TF. Periodontitis. Ann Priodontol 1999;4:32. progression of periodontal disease. Periodontol 2000;2:1993.

PART IV Periodontal Pathology Periodontal 26 ChapterChapter

Aggressive Periodontitis

 LOCALIZED AGGRESSIVE PERIODONTITIS • Immunology • Historical Background • Treatment • Clinical Features  GENERALIZED AGGRESSIVE PERIODONTITIS • Radiographic Findings • Clinical Characteristics • Histopathologic Features • Radiographic Findings • Bacteriology • Risk Factors

INTRODUCTION LOCALIZED AGGRESSIVE PERIODONTITIS/ LOCALIZED JUVENILE PERIODONTITIS Aggressive periodontitis is characterized by the rapid loss of attachment and bone loss occurring in an otherwise Historical Background clinically healthy patient with the amount of microbial deposits inconsistent with disease severity and familial • In 1923, Gottlieb reported a case as diffuse atrophy of aggregation of diseased individuals. Aggressive alveolar bone characterized by the loss of collagen fibers periodontitis was formerly classified as early onset in the periodontal ligament and loss of alveolar bone. periodontitis, i.e. localized juvenile periodontitis (LJP) has • In 1928, Gottlieb attributed this condition to the inhibition been changed to localized aggressive periodontitis; of cementum formation and termed the disease as generalized aggressive periodontitis was previously cementopathia. classified as generalized juvenile periodontitis (GJP) and • In 1938, Wannenmacher described incisor, first molar rapidly progressive periodontitis (RPP). involvement and called the disease as periodontitis 226

marginalis progressiva. Unlike others, he considered this Generalized juvenile periodontitis is defined as destructive as an inflammatory disease. periodontitis in individuals under the age of 30 years affecting • In 1940, Thoma and Goldman used the term paradontosis more than fourteen teeth, i.e. generalized to an arch or an and reported that the initial abnormality was located in entire dentition. the alveolar bone rather than in the cementum. • In 1942, Orban and Weinmann introduced the term Clinical Features and on the basis of autopsy case, described Age and Sex Distribution three stages in the development of the disease. Affects both the sexes and is seen mostly between puberty PART IV Stage 1: Involves the degeneration of principle fibers of the and 20 years of age. Some studies show predilection to periodontal ligament, which induces cessation of cementum female patients. formation and resorption of alveolar bone. In this stage, tooth migration occurs without detectable inflammatory Distribution of Lesions involvement. Three areas of localization of bone loss have been described: Stage 2: The lack of periodontal fibers results in the rapid 1. First molar and/or incisors. proliferation of the junctional epithelium along the root and 2. First molar and/or incisors + additional teeth (not earliest signs of inflammation appear. exceeding 14 teeth). Stage 3: It is characterized by progressive inflammation and 3. Generalized involvement. the development of deep, infrabony periodontal pockets. For localized juvenile periodontitis, classic distribution

Periodontal Pathology Periodontal Most of these studies considered ‘periodontosis’ as a is in the first molars and incisors with least destruction in degenerative disease caused by unknown systemic factors. the cuspid, premolar area. Other investigations denied the existence of a degenerative Limitations of destruction to certain teeth could be for type of periodontal disease and attributed the changes the following reasons: observed to trauma from occlusion. • Production of opsonizing antibodies against In 1996, the World Workshop concluded that A. actinomycetemcomitans called burn-out pheno- periodontosis as a degenerative entity was unsubstantiated menon. and the term should be eliminated from periodontal • Bacteria antagonistic to A. actinomycetemcomitans may nomenclature. develop, thereby decreasing the number of colonization The term juvenile periodontitis was introduced by sites. Chaput and colleagues in 1967 and by Butler in 1969. In • A. actinomycetemcomitans may loose its leukotoxin 1971, Baer defined it as ‘a disease of periodontium occurring producing ability for unknown reasons. in an otherwise healthy adolescent which is characterized • Localization of the lesions could also be due to the defect by a rapid loss of alveolar bone, about more than one tooth in cementum formation (hypoplastic/aplastic of the permanent dentition. The amount of destruction is cementum). not commensurate with the amounts of local irritants’. A more recent definition by Genco et al in 1986 Clinical Findings (Figs 26.1 and 26.2) describes localized juvenile periodontitis as a disease 1. The most striking feature is lack of clinical inflammation occurring in otherwise healthy individuals under the age of despite the presence of deep periodontal pockets. 30 years with destructive periodontitis localized to the first 2. There is a small amount of plaque, which forms a thin permanent molars and incisors not involving more than two film on the tooth and rarely mineralizes to become other teeth. calculus. CHAPTER 26 Aggressive Periodontitis 227 aggressive periodontitis Radiographic appearance of localized Radiograph showing progressive bone loss Radiograph showing progressive bone

Fig. 26.4: Fig. 26.3: distal surface of 2nd premolar to mesial surface of 2nd molar.” occurs, called as “mirror image pattern”. Pathogenesis of aggressive periodontitis is due to an • bilaterally symmetrical patterns of bone loss Frequently, interplay of several factors, these include the specific microbiology of subgingival plaque, defects in cementum, hereditary factors, impaired PMNs function and disorders of the immune system. Clinical appearance of localized in a 30-year-old patient aggressive periodontitis Generalized aggressive periodontitis

Fig. 26.2: Fig. 26.1: incisors in an otherwise healthy teenagers is a diagnostic sign of classic juvenile periodontitis. The pattern appears to be, “Arc-shaped loss of alveolar bone extending from migration of first molars and incisors. Classically, a migration of first molars and incisors. Classically, distolabial migration of the maxillary incisors with diastema formation occurs, lower incisors rarely migrate compared to upper incisors, all changes followed by sequelae of migration are seen. periodontal deep dull radiating pain, surface sensitivity, abscess formation and regional lymph node enlargement may occur. Radiographic Findings (Figs 26.3 and 26.4) • or angular bone loss around the first molars and Vertical 3. Most common initial symptoms are mobility and 4. As the disease progresses, other symptoms like root 228

Histopathology/Microscopic Features 1. Extraction: Extraction of involved teeth especially first molars results in uneventful healing. These are the same as those seen during pocket formation. Transplantation of developing third molars into the • Like ulcerated pocket epithelium. sockets of previously extracted 1st molars has been tried • Accumulation of various inflammatory cells in the but with limited success. connective tissue mainly leukocytes, plasma cells and 2. Standard periodontal therapy: Includes scaling, root small number of lymphocytes and macrophages. planing, curettage, flap surgery with/without bone grafts, • Electron microscopic studies of juvenile periodontitis root amputation, hemisection, occlusal adjustment and revealed bacterial invasion of connective tissue that strict plaque control has been tried. PART IV reaches the bone surface. However, response is unpredictable and frequent • The flora involves A. actinomycetemcomitans, Capno- maintenance visits are a must. cytophaga sputigena and others. 3. Antibiotic therapy: Several authors reported successful Bacteriology results using antibiotics as adjuncts to standard therapy. • Genco and coworkers reported scaling and root Two types of bacteria are considered to be pathogens in planing and tetracycline 250 mg qid for 14 days every localized aggressive periodontitis— A. actinomycetem- 8 weeks. comitans and Capnocytophaga. A. actinomycetemcomitans • Several other investigations have also noticed is a short, facultatively anaerobic, non-motile Gram-negative excellent bone fill in cases of localized juvenile rod. periodontitis treated with tetracycline, flap surgery Virulence factors associated with A. actinomycetem- and placement of grafts. Periodontal Pathology Periodontal comitans are:

Factors Significance Current Approach to Therapy Leukotoxin Destroys polymorphonuclear leukocytes and • In almost all cases, systemic tetracycline hydrochloride macrophages. 250 mg qid for atleast a week should be given in Endotoxin Activates host cells to secrete inflammatory mediators (prostaglandins, interleukin’s conjunction with local mechanical therapy. If surgery is 1 and 3, tumor necrosis factor-α). indicated, systemic antibiotics are advised with patient Bacteriocin May inhibit IgG and IgM production instructed to begin taking the antibiotic approximately Collagenase Causes degradation of collagen 1 hour before surgery. Chemotactic May inhibit neutrophil chemotaxis • Doxycycline 100 mg/day may also be used. inhibition factors • Chlorhexidine rinses should be prescribed. • In refractory cases, tetracycline resistant Actinobacillus Immunology species have been suspected. In such cases, a combination of amoxicillin and metronidazole has been Immune defects that have been implicated in the pathogenesis suggested. of localized aggressive periodontitis are functional defects of polymorphonuclear leukocytes/monocytes, thereby it impairs the chemotactic attraction of PMNLs GENERALIZED AGGRESSIVE (polymorphonuclear leukocytes) to the site of infection. PERIODONTITIS Previously classified as Generalized Juvenile Periodontitis Treatment (GJP) and Rapidly Progressive Periodontitis (RPP). Prognosis is no more considered as poor for patients with Generalized aggressive periodontitis is usually aggressive periodontitis. The following treatment has been characterized by ‘generalized interproximal attachment loss tried in the past with varying results: affecting atleast three permanent teeth other than first molars CHAPTER 26 Aggressive Periodontitis 229 , which explains sub-species and . Mycoplasma A. actinomycetemcomitans , also associated with a 40 percent A. actinomycetemcomitans . is one of the factors that can influence the extent A. actinomycetemcomitans aggressive periodontitis (LAP) have dysfunctional aggressive periodontitis are seen as decreased in the neutrophils, which agents, chemotactic response to several chemotactic C5a, N-formyl- including the complement component and leukotriene methionyl leucylphenylalanine (FMLP) The defect is B4. on the neutrophil deficiency in glycoprotein, GP110, surface. response to the dominant the limitation of the infection. In LAP to antigens serum antibody is IgG2 type which is specific of associated with microbial patterns including organisms Host chronic periodontitis have been implicated. defects in either response is often characterized by neutrophils or monocytes. of destruction seen in young patients. Especially, smokers of destruction seen in young patients. Especially, with generalized aggressive periodontitis exhibit more Genetic Factors Some of the above mentioned immunologic defects seen in aggressive periodontitis may have a genetic basis, i.e. familial clustering of neutrophil abnormalities may be seen. It has been suggested by some authors that, a major gene plays a role in aggressive periodontal disease, which could be transmitted through an autosomal dominant mode of inheritance. Environmental Factors Smoking Immunologic Factors in defects that have been implicated Some of the immune localized aggressive periodontitis are: the pathogenesis of a. localized 75 percent of patients with Approximately b. Patients with LAP demonstrate a strong antibody c. In generalized form of aggressive periodontitis diverse have been identified as have been Capnocytophaga sputigena Spirochetes , . , may be seen in Bacteroids forsythus Bacteroids : It affects persons between has been implicated as the Porphyromonas gingivalis Porphyromonas , and : No specific pattern is observed, Distribution of lesion types of gingival responses Two and general such as weight loss, mental depression malaise. puberty and 35 years (but may be older). No sex puberty and 35 years (but may be discrimination is seen. all or most of the teeth are affected. One is severe, generalized aggressive periodontitis. proliferating, acutely inflamed tissue which is often bleeding and ulcerated and fiery red, spontaneous other cases, the suppuration are commonly seen. In the of inflammation gingival tissue may appear pink and free by probing. but deep pockets can be demonstrated Age and sex distribution A. actinomycetemcomitans primary pathogen associated with this disease. the lesions of localized aggressive Microscopically, periodontitis have revealed bacterial invasion of connective These invading bacteria tissue that reaches the bone surface. Microbiologic Factors A. actinomycetemcomitans Risk Factors for Aggressive Forms Risk Factors for of Periodontitis No definite pattern of distribution occurs but the radiographic picture can range from severe bone loss associated with the minimal number of teeth, to advanced the majority of teeth in the dentition. bone loss affecting Radiographic Findings b. c. d. systemic manifestations Some of the patients may have a. Clinical Characteristics and incisors.’ Patients with generalized aggressive form may aggressive Patients with generalized and incisors.’ of microbial plaque associated with exhibit minimal amounts the amount of plaque i.e. quantitatively, the affected teeth, with the amount of periodontal seems to be inconsistent most pathogenic organisms destruction; qualitatively, e.g. may be associated, 230

number of teeth affected by loss of clinical attachment than non-smokers with generalized aggressive periodontitis. KNOW MORE ...

Treatment of Aggressive Periodontitis It also includes full mouth disinfection which has been Juvenile Periodontitis proposed by Quirynen et al. Since it was observed that It is defined as “a disease of periodontium occurring in A. actinomycetemcomitans has the ability to translocate an otherwise healthy adolescent which is characterized from one person to another and from site to site, full by a rapid loss of alveolar bone, about more than one mouth disinfection was implemented. It includes the following steps:

PART IV tooth of the permanent dentition. The amount of a. Full mouth scaling and root planing (in 2 sessions destruction is not commensurate with the amount of within 24 hours). local irritants. b. Brushing the dorsum of the tongue with an 1. Previously classified as generalized juvenile antimicrobial agent (1% chlorhexidine gel) for one periodontitis (GJP) and rapidly progressive periodontitis minute. (RPP). c. Mouthrinsing with antimicrobial agents. 2. Usually affects individuals under the age of 30, but older d. Home irrigation systems. patients may also be affected. Other Treatment Options 3. They usually produce a poor antibody response to the • Local drug delivery system. • Host modulation and photodynamic therapy. pathogens present. 4. Two types of gingival responses may be seen, one is a severe form, which is characterized by acute inflam- BIBLIOGRAPHY matory changes in the gingival tissue. Other cases, the 1. Jan Lindhe. Clinical Periodontology and Implant Dentistry, 4th gingival tissue may appear pink, free of inflammation

Periodontal Pathology Periodontal edition, Blackwell Munksgaard Publication, 2003. but in the presence of deep pockets. 2. Lang N, Bartold PM, Cullinan M et al. Consensus report: 5. There is no specific pattern for distribution of lesions, Aggressive periodontitis. Ann periodontol 1999;4:53. radiographically again no definite pattern of distribution 3. Tonnetti MS, Mombelli A. Early onset periodontitis. Ann seen. periodontol 1999;4:39. 27 ChapterChapter Necrotizing Ulcerative Periodontitis, Refractory Periodontitis and Periodontitis as a Manifestation of Systemic Disease

 NECROTIZING ULCERATIVE  PERIODONTITIS AS A MANIFESTATION OF PERIODONTITIS SYSTEMIC DISEASE • Non-AIDS type • Papillon-Lefévre Syndrome • AIDS associated • Chédiak-Higashi Syndrome  REFRACTORY PERIODONTITIS • Down’s Syndrome • Etiology • Hypophosphatasia • Clinical Features • Neutropenia • Treatment • Leukocyte Adhesion Deficiency

NECROTIZING ULCERATIVE all the characteristic clinical features of necrotizing ulcerative PERIODONTITIS (NUP) gingivitis are seen, i.e. i. Ulceration and necrosis of gingival margin, which gets Necrotizing ulcerative periodontitis occurs as a result covered by a pseudomembranous slough. of extension of necrotizing ulcerative gingivitis into the periodontal structures, leading to loss of attachment and ii. The ulcerated margins are surrounded by an bone loss. There are two types of necrotizing ulcerative erythematous halo. periodontitis described, based on its relationship to acquired iii. The lesions are extremely painful and bleed immunodeficiency syndrome (AIDS): Non-AIDS type spontaneously. necrotizing ulcerative periodontitis and AIDS-associated iv. Localized lymphadenopathy, fever and malaise. These necrotizing ulcerative periodontitis. lesions, especially in long-standing cases, can extend to the deeper periodontal structures resulting in deep, Non-AIDS Type Necrotizing crater-like osseous lesions especially in interdental Ulcerative Periodontitis areas. Such cases are identified as necrotizing ulcerative periodontitis (NUP), most striking feature Clinical Features of this condition is absence of deep conventional Since necrotizing ulcerative periodontitis occurs after pockets associated with deep interdental osseous repeated attacks of necrotizing ulcerative gingivitis (NUG), craters. This is because the necrotizing and ulcerative 232

properties of the gingival lesion destroys the marginal Etiology epithelium, resulting in total destruction of the marginal tissue leading to recession. Risk Factors Responsible for Refractory Cases a. Abnormal host response. AIDS-Associated Ulcerative Periodontitis b. Resistant strains of pathogenic periodontal microflora. (Discussed in detail elsewhere in this book) c. Failure to eliminate plaque-retentive factors, such as Gingival and periodontal lesions of HIV positive patients furcation involvement, irregular root surface, palato- gingival groove, etc. which may in turn interfere with PART IV appear to have similar findings that are seen in non-AIDS- associated necrotizing ulcerative periodontitis patients, in complete plaque removal. addition, they may exhibit certain complications such as: d. On the other hand, smoking and systemic diseases may 1. Large areas of soft tissue necrosis with exposure of bone result in generalized lesions, which may not respond and sequestration of bone. favorably to treatment. 2. Sometimes these lesions may extend onto the buccal Specific microorganisms have been identified in lesions vestibule or the palate and become necrotizing stomatitis. of refractory periodontitis. Haffajee et al. (1988) reported three major microbial complexes in refractory periodontitis REFRACTORY PERIODONTITIS cases. 1. B. forsythus, F. nucleatum and C. rectus. According to American Academy of Periodontology, 2. S. intermedius, P. gingivalis and P. micros. refractory periodontitis has been defined as “those cases

Periodontal Pathology Periodontal 3. S. intermedius and F. nucleatum. which do not respond to any treatment provided, whatever the thoroughness or frequency”. It should be differentiated Clinical Features from the cases of recurrent periodontitis, in which, after remission of the disease, recurrence follows due to In the classification proposed by the American Academy of inadequate plaque control either by the patient or clinician. Periodontology (1999), the term refractory periodontitis has Hence recurrent periodontitis, which is recurrence of the been removed as a single entity due to the diversity of disease due to incomplete treatment should be differentiated clinical conditions and treatments under which periodontal from refractory cases whose reasons for not responding to therapy fails to arrest the progression of periodontitis. adequate treatment, in certain cases, is still not clearly Therefore, the participants of the workshop have concluded understood (Table 27.1). that, rather than a single disease entity, the ‘refractory’

Table 27.1: Distinction between recurrent and refractory periodontitis

Disease Recurrent periodontitis Refractory periodontitis

Definition Sites are successfully treated but disease Sites do not respond to conventional therapy; returns, may refer to site/patients. usually refers to patients but may refer to sites. Phase of therapy May be because of inadequate therapy May be because of inadequate therapy during during maintenance/no maintenance. active treatment/other factors. Etiology May be because of re-infection, with May be because of infection with tissue invasive microbes that were suppressed but not microbes that cannot be eliminated with conven- eliminated. Re-infection with eliminated tional therapy or because of immunoincompetence. organisms or new bacteria. Immune system Immunocompetent. May not be immunocompetent. Antibiotic therapy Not usually needed. Usually needed. CHAPTER 27 Necrotizing Ulcerative Periodontitis, Refractory Periodontitis 233 Another approach in treating refractory periodontitis is refractory periodontitis in treating Another approach severe destruction of the periodontium. palms, soles, knees and elbows. that lead to bone loss and exfoliation of teeth. Primary The permanent teeth are lost by 5 or 6 years of age. dentition erupts normally but within few years the permanent teeth are also lost. PERIODONTITIS AS A MANIFESTATION OF MANIFESTATION A AS PERIODONTITIS SYSTEMIC DISEASE through modulation of host by sub-antimicrobial doses of by sub-antimicrobial of host through modulation drugs anti-inflammatory or non-steroidal doxycycline The with conventional therapy. (NSAIDs) in conjunction low dose doxycycline helps to prevent sub-antimicrobial or by controlling the production the periodontal destruction whereas flurbiprofen, indometha- of collagen and gelatinase, may reduce the production of inflam- cin and naproxen chronic periodontal disease. matory mediators during Papillon-Lefévre Syndrome (Fig. 27.1) Papillon-Lefévre Syndrome (Fig. 1. skin lesions and This is characterized by hyperkeratotic 2. These changes may appear before the age of 4 years. 3. are—hyperkeratosis of localized areas on Skin lesions 4. Periodontal involvement is early inflammatory changes Chédiak-Higashi Syndrome (CH Syndrome) This is a rare syndrome characterized by recurrent bacterial infections. It exhibits oral ulceration and rapidly destructive periodontitis. Chédiak-Higashi syndrome is a hereditary disease with defects in both neutrophils and monocytes. Severe periodontitis has been observed in patients who Severe periodontitis has been observed or defective exhibit either defective numbers of neutrophils associated with neutrophil function. Some of the conditions defective neutrophils are: a. syndrome. Papillon-Lefévre b. Chédiak-Higashi syndrome. c. syndrome. Down’s d. Hypophosphatasia. e. Neutropenia. f. deficiency. Leukocyte adhesion 250 mg + 125 mg thrice for 2 weeks 150 mg of qid for 1 week R Table 27.2: Drugs used to treat refractory sites Table Antibiotic therapy aims to reinforce mechanical perio- Antibiotic therapy aims to reinforce with 10 percent In addition to this, intrasulcular irrigation delivery system In cases of localized lesions, local drug Hence, refractory periodontitis in no way differs from Hence, refractory Clindamycin hydrochloride daily Clavulanate potassium (Augmentin) Combination of the above drugs, i.e. metronidazole/ amoxicillin, metronidazole doxycycline are also used. Drug hydrochlorideTetracycline Amoxicillin 250 mg of qid Dosage dontal therapy and also helps the host defence system by dontal therapy and also helps the host after conventional killing subgingival pathogens that remain Many antibiotics have been mechanical periodontal therapy. 27.2). used to treat the refractory sites (Table solution have povidone-iodine solution and chlorhexidine also been used successfully. advantages of this are The has been tried successfully. therapies These local smaller doses and minimal side effects. or chips. are available in the form of gels, fibers Antimicrobial therapy along with mechanical debridement Antimicrobial therapy along with mechanical the microbial in reducing has been found to be effective population at the refractory sites. Treatment other forms of periodontitis. Magnusson et al. (1991) noticed other forms of periodontitis. of plaque in relation to the sites no changes in the amount sites that showed the however, that have been treated, on also showed persistent bleeding attachment loss had by cases can be identified either The refractory probing. of attachment loss or progressive presenting new areas already treated sites. attachment loss in designation could be applied to all forms of periodontitis, could be applied designation aggressive refractory chronic periodontitis, e.g. refractory and others. periodontitis

234 PART IV

Fig. 27.2: Gingival changes associated with Down’s syndrome

Hypophosphatasia This is a rare familial skeletal disease characterized by rickets, poor cranial formation, premature loss of primary Fig. 27.1: A case of Papillon-Lefévre syndrome dentition particularly incisors. Patients have low level of

Periodontal Pathology Periodontal serum alkaline phosphatase. Teeth are lost with no clinical Down’s Syndrome (Mongolism, Trisomy 21) evidence of gingival inflammation and show reduced cementum formation. This is a congenital disease caused by a chromosomal abnormality and is characterized by mental deficiency and Neutropenia growth retardation. It is a condition where the circulating neutrophils are The oral findings include presence of plaque, calculus, reduced, i.e. less than 1,500 per ml. Destructive generalized and other local factors, like diastema, crowding of teeth, periodontal lesions have been described in children with high frenal attachment and malocclusion. neutropenia. Neutropenia could be inherent or acquired. Periodontitis in Down’s syndrome include the formation Certain drugs and infections can lead to reduction in number of deep periodontal pocket associated with plaque accumu- of neutrophils. lation and moderate gingivitis, usually generalized but more severe in the lower anterior region; marked recession is also Leukocyte Adhesion Deficiency seen in this region (may be due to high frenal attachment). Acute necrotizing lesions are also common (Fig. 27.2). These cases are rare, and begin during or immediately after Two factors have been proposed to explain high eruption of the primary teeth. Extreme acute inflammation prevalence and increased severity of periodontal destruction and proliferation of gingival tissues accompanied by rapid in Down’s syndrome: bone loss is found, profound defects in peripheral blood 1. Reduced resistance to infections because of poor neutrophils and monocytes are seen. Hence they are absent circulation (especially peripheral). in gingival tissues. Patients with LAD (Leukocyte adhesion 2. Defect in T-cell maturation and polymorphonuclear deficiency) also have frequent respiratory tract infections leukocyte chemotaxis. and sometimes otitis media. CHAPTER 27 Necrotizing Ulcerative Periodontitis, Refractory Periodontitis 235 A, Fernandez-Novoa MC, et al. Late A, Fernandez-Novoa MC, BIBLIOGRAPHY REVIEW QUESTION irrigation may be helpful in flushing of the deep lesions be helpful in flushing irrigation may the to alleviate should be considered and analgesics infection and pain. onset Paillon-Lefèvre syndrome. J Clin Periodontol 1993;20: onset Paillon-Lefèvre syndrome. J Clin Periodontol 662. subjects. J microbiological features of refractory periodontitis Clin Periodontol 1998;25:169. study. associated with Down syndrome—Clinical interventional Ann Periodontol 1998;3:370. Ann Periodontol 1999;4:1999. from a family of 4 unusual periodontal findings. Observations members. J Clin Periodontol 1998;25:181. of subjects with microbiological and immunological features 1988;15:390. refractory periodontal disease. J Clin Periodontol its relationship to chemotaxis in Down syndrome patients and periodontal disease. J Periodontol 1989;60:238. microbiological and immunological characteristics of subjects with “refractory” periodontitis. J Clin Periodontol 1991;18: 291. WB Saunders. in the treatment of refractory periodontitis. J Periodontol 1993; 64:772. periodontitis. 1. Pascual Bullon P, 2. Dewhirst FE, et al. Clinical and AD, Haffajee AP, Colombo 3. L, Grimm WD. Early onset periodontitis Crawford Ciclon P, 4. by systemic factors. Periodontitis modified Kinane Denis F. 5. Fardalo, Drangsholt E, Olsen I. Palmar plantar keratosis and 6.AD, Socransky SS, Dzink JL, et al. Clinical, Haffajee 7. S, Shinozuka O, et al. Defective neutrophil Sugiyama Y, Izumi 8.WB, et al. Clinical, Clark Magnusson I, Marks RG, 9. 9th edition, Carranza. Clinical periodontology, Newman, Takei, • with copious instrumentation The use of ultrasonic • antibiotics antimicrobials, systemic Locally applied 10. role of antibiotics A CB, Gordan JM, Magnusson I, et al. Walker 1. ulcerative Describe the features of necrotizing KNOW MORE ... acquired immunodeficiency syndrome (AIDS). Non-AIDS acquired immunodeficiency NUP. AIDS-associated type NUP and ulcerative gingivitis). of NUG (Necrotizing of the features of non-AIDS type, ontitis) shares most tissue necrosis with exposure of soft but with larger areas of bone and sequestration of bone fragments. whatever the do not respond to any treatment, provided, It should be differentiated thoroughness or frequency.” the after from recurrent periodontitis cases, in which, follows due to remission of the disease, recurrence or the patient inadequate plaque control either by the clinician. the term 1999) Academy of Periodontology, (American as a single refractory periodontitis has been removed entity. severe number or function of neutrophils exhibit are, Papillon- periodontitis. Some of the conditions Down Lefèvre syndrome, Chediak-Higashi syndrome, neutropenia and syndrome, hypophosphatasia, leukocyte adhesion deficiency. periodontal structures, it results in loss of attachment in loss of it results periodontal structures, condition is termed as necrotizing and bone loss. This (NUP). ulcerative periodontitis planing • Oral hygiene instructions Treatment of Necrotizing Ulcerative Periodontitis Treatment • debridement of lesions with scaling and root Local 3.repeated attacks non-AIDS type occurs as a result of A 4. period- NUP (Necrotizing ulcerative AIDS-associated 5. Refractory periodontitis is defined as, “those cases which 6.AAP to the classification proposed by According 7. conditions associated with defective Many systemic 2. relationship to based on its It can be of two types, 1. into the gingivitis extends deeper When ulcerative 28 ChapterChapter

AIDS and the Periodontium

 HIV OPPORTUNISTIC INFECTIONS • Necrotizing Stomatitis  CLASSIFICATION OF PERIODONTAL DISEASES • CDC Surveillance Care Classification ASSOCIATED WITH HIV INFECTION  MOST COMMON ORAL AND PERIODONTAL • Linear Gingivitis MANIFESTATIONS OF HIV INFECTION • Necrotizing Ulcerative Gingivitis • Necrotizing Ulcerative Periodontitis  MANAGEMENT

HIV OPPORTUNISTIC INFECTIONS width of the attached gingiva that may occur in the presence of excellent oral hygiene. Most of the opportunistic infections seen in HIV-positive 2. HIV-associated periodontitis (HIV-P): Characterized by patients are caused by, protozoan, fungal, or viral pathogens. rapid loss of attachment, connective tissue destruction This is because the effective immune defence for these and deep bone pain. pathogens is the cell-mediated response which is impaired 3. HIV-necrotizing gingivitis (HIV-NG). by HIV infection. Of the various types of oral lesions found 4. Necrotizing stomatitis (NS): In which spontaneous in the HIV-positive population, the most destructive and sequestration of interdental bone along with extensive problematic are those of bacterial origin. Bacterial infections soft tissue necrosis occurs. seen in HIV-positive patients include diseases caused by Since it was felt that the prefix ‘HIV’ was over- encapsulated or enteric bacteria such as Campylobacter, descriptive and caused potential, ethical and legal Klebsiella, Salmonella and Streptococcus. problems with confidentiality, the new classification has dropped the term HIV from individual disease titles. CLASSIFICATION OF PERIODONTAL DISE- • HIV-G has been changed to linear gingivitis. ASES ASSOCIATED WITH HIV INFECTION • HIV necrotizing gingivitis has been changed to Four distinct disease types are seen, necrotizing ulcerative gingivitis (NUG). 1. HIV-associated gingivitis (HIV-G): A distinctive linear • HIV-P has been changed to necrotizing ulcerative inflammation is seen around the gingival margin with periodontitis (NUP). possible punctate erythema extending throughout the • Necrotizing stomatitis. CHAPTER 28 AIDS and the Periodontium 237 . 3 of the interdental papilla Lesions seen in HIV infection Marginal gingival erythema and early necrosis Marginal gingival erythema and interproximal cratering with soft tissue there is a loss of crestal bone coinciding destruction gingival inflammation has been reported cell count below 200 cells/mm to grayish necrosis is observed on the tip of the to grayish necrosis is observed on gingiva. interdental papilla and margins of the to the soft tissue of the periodontium. Fig. 28.2: Necrotizing Ulcerative Periodontitis (Figs 28.1 and 28.2) • Severe pain, localized soft tissue necrosis, ulceration • Not associated with deep pocket formation but instead • the absence of severe Rapid horizontal bone loss in • mobility is a common feature Tooth • with CD4+ Associated with severe immune suppression • gingiva appears fiery-red and swollen and yellow The • Mostly anterior gingiva is affected and normally limited II Group III Lesions less commonly Oral Lesions Associated with HIV Infection A case of necrotizing ulcerative periodontitis A gingivitis periodontitis •• LGE: Linear gingival erythema NUG: Necrotizing ulcerative• NUP: Necrotizing ulcerative 6. Bacterial infections 7. Exacerbation of apical periodontitis generally involving all the teeth gingiva a bright-red appearance to the amount of erythema measures. scaling, root planing and plaque control Fig. 28.1: Oral lesions strongly associated Group I Group with HIV infection1. Candidiasis2. Hairy leukoplakia3. lymphoma Non-Hodgkin’s 4. sarcoma Kaposi’s 5. diseases Periodontal 3. Viral infection associated with HIV infection 2. Melanotic hyperpigmentation 1. Salivary gland diseases 5. 4. 2. Necrotizing stomatitis Bacterial infections Osteomyelitis 1. 3. Recurrent aphthous stomatitis Sinusitis 5. Cytomegalovirus infection 4. Fungal lesions other than candidiasis • toothbrushing. Sudden onset, bleeding on • Pain and characteristic halitosis. Necrotizing Ulcerative Gingivitis (NUG) Necrotizing Ulcerative Gingivitis • entire Punctate lesions appear to coalesce giving the • Spontaneous bleeding or bleeding on probing • The amount of supragingival plaque is not proportional • is seen No ulceration, no loss of attachment • plaque by intensive Does not respond to the removal of Linear Gingivitis It is characterized by: • linear erythema across the attached gingiva Marginal 238

Necrotizing Stomatitis 3. Kaposi’s sarcoma: Multifocal, vascular neoplasm manifest as nodules, papules or non-elevated macules • Extensive soft tissue and bony necrosis with that are usually brown, blue or purple in color. sequestration. 4. Bacillary angiomatosis: It is an infectious vascular, • It resembles noma and cancrum oris and represents the proliferative disease. It appears as red, purple or blue most severe form of periodontal infection seen in edematous soft tissue lesions that may cause destruction association with HIV. of periodontal ligament and bone. All of the above mentioned conditions may occur in

PART IV 5. Oral hyperpigmentation isolation or in combination in any one patient. A common 6. Atypical ulcers and delayed healing. feature of these periodontal diseases which distinguishes them from conventional periodontal conditions are, a lack MANAGEMENT of response to the removal of plaque and to the patients maintenance of good oral hygiene. Step I: Thorough medical and dental history (should be kept confidentially). CDC Surveillance Care Classification (1993) Step II: Periodontal therapy

AIDS patients have also been grouped as follows: Category A: Includes patients with acute symptoms or TREATMENT OF LINEAR GINGIVAL asymptomatic diseases, along with individuals with ERYTHEMA AND NECROTIZING

persistent generalized lymphadenopathy, with or without ULCERATIVE GINGIVITIS Periodontal Pathology Periodontal malaise, fatigue or low grade fever. • Medical history and appropriate medical consultation. Category B: Patients have symptomatic conditions such as • Scaling of affected areas and oral hygiene instructions. oropharyngeal or vulvovaginal candidiasis, herpes zoster, • Intrasulcular irrigation using 10 percent povidone iodine. oral hairy leukoplakia, idiopathic thrombocytopenia or • 0.12 percent chlorhexidine mouth-rinse twice daily. constitutional symptoms of fever, diarrhea and weight loss. • Antifungal agents like nystatin oral suspension and Category C: Are those with outright AIDS as manifested clotrimazole. by life-threatening conditions identified by CD4+T4 Disadvantages of oral antifungal agents are, lack of patients lymphocyte levels of less than 200 cells/mm3. compliance because of strong, sweet flavor and also high sucrose content in them preventing its use for long term MOST COMMON ORAL AND PERIODONTAL (risk of rampant tooth decay). MANIFESTATIONS OF HIV INFECTION Hence, systemic antifungal agents are recommended. Ketoconazole (may cause liver toxicity), fluconazole– 1. Oral hairy leukoplakia 200 mg tablets once and twice daily (most preferred). • Found on lateral borders of tongue • Follow-up one day and one week post-initial therapy. • Caused by Human Papillomavirus • Recall every 4 weeks until periodontal condition is • Keratotic, asymptomatic area with vertical striations stable, then every 3 to 6 months. giving a corrugated appearance • When dried appears hairy and does not rub off Treatment of Necrotizing Ulcerative Periodontitis 2. Oral candidiasis manifested as • Pseudomembranous (thrush) candidiasis • Medical history • Erythematous candidiasis • Scaling of affected areas under local anesthesia • The hyperplastic candidiasis • Remove necrotic bone and soft tissue • Angular cheilitis • Perform 10 percent povidone iodine irrigation CHAPTER 28 AIDS and the Periodontium 239 ELISA (Enzyme Linked ELISA (Enzyme Immunosorbent Assay) Western blot assay reaction. Polymerase chain → → → BIBLIOGRAPHY REVIEW QUESTION 4th edn, Blackwell Munksgaard Publication, 2003. 4th edn, Blackwell Munksgaard Publication, Curropin Periodontol 1993;111-28. with HIV. 9th edn, WB Saunders Co, 2002. 2000;6: by human immunodeficiency virus. Periodontol 1994. Periodontics. CV Mosby Company Publication 1990. Periodontol 1992;19:609. periodontal disease in HIV seropositive patients. J Periodontol 1993;64(7):651. infection? 1. Jan Lindhe. Clinical periodontology and implant dentistry. 2. considerations in the patients Periodontal I Ryder. Mark 3. Carranza. Clinical periodontology. A Fermin Takei, Newman 4. Periodontal diseases in patients infected Murray. A Patrica 5. Robert J Genco, Henry M Goldman. Contemporary 6. infection. J Clin Periodontal disease and HIV Robinson P. 7. GJ, Cooper DA, et al. Progression of SCH, Stewart Young Role of Antiretroviral Drugs in Drugs Role of Antiretroviral of HIV/AIDS the Management different so far act at that are developed The agents of HIV: stages of the life cycle a.virus to the target cell. They can block the binding of b. block the viral RNA cleavage. They can c. transcriptase. One that inhibits enzyme reverse Antibodies for HIV Testing a. Screening test b. Confirmatory test 1. What are the various periodontal manifestations of HIV : KNOW MORE ... : Lesions seen in HIV infection. : Lesions less commonly associated with HIV : Lesions less commonly associated with : Oral lesions strongly associated with HIV : Oral lesions strongly associated with Four distinct types of periodontal diseases associated Four distinct types of periodontal diseases with HIV infection are: a. gingivitis (HIV-G) HIV-associated b. periodontitis (HIV-P) HIV-associated c. (NS) Necrotizing stomatitis d. gingivitis (HIV-NG) HIV-necrotizing could be Oral lesions associated with HIV infection classified under Group I infection. Group II infection. Group III a. Oral hairy leukoplakia b. Oral candidiasis c. Kaposi’s sarcoma d. Bacillary angiomatosis e. Oral hyperpigmentation f. delayed wound healing Atypical ulcers and Most common oral and periodontal manifestations of Most common oral and periodontal manifestations HIV infections are Acquired Immunodeficiency Syndrome (AIDS) It is a disease due to infection with the human immunodeficiency virus. 1. 2. 3. Treatment of Necrotizing Stomatitis Treatment if + protect lesion with mouthguard Same steps followed possible. • hygiene instructions Oral • mouth-rinse percent Chlorhexidine 0.12 • Systemic analgesics • metronidazole Consider systemic antibiotic such as • Antifungal agents • 1 to 6 months) Follow-up (1 day to 4 weeks, 29 ChapterChapter

Diagnosis of Periodontal Diseases

 PERIODONTAL DIAGNOSIS • Key Stages of Periodontal Diagnosis  PRINCIPLES OF DIAGNOSIS • Diagnosis with Detailed Case History Recording  CLINICAL DIAGNOSIS  CASE HISTORY PROFORMA

PERIODONTAL DIAGNOSIS CLINICAL DIAGNOSIS

Proper periodontal diagnosis is essential for successful Periodontal diagnosis is mainly based on careful analysis treatment. Hence, diagnosis should first determine whether of the case history and recording clinical findings with the disease is present; then identify its type, extent, distribution help of various aids. One must remember that the importance and severity and finally provide an understanding of the should be given to the patient who has the disease and not simply the disease itself. The clinical findings are recorded underlying pathologic processes and their cause. Hence, in a systematic manner, when pieced together should provide diagnosis may be defined as, identifying disease from an a meaningful explanation. evaluation of the history, signs and symptoms, laboratory tests and procedures. Key Stages of Periodontal Diagnosis

PRINCIPLES OF DIAGNOSIS

This includes: Sensitivity—refers to the ability of a test or observation to detect the disease whenever it is present. Specificity—refers to the ability of a test or observation to clearly differentiate one disease from another. Predictive value—refers to the probability of the test results. CHAPTER 29 Diagnosis of Periodontal Diseases 241 Diagnosis Examination Investigations Clinical Diagnosis with Detailed Case History Recording Detailed Case Diagnosis with Clinical History Recording

242

PART IV Periodontal Pathology Periodontal

CASE HISTORY PROFORMA Drug allergy: Habits: Name: OP No: Clenching [ ] Tonguethrusting [ ] Sex: Age: Mouthbreathing [ ] Pan-chewing [ ] Address: Occupation: Bruxism [ ] Cigarette/pipe-smoking [ ] Date: Chronic biting of Chief Complaint cheek/tongue [ ] Tobacco chewing [ ]

History of present illness: Oral Hygiene Methods Past dental history: 1. Toothbrushing: Medical history: Age of brush: Family history: CHAPTER 29 Diagnosis of Periodontal Diseases 243 Upper right posteriorUpper left posterior Upper anterior Lower right posteriorLower left posterior Lower anterior Attrition: Abrasion: Erosion: Wasting disease: Wasting Fillings/restorations on percussion Tender Pulp/periapical problem: Pathologic migration Angles classification: jet: Overbite and over Openbite: Premature contact: Crossbite: Plunger cusps: Edge to edge bite: Prematurities: Color Contour Size Consistency Stippling Position Bleeding on probing Exudation Color Contour Size Consistency Stippling Position Bleeding on probing Exudation Occlusal Analysis: Gingival Status Lip seal: Halitosis: Buccal/labial mucosa: Palate: Floor the mouth: Lips: Vestibule: Tongue: Missing teeth: Carious teeth: Restored teeth: Loss of proximal contact: Crowding of teeth: Symmetry of face: TMJ: Tenderness: Clicking: Jaw deviation: nodes: Lymph Submental: Submandibular: Cervical: Type of brush: Type Methods: HorizontalCircularFrequency of brushing: Estimate of time spent: ] [ ] [ Vertical ] [ Soft Tissue: (Teeth): Hard Tissue Intraoral Extraoral Clinical Examination 2. Dental floss3. Toothpicks4. Interproximal brushes5. Mouthwashes6. [ ] Others specify [ ] ] [ ] [ [ ] 244

Investigations Other Investigations

Diagnosis Radiological Investigations (IOPA/OPG)

Horizontal bone loss: Prognosis Vertical bone loss: Individual: Furcation involvement: Good [ ]

Endodontic treatment/overhanging restorations: Fair [ ] PART IV Periapical pathology Poor [ ] Impacted/supernumerary/embedded teeth: Overall: Caries: Good [ ] Crown/root-ratio: Fair [ ] Poor [ ] Special Investigations

Biopsy: Bacterial smear:

Surgical Assessment Periodontal Pathology Periodontal CHAPTER 29 Diagnosis of Periodontal Diseases 245 BIBLIOGRAPHY Periodontol 1996;1:37-215. J Periodontol reivew. literature A of periodontal disease. 1984;55:684. 2nd management and occlusal and restorative interrelationshpis. edition, Lea and Febiger publication, 1977. 1992. Advances in Periodontics, QB Publishing Company, 1.Ann Armitage. Periodontal Diseases: Diagnosis. Gary C 2. in the diagnosis The role of bleeding upon probing Greenstein G. 3. phenomena, clinical Periodontal diseases, basic Saul Schluger. 4. Thomas G Wilson, Kenneth S Korman, Michael G Newman. Factors that can Influence the Accuracy of Probing the Accuracy of can Influence Factors that • probe qualities of a Physical • probing Angulation of the • Force applied during probing • status of the tissue Inflammatory • a reference point. Availability of KNOW MORE ... KNOW MORE It includes, measurement of probing depths, clinical It includes, measurement of probing trauma mobility, attachment loss, furcation involvement, migration (given in from occlusion and pathologic tooth detail in Chapter No. 9). Periodontal Examination Phase I therapy (Etiotropic phase) Phase I therapy (Etiotropic phase) Phase II therapy (Surgical phase) Phase III therapy (Restorative phase) Phase IV therapy (Maintenance Treatment Plan Treatment Phase Phase/Emergency Preliminary 30 ChapterChapter

Determination of Prognosis

 DEFINITION, DIFFERENCES BETWEEN • Systemic/Environmental Factors PROGNOSIS AND RISK • Local Factors  DETERMINATION OF A PROGNOSIS  RELATIONSHIP BETWEEN DIAGNOSIS AND  FACTORS FOR DETERMINATION OF PROGNOSIS PROGNOSIS  RE-EVALUATION OF PROGNOSIS AFTER • Overall Clinical Factors PHASE I THERAPY

DEFINITION OF PROGNOSIS There are certain situations where risk factors and prognostic factors are similar, for example, patients with It is a prediction of the probable course, duration and diabetes and smokers are more at risk for developing outcome of a disease based on a general knowledge of the periodontal diseases, and once they acquire it, they are pathogenesis of the disease and the presence of risk factors considered to have a poor prognosis. for the disease. It is established after the diagnosis is made and before the treatment plan is established. Prognosis is often confused DETERMINATION OF PROGNOSIS with the term risk. The differences between prognosis and It is based on the factors to be considered while determining risk are given in Table 30.1. the prognosis. Prognosis may be: i. Excellent prognosis: No bone loss, excellent gingival Table 30.1: Differences between prognosis and risk condition, good patient cooperation, no systemic/ Prognosis Risk environmental factors. i. It is the prediction of the i. Deals with the likelihood ii. Good prognosis: One or more of the following: adequate duration, course and the that an individual will termination of disease and get a disease in a remaining bone support, possibilities to control etiologic its response to treatment. specified period. factors and establish a maintainable dentition, adequate ii. Prognostic factors are ii. Risk factors are those patient co-operation, no systemic/ environmental factors characteristics that characteristics of an predict the outcome of individual that put or if present are well-controlled. disease once the them at increased risk iii. Fair prognosis: One or more of the following: less than disease is present. for getting a disease. adequate remaining bone support, some tooth mobility, CHAPTER 30 Determination of Prognosis 247 In two patients with comparable levels of

: i. Overall clinical factors. ii. Systemic/Environmental factors. iii. Local factors. iv. Prosthetic/restorative factors. Patient age remaining connective tissue attachment and alveolar bone, the prognosis is better in the older of the two. In younger patient, the prognosis is not as good because of the increased periodontal destruction in a shorter time frame. The cause may be aggressive type of periodontitis or the progression of disease may be increased due to systemic diseases or smoking. to assess the tissue response to scaling, oral hygiene and to assess the tissue response to scaling, agents root planing and also the use of chemotherapeutic where indicated. Factors for Determination of Prognosis (Fig. 30.1) Overall Clinical Factors a. Factors for determination of prognosis Fig. 30.1: One or more of the following: : One or more of the following: : One or more of the following: moderate : advanced bone loss, non-maintainable areas, extraction indicated, presence of uncontrolled systemic/ environmental factors. It is advisable to establish a provisional prognosis to advanced bone loss, tooth mobility, grade I and II to advanced bone loss, tooth mobility, co-operation, furcation involvements, doubtful patient of systemic/ difficult to maintain areas, presence environmental factors. Questionable prognosis advanced bone loss, grade II and III furcation involve- inaccessible areas, systemic/ ments, tooth mobility, environmental factors. Hopeless prognosis grade I furcation involvement, adequate maintenance, grade I furcation involvement, adequate of limited acceptable patient co-operation, presence systemic/environmental factors. Poor prognosis until phase I therapy is completed and evaluated. The provisional prognosis allows initiating treatment of teeth having a doubtful outlook. The re-evaluation phase allows v. vi. iv. 248

b. Disease severity: It is determined by recording the No heroic attempts should be made to retain patient’s past history of periodontal disease; for this the hopelessly involved tooth because it may indirectly following variables should be carefully recorded: affect the health of adjacent teeth. i. Pocket depth. c. Plaque control: Plaque is the primary etiological factor ii. Level of attachment. for periodontal disease. Therefore, effective removal of iii. Degree of bone loss. plaque is important for the success of periodontal therapy iv Type of bony defect. and to the prognosis.

PART IV PART These can be determined by clinical and radiographic d. Patient compliance and co-operation: The prognosis for evaluation. patients with gingival and periodontal disease is i. Pocket depth: This is not necessarily related to bone dependent on patient’s attitude; desire to retain the loss. A tooth with deep pockets and little attachment natural teeth, willingness and ability to maintain good and bone loss has a better prognosis than one with oral hygiene. If the patient is unwilling or unable to shallow pockets and severe attachment and bone perform adequate plaque control and receive periodic loss. maintenance checkups, the treatments to be considered ii. Level of attachment: Reveals the approximate extent are: of root surface that is devoid of periodontal 1. Refuse to accept the patient for treatment. ligament; the radiographic examination reveals the 2. Extract teeth that have a hopeless or poor prognosis amount of root surface still invested in bone. and perform scaling and root planing on the

Periodontal Pathology Periodontal Prognosis is adversely affected if the base of the remaining teeth. pocket is close to the root apex. The presence of apical disease as a result of endodontic involvement Systemic/Environmental Factors also worsens the prognosis. a. Smoking: It is the most important environmental risk iii. Degree of bone loss: The prognosis can also be factor affecting the development and progression of related to the height of the remaining bone. The periodontal disease. There is a direct relationship height of the remaining bone is usually somewhere between smoking and the prevalence and incidence of in between making bone level assessment alone periodontitis. It even affects the healing potential of the insufficient for determining the overall prognosis. periodontal tissues. Therefore, the prognosis in patients iv. Type of bony defect: The prognosis for horizontal who smoke and have slight to moderate periodontitis is bone loss depends upon the height of the existing generally fair to poor. But with the cessation of smoking, bone. The prognosis for angular, intrabony defects the prognosis may be upgraded from fair to good in case depends upon the contour of the existing bone and of slight to moderate periodontitis and poor to fair in the number of osseous walls. The chance to regenerate bone in vertical bony defect is excellent case of severe periodontitis. as compared to horizontal bony defects. b. Systemic disease/condition: Studies have shown that When greater bone loss has occurred on one patients with type I and type II diabetes have increased surface of a tooth, the bone height on the less severity of periodontitis than in those without diabetes. involved surfaces should be considered when Prognosis in these cases is dependent on patient determining the prognosis. Because greater the compliance relative to both their medical and dental height of bone in relation to other surfaces, the status well-controlled diabetics. center of rotation of the tooth will be nearer the In patients with uncontrolled diabetes, the prognosis crown which results in favorable distribution of is questionable when surgical periodontal treatment is forces to the periodontium and less tooth mobility. required. In well-controlled diabetic patients with mild CHAPTER 30 Determination of Prognosis 249 : Anatomic factors that : Contribute to increased plaque : Contribute prognosis is dependent on the ability of the patient and ability of the patient is dependent on the prognosis etiologic factors. to remove these the clinician restorations Subgingival inflammation and increased bone accumulation, increased can have negative impact on the loss. Overhangs amount of destruction is mainly periodontium. The size of these discrepancies and the dependent upon the have been present. In general, a tooth amount of time they has a poorer its subgingival margins with a discrepancy in with well-contoured, supragingival prognosis than a tooth margins. Anatomic variations/factors include short, predispose the periodontium to disease crowns, cervical enamel tapered roots with large intermediate projections (CEP) and enamel pearls, developmental bifurcation ridges, root concavities and furcation involvement and tooth grooves, root proximity, mobility. Prognosis is poor for teeth with short, tapered roots disproportionate and relatively large crowns because of surface area crown to root ratio and reduced root The periodontium may available for periodontal support. be injured by occlusal forces. flat, ectopic Cervical enamel projections (CEP) are the normal extensions of enamel that extend beyond They may also contours of the cemento-enamel junction. found on buccal extend into furcations, most likely Enamel pearls are surfaces of maxillary second molars. found in round deposits of enamel that can be larger, furcations or other areas of root surface. They are less the presence of these enamel pearls frequent than CEP, on the root surface interferes with the attachment apparatus and may prevent regenerative procedures from Therefore, it has a achieving their maximum potential. negative effect on the prognosis of individual teeth. Scaling and root planing is a fundamental procedure Anatomic factors that decrease in periodontal therapy. a negative impact of this procedure have the efficiency on prognosis. Root concavities exposed through loss of attachment can vary from shallow flutings to deep depressions. These concavities increase the attachment b. c. Genetic polymorphisms in the inter- Genetic polymorphisms : It is the most important local factor in antibody titers and the expression of antibody titers and the expression 2 , have been associated with a significant β : Physical and emotional stress as well as substance RII receptors on the neutrophil, both of which may RII receptors on the neutrophil, both γ Fc Other genetic be significant in aggressive periodontitis. deficiency type I disorders such as leukocyte adhesion an additional can influence neutrophil function, creating risk factor for aggressive periodontitis. Detection of genetic variations that are linked with the prognosis periodontal disease can potentially influence of patients at risk in several ways. First, early detection implementation due to genetic factors, can lead to early Second, of preventive and treatment measures. the course of identification of genetic risk factors during such treatment can influence treatment recommendations Finally, therapy. as the use of adjunctive antibiotic identification of young individuals who are identified as being at risk because of the familial aggregation seen in aggressive periodontitis can lead to the development of early intervention strategies. Early diagnosis, intervention and/or alterations in the treatment regimen may lead to an improved prognosis for the patient. Stress abuse alter the patients ability to respond to periodontal treatment. leukin–1 (IL-1) genes, resulting in increased production leukin–1 (IL-1) genes, in IL1– chronic increase in risk for severe, generalized, to influence periodontitis. Genetic factors also appear serum IgG to moderate periodontitis, who comply well to who comply periodontitis, to moderate have well and hence instructions, respond recommended with incapacitating patients Similarly, good prognosis. systemic disorders can affect the conditions and other hence correction of systemicprogression of disease, the prognosis. Newer automated problem may improve like electric tooth brushes may help oral hygiene devices oral disease to maintain patients with Parkinson’s improve their prognosis. hygiene and thereby Genetic factors: Plaque/calculus periodontal diseases. In most cases, having a good d. c. Local Factors a. 250

area and produce a root shape that may be more resistant jeopardises the stability of teeth and adversely affects the to torquing forces, and also create areas that can be response to periodontal treatment. The periodontal prognosis difficult for dentist and patients to clean. of treated non-vital teeth is not different from that of vital Other anatomic factors that present accessibility teeth. New attachment can occur to cementum of both non- problems include developmental grooves, root proximity vital and vital teeth. and furcation involvements. The presence of any of these can worsen the prognosis. The developmental grooves, OVERALL VERSUS INDIVIDUAL

PART IV PART which initiates on enamel can extend to a significant TOOTH PROGNOSIS distance on the root surface. It provides plaque-retentive Prognosis can be divided into overall and individual tooth areas that are difficult to clean by the instrument. Root prognosis. proximity results in interproximal areas that are difficult for the clinician and patient to access. Furcation areas Overall Prognosis are also difficult to access. d. Tooth mobility: The principal causes are loss of alveolar It is determined for the whole dentition and it addresses bone, inflammatory changes in the periodontal ligament some important questions such as— and trauma from occlusion. Tooth mobility caused by • Should treatment be undertaken? inflammation and trauma from occlusion may be • Is treatment likely to succeed? correctable but tooth mobility caused by loss of alveolar • When prosthetic replacement is needed, are the bone is not likely to be corrected. The stabilization of Periodontal Pathology Periodontal remaining teeth able to support the added burden of the tooth mobility through the use of splinting may have a prosthesis? beneficial impact on the overall and individual tooth Factors influencing the overall prognosis are: prognosis. • Patient’s age Prosthetic/Restorative Factors • Current severity of disease • Systemic factors The overall prognosis requires general consideration of bone • The presence of plaque, calculus and other local factors levels and attachment levels to establish whether teeth can • Patient compliance be saved for functional and aesthetic purposes or to serve • Smoking as abutments for prosthesis. When few teeth remain, the • Prosthetic possibilities. prosthodontic need become more important and sometimes periodontally treatable teeth may have to be extracted if Individual Tooth Prognosis they are not compatible with the design of the prosthesis. Teeth that serve as abutments are subjected to increased It is determined for a single tooth and it is determined after functional demands. A tooth that has undergone endodontic the overall prognosis. Individual tooth prognosis is affected treatment post is more likely to fracture when serving as a by overall prognosis. For example, in a patient with a poor distal abutment supporting a distal removable partial overall prognosis, the dentist likely would not attempt to denture. Special oral hygiene measures should be instituted retain a tooth that has a questionable prognosis because of in these areas. local conditions. Caries, non-vital teeth and root resorption: Teeth with extensive caries should be adequately restored and Factors Influencing the Individual Tooth Prognosis endodontic therapy should be considered before undertaking • Plaque and calculus periodontal treatment. Extensive idiopathic root resorption • Subgingival restorations or root resorption as a result of orthodontic therapy, CHAPTER 30 Determination of Prognosis 251 : Most of the linked to manage- Prognosis : Drug-influenced gingival enlargement is gingival : Drug-influenced like lichen planus, pemphi-goid, pemphigus vulgaris, of the associated ment erythema multiforme, lupus erythematosis. dermatologic conditions. body reactions, Mechanical and thermal trauma. Condition Plaque-induced gingival diseases modified by diseases modified gingival Plaque-induced medications and nifedipine with phenytoin, cyclosporin, often seen gingivitis. Plaque control oral contraceptive-associated the development of the lesions alone does not prevent correct intervention is usually necessary to and surgical of the Continued use contour. the alterations in gingival of the enlargement even drug causes recurrences intervention. Therefore, prognosis is following surgical problem systemic the patient’s dependent on whether an alternative medication. In oral can be treated with gingivitis, frank signs of contraceptive associated the presence of gingival inflammation can be seen in these patients is relatively little plaque. Prognosis in dental plaque, but dependent not only on the control of use of the oral also on the likelihood of continued contraceptive. Gingival diseases modified by malnutrition importance of clinical studies have disproved the Prognosis malnutrition in developing gingival disease. the severity and in these cases may be dependent on of reversing duration of deficiency and on the likelihood the deficiency through dietary supplementation. i. Dermatological disorders is It ii. Allergic, toxic and foreign Table 30.2: Distinction between condition and prognosis Table Nonplaque-induced Gingival Lesion variety of bacterial, It can be seen in patients with a is dependent fungal and viral infections. Prognosis agent. on elimination of the source of infectious with Periodontitis Prognosis for Patients 30.3. See Table • • : The : The systemic factors which influence the The : inflammatory response to bacterial plaque include endocrine related changes associated with puberty, menstruation, pregnancy and diabetes and the presence of blood dyscrasias, prognosis for these patients depends on not only control of bacterial plaque but also on control or correction of the systemic factors. Gingivitis associated with dental plaque only Gingivitis associated with dental plaque with only prognosis for patients with gingivitis associated dental plaque is good, provided all local irritants are eliminated, i.e. other local factors contributing to plaque retention are eliminated, gingival contours conducive for the preservation of health are attained and the patient co- operates by maintaining good oral hygiene. Plaque-induced gingival diseases modified by systemic factors — tapered roots Short, — projections Cervical enamel — Enamel pearls —ridges Bifurcation — Root concavities — Developmental grooves — Root proximity — Furcation involvement. — Abutment selection — Caries — Non-vital teeth — Root resorption RELATIONSHIP BETWEEN DIAGNOSIS RELATIONSHIP AND PROGNOSIS Dental Plaque-induced Gingival Disease Plaque-induced Dental • • Prognosis for Patients with Gingival Disease with Prognosis for Patients Factors such as patient’s age, severity of disease, genetic age, Factors such as patient’s disease are all susceptibility and presence of systemic the condition. These important criteria in the diagnosis of 30.2). (Table are also important in developing a prognosis • and restorative factors Prosthetic • Mobility • Anatomic factors 252

Table 30.3: Distinction between chronic and aggressive periodontitis

Chronic periodontitis Aggressive periodontitis i. Slowly progressive disease associated with i. Rapidly progressive disease with minimal/no local factors local environmental factors. with increased level of Aa and P gingivalis. ii. Can be localized or generalized. ii. Can be localized or generalized. iii. In case of not advanced attachment loss, iii. Two common features are observed. prognosis is generally good. But inflammation a. Rapid attachment loss and bone destruction in an has to be controlled through good oral hygiene otherwise clinically healthy person.

and removal of local plaque-retentive factors. b. A familial aggregation. PART IV PART iv. In cases of severe disease with furcations iv. Localized type, which occurs around the age of puberty and involvement and increasing clinical mobility/ is localized to first molars and incisors, if diagnosed early can who are non-compliant with oral hygiene, be treated conservatively with oral hygiene instructions and prognosis is down graded from fair to poor. systemic antibiotic therapy. Resulting in excellent prognosis. In advanced cases, the prognosis is still good if the lesions are treated with debridement, local and systemic antibiotics and regenerative therapy. v. In generalized type, also seen in young patients with generalized interproximal attachment loss and poor antibody response. Secondarily aggravated by cigarette smoking does not respond well to conventional periodontal therapy, therefore prognosis is often fair, poor or questionable and the use of

systemic antibiotics should be considered. Periodontal Pathology Periodontal

Periodontitis as a Manifestation of Systemic Disease control of both the bacterial plaque and the secondary It can be divided into two categories: factors, the prognosis is good. i. Associated with hematological disorders such as In necrotizing ulcerative periodontitis cases the leukemia and acquired neutropenias. treatment is not only reducing local and secondary factors ii. Associated with genetic disorders such as familial and but also in dealing with the systemic problem. Prognosis cyclic neutropenia, Down syndrome, hypophos- depends on management of disease. phatasia, Papillon-Lefévre syndrome. In both these cases, prognosis may be fair to poor RE-EVALUATION OF PROGNOSIS and is mainly dependent on the treatment of systemic AFTER PHASE I THERAPY disease. A frank reduction in pocket depth and inflammation after Necrotizing Periodontal Disease phase I therapy indicates favourable response to treatment Necrotizing periodontal disease can be divided into necrotic and is suggestive of a better prognosis and in vice versa diseases that affect the gingival tissues [NUG] and necrotic cases the overall prognosis may be unfavourable. diseases that affect deeper tissues of the periodontium, resulting in loss of connective tissue attachment and alveolar bone [NUP]. In these [NUG] cases, the predisposing factor 1. Prognosis is defined as the prediction of the probable is bacterial plaque. The disease is further complicated by course, duration and outcome of a disease based on a general knowledge of the pathogenesis of the both presence of secondary factors such as acute psycho- disease and the presence of risk factors for the disease. logical stress, tobacco smoking and poor nutrition, all of 2. Prognosis is established after the diagnosis and before which can contribute to immunosuppression. With the the treatment plan. CHAPTER 30 Determination of Prognosis 253 BIBLIOGRAPHY publication, 1988. in Publication Data, 1995. British Library Cataloguing periodontal patients under maintenance survey of two related care. J Periodontol 1991;62:51. parameters in accurately predicting The effectiveness of clinical 1996;67:666. tooth survival. J Periodontol IL-1 genotype in The effectiveness of clinical parameters and tooth survival. accurately predicting prognosis and J Periodontol 1999;70:49-56. 9th edn, 2002, WB Saunders Co. 1. 6th edn. Mosby Stern. Listgarten Periodontics. Grant, 2. of Periodontics. 3rd edn, Manson JD and Eley BM. Outline 3. outcome: a long term McGuire MK. Prognosis versus actual 4. actual outcome III. McGuire MK, Nunn ME. Prognosis versus 5. outcome IV. MK, Nunn ME. Prognosis versus actual McGuire 6. Periodontology. Carranza. Clinical A Fermin Newman Takei, severity, systemic restorative and environmental severity, compliance and patient factors and local factors, prosthetic possibilities. restorations, caries, non- plaque/calculus, subgingival teeth and root resorption. vital REVIEW QUESTIONS able, and hopeless. able, and tooth prognosis. individual prognosis are: a. disease like age of the patient, Overall clinical factors b. individual tooth prognosis are– Factors influencing overall prognosis. prognosis. 3. question- poor, excellent, good, fair, Prognosis may be 4.and prognosis can be divided into, overall Prognosis 5. considered while determining the Factors that are to be 2. Describe the factors to be considered for determining 1. Define prognosis and describe the factors influencing 31 ChapterChapter

Related Risk Factors Associated with Periodontal Diseases

 DEFINITION  CLINICAL RISK ASSESSMENT  RISK FACTORS • Demographic Data  RISK DETERMINANTS/BACKGROUND • Medical History CHARACTERISTICS • Dental History  RISK INDICATORS • Clinical Examination  RISK MARKERS/PREDICTORS

DEFINITION 2. Diabetes: Diabetes is a risk factor for periodontitis. Prevalence and severity is higher in diabetes than in those Risk is the probability that an individual will develop a without diabetes. specific disease in a given period which may vary from one 3. Pathogenic bacteria and microbial tooth deposits: individual to another. Risk assessment involves identifying • Quantity of plaque present on teeth is not of major elements that either may predispose a patient to developing importance. Composition or quality of the plaque periodontal disease or may influence progression of disease biofilm is of importance. that already exists. • In terms of plaque, three specific bacteria have been identified as etiologic agents: RISK FACTORS FOR PERIODONTAL DISEASE a. Actinobacillus actinomycetemcomitans Risk factors may be environmental, behavioral or biologic b. Porphyromonas gingivalis factors that, when present, increases the likelihood that an c. Bacteroides forsythus individual will develop the disease. Following are the risk 4. Anatomic factors: Such as furcations, root concavities, factors: developmental grooves, cervical enamel projections, 1. Tobacco smoking: A direct relationship exists between enamel pearls and bifurcation ridges. All predispose to smoking and prevalence of periodontal disease. Smoking periodontitis, as they harbor bacterial plaque and present has a negative impact on response to therapy. a challenge to clinician during instrumentation. 255

Presence of calculus: It serves as a reservoir for bacterial • There is an apparent link between psychosocial plaque. factors and risk behavior such as smoking, poor oral hygiene and chronic periodontitis. RISK DETERMINANTS/BACKGROUND • Individuals with financial strain, distress, depression HPE 31 CHAPTER CHARACTERISTICS FOR PERIODONTAL and inadequate coping mechanisms have more loss DISEASE of attachment.

It is defined as those risk factors that cannot be modified. RISK INDICATORS FOR 1. Genetic factors: Genetic factors influence clinical PERIODONTAL DISEASE measures of gingivitis probing pocket depth, attachment loss and interproximal bone height. Risk indicators are probable or putative risk factors that have

• A specific interleukin-1 (IL-1) genotype has been been identified in cross-sectional studies but have not been Related Risk Factors Associated with Periodontal Diseases Periodontal with Associated Factors Risk Related associated with severe chronic periodontitis. confirmed through longitudinal studies. • Immunologic alterations such as neutrophil Following are the risk indicators: abnormalities are under genetic control. 1. HIV/acquired immunodeficiency syndrome: It has been • Genetics plays a role in regulating the titre of hypothesized that immune dysfunction associated with

protective IgG2 antibody response to A. actinomy- high HIV infection and AIDS increases the susceptibility cetemcomitans in patients with aggressive to periodontal disease, though the evidence is not periodontitis. conclusive. 2. Age: 2. Osteoporosis: Osteoporosis does not by itself initiate • Both the prevalence and severity of periodontal periodontitis, there is reduced bone mass in osteoporosis, disease increases with age. this may enhance the progression of periodontal disease. • Attachment loss and bone loss seen in elderly 3. Infrequent dental visits: Some studies have shown individuals is a result of prolonged exposure to other increased risk for severe periodontitis in patients who risk factors over a longer period of time. have not visited dentist for 3 or more years (although • Changes related to old age such as intake of age factor also plays a role). medications, decreased immune functions and altered nutritional status may increase susceptibility RISK MARKERS/PREDICTORS to periodontitis. These are associated with increased risk for disease, but do 3. Gender: not cause the disease. These factors also are identified in • Males have more attachment loss than females and cross-sectional and longitudinal studies. A risk factor that have a poorer oral hygiene, therefore more males can be used to predict the future course of disease, is known are prone to periodontal diseases. as a risk marker. 4. Socioeconomic status: 1. Previous history of periodontal disease. • Poor oral health is seen in lower socioeconomic 2. Bleeding on probing: Bleeding on probing along with status. This can be attributed to: increased pocket depth may serve as an excellent 1. Decreased dental awareness. predictor for future loss of attachment. 2. Decreased dental visits. 5. Stress: Incidence of ANUG increases during stressful CLINICAL RISK ASSESSMENT FOR situations. PERIODONTAL DISEASE • Emotional stress may interfere with normal immune function. It is done by careful evaluation of the following: 256

Demographic Data

Age 1. Risk factors may be environmental, behavioral or biologic in nature that when present increases the • Duration of exposure to the risk elements likelihood of a disease, e.g. smoking, diabetes, presence • Postmenopausal women of pathogenic bacteria. • Evidence of aggressive disease 2. Risk determinants are those risk factors that cannot be modified, e.g. age, gender, socioeconomic status, stress. 3. Risk indicators are probable or putative risk factors that Gender have been identified in cross-sectional studies but not confirmed through longitudinal studies, e.g. AIDS,

• Males osteoporosis, infrequent dental visits. PART IV • Frequency of care and preventive practices 4. A risk factor that can be used to predict the future course of disease, is known a risk marker, e.g. previous history of periodontitis, bleeding on probing. Socioeconomic Status 5. In conclusion, risk assessment may have a role at two levels, one involving identification of factors that may • Dental awareness predispose to developing periodontal disease, secondly, • Frequency of care may influence the progression of already existing disease.

Medical History The following conditions either predispose or make the patient more susceptible to periodontitis. KNOW MORE ... • Diabetes Periodontal Pathology Periodontal • Tobacco smoking Hill’s Criteria In order to confirm a risk factor as a part of the casual • HIV/AIDS chain, Hill’s criteria are usually quoted: • Osteoporosis • Strength of association between factor and disease. • Stress • Consistency of association in different populations. • Temporal sequence: A factor must precede outbreak of the disease (principle of cause and effect). Dental History • Specificity of association. • Dose-response effect. • Genetic predisposition to aggressive disease. • Biological plausibility. • Previous history of periodontal disease. • Experimental evidence. • Frequency of dental care.

REVIEW QUESTIONS Clinical Examination 1. Define risk, risk factors, risk indicators, risk markers • Plaque accumulation and risk determinants. • Calculus 2. Enumerate various risk factors for periodontal disease. • Bleeding on probing • Extent of loss of attachment BIBLIOGRAPHY • Tooth examination - Plaque retentive areas 1. Blieden TM. Tooth related issues. Ann Periodontol 1999;4: 91-6. - Anatomic factors 2. Carranza, Newman, Takei. Clinical Periodontology, 9th edn, WB • Restorative factors Saunders Co, 2002. • Once a risk patient is identified and a diagnosis is made, 3. Genco Robert J. Current view of risk factors for periodontal treatment plan may be modified accordingly. diseases. J Periodontol 1996;67:935-45. 32 ChapterChapter

Various Aids including Advanced Diagnostic Techniques

 AIDS USED IN CLINICAL DIAGNOSIS  AIDS IN IMMUNOLOGICAL DIAGNOSIS • Periodontal Probes • Immunofluorescence • Conventional Probes • Latex Agglutination • ELISA • PSR • Flow Cytometry  AIDS USED IN RADIOGRAPHIC DIAGNOSIS  BIOCHEMICAL DIAGNOSIS • Orthopantomograph • Prostaglandins • Xeroradiography • Collagenase • Advanced Radiographic Techniques  OTHER DIAGNOSTIC AIDS  AIDS IN MICROBIOLOGICAL DIAGNOSIS • BANA Test • Identification of Bacteria • FSEIA • Speciation Techniques • PCR

AIDS USED IN CLINICAL DIAGNOSIS Periodontal Probes

a. Millimeter probe for gingival bleeding. Uses of Probes b. Measurement of gingival crevicular fluid flow with the help of a filter paper. Newer method is by use of a 1. Periodontal probes are used to measure the pocket depth. periotron 6000. 2. Quantification of bacterial plaque and gingival c. Measurement of temperature by pressure-sensitive inflammation. probes. PeriotempTM probe (AbiodentTM). 3. Determination of mucogingival relationship. d. Mouth odors—olfactometer. 4. Measurement of gingival recession. e. Tooth mobility—mobilometer/periodontometer. 5. Location of calculus. f. PSR (Periodontal screening and recording). 6. Identification of tooth irregularities. 258

7. Identification of tissue characteristics. Third generation probes are the computerized probes. Gibbs 8. Determination of bleeding tendency. et al designed Florida probe. Other examples are—Foster 9. Evaluation of bone support in the furcation areas of Miller probe, Toronto automated probes, which can detect bifurcated and trifurcated teeth. the cementoenamel junction.

Types of Conventional Periodontal Probes (Fig. 32.1) Limitations of Conventional Probes

1. Marquis color coded probe: Calibrations are in 3 mm 1. Probing depth obtained with periodontal probe does not sections. coincide with the histological pocket depth, because the

PART IV 2. The University of North Carolina-15 probe (UNC-15): probe normally penetrates the coronal level of the 15 mm long and markings are at 1 mm and color coding junctional epithelium. at the 5th, 10th and 15 mm. 2. Another limitation is related to the reproducibility, which 3. The University of Michigan O probe with Williams has been correlated with the variation in the probing force. markings (at 1, 2, 3, 5, 7, 8, 9) 4 and 6 missing. Other factors that are likely to influence clinical 4. The Michigan ‘O’ probe with markings at 3, 6, and 8 measurement of attachment level include intra and inter- mm. examiner reliability, patient discomfort, accuracy of probe 5. The WHO probe, which has a 0.5 mm ball at the tip and markings and anatomical variations in tooth contours or millimeter markings at 3.5, 8.5 and 11.5 mm and color position. coding from 3.5 to 5.5 mm. 6. Furcation areas can best be evaluated with the curved, Limitations of all Automated Controlled

Periodontal Pathology Periodontal blunt Naber's probe. Force Probes Periodontal probes may be divided into: 1. Reduced tactile sense of the operator. First generation probes are conventional, hand held probes, 2. Increased patient discomfort. e.g. conventional periodontal probes. 3. Presence or absence of inflammation often produced Second generation probes are the pressure-sensitive probes. inaccurate measurement. It has been shown that, with forces up to 30 grams, the probe tip remains within junctional epithelium and forces up to Periodontal Screening and Recording (PSR) 50 grams are necessary to diagnose osseous defects. This It is designed for easier and faster screening and recording probe did solve many of the problems of the conventional of the periodontal status of a patient or a group of population. probes, but lacked tactile sensitivity. It uses a specially designed probe that has a 0.5 mm ball tip and is color-coded from 3.5 to 5.5 mm. The patient's mouth is divided into six sextants— maxillary right quadrant, left quadrant and anteriors, mandibular left and right quadrants and anteriors, and at least six points around each tooth is examined. The deepest finding is recorded in each sextant, according to the following code. Code 0: In the deepest sulcus of the sextant, the probes colored band remains completely visible, gingival tissue is healthy and does not bleed on gentle probing. No calculus or defective margins are found. These patients require only Fig. 32.1: Florida probe appropriate preventive care. 259

Code 1: The colored band remains completely visible in 1. Thirty to sixty percent of the mineral content of the bone the deepest sulcus of the sextant. No calculus or defective must be lost to visualize the change in the radiographic margins are found but some bleeding after gentle probing image, hence though very specific, lacks sensitivity. is found. Treatment for these patients include subgingival 2. Actual damage is more extensive than radiographs. HPE 32 CHAPTER plaque removal and appropriate oral hygiene instructions. 3. Radiographs are a two-dimensional representation of a three-dimensional anatomy. Code 2: The probe's colored band is still completely visible, Techniques are available to minimize this source of but there is bleeding on probing. Supragingival or distortion. First a long cone should be used (because parallel subgingival calculus and/or defective margins are found. rays will minimize distortion). Treatment includes plaque and calculus removal, correction Secondly, the use of parallel positioning devices helps of plaque retentive margins of restorations and oral hygiene to standardize the relationship between film, object and instructions.

X-ray source, e.g. RINN XPR. Techniques Diagnostic Advanced including Aids Various Code 3: The colored band is partially-submerged. This Disadvantage: Only a limited view of the osseous crest is indicates the need for a comprehensive periodontal available. Hence the use of extended cone projection examination and charting of the affected sextant to instruments is recommended. determine the necessary treatment plan. If two or more Bite-wing: It is an often forgotten radiograph in periodontal sextants score code 3, a comprehensive full mouth diagnosis. On a bite-wing radiograph we can visualize both examination and charting is indicated. maxillary and mandibular teeth along with the interdental Code 4: The colored band completely disappears in the alveolar bone. Thus, it can provide us with the vital pocket, indicating a depth greater than 5.5 millimeters. In information regarding the presence of local irritating factors, this case, a comprehensive full-mouth periodontal e.g. calculus. examination, charting and treatment planning are needed. Code*: When any of the abnormalities are seen, an asterisk Orthopantamograph (OPG) (*) is entered, in addition to the code number, (for example, When compared with IOPA radiograph, they have a furcation involvement, tooth mobility, mucogingival tendency to underestimate minor bone changes. The major problem or gingival recession extending to the colored band disadvantages of OPG are magnification, unsharpen and of the probe). distortion. However, the clarity of panoramic image obtained from digital machines are superior to analogue machines. AIDS USED IN RADIOGRAPHIC DIAGNOSIS Xeroradiography Radiographs are used to obtain a visual image of the bone support around a tooth or dental implant. The radiographic It does not involve wet chemical processing or the use of a image is the result of X-ray beam passing through the area dark room. Instead of X-ray film, xeroradiography uses a of interest and exposing the silver halide emulsion on the uniformly charged selenium plate held in a light tight radiographic film. cassette. Exposure to X-ray and adequate processing produces a real image on opaque paper, which is viewed by The most commonly used radiographs in periodontal reflected light. diagnosis are transmission radiographs. Transmission radiographs, including periapical and bite-wing films are Advantages: Less expensive, edge enhancement. used to detect the amount of bone loss in any type of Advanced Radiographic Techniques periodontitis. They should be used with less exposure to avoid any cervical burnout effect. Techniques have been developed to enhance the ability to Though there are many advantages of radiographs there "see" small changes over a period of time in the bone. They is also equal number of disadvantages: are: 260

Iodine-125 Absorptiometry two X-rays. A video camera measures the light transmitted through a radiograph and the signals from the camera are A nonradiographic method to analyze the periodontal bone converted into gray levels. The images can be stored in mass changes. It is based on the absorption by bone of a the computer. low energy gamma beam, originating from a radioactive source of 125-1. This method has shown to measure bone Computerized Tomography changes with a high degree of accuracy and precision. Disadvantage: Technical considerations limit the use of this Unlike conventional radiography, which is a two- system on posterior sites. To overcome this, photo- dimensional representation of a three-dimensional object.

PART IV densitometric analysis has been developed. Computed tomography gives an exact picture of the bone levels in coronal, axial and sagittal plane by which all the Photodensitometric Analysis osseous defects can be visualized accurately.

A beam of light is passed onto the radiographic film and Nuclear Medicine Bone Scan the image is shown on an aluminium scale and then it transforms the density readings into millimeter of aluminium This involves the detection of changes in bone metabolism— equivalents. It is mainly developed to evaluate bone hence can detect the earliest stage of bone loss. A bone resorption especially in furcation areas. This technique seeking radiopharmaceutical diphosphonate compound is mainly enables the clinician to detect the variations in the injected intravenously and after a waiting period, the uptake bone density that cannot be detected by visual inspection. by the bone is measured by the semiconductor probe

radiation detector. This technique has the ability to detect Periodontal Pathology Periodontal Digital Radiography bone changes before structural alterations occur. This is useful in detecting small changes in hard tissues AIDS IN MICROBIOLOGICAL DIAGNOSIS that occur between examinations. The purpose of digital subtraction radiography is to remove all unchanging It is based on the concept of bacterial specificity. These structures from a set of two films and to display only the microbiological tests may have the potential not only to area of changes in periodontal defects. diagnose various forms of periodontal diseases but also to determine the sites which are at a higher risk of undergoing Substraction Radiography active destruction. Two radiographs are taken and the changes are noted Predictive treatment model: It is a combination of clinical depending on their gray levels. and microbiological parameters to predictably recommend specific therapy. Digital Substraction Radiography Microbiology and Disease Progression Digitization is done before subtraction, i.e. serial radiographs are converted into digital images. These images Because bacteria are the causative agents in periodontal are superimposed and are used on a video screen. Light diseases it makes sense to look for specific bacteria as areas indicate bone gain and dark areas indicate bone loss. indicators of disease activity.

Computer Assisted Densitometric Identification of Bacteria Image Analysis (CADIA) 1. Direct examination—microscopy In this technique, parallelization errors can also be • Light corrected and values of difference are shown between • Dark field 261

2. Culture and sensitivity assay i. Culture techniques • Aerobic • Anaerobic HPE 32 CHAPTER ii. Speciation techniques • GLC (Gas liquid chromatography) • DNA homology Direct microscopy: Specimens are viewed directly under the light. They are of two types: a. Light microscopy: Under this stained or unstained specimens can be read. Fig. 32.2: Microbial sampling method Techniques Diagnostic Advanced including Aids Various Gram's staining: Differentiates Gram-positive and Gram-negative organisms. Gram-positive appears violet. Gram-negative appears pink under the microscope. This • Paper points may be important because it differentiates between • Irrigation health and disease. • Surgical excision b. Dark field and phase contrast microscopy: Fresh, For the identification of anaerobes from the clinical unstained samples are examined. It uses a special material, many artificial media and culture techniques are condenser in which the light rays are either reflected or available. refracted off bacterial cell surface. So the outline of the Different Kinds of Media bacterium is dark against the light background in phase contrast microscopy and light against a dark background Supportive media: Only allows growth of non-fastidious in dark-field microscopy. organisms. Advantages of direct microscopy: It is quick, easy and Enriched media: Encourages the growth of organisms. inexpensive means of screening a microbial sample for Nonselective media: Permits the growth of most oral micro- major morphotypes. organisms without specific inhibitory agents. Disadvantages Selective media: Contains dyes, antibiotics that are • Inability to identify species. inhibitory to all organisms except those being sought. • Specimens have to be examined as soon as they are collected from the patients. Different Culture Techniques

Culture methods: These are used for cultivation and a. Jar technique: Removes air/oxygen within the jar and identification of organisms, then to determine its is replaced by oxygen-free gas containing 80 to 90 susceptibility or resistance to various antimicrobial agents. percent nitrogen, 5 to 10 percent hydrogen and 5 to 10 Types of specimens are: percent carbon dioxide. • Blood samples. b. PRAS: Pre-reduced anaerobically sterilized roll tubes • Mucosal surfaces. contain a medium which is boiled to remove the • Periodontal pockets. dissolved air and is then flushed with oxygen-free gas. Subgingival plaque sampling methods (Fig. 32.2) are: c. Anaerobic chamber techniques. • Nickel-plated curettes d. Enzyme reduction technique: It contains certain enzymes • Scalers which can sweep the oxygen out. 262

Speciation Techniques a. Gas Liquid Chromatography (GLC): In which various metabolic products of anaerobes are studied which are unique enough to serve as markers for identification. b. DNA probes in the identification of periodontal pathogens: It is based on the ability of DNA to hybridize or bind to the complementary strands of DNA having

the exact base sequence. PART IV Procedure: The plaque is first denatured to obtain single Fig. 32.3: Direct immunofluorescence strain bacterial DNA and then incubated on a membrane such as nitrocellulose. The specific labeled DNA probe is incubated on the membrane to allow hybridization and then washed off. The plaque sample contains complementary DNA; hybridization of the two single strains takes place, which can be visualized via the label of the probe.

METHODS/AIDS IN IMMUNOLOGICAL DIAGNOSIS

Immunofluorescence Periodontal Pathology Periodontal This method permits the identification of specific bacteria Fig. 32.4: Indirect immunofluorescence in bacterial smears. It not only identifies but also quantifies the percentage Antiserum: A serum that contains antibody or antibodies, it of the pathogens in the latex smear. may be obtained from an animal that has been immunized Others are: either by injecting the antigen into the body or by infecting • Enzyme-linked immunosorbent assay (ELISA). with microorganisms containing the antigen. • Flow cytometry. Direct Immunofluorescence (Fig. 32.3) Latex Agglutination (Fig. 32.5) Antiserum to a microorganism is conjugated to fluorescein. The conjugate is incubated on a clinical smear containing It is based on the binding of protein to latex. Latex beads the microorganisms and then washed off. The antigen are coated with species specific antibody and when these antibody reactions take place and organism is visualized by beads come in contact with the microbial cell surface, its fluorescent outline, when observed under a fluorescent antigens cross-linking occurs and its clumping/agglutination microscope, if the microorganism is not present, it appears is made visible within 2 to 5 minutes. dark with no fluorescence. Enzyme-linked Immunosorbent Indirect Immunofluorescence (Fig. 32.4) Assay (ELISA) (Fig. 32.6) It is a two step procedure. Antiserum to the microorganism In this, bacterial antigens are incubated in a well, on a plastic is incubated on the clinical smear and washed off, then a plate to allow coating by the material. After washing to conjugate of a fluorescent dye and an antiserum to the first remove the free antigen, the plates are ready for tests. antisera are incubated and then washed off. Samples containing suspected antibodies and controls are 263

BIOCHEMICAL DIAGNOSIS By-products of the cells (PMNLs), complement cleavage, e.g. C3, C4 in gingival crevicular fluid are studied. HPE 32 CHAPTER Prostaglandins

Levels of prostaglandin E2 are studied which can differentiate between gingivitis and periodontitis, e.g. aggressive forms showed higher levels than chronic Fig. 32.5: Principle of latex agglutination test periodontitis. Active sites exhibited five fold increase in

PGE2 levels than inactive sites.

PGE2 levels are studied by RIA (Radioisotope assay). Techniques Diagnostic Advanced including Aids Various

Collagenase

It showed positive correlation with disease activity. It is studied by sodium dodecylsulphate polyacrylamide gel electrophoresis (PAGE). In this they studied breakdown products resulting from incubation of collagen with gingival crevicular fluid.

OTHER DIAGNOSTIC AIDS Fig. 32.6: Principle of ELISA assay a. BANA test b. FSEIA then incubated in separate wells to allow antibodies bind the antigen on the surface of the wells. After washing to c. PCR (Polymerase chain reaction) remove unbound serum components, antisera to the antibody N-benzoyl-DL-arginine 2-naphthylamide is conjugated to either alkaline phosphatase or horseradish peroxidase then incubated in the wells. (BANA) A positive reaction is visualized by addition of a Can identify: chromogen which changes from a colorless to colored • B. forsythus Have a common trypsin-like solution. • P. gingivalis enzyme, which hydrolyzes • Treponema denticola the colorless substrate. Flow Cytometry • Capnocytophaga This is for rapid identification of oral bacteria. This involves N-benzoyl-DL-arginine-2-naphthylamide—when labeling bacterial cells from a patient plaque sample with hydrolysis takes place, it releases the chromophore beta- both species specific antibody and a second fluorescein naphthylamide, which turns orange-red when a drop of fast conjugated antibody. The suspension is then introduced into garnet is added to the solution. the flow cytometer, which separates the bacterial cells into an almost single cell suspension by means of a laminar flow Filter Separation Enzyme through a narrow tube. After incubation, the cells are passed Immunoassay (FSEIA) through a focussed laser beam. The cells then scatter the light at low and wide angles, and the fluorescent emission It can identify A. actinomycetemcomitans, P. intermedia, P. can be measured by appropriate detectors. gingivalis. 264

The clinician mixes the plaque sample taken with a paper point with this reagent to produce a colored reaction which 1. Probes are commonly used to detect and measure the may be positive or negative. It requires 10 to 15 min of the pockets. office time. 2. Periodontal probes can be divided into first generation, second generation and third generation probes. Polymerase Chain Reaction (PCR) 3. First generation probes are conventional probes which are calibrated with or without color coding. Whereas History second and third generation probes are pressure- sensitive, and also third generation probes can

Kary Mullis had just conceived a simple method of automatically detect the CEJ with computerized data PART IV producing virtually unlimited copies of a specific DNA capture. 4. Radiographs are used to obtain a visual image of the bone sequence in a test tube and introduced to the scientific support around the teeth or implants. The most commonly community at a conference in Oct, 1985. used radiographs are, intraoral periapical and bite wing X-rays. DNA Hybridization 5. Various advanced radiographic techniques include, photodensitometric analysis, digital radiography, The chemistry of PCR, as with much of molecular biology computerized tomography and nuclear medicine bone depends on the complementary's of DNA bases. scan. 6. Identification of bacteria can be done by direct examination using light microscopy, phase contrast and dark field Mechanism of Action of PCR microscopy. 7. Methods used in immunological diagnosis include, 1. The PCR is a test tube system for DNA replication that immunofluorescence, latex agglutination, ELISA and flow Periodontal Pathology Periodontal allows a "target" DNA sequence to be selectively cytometry. amplified, or enriched, several million fold in just a few hours. 2. It involves a series of enzyme-mediated reactions whose end result is a copy of the entire genome. KNOW MORE ... 3. PCR uses just one indispensable enzyme DNA Second Generation Probes polymerase to amplify a specific fraction of a genome. Some of the examples of second generation probes: 4. DNA acts as "Priming site" for the attachment of DNA • Pressure probe (Vander Volden) • Pressure sensitive probe (PSP) polymerase, two different primer sequences are used to • Borodontic probe bracket the target region to be amplified, one primer is • Hunton probe (disposable probe) complementary to one DNA strand at the beginning of • Yeaphe probe (to assess dentinal hypersensitivity). the target region and second primer is complementary Newer Generation Probes to a sequence on the opposite DNA strand at the target Watts in the year 2000 has added two more generations to it: region. • Generation IV and V Advantages Fourth generation probes These are three-dimensional probes, currently under a. It is a quick, reliable method for detecting all manner of development, these are aimed at sequential probe positions along the gingival sulcus. mutations associated with genetic diseases from Fifth generation probes insertions to deletions and to point mutations. This is the only noninvasive three-dimensional probe. b. Used for detection of tiny amounts of human immuno- These will have an ultrasound attached to the fourth deficiency virus and numerous genetic anomalies. generation probe. 265

Some of the commercially available kits for identification of bacteria and its products are:

Assay Kit Manufacturer/supplier Comments

Culture and biochemical Laboral Laboral, France Quantification/identification after bacterial 32 CHAPTER identification culture of A. a,B. f, C. r, F. n, P. i, P. g, P. m (GOLD STANDARD) Prognostic Dentsply Aids in detection of proteinase, elastase Immunological detection Evalusite test Kodak Eastman Detects bacterial antigens of A.a, P. i, (ELISA) company (Switzerland) P. g. can be used at chairside. Bacterial enzymes Perioscan Oral B laboratories Detects enzymatic activity of A.a, B.f, P.g BANA periodontal test OraTec Corporation Detects enzymatic activity of B. f, P. g, T. d Manassas (USA)

Bacterial toxins TOPAS Affinity Labeling Detects toxins derived from anaerobic Various Aids including Advanced Diagnostic Techniques Diagnostic Advanced including Aids Various Technologies (USA) metabolism and measures GCF protein level. Host enzymes Periocheck Collagenex Detects enzymatic activity derived from pharmaceuticals GCF (Matrix metalloproteinases and neutral protease enzymes) Nucleic acid technology Affirm DP Microprobe (USA) DNA probes for A. a, B. f, P. i, P. g, T. d BTD test BioTechnica DNA probes for A.a, C.r, E.c, F.n, P.i, P.g. OMTL test, Diagnostic (USA) DNA probes for B. f, P. g Omnigene USC (USA) Omnigene (USA) DNA probes for A. a, P.i, P. g, E. c, F. n, T. d, C. r, B.f A. a: Aggregatibacter actinomycetemcomitans, B. f: Bacteroides forsythus, C. r: Campylobacter rectus, E. c: Eikenella corrodens, P.m: Peptostreptococcus micros, P. g: Porphyromonas gingivalis, P. i: Prevotella intermedia, T. d: Treponema denticola.

BIBLIOGRAPHY 5. Jeffcoat MK. Radiographic methods for the detection of progressive alveolar bone loss. J Periodontol 1992;63:367. 1. Beck JD. Issues in assessment of diagnostic tests and risk for 6. Newman, Takei, Fermin A Carranza. Clinical periodontology, periodontal diseases. Periodontol 2000, 1995;7:100. 9th edn, WB Saunders and Co, 2002. 2. Bragger U, Pasquali L, Rylander H, et al. Computer assisted 7. Roy E Mintzer, John P Derdivanis. Automated periodontal densitometric image analysis in periodontal radiography. A probing and recording. Curr Opin Periodontol 1993;60-67. methodological study. J Clin Periodontol 1998;15;27. 8. Socransky SS, Haffajee AD, Cuginity, et al. Microbial complexes 3. Clark WB, Yang MCK, Magnusson I. Measuring clinical in subgingival plaque. J Clin Periodontol 1998; 25:134. attachment: Reproducibility and relative measurements with an 9. Thomas G Wilson Jr. The current status of determining electronic probe. J Periodontol 1992;63:831. periodontal prognosis. Curr Opin Periodontol 1993;67-74. 4. Jeffcoat MK. Diagnosing periodontal disease : New tool to solve 10. Thomas G Wilson, Kenneth S Kornman. Advances in old problems. J Am Dent Assoc 1991;122:54. Periodontics. Quintessence publishing Co, 1992. 33 ChapterChapter

Treatment Plan

 SEQUENCE OF THERAPEUTIC  PREFERRED SEQUENCE OF PROCEDURES PERIODONTAL THERAPY

INTRODUCTION Phase I Therapy (Etiotropic Phase)

The aim of the treatment plan is total treatment, i.e. co- • Plaque control. ordination of all treatment procedures for the purpose of • Diet control. creating a well-functioning dentition in a healthy periodontal • Removal of calculus and root planing. environment. Treatment plan is the blueprint for the • Correction of restorative and prosthetic irritational factors. management of a case and establishment of periodontal • Excavation of caries and restorations (Temporary or final). health. Treatment procedures should be performed in • Antimicrobial therapy. a systematic sequence and should be planned well in • Occlusal therapy. advance. • Minor orthodontic movement. • Provisional splinting. SEQUENCE OF THERAPEUTIC PROCEDURES Evaluation of Response to Phase I Rechecking: Preliminary Phase or Emergency Phase • Pocket depth and gingival inflammation. Treatment of emergencies. • Plaque and calculus, caries. • Dental or periapical abscess. • Periodontal abscess. Phase II Therapy (Surgical Phase) Extraction of hopeless teeth and provisional replacement • Periodontal surgery including placement of implants if needed. • Root canal treatment. 267

Phase III Therapy (Restorative Phase) PREFERRED SEQUENCE OF • Final restorations. PERIODONTAL THERAPY • Fixed and removable prosthesis.

• Evaluation of response to restorative procedures. 33 CHAPTER • Periodontal examination.

Phase IV Therapy (Maintenance Phase)

• Periodic recall visits. • Checking for plaque and calculus. • Gingival condition (Pockets, inflammation).

• Occlusion, tooth mobility and other pathologic changes. Plan Treatment 34 ChapterChapter

Rationale for Periodontal Treatment

 OBJECTIVES OF PERIODONTAL THERAPY  HEALING AFTER PERIODONTAL THERAPY  FACTORS WHICH AFFECT HEALING • Regeneration • Local Factors • Repair • Systemic Factors • Reattachment

OBJECTIVES OF PERIODONTAL THERAPY of primary consideration in local therapy. Systemic therapy may be used as an adjunct to local measures especially if it If properly performed, periodontal treatment can accomplish is indicated in localized juvenile periodontitis and rapidly the following: progressing periodontitis cases. Here the systemic antibiotics • Eliminate pain. are used to completely eliminate the bacteria that invade • Eliminate gingival inflammation. gingival tissues. The accumulation of plaque can be favored • Eliminate gingival bleeding. by a variety of local factors such as calculus, overhanging • Eliminate infection. margins of restorations, food impaction. Hence the primary • Reduces periodontal pockets and mobility of the teeth. consideration in local therapy should be removal of plaque • Stops pus formation. and all the factors that favor its accumulation. Systemic • Arrests the destruction of soft tissue and bone. therapy may be employed as an adjunct to local measures • Establishes optimal occlusal function. and for specific purposes such as systemic complications • Restores tissue destroyed by disease. from acute infections, post-treatment bacteremia, control • Re-establishes the physiologic gingival contour. of systemic diseases that aggravate the patient’s general • Prevent the recurrence of disease. periodontal condition. Evidence has shown that some • Reduces tooth loss. nonsteroidal anti-inflammatory drugs such as flurbiprofen The treatment of periodontal disease is based on the fact and ibuprofen can slow down the development of that it is caused by bacterial plaque. Hence, the removal of experimental gingivitis and the studies have shown that plaque and all factors that favor its accumulation is therefore it can also inhibit alveolar bone loss in periodontitis. 269

Another drug that has been shown to reduce bone loss HEALING AFTER PERIODONTAL THERAPY associated with periodontitis, in experimental animals is (FIGS 34.1 AND 34.2) alendronate, a biphosphonate which is also used to treat Regeneration, repair and new attachment are the aspects of Paget’s disease and other metabolic diseases. Although some healing that have a special bearing on the outcome of 34 CHAPTER of the systemic conditions associated with periodontal periodontal treatment. diseases are treated primarily by other than local measures, a. Regeneration: It is the biologic process by which the local therapy is indicated to reduce or prevent the progression architecture and function of lost tissues are completely of periodontal disease. restored by formation of new periodontal ligament, alveolar bone and cementum. FACTORS WHICH AFFECT HEALING b. Repair: It is the healing of tissues without completely

As elsewhere in the body, healing is affected by local and restoring the lost tissues. Treatment Periodontal for Rationale systemic factors. c. New attachment: This is the reunion of connective tissue with a root surface that has been pathologically Local Factors exposed. Healing is delayed due to contamination of micro- d. Reattachment: This is the reunion of connective tissue organisms; irritation from plaque, food debris, necrotic and a root surface that have been separated by incision tissue remnants and trauma from occlusion. Excessive tissue or injury. manipulation during treatment, trauma to the tissues can delay healing. In addition, repetitive treatment procedures which affect the orderly cellular activity in the healing process, topically applied cortisone and ionizing radiation can retard healing. Healing is improved by a local increase in temperature, debridement, immobilization of the healing area and pressure on the wound.

Systemic Factors

Healing is delayed in: • Older patients (Because of atherosclerotic vascular changes which results in reduced blood circulation). • Generalized infections especially in patients with diabetes and other debilitating diseases. • By insufficient food intake, vitamin C deficiency, deficiency of proteins and other nutrients. • Increased levels of hormones such as cortisone hinder repair by depressing the inflammatory reaction or inhibiting the growth of fibroblasts, the production of collagen and the formation of endothelial cells. • Systemic stress, thyroidectomy, testosterone, adrenocor- ticotropic hormone and large doses of estrogen suppresses the formation of granulation tissue and retard healing. Figs 34.1A and B: Healing after periodontal therapy

270 PART IV

Fig. 34.3: Sources of cells that populate the pocket area

cells that can synthesize and remodel the three connective

tissues of the supporting structures of periodontium. Periodontal Pathology Periodontal

Fig. 34.2: Outcome of periodontal therapy 1. If periodontal treatment is properly performed it can restore the normal health of the periodontal tissues. 2. The periodontal treatment consists of both local and systemic therapy. During the healing stages of periodontal pockets, the 3. The primary objective of local therapy is removal of plaque area is invaded by cells from four different sources: oral and all those factors that may favour its accumulation. 4. Systemic therapy is used as an adjunct to local therapy epithelium, gingival connective tissue, bone and periodontal and is mainly indicated in localized and generalized ligament (Fig. 34.3). aggressive periodontitis. The final outcome of periodontal pocket healing depends 5. Healing is affected by local and systemic factors. Under local factors, those factors that can delay the healing are on the sequence of events during the healing stages. If the excessive tissue manipulation, unnecessary trauma to epithelium proliferates along the tooth surface before the cells the tissue, presence of foreign bodies etc. Healing is improved mainly by good debridement and proper from other tissues reach the area, the result will be a long immobilization of the wound. junctional epithelium. If the cells from connective tissue 6. Systemic conditions that may have an effect on healing populate, the result will be fibers parallel to the tooth surface are infections like diabetes, and other debilitating diseases, malnutrition, increased levels of hormones, and remodelling of bone and no attachment to the cementum. systemic stress. If bone cells arrive first, root resorption and ankylosis may 7. During healing, the area may be invaded by cells from occur. Finally, when only cells from the periodontal ligament four different sources: a. Oral epithelium—results in long junctional proliferate coronally, there is new formation of cementum epithelium. and periodontal ligament. Hence, Melcher pointed out that b. Gingival connective tissue results in fibres parallel to root surface. the regeneration of the periodontal ligament is the key to c. Bone cells—root resorption and ankylosis. new attachment because it provides continuity between the d. Only cells from periodontal ligament—results in new alveolar bone and the cementum and also because it contains attachment. 271

REVIEW QUESTIONS KNOW MORE ... 1. Describe factors that can affect the healing following periodontal treatment.

Events Occurring during the Development and 2. Define regeneration, repair, new attachment and 34 CHAPTER during the Regeneration of Periodontal Tissues reattachment. Periodontal Periodontal development regeneration BIBLIOGRAPHY

Cells at site of Marrow- 1. McCulloch CAG. Basic considerations in periodontal wound tooth development derived cells healing to achieve regeneration. Periodontol 2000; 1:1993. Disruption of Clot formation 2. Caton Jack G, Greenstein Gary. Factors related to periodontal epithelial root sheath regeneration. Periodontol 2000;1:1993. Treatment Periodontal for Rationale Inflammatory 3. Salomon Amar, Kong Mun Chung. Clinical implications of Cell-cell; cell-matrix response cellular biologic advances in periodontal regeneration. Curr Opin interactions; growth (cytokines/ Periodontol 1994;187-93. factors/cytokines growth factors) 4. Takashi Takata. Oral wound healing concepts in periodontology. Reorganization of Granulation Curr Opin Periodontol 1994;187-93. cells between tissue tooth and bone

Migration/ Migration/ attachment/ attachment/ orientation/ orientation/ proliferation proliferation factors factors

Progenitor cells Progenitor cells

Differentiation Differentiation factors factors

PDL, bone, PDL, bone, cementum cementum 35 ChapterChapter

Periodontal Instrumentarium

 PERIODONTAL INSTRUMENTS • Scaling and Curettage • Diagnostic • Ultrasonic and Sonic • Surgical • Cleansing and Polishing Instruments

PERIODONTAL INSTRUMENTS Periodontal instruments are designed for specific purposes, such as removing calculus, planing root surfaces, curetting the gingival wall or removing diseased tissue. Fig. 35.1: Parts of an instrument Periodontal instrument (Fig. 35.1) is composed of: a. Blade b. Shank b. For subgingival scaling: c. Handle • Hoe scaler, chisel and file scalers are used to remove tenacious subgingival deposits. Classification of Periodontal Instruments • Curettes are used to plane the root surfaces by Diagnostic Instruments removing altered cementum and also, for scraping the soft tissue wall of the pocket. • Periodontal probes are used to locate, measure and mark pockets. c. Sonic and ultrasonic instruments. • Explorers are used to locate calculus deposits and caries. The Periodontal Endoscope

Scaling, Root Planing, and Curettage Instruments Used to visualize deep pockets and furcations during scaling Scaling and root planing instruments are classified as follows: and root planing. a. For supragingival scaling: Cleansing and Polishing Instruments • Sickle scalers, cumine universal scaler, posterior Jacquette scaler, Morse scaler, surface scaler, • Rubber cups, brushes, dental tapes cingulum scaler. • Air-powder abrasive system. 273

Surgical Instruments Excisional and incisional instruments, surgical curettes and sickles, periosteal elevators, surgical chisels, Hoes files,

scissors and nippers. 35 CHAPTER

Periodontal Probes

A typical probe is a tapered rod-like instrument calibrated in millimeters with a blunt, rounded tip. Periodontal probes are used to measure the depth of the pocket and to determine their configuration.

When measuring a pocket, the probe is inserted with a Periodontal Instrumentarium Periodontal firm gentle pressure to the base of the pocket. The shank should be aligned with the long axis of the tooth surface to be probed. Furcation areas can be best evaluated with the curved, blunt Naber’s probe (Figs 35.2 to 35.4).

Fig. 35.3: Types of periodontal probes

Fig. 35.4: Diagnostic instruments

a. The Marquis color-coded probe: The calibrations are in 3 millimeter sections. b. The University of North Carolina-15 probe (UNC-15): Figs 35.2A to E: Different types of probes It is a 15 mm long probe with millimeter markings at each millimeter and color coding at the 5th, 10th, and Types of Periodontal Probes 15th mm. • Color-coded c. Williams probe: Has both color and non-color coding • Noncolor-coded with markings at 1,2,3,5,7,8,9 and 10 mm. 274

d. The Michigan ‘O’ probe with Williams marking: At 1, 2, shanks are designed for use on anterior teeth and premolars. 3, 5, 7, 8, 9, 10 mm (4 and 6 are missing). Sickle scalers with contra-angled shanks adapt to posterior e. The Michigan ‘O’ probe with markings: At 3, 6, and 8 teeth. mm. f. The WHO probe: It has a 0.5 mm ball at the tip and millimeter marking at 3.5, 8.5 and 11.5 mm and color coding from 3.5 to 5.5 mm

Explorers PART IV They are used to locate subgingival deposits in various areas, and to check the smoothness of the root surfaces after root Fig. 35.6: Sickle scaler planing. Explorers are designed with different shapes and angles for a variety of use.

Scaling and Curettage Instruments (Figs 35.5 to 35.8) Sickle scalers: Sickle scalers have a flat surface and two cutting edges that converge in a sharply-pointed tip. The arch-shape of the instrument makes the tip so strong that it Periodontal Pathology Periodontal will not break off during use. They appear triangular in cross- section. The sickle scaler is inserted under ledges of calculus no more than 1 mm below the gingival sulcus. It is used with a pull stroke. The Morse sickle has a very small, miniature blade; it is useful in the mandibular, anterior area where there is Figs 35.7A to E: Basic scaling instruments narrow, interproximal space. Sickles with straight

Fig. 35.5: Scaling instruments Figs 35.8A and B: Basic characteristics of scalers and curettes 275

Curettes (Figs 35.9 to 35.11): The curette is the instrument The curved blade and rounded toe of the curette allows the of choice for removing deep subgingival calculus, altered blade to adapt better to the root surface. In cross-section, cementum, for root planing and for removing the soft tissue the blade appears to be semicircular with a convex base. lining the periodontal pocket. There are two basic types of curettes. HPE 35 CHAPTER Curette can be adapted to provide good access A. Universal to deep pockets, with minimal soft tissue trauma. B. Area-specific There are cutting edges on both sides of the blade. Universal curettes: Universal curettes have cutting edges Both single and double-ended curette may be obtained that may be inserted in most areas of the dentition by altering depending upon the preference of the operator. and adapting the finger rest, fulcrum and hand position of the operator. The face of the blade of every universal curette is at a 90 degree angle to the lower shank, when seen in cross Instrumentarium Periodontal section from the tip. Examples of universal curettes: Barnhart curettes # 1-2 and 5-6 and Columbia curettes # 13-14, 2R-2L and 4R-4L. Other universal curettes include Younger-Good # 7-8, the McCalls # 17-18, and Indiana University # 17-18. Area-specific curettes: Gracey curettes: They are area-specific curettes, designed and angled to adapt to specific anatomic areas of the Fig. 35.9: Types of curettes dentition. These curettes and their modifications are probably the best instruments for subgingival scaling and root planing because they provide the best adaptation to complex root anatomy. The term offset blade is used to describe Gracey curettes, because they are angled approximately 60–70 degrees from the lower shank. This unique angulation allows the blade to be inserted in a precise position, necessary for subgingival scaling and root planing, provided that the lower shank is Figs 35.10A and B: Universal and Gracey curette. Note: parallel to the long axis of the tooth surface being scaled. offset blade angulation of Gracey curette Double-ended Gracey curettes are paired in the following manner: Gracey # 1-2 and 3-4 : for anterior teeth Gracey # 5-6 : for anterior teeth and premolars Gracey # 7-8 and 9-10 : posterior teeth; facial and lingual Gracey # 11-12 : posterior teeth; mesial Gracey # 13-14 : posterior teeth; distal Recent additions to Gracey set are: Gracey # 15-16 : #15-16 is a modification of and 17-18 #11-12; # 17-18 is a modifica- Fig. 35.11: Gracey curette blade. Note that the Gracey curette is 50 percent shorter and the tip of the blade is turned upwards tion of # 13-14. It has a shank as compared to a standard Gracey curette blade elongated by 3 mm. 276

Distinction between Gracey and universal curettes is blade is curved slightly upward. This curvature allows the given in Table 35.1. curettes to adapt, more closely to the tooth surfaces. Langer and mini Langer curettes: This set of 3 curettes Table 35.1: Distinction between Gracey combines the shank design of the standard Gracey # 5-6, and universal curettes 11-12, and 13-14 curettes with a universal blade honed at Gracey curette Universal curette 90 degrees rather than the offset blade of the Gracey curette. Area of use Set of many curet- One curette designed Hence, these curettes offer a blend of both Gracey and tes designed for for all areas and sur- specific areas and faces. universal curette and can be adapted both on the mesial and surfaces. PART IV distal surfaces without changing instruments. Cutting edge One cutting edge Both cutting edges used, work is done used, work is done Schwartz periotrievers: They are a set of two double-ended, with the outer with outer or inner highly-magnetized instruments designed for the retrieval edge only. edge. Curvature Curved in 2 planes, Curved in one plane, of broken instrument tips from the periodontal pocket. blade curves up blades curves up and Plastic instruments for implants: It is imperative that plastic and to the side. not to the side. Blade angle Offset blade, face Not offset, face of rather than metal instruments be used, to avoid scarring and of blade beveled blade beveled at 90 permanent damage to the implants. at 60 degrees to degrees to the shank. the shank. Hoe scalers: They are used for scaling ledges or rings of calculus. The blade is bent at a 99 degree angle; the cutting Extended Shank Curettes or After Five Curettes edge is beveled at 45 degrees. The Hoe scalers are used in

Periodontal Pathology Periodontal the following manner: Hu Friedy After Five Curettes are modifications of the a. The blade is inserted to the base of the periodontal standard Gracey curette design. The shank is 3 mm longer, allowing extension into deeper periodontal pockets of 5 mm pocket, so that it makes a two point contact with the or more, other features include a thinned-blade for smoother tooth. This stabilizes the instrument and prevents nicking subgingival insertion or reduced tissue distention with a of the tooth. large diameter, tapered shank. b. The instrument is activated with a firm pull stroke All the standard Gracey numbers except # 9-10 are towards the crown, with every effort being made to available in the After Five series. preserve the two point contact with the tooth. McCalls Hoe scalers # 3, 4, 5, 6, 7 and 8 are a set of Mini-bladed curettes: They are modifications of After Five six Hoe scalers designed to provide access to all the Curettes. The shorter blade allows easier insertion and tooth surfaces. adaptation in deep, narrow pockets, furcations, developmental grooves, line angles, and deep, tight, facial, Files: They have a series of blades on a base. Their primary lingual, or palatal pockets. As with the After Fives, the Mini function is to fracture or crush tenacious calculus. Files can Fives are available in all standard Gracey number except easily gouge and roughen root surfaces when used for the # 9-10. improperly. Therefore they are not suitable for fine scaling and root planing. They are sometimes used for removing Gracey curvettes: They are another set of four mini-bladed overhanging margins of dental restorations. curettes. Sub-0 and # 1-2—anterior and premolars Chisel scalers: Usually used in the proximal surfaces of # 11-12—posterior mesial surfaces. anterior teeth (too closely spaced). It is a double-ended # 13-14—posterior distal surfaces. instrument with a curved shank at one end and a straight The blade length of these instruments is 50 percent, shank at the other. The instrument is activated with a push shorter than that of conventional Gracey curette and the motion. 277

Quétin Furcation Curettes: These are the curettes specifically • It consists of reusable fiberoptic endoscope, over which designed to fit into the roof or floor of the furcation. These there is a sterile sheath. The fiber optic endoscope fits curettes are nothing but hoe scalers with a shallow, half onto the periodontal probes and ultrasonic instruments moon radius and the tip is curved in such a way that it also that have been designed to accept it. HPE 35 CHAPTER fits into the developmental depressions. They are available • The sheath delivers water for irrigation that flushes the in two widths, namely the B-L (buccolingual) and pocket while the endoscope is in use, and it keeps the M-D (mesiodistal). These instruments can remove field clear. burnished calculus from furcation areas where even the • This device allows clear visualization, subgingivally, in mini-bladed Gracey curettes are often too large to gain deep pockets and in furcations. It enables the operator access. to detect the presence and location of subgingival deposits and guides the operator in their thorough Ultrasonic and Sonic Instruments (Fig. 35.12) removal. Instrumentarium Periodontal • Using this device it is possible to achieve levels of root Used for removing plaque, scaling, curetting and removing debridement and cleanliness that are much more difficult stains to produce without it. Two types of ultrasonic units are: The EVA system: They are most efficient and least traumatic • Magnetostrictive: Vibration of the tip is elliptical; hence instruments, for correcting overhanging or overcontoured all the sides can be used. proximal alloy and resin restorations. • Piezoelectric: Pattern of vibration of the tip is linear; only two sides of the tip are active. Cleansing and Polishing Instruments Ultrasonic vibrations range from 20,000 to 45,000 cycles/second. They operate in a wet field and have attached Rubber cups: They consist of a rubber shell with or without water outlets. configuration in the hollow interiors. They are used in the hand piece with special prophylaxis Dental Endoscope angle. A good cleansing and polishing paste that contains fluoride should be used. It is introduced for use subgingivally, in the diagnosis, treatment of periodontal diseases. Produced by Dentalview Bristle brushes: Available in wheel and cup shapes, used in hand piece with a polishing paste Inc. and called as the perioscopy system. Dental tape: It is used with a polishing paste and is used for polishing proximal surfaces that are inaccessible to other polishing instruments. Air powder polishing: A specially designed hand piece that delivers air powdered slurry of warm water and sodium bicarbonate, this instrument is called prophy-jet. Effective for the removal of extrinsic stains and soft deposits. Disadvantages: Tooth substance can be lost, damage to gingival tissue is transient and insignificant clinically, but amalgam restorations, composite resins and cements can be roughened. Contraindications: Patients with medical histories of Fig. 35.12: Ultrasonic scaler (EMS scaler) respiratory illness, hypertension, and patients on 278

medications affecting the electrolyte balance are 4. Surgical chisels and hoes: They are used during contraindicated. periodontal surgery for removing and reshaping bone. Chisels are used with a push stroke whereas surgical Surgical Instruments (Fig. 35.13) hoes are used with a pull stroke. 1. Excisional and incisional instruments: Example: • Periodontal knives (Gingivectomy knives): Example • Ochsenbein #1-2, chisel. Kirkland knife (Fig. 35.14). • Rhodes chisel. • Interdental knives (Fig. 35.15): Example, Orban knife 5. Surgical files: They are used primarily to smoothen rough,

# 1-2, Merrifield knife # 1, 2, 3 and 4. bony, ledges and to remove all areas of necrotic bone. PART IV • Surgical blades: Example, # 12D, 15 and 15C. Example: Schluger and Sugarman files. • Electrosurgery techniques and instrumentation (Fig. 35.16): – Electrosection used for incisions, excisions and tissue planing. – Electrocoagulation, coagulation or hemorrhage control. – Electrofulguration not in general use in dentistry. Fig. 35.14: Kirkland knife – Electrodessication not in general use in dentistry. 2. Surgical curettes and sickles: Required for the removal

of granulation tissue, fibrous interdental tissue, and Periodontal Pathology Periodontal tenacious subgingival deposits. Examples: • Kramer curettes # 1, 2, 3 and Langer curettes. • Kirkland surgical instruments. Fig. 35.15: Orban Interdental knife • Ball scaler # B2-B3. 3. Periosteal elevators: Necessary to reflect and move the flap after the incision has been made for flap surgery. Example: Goldman Fox #14.

Fig. 35.13: Surgical instruments Fig. 35.16: Electrosurgery unit 279

6. Scissors and nippers: Used for removing tabs of tissue BIBLIOGRAPHY during gingivectomy, trimming the margins of flaps, enlarging incisions in periodontal abscesses and removing 1. Jill, S Nield-Gehrig. Fundamentals of Periodontal Instrumenta- muscle attachments in mucogingival surgery. tion, 4th edn, Lippincott Williams and Wilkins, 2000. HPE 35 CHAPTER Example: Goldman – Fox # 16 scissors. 2. Newman, Takei, Fermin A Carranza. Clinical Periodontology, 9th edn, WB Saunders, 2002. 7. Needle holders: They are used to suture the flap at the 3. Wilkins EM. Clinical Practice of the Dental Hygienist, 7th edn, desired position. Baltimore, Williams and Wilkins, 1994. Example: Castroviejo needle holder.

KNOW MORE ... Instrumentarium Periodontal

Advantages and Disadvantages of Hand and Ultrasonic Instruments

Advantages Disadvantages

Hand • Superior tactile sensation Correct angulation is instruments • Good access mandatory • Good adaptation Frequent sharpening • No aerosol production required • No heat development Considerable working force is required Tiring for operator Negative time factor Ultrasonic • Instrumentation without Poorer tactile instruments pressure sensation • Highly accessible to Aerosols are difficult to reach areas highly contaminated • Disruption of biofilm Not all hand by cavitation pieces can be • Minimal soft tissue autoclaved damage Possible risk for • Requires less time patients with pace • Pocket irrigation makers is possible Contraindicated in • No sharpening of tips infectious patients • Better patient acceptance • Less tiring for the operator SECTION 2(A): Nonsurgical Therapy

36 ChapterChapter

Principles of Periodontal Instrumentation including Scaling and Root Planing

 POSITIONING OF PATIENT AND OPERATOR  INSTRUMENT ACTIVATION

 VISIBILITY, ILLUMINATION AND RETRACTION  PRINCIPLES OF SCALING AND ROOT PLANING  CONDITION OF INSTRUMENTS  ULTRASONIC INSTRUMENTS  MAINTAINING A CLEAN FIELD  INSTRUMENT STABILIZATION  AEROSOL PRODUCTION

INTRODUCTION • Thighs parallel to the floor. • Hip angle of 90 degrees. Effective instrumentation is governed by a number of general • Seat height positioned low enough so that the heels of principles that are common to all periodontal instruments. your feet touch the floor. Proper position of the patient and the operator, illumination • When working from clock positions 9-12:00, spread feet and retraction for optimal visibility and sharp instruments apart so that your legs and the chair base form a tripod are the fundamental prerequisites. which creates a stable position. ACCESSIBILITY (POSITIONING OF PATIENT • Avoid positioning your legs under the back of the AND OPERATOR) patient’s chair. • Back straight and the head erect. It facilitates thoroughness of instrumentation. The position of the patient and operator should provide maximal Patient’s Position accessibility to the area of operation. Inadequate accessibility impedes thorough instrumentation, prematurely The patient should be in a supine position and placed in tires the operator, and diminishes his or her effectiveness. such a way that the mouth is close to the resting elbow of the clinician.

Neutral Seated Position for the Clinician Body: The patient’s heels should be slightly higher than • Forearm parallel to the floor. the tip of his or her nose. The back of the chair should be • Weight evenly balanced. nearly parallel to the floor for maxillary treatment areas. CHAPTER 36 Principles of Periodontal Instrumentation including Scaling and Root Planing 281 Direct and indirect vision

: When transilluminating a tooth, the : Figs 36.1A and B: – Good image quality – Easily scratchable Concave surface – Image is magnified – Distortion of the image. Plane (Flat surface) – Produces double image – image is distracting. Double • • mirror is used to reflect light through the tooth surface. Various Uses of a Dental Mirror Uses of a Dental Various 1. Indirect vision 2. Retraction 3. Indirect illumination 4. Transillumination. Transillumination head. Left-handed clinician left-handed clinicians : If the head rest is adjustable, it should be raised : If the head rest is Table 36.1: Clinical positions for right and Table : The foremost of the patient’s head should be even head should be of the patient’s The foremost : Front surface Front – Produces clean clear image with no distortion There are four basic clinical positions for the right- There are four basic front of the patient’s head.head. patient’s the of side of the patient’s head. front head. patient’s the of back side of the patient’s head. to the back of the patient’s tly behind the patient’shead. tly behind the patient’s head. Right-handed clinician • o’ clock position to the 7 • • o’ clock position to the 9 5 o’ clock position, to the •theto clock, o’ •11 to 10 3 o’ clock position, to the •• to 10 o’ clock position, 2 12 o’ clock position, direc- •direc- position, clock o’ 12 VISIBILITY, ILLUMINATION AND ILLUMINATION VISIBILITY, AND B) RETRACTION (FIGS 36.1A • Various Types of Mirror Surfaces Types Various It is a hand instrument which has a reflecting mirrored It is a hand instrument which has a cannot be seen by surface used to view tooth surfaces that direct vision. Dental Mirror Dental handed and left-handed clinician (Table 36.1). clinician (Table handed and left-handed direct illumination Whenever possible, direct vision with If this is not possible, from the dental light is most desirable. a mouth mirror to indirect vision may be obtained by using vision and indirect reflect light where it is needed. Indirect illumination are often used simultaneously. or lowered, so that the patient’s neck and head are aligned neck and head the patient’s or lowered, so that with the torso. Head rest with the upper edge of the head rest. with the upper edge • down position. For mandibular areas—chin • up position. Maxillary areas—chin Head The chair back may be raised slightly for mandibular slightly for back may be raised The chair areas. treatment 282

The transilluminated-tooth almost will appear to glow. It is 3. Reduced number of strokes. effective only with anterior teeth because they are thin 4. Increased patient comfort. enough to allow the light to pass through them. 5. Reduced clinician fatigue. Ideally, it is best to sharpen your instruments after Procedure: autoclaving and then reautoclave them prior to patient Step 1 : Position yourself in 12 o’ clock position. treatment. Dull instruments may lead to incomplete calculus Step 2 : Using a modified pen grasp, hold the mirror in the removal and unnecessary trauma because of excess force non-dominant hand. Bring the arm up and over applied. the patient’s face. Gently rest your ring finger on

PART IV the side of the patient’s lip or cheek. MAINTAINING A CLEAN FIELD Step 3 : Hold the dental mirror behind the central incisors so that the reflecting surface is parallel to the Despite good visibility, illumination and retraction, lingual surface. Position the unit light so that the instrumentation can be hampered if the operative field is light beam shines on the dental mirror at a 90 obscured by saliva, blood and debris. Adequate suction is degree angle to the mirrors reflecting surfaces. essential and can be achieved with a saliva ejector or, an Step 4 : Properly-positioned light and the mirror will result aspirator. in glow. Blood and debris can be removed from the operative field with suction and by wiping or blotting with gauze Retraction: It provides visibility, accessibility and squares. The operative field should also be flushed illumination. The following methods are effective for occasionally with water. Compressed air and gauze square retraction:

Periodontal Pathology Periodontal can be used to facilitate visual inspection of tooth surfaces 1. Use of the mirror to deflect the cheek while the fingers just below the gingival margin during instrumentation. of the non-operating hand retract the lips and protect Retractable tissue can also be deflected away from the tooth the angle of the mouth from irritation by the mirror by gently packing the edge of gauze square into the pocket handle. with the back of a curette. 2. Use of the mirror alone to retract the lips and cheek. 3. Use of fingers of the non-operating hand to retract the INSTRUMENT STABILIZATION lips. Stability of the instrument and the hand is the primary 4. Use of the mirror to retract the tongue. requisite for controlled-instrumentation. Stability and 5. Combination of the preceding methods. control is essential for effective instrumentation and to avoid While retracting, care should be taken to avoid irritation injury to the patient or clinician. The two factors that provide to the angles of the mouth. stability are, instrument grasp and finger rest (Table 36.2).

CONDITION OF INSTRUMENTS Instrument Grasp (Figs 36.2 and 36.3) (SHARPNESS) A proper grasp is essential for precise control of movements Prior to any instrumentation, all instruments should be made during periodontal instrumentation. The most effective inspected to make sure that they are clean, sterile and in and stable grasp for all periodontal instruments is the good condition. The working ends of pointed or bladed modified pen grasp. This grasp allows precise control of instruments must be sharp to be effective. the working end, permits a wide range of movements and facilitates good tactile conduction. Advantages of Sharpness The palm and thumb grasp is useful for stabilizing 1. Easier calculus removal. instruments during sharpening and for manipulating air and 2. Improved stroke control. water syringes (Fig. 36.4). CHAPTER 36 Principles of Periodontal Instrumentation including Scaling and Root Planing 283 Palm and thumb grasp

Fig. 36.4: Finger rests may be generally classified as intraoral Finger rests may be generally classified of stress to the hand and fingers. Finger Rest and the instrument The finger rest serves to stabilize the hand are made to by providing a firm fulcrum, as movements rest prevents injury good finger A activate the instrument. The tissues. and laceration of the gingival and surrounding for the finger ring finger is preferred by most clinicians the middle finger is rest. Maximal control is achieved when the fourth finger. kept between the instrument shank and of the wrist-forearm This built-up fulcrum is an integral part stroke for calculus action that activates the powerful working removal. finger rests or extraoral fulcrums. Intraoral Finger Rest Standard The finger rests on a stable tooth surface immediately adjacent to the working area. Advantages • secured support for the hand. Provides the most stable, • Provides leverage and power for instrumentation. •tactile transfer to the fingers. Provides excellent • Permits precise stroke control. • Allows forceful stroke pressure with the least amount • Decreases the likelihood of injury to the patient. Pen grasp position and function position and Modified pen grasp Fig. 36.2: Fig. 36.3: The finger pads rest opposite to each other at pads rest opposite The finger exists and a tiny space They do not overlap is held in a relaxed The instrument between them. curve The index finger and thumb manner. The main in a C-shape. outward from the handle instrument. is to hold the function of these digits other side of the finger instrument shank. The It helps to guide rests against the ring finger. pad also feel the vibration. the working end and The finger the weight of the hand and instrument. strong is held straight and upright to act as a support beam for the hand. function. Table 36.2: Correct finger placement Correct finger 36.2: Table Digit Recommended Thumb and index and the shank. or near the junction of the handle Middle lightly on the One side of the finger pad rests Ringbalances firmly on the tooth to support Finger tip Little It should be held in a relaxed manner with no 284

Disadvantages Disadvantages • May not be practical for use in edentulous areas. • Decreases tactile information • May be difficult to obtain parallelism of the lower shank • Uncomfortable for patients with TMJ prob- to the tooth surface for accessing deep pockets. lems. e. Finger-on-finger fulcrum: It is accomplished by resting Advanced Intraoral Finger Rests the ring finger on the index finger. a. Modified intraoral fulcrum: It is achieved by combining Advantages an altered modified pen grasp with a standard intraoral • Provides stable rest to fulcrum finger.

fulcrum. It is useful while instrumenting the maxillary • Improves access to deep pockets. PART IV teeth. It alters the point of contact between the middle Disadvantage and ring fingers in the grasp. Non-dominant hand cannot be used for retraction or to Advantages hold the mirror. • Provides good stable support for the clinician’s hand. f. Basic extraoral fulcrums: They are essential for effective • Provides leverage, strength and good stroke control. instrumentation of some aspects of maxillary posterior • Provides good tactile sensitivity to clinician’s finger. teeth. • Improves access to deep pockets on maxillary teeth I. Knuckle-rest technique or palm up technique: The and facilitates parallelism of lower shank to proximal clinician rests the Knuckle against the patients chin root surfaces. or cheek. Disadvantage II. Chin-cup technique or palm down technique: The

Requires more muscle control. clinician cups the patients chin with the palm of Periodontal Pathology Periodontal b. Piggy-backed fulcrum: The middle finger rests on top the hand. of the ring finger. Advantage Advantages Facilitates instrumentation of the proximal root surfaces • Improved access to mandibular posterior aspects of maxillary molars. away from the clinician. Disadvantages • Enhances the whole hand working together as • Least effective of all fulcrum techniques. a unit. • Stroke control is more difficult and decreases tactile Disadvantage information. In patients with limited opening it cannot be used. c. Cross-arch fulcrum: It is accomplished by resting the INSTRUMENT ACTIVATION ring finger on a tooth on the opposite side of the arch • Adaptation from the teeth being instrumented. • Angulation Advantage • Lateral pressure Allows improved access to the lingual aspect of • Strokes mandibular posterior teeth. Disadvantage Adaptation Decreases tactile sensitivity and makes strokes difficult. It refers to the manner in which the working end of a d. Opposite arch fulcrum: It is accomplished by resting periodontal instrument is placed against the surface of a the ring finger on the opposite arch. tooth. The object of adaptation is to make the working Advantage end of the instrument conform to the contour of the tooth Facilitates access to deep pockets. surface. CHAPTER 36 Principles of Periodontal Instrumentation including Scaling and Root Planing 285 Blade angulations

Basic stroke directions Fig. 36.5: Fig. 36.6: The placement stroke is used to position the working The placement stroke Strokes (Fig. 36.6) Strokes four types of strokes: There are 1. Placement stroke. 2. stroke or assessment stroke. Exploratory 3. Scaling stroke. 4. stroke. Root planing the apical to a calculus deposit or at end of an instrument are pocket. Characteristics of strokes base of a sulcus or 36.3. Table described in Precise adaptation must be maintained with all Precise adaptation The cutting edge has three imaginary sections: edge has three imaginary The cutting Repeated application of excessively heavy strokes will tooth surface angulation should be an angle between tooth surface angulation should be 0 to 40 degrees. depends on to 90 degrees. The exact blade angulation procedure being the amount and nature of calculus, the scaling or root performed and condition of tissue during 45 degrees, the planing, with angulation of less than smoothening cutting edge will slide over the calculus is indicated, or burnishing it. When gingival curettage is deliberately angulation greater than 90 degrees established. instruments to avoid trauma to the soft tissues and root instruments to avoid of ensure maximum effectiveness surfaces and to instruments such as curette and instrumentation. Bladed such as explorers are more sharp pointed instruments to adapt. difficult 1. often during instrumentation. third—used more Leading 2. third. Middle 3. Heel third. nick or gouge the root surface. The careful application of The nick or gouge the root surface. varied and controlled amounts of lateral pressure during scaling and instrumentation is an integral part of effective root planing techniques. It refers to the pressure created when force is applied against the surface of a tooth with the cutting edge of a bladed instrument. Exact amount of pressure depends upon the procedure performed. It may be firm, moderate or light when insufficient lateral pressure is applied rough ledges or lumps may be shaved to thin, smooth sheets of burnished calculus. Lateral Pressure 2. removal, angulation should be between 45 For calculus It refers to the angle between the face of a bladed instrument It refers to the angle between the face of and the tooth surface. 1. the face to For insertion beneath the gingival margin, Angulation (Fig. 36.5) Angulation (Fig. 286

Table 36.3: Characteristics of strokes PRINCIPLES OF SCALING AND

Assessment Calculus removal/ Root planing ROOT PLANING stroke scaling stroke stroke Purpose Assess tooth– Remove calculus Remove resi- Scaling anatomy. deposits. dual calculus, This is the process by which plaque and calculus are Level of bacterial pla- attachment. que and by- removed from both supragingival and subgingival tooth Detect cal- products. surfaces. culus and other plaque Root Planing

PART IV retentive factors. This is the process by which residual embedded calculus Used Probes/explo- Sickle scalers, Curettes and portions of cementum are removed from the roots to with rers, curettes. curettes, files. Insertion 0 to 40 degrees 0 to 40 degrees 0 to 40 produce a smooth, hard, clean surface. degrees The prime objective of scaling and root planing is to Working 50 to 70 70 to 80 degrees 60 to 70 restore gingival health by completely removing the tooth angula- degrees degrees tion surface elements that provoke gingival inflammation. Lateral Contacts tooth Moderate to firm Light to pressure surface, but no scraping. moderate. Principles of Curettes pressure • Universal applied. • Gracey Character Fluid stroke Powerful strokes Lighter

Periodontal Pathology Periodontal of moderate short in length. strokes of Universal curettes: The working ends of the universal curettes length. moderate length. are designed in pairs so that all surfaces of the teeth can be Direction Vertical, Vertical, oblique, Vertical, treated with one-double ended instrument or a matched pairs oblique, horizontal. oblique, of single-ended instruments. horizontal. horizontal. In any given quadrant, one end of universal curette will Number Many, covering Limited, to area Many, cover- entire root where needed. ing entire adapt to the mesial surface and the other end to the distal surface. root surface. surface. The end that adapts to the mesial surface of the facial aspects also adapts to the distal surface on the lingual Stroke Direction aspect and vice versa. When adapting the universal curette blade, as much of the cutting edge should be in contact Instrument strokes are initiated using a pull stroke in a with the tooth surface. Although the entire cutting edge coronal direction away from the junctional epithelium. should contact the tooth, pressure should be concentrated Pull strokes may be made in vertical, oblique or horizontal on the lower-third of blade during scaling stroke. During directions. root planing stroke, however, lateral pressure should be Vertical strokes : Facial, lingual, proximal distributed evenly along the cutting edge. surfaces of anterior teeth, In the posterior teeth, a single working end can be used mesial and distal surfaces to treat both mesial and distal surfaces by using both of its of posterior teeth. cutting edges. Oblique strokes : Facial and lingual surfaces of anterior and posterior teeth. Gracey curettes Horizontal strokes or : Line angles of posterior 1. Determine the cutting edge by visually inspecting the circumferential strokes teeth, furcation areas. blade and confirmed by lightly adapting the chosen CHAPTER 36 Principles of Periodontal Instrumentation including Scaling and Root Planing 287 : Although : . instrumentation zone The direction and length of the strokes are limited by the strokes are limited and length of The direction a modified pen grasp and a stable The curette is held with ULTRASONIC INSTRUMENTS ULTRASONIC adjacent pocket wall. The curette is preferred by most curette is preferred The pocket wall. adjacent because and root planing for subgingival scaling clinicians afforded by its design. Hoes, files and of the advantages are also used for subgingival scaling ultrasonic instruments but are more hazardous than the curette of heavy calculus, to the root surface and the surrounding in terms of trauma tissues. correct cutting edge is slightly The finger rest is established. to with the lower shank kept parallel adapted to the tooth, The working angulation is established the tooth surface. of controlled and calculus is removed by a series utilizing wrist overlapping, short powerful strokes primarily lighter root planing strokes are then arm motion. Longer, the root surface is activated with less lateral pressure until and root planing completely smooth and hard. Scaling position of the tooth strokes should be confirmed to the This zone is is found. where calculus or altered cementum known as planing Evaluation of scaling and root and root planing smoothness is the criteria by which scaling is based on tissue are evaluated, the ultimate evaluation be conducted earlier response. Clinical evaluation should not of wound Re-epithelialization than 2 weeks postoperatively. Any 1 to 2 weeks. created during instrumentation takes this interval is due gingival bleeding on probing noted after by residual deposits. to persistent inflammation produced Positive clinical changes after instrumentation often continues for weeks or months. So longer period of evaluation is indicated deciding whether to intervene to further instrumentation or surgery. They use a water-cooled instrument tip, vibrating at high supragingival and subgingival calculus to remove frequency, deposits from the tooth and bacterial plaque from The two categories of mechanized periodontal pocket. instruments are ultrasonic and sonic hand piece. Ultrasonic a handpiece and units are comprised of electric generator, be instrumented. in a built-up fulcrum for middle fingers together and wrist-arm action. maximum control when working on the maxillary optimal angulation posterior teeth. calculus removal. stroke, rather than flexing the fingers. end is advanced to keep the blade adapted as the working around line angles and into concavities. depending on the nature of calculus. cutting edge to the tooth with the lower shank parallel the lower shank to the tooth with cutting edge of the tooth. to the surface Sickles, curettes and ultrasonic and sonic instruments Sickles, curettes and ultrasonic and 3. rests, keep the fourth and When using intraoral finger 4.finger rests for extraoral fulcrum or mandibular Use 5. for on using the cutting edge (lower) Concentrate 6. Allow the wrist and forearm to carry the burden of the 7. handle slightly between the thumb and fingers Roll the 8. Module lateral pressure from firm to moderate to light 2. to the surface to shank is parallel Make sure the lower Subgingival Scaling and Root Planing Technique Subgingival calculus is usually harder than supragingival calculus and is often locked into root irregularities, making it more tenacious. are most commonly used for the removal of supragingival are most commonly used for the removal To frequently used. calculus. Hoes and chisels are less sickle is held with perform supragingival scaling, the modified pen grasp and a firm finger rest is established on The blade is adapted the teeth adjacent to the working area. at an angulation of slightly less than 90 degrees to the surface The cutting edge should engage the apical being scaled. of supragingival calculus while short, powerful, margin overlapping scaling strokes are activated coronally in a vertical or oblique direction. Supragingival Scaling Technique and less calcified Supragingival calculus is less tenacious are not confirmed than subgingival calculus. Scaling strokes by surrounding tissues. 288

interchangeable instrument tip. Ultrasonic devices work by Use of barriers, surface disinfec- converting electrical current to mechanical energy in the tants, protective clothing and form of high frequency vibration of instrument tip. They laminar airflow system are operate at frequencies 18,000 to 50,000 cycles/sec. Two recommended. types of ultrasonic units are magnetostrictive and Aerosol production is reduced by piezoelectric units. proper patient position (Supine, Ultrasonic instrument tip must be cooled by fluid to head turned), pretreatment rinse prevent overheating of the vibrating instrument tip. They with antimicrobial solution,

have been shown to be as effective as hand instruments in cupping of cheeks or lips for water PART IV subgingival calculus removal, removal of attached and containment, and use of high unattached subgingival plaque, removal of toxins from root volume suction tip. surfaces, and in reduction and maintenance of pocket depth. Personal protection: Clinician should always use The water lavage has three benefits on the treatment recommended personal protection site. equipment, like gown is high neck • Flushing action–flushes calculus, blood, bacteria, plaque and long sleeves, hair covering, from treatment site. mask, protective eyewear, face • Cavitation. shield, and gloves. • Acoustic streaming. Patients should rinse with As the water exits from instrument tip, it forms a spray antimicrobial solution prior to start

of tiny bubbles that collapses and releases shock waves in a of ultrasonic or sonic procedures. Periodontal Pathology Periodontal process known as cavitation. It causes lysis of bacterial Patient protection: Personal protection gear for the cell wall. patient includes; plastic drape, The continuous stream of water produces tremendous towel or bib, protective eye wear, pressure within the confined space of periodontal pocket. and hair covering cap. This effect is called acoustic streaming. Bacteria, Gram- Water control: Use a disposable high-volume negative rods are sensitive to acoustic streaming. evacuation tip for suction, water control reduces aerosol produc- Equipment and Armamentarium for Ultrasonic tion, improves the visibility of the and Sonic Instrumentation treatment area, and increases Unit selection: When purchasing equipment, look patient comfort. for a unit with adjustable power and Power level: Thin tips may damage the root a selection of varied instrument tip surface if used on high power designs. setting. All tip designs should be Instrument selection: Larger, stronger tip should be used used at lowest frequency power for heavy calculus removal, thin tip setting, the high setting should be should be used on light deposits, avoided. de-plaquing, and endotoxin Water: The water spray around the removal. instrument tip should create a light Infection control: Ultrasonic and sonic instruments mist or halo effect with no excess produce a high level of aerosol dripping of water. Insufficient contamination in dental operatory. water can result in trauma to pulp. CHAPTER 36 Principles of Periodontal Instrumentation including Scaling and Root Planing 289 , aerosols , which filters the organisms in , which filters the organisms : These are used with a light grasp and used with a light : These are – Sickle scalers. – scalers. Surface – Jacquette scalers. – Hoe scalers. – scalers. Chisel – Root scalers. • Supragingival scalers. • Subgingival scalers. • Ultrasonic scalers. • Supragingival scalers: • Subgingival scalers: • Ultrasonic scalers. a. Diagnostic instruments–Probes, explorers. b. Scaling instruments. Laminar airflow system composite resin-restoration, demineralized enamel composite resin-restoration, demineralized surface, or dentinal hypersensitivity. pulp chamber Newly-erupted and primary teeth have large by instruments. that are more susceptible to heat generated Technique for use Technique to the clinician. is less fatiguing pressure which 1. Periodontal instruments are classified as: AEROSOL PRODUCTION into surrounding environment. These aerosols contain into surrounding saliva, and oral debris. Micro- microorganisms, blood, up to 24 hours. Hence, patient should organisms can survive solution prior to treatment. rinse with antimicrobial is recommended. air, Dental procedures produce airborne particles called Dental procedures produce Contraindications contraindicated in Use of ultrasonic instruments is patients with: 1. pacemaker. Cardiac 2. Communicable disease. 3. in breathing. Respiratory disease or difficulty 4. in swallowing. compromised gag reflex, or difficulty With 5. porcelain crown, titanium dental implants, With 6. may damage growing tissue. Vibrations In children: 3. 4. easily. Overhangs can be removed : Modified tips are significantly Position the patient in normal supine patient in normal Position the This position reduces position. and gagging, aerosol production facilitates proper instrumentation. to pool in This causes the water aerosol the cheek, minimizing production. last several Adapt the side of tip to tooth millimeters of the the tip should surface. Length of be parallel to the long axis of tooth. Direct contact of tip to tooth surface should be avoided. Strokes overlap one another in a sweeping or erasing type motion. Multidirectional strokes are used. To Keep the tip moving at all times. remove heavier deposits, keep the tip in constant motion while making light strokes in sweeping motion, back and forth, over the teeth. n: should be turned to a side. The head : so less tissue damage. approach to subgingival debridement. Design of modified tip tips are easier smaller than hand-activated curettes. Thin to insert and easier to adapt to root surface concavities and furcation. • Entire length of tip is active. • Tips have no cutting edge to cut or tear the tissue, • Removes less cementum so more conservative lavage Water • calculus, debris and plaque. Flushes • and debris allowing better vision. Removes blood • Endotoxin removal. • Antimicrobial effect. 1. 2. Advantages of Ultrasonic and Sonic Instruments Advantages of Ultrasonic and Sonic Patient chair position: Patient Patient head positio Adaptation: Stroke pressure:Stroke pattern: strokes Light Stroke technique: 290

c. Root planing and curetting instruments 3. Describe the characteristics of a sickle scaler. • Gracey curettes. 4. How are curettes different from scalers? • Universal curettes. d. Cleansing and polishing instruments 5. What are the modifications in curettes? • Rubber cups, bristle brushes. 6. Name some differences in Universal and Gracey • Dental tape, air powder polishing. curettes. e. Surgical instruments 2. Fundamental prerequisites for effective instru- 7. What are the principles of periodontal instrumen- mentation are governed by a number of general tation? principles, like, proper position of the patient and the 8. Define scaling and root planing. operator, illumination and retraction for optimal visibility

and sharp instruments. 9. What are the different types of instrument grasps and PART IV 3. Stabilization of the instrument is very essential to avoid finger rests? any injury to the patient or clinician. 4. There are four types of strokes used in periodontal 10. What are the different types of strokes used in instrumentation, placement stroke, exploratory stroke periodontal instrumentation? or assessment stroke, scaling stroke and root planing stroke. 5. Scaling is the process by which plaque and calculus BIBLIOGRAPHY are removed from both supragingival and subgingival tooth surfaces where as root planing is the process by 1. Drisco CL. Scaling and root planing without over instrumentation: which residual embedded calculus and portions of Hand versus power-driven scalers. Curr Opin Periodontol cementum are removed from the roots to produce a smooth, hard, clean surface. 1993;78. 6. The objective of scaling and root planing is to restore 2. Drisko CL, Cochran DL et al. Position paper sonic and ultrasonic gingival health by completely removing all the tooth scalers in periodontics. J Periodontol 2000;71(ll):1792. surface elements that can provoke gingival Periodontal Pathology Periodontal 3. Jill and Nield Gegrig. Fundamentals of Periodontal inflammation. Instrumentation, 4th edn, Lippincott Williams and Wilkins, 2000. REVIEW QUESTIONS 4. Newman, Takei, Fermin A Carranza. Clinical periodontology, 9th edn. WB Saunders and Co, 2002. 1. How do you classify periodontal instrumentarium? 5. Wilkins EM. Clinical Practice of the Dental Hygienist, 7th edn 2. What are the various types of probes? Baltimore, Williams and Wilkins 1994. 37 ChapterChapter

Plaque Control

 DEFINITION • Manual Toothbrushes  GOALS OF PLAQUE CONTROL MEASURES • Powered Toothbrushes  RATIONALE • Interdental Aids  BASIC APPROACHES FOR PLAQUE CONTROL • Others • Mechanical  CHEMICAL PLAQUE CONTROL • Chemical • Ideal Properties of Mouthwash  MECHANICAL PLAQUE CONTROL • Classification of Antimicrobial Agents

DEFINITION OF PLAQUE CONTROL BASIC APPROACHES FOR PLAQUE CONTROL It is the removal of microbial plaque and the prevention of its accumulation on the teeth and adjacent gingival surfaces. There are two basic approaches for plaque control: 1. Mechanical: GOALS OF PLAQUE CONTROL MEASURES • Individual 1. Plaque control retards the formation of calculus. • Professional—for subgingival plaque control, e.g. 2. Removal of plaque leads to resolution of gingival scaling and root planing. inflammation. 2. Chemical: 3. Good plaque control facilitates return to and preservation • Individual of oral health. • Professional.

RATIONALE MECHANICAL PLAQUE CONTROL

Controlling periodontal disease by regular plaque removal Individual mechanical plaque control is achieved by: is based on the fact that if supragingival plaque is left I. Toothbrush: Manual or powered undisturbed, it will become subgingival with the potential II. Interdental aids: to become colonized by pathogenic bacteria. • Dental floss: 292

– Unwaxed b. ADA specifications of a toothbrush: The head of the – Waxed brush should be: • Triangular toothpicks: i. 1 inch to 1¼ inches long. – Hand-held ii. 2-4 rows of bristles. – Proxa-pic iii. 5/16 inch to 3/8 inches wide. • Brushes: Proxa brush, bottle brushes iv. 5-12 tufts per row. • Yarns, gauze strips, pipe cleaners. v. 80-86 bristles per tuft. III. Others: c. Design of the toothbrush: A toothbrush consists of

• Rubber tip stimulator handle, shank and head. It has bristles which when PART IV PART • Water irrigators. bunched together are called tufts. The extreme end of the head is toe and that, close to the handle is the heel. Toothbrushes (Fig. 37.1) • Size—Large, medium and small. The following aspects are discussed: • Lateral profile—Flat, convex, concave and scalloped. a. Historical background. Bristles: Two types of bristles are available, nylon b. ADA specification of a toothbrush. (synthetic) and natural (hog). Nylon bristles are c. Design of the toothbrush. preferred. Natural bristles are more susceptible to d. Brushing techniques. breakage and fraying, contamination with bacteria is e. Instruction in toothbrushing. high. a. Historical background Hardness: Depends on material, diameter and length. i. Initially aromatic plants like chewing twigs were Periodontal Pathology Periodontal • Nylon bristles are more flexible. used and Miswak from arrack trees were used. • Soft: 0.007 inches to 0.009 inches (No. 7, 8, 9) ii. Then Chinese invented the modern toothbrush in • Medium: 0.010 inches to 0.012 inches (No. 10, 11, the year 1600. 12) iii. In 1,780, William Addis designed a toothbrush with • Hard: 0.013 inches to 0.014 inches (No. 13, 14) bone handle and hog bristles. • Extra hard: 0.015 inches (No. 15) iv. In 1,900 celluloid (plastic) brushes with bone handle were introduced. If the bristles are soft, they should be set close. If they v. World War II—Nylon bristles were introduced. are hard they should be more widely spaced. Handle design: i. Straight ii. Angulation in the shank. iii. Indentation of handle for a better grip. • Frequency of brushing—Every 12 hours. • Frequency of change of brush—Every 3 months. • Length of brushing time—Initially 10-20 minutes is required until the patient becomes more precise. Later 3-5 minutes may suffice. d. Brushing motions in brushing techniques: i. Horizontal: • Reciprocating (Scrub) ii. Vibratory: Fig. 37.1: Different types of toothbrushes • Bass method CHAPTER 37 Plaque Control 293 The first part of the With Stillman’s technique Stillman’s With It removes soft deposits from cervical areas. As described by Perry and Schmid As described interproximal portions of the teeth, where most of the teeth, where most portions of the interproximal the gingivae is located. detrimental to dental plaque When the brush is activated, into the gingival sulcus. and tooth surfaces are neglected; the gingival margin gingiva and alveolar mucosa are whereas the attached traumatized. brush cleans the Activating the into the gingival sulci. surfaces and facial surfaces but misses the interproximal surfaces along the gingival margin. between the allowed to slide down, creating an angle This the brush. occlusal plane and the long axis of from adequately prevents the main bulk of bristles the gingival penetrating interproximally and into sulci. Once the bristles are in place, pressure is applied to with the bristle ends resting partly on the cervical portion of the teeth and partly on the adjacent gingiva, pointing in an apical position, directed at an oblique angle to the long axis of the teeth. 2. and on the cervical action is concentrated Cleaning Errors: 1. gingiva, rather than of bristles on the attached Placement 2. teeth rather than directed Bristles are pressed against the 3. arm owing to tiredness so that the brush is Relaxing the Modified Bass method (Fig. 37.2): The the Bass method. modified Bass method is identical to bristles downwards modification consists of sweeping the completing the over the tooth surface occlusally after vibratory motion in the gingival sulci. method (Fig. 37.3): Stillman’s with the bristles the bristle ends are placed at a 45° angle, on the cervical portion placed partly on the gingiva and partly of the teeth. blanch the gingiva and a gentle but firm vibratory rotary motion is applied to the brush with the bristles remaining in the same position. Advantage: technique: Modified Stillman’s 1. The soft or medium, multitufted brush should be placed Also called as intrasulcular method. • Rolling stroke • Modified bass • Stillman’s Modified • Leonard • technique) Smithbell (Physiological • method Stillman’s • method Charter’s To reach occlusal surfaces, press the bristles firmly reach occlusal To reach distal surfaces of the last tooth in the arch, To iii. sweeping: Vertical iv. Rotary–Fones. plane, with the brush head covering three teeth, plane, with the brush head covering arch. beginning at the most distal tooth in the the teeth. angle of 45 degrees to the long axis of of the bristles. forth motions without dislodging the tips as well as into This forces the bristle ends into the sulci, should produce interproximal embrassures and perceptible blanching of the gingiva. help reach the lingual surfaces for next three teeth. To too large, insert of the anterior teeth, if the brush seems the heel of the brush into the Press the brush vertically. gingival sulci and proximal surfaces at a 45° angle to Activate the brush with 20 the long axis of the teeth. short vibratory strokes. the brush into 20 short Activate into the pits and fissures. back and forth strokes, advancing section by section until all posterior teeth in all quadrants are cleaned. open the mouth wide and vibrate the tip of the brush against that surface, 20 times for each tooth. BRUSHING TECHNIQUES Technique: 1. head of a soft brush parallel to the occlusal Place the 2. establishing an Place the bristles at the gingival margin, 3. back and Exert gentle vibratory pressure, using short 4. Complete 20 strokes in the same position. 5. repeat the process Lift the brush, move it anteriorly and Advantages 1. is easy to master. Short back and forth motion The Bass method: 294

To reach lingual surfaces of the maxillary and mandibular incisors, the handle of the brush is held in a vertical position, engaging heel of the brush. With this technique the sides rather than the ends of the bristles are used, penetration of the bristles into gingival sulci is avoided.

Advantages: The modified Stillman method may be recommended for cleaning areas with progressing gingival

PART IV PART recession and root exposure to prevent abrasive tissue destruction.

The Charter’s method (Fig. 37.4) 1. A soft or medium, multitufted brush is placed on the tooth with bristles pointing towards the crown at a 45° angle to long axis of the teeth. 2. The sides of bristles are flexed against the gingiva, and the back and forth vibratory motion is used to massage the gingiva. Advantages: This method is effective particularly in cases

with receded interdental papillae, it is suitable for gentle Periodontal Pathology Periodontal plaque removal and gingival massage, when using soft brush, and this technique can be recommended for temporary cleaning in areas of healing wounds after periodontal surgery. Fig. 37.2: Modified Bass method Roll method/Fones technique: Technique: The bristles are first directed apically and then swept in an occlusal direction with a rolling motion. Advantages: It is popular because it is very easy to learn.

Disadvantage: Rolled-gingival margins prevent removal of plaque from sulcus area.

Fig. 37.3: Modified Stillman method

2. Pressure is applied laterally against the gingival margin to produce a perceptible blanching. 3. The brush is activated with 20 short back and forth strokes and is simultaneously moved in a coronal direction along the attached gingiva, the gingival margin and tooth surface. This process is repeated on all the teeth. Fig. 37.4: Charter’s method CHAPTER 37 Plaque Control 295 2 ) 4 (PO 3 , Ca 3 Less than 1 percent. Less than 1 Powered toothbrush Up to 2 percent strontium salts, Synthetic sodium carboxy-methyl 1 to 2 percent soap/detergent, e.g. 1 to 2 percent soap/detergent, Such as benzoic acid. 20 to 40 percent; maintains moisture, e.g. 20 to 40 percent; maintains moisture, such as 20 to 40 percent CaCO 20 to 40 percent. , granular polyvinylchloride are used. 3 Figs 37.5A and B: e.g. mint and others. mannitol. O 2 Humectants: glycol. glycerine, sorbitol, mannitol, propylene Preservatives: both of which react with fluoride. Now, silicon oxides, both of which react with fluoride. Now, Al Abrasives Thickening agents: cellulose is used. Water: sodium fluoride, formalin, potassium nitrate and others. Coloring and preservatives: Foaming agents: sodium lauryl sulphate. Flavoring and sweetening agents: • oils and synthetic flavors, percent essential Two • sorbitol, Sweetening agents such as saccharine, Desensitizing agents: 2. 3. 1. 4. 5. 9. 6. 7. 8. Composition of toothpaste: Poor plaque removal causes cervical abrasion Poor plaque removal In conclusion, no specific toothbrush can be It is easy to master. wedge-shaped defects in the cervical areas of root wedge-shaped defects in the cervical This gingiva. surfaces and painful ulceration of the identified and type of brushing technique should be discouraged. to fray. replaced as soon as the bristles begin who need to have their teeth cleaned by someone else. i. be started on the last/terminal teeth. It should v. must be toothbrushes cleaning efficacy maintain To ii.at a time. Three teeth are covered iv. Overzealous brushing can lead to gingival recession, iii. 20 strokes are used in each area. surfaces. Instructions in brushing: and moving them back and forth or scrubbing. and moving them back i. Reciprocal or back and forth. i. Individuals lacking fine motor skills. ii. Circular. ii. Small children or handicapped or hospitalized patients iv. Patients who prefer them. iii. Elliptical or combination. iii.with orthodontic appliances. Patients • They are used in the form of powders, pastes and gels. Dentifrices • for cleaning and polishing of teeth These are the aids They were introduced in 1939. Various types of motions Various They were introduced in 1939. used in powered toothbrushes are: for: Powered toothbrushes are recommended Conclusion: singled out as clearly superior for the routine removal of greatly among microbial deposits from the teeth. It differs individuals and should be recommended after considering factors such as the morphology of the dentition, periodontal health and manual dexterity. Powered Toothbrushes (Figs 37.5A and B) 37.5A (Figs Powered Toothbrushes e. Disadvantage: and gingival recession. Advantage: Scrub technique: • method. It is the simplest • Consists of merely placing the bristles next to the teeth 296

10. Anticaries agents: Like sodium monofluorophosphate, sodium fluoride, formalin. Dentifrices containing pyrophosphates or zinc compounds have reportedly shown 10 to 50 percent reduction in calculus. They are thought to produce this effect by the fact that they are absorbed on to hydroxyapatite crystals thus inhibiting the growth of larger organized crystals.

Interdental Cleaning Aids (Fig. 37.6) PART IV PART Toothbrush regardless of the brushing method used does not completely remove interdental plaque either in individuals with healthy periodontal support or in periodontally-involved patients, with open embrasures. Interdental plaque removal is of importance because most

of the pathogenic organisms originate in the interproximal Figs 37.7A to C: Types of embrasures with interdental areas. Among the numerous aids available, dental floss and cleansing aids interdental cleansers such as wooden or plastic tips and interdental brushes are most commonly recommended. Dental floss: It is the most commonly recommended method Factors determining the selection of interdental aids are of removing plaque from interdental areas. Periodontal Pathology Periodontal the type of embrasures (Figs 37.7A to C) • Type 1: The interdental papilla fills up the embrasure. Types of dental floss: Dental floss is advised 1. Twisted or non-twisted • Type 2: Moderate papillary recession is seen in such 2. Bonded or non-bonded situations, miniature interdental brushes and 3. Waxed or unwaxed wood tips are recommended. 4. Thick or thin. • Type 3: Where there is complete loss of papilla and Factors determining the choice of dental floss: interdental gingiva is tightly bound to under- a. Tightness of tooth contacts. lying bone (seen in diastema). Unitufted b. Roughness of proximal surfaces. brushes are recommended. c. The patient’s manual dexterity. The floss must contact the proximal surface from line angle to line angle to clean effectively. It should also cover the entire proximal surface, not just slipped apical to the contact area. Technique: The floss should be at least 12 to 18 inches long. It is wrapped around the fingers or the ends may be tied together in a loop. After stretching the floss between thumb and forefinger, pass it gently through each contact area in a back and forth motion. Once the floss is apical to the contact area, move it up Fig. 37.6: Interdental aids along the tooth till the contact area and down into the sulcus CHAPTER 37 Plaque Control 297 They are of several types, one can They are of several The ADA Council on Dental Therapeutics has adopted Council on Dental ADA The 1. Eliminate pathogenic microorganisms only. 2.of resistant bacteria. Prevent development 3. Exhibit substantivity. CHEMICAL PLAQUE CONTROL Ideal Properties of a Mouthwash It should Mechanical plaque removal remains to be a primary Mechanical plaque removal remains and it should preventive method to control dental diseases control. However, not be replaced by chemical plaque as an adjunct to chemical plaque control can be used and prevent the control gingival inflammation effectively disease. Chemical recurrence or progression of periodontal for during phase I therapy, methods are very effective plaque control patients with recurrent problems, ineffective or oral surgery. for any reason and for use after periodontal The a program for acceptance of plaque control agents. agents must be evaluated in placebo-controlled clinical trials of 6 months or longer and demonstrate significantly date, To improved gingival health compared with controls. for treatment ADA only two agents have been accepted by of gingivitis: chlorhexidine digluconate mouth wash and essential oil mouth rinse. factors can provide substantial protection against protection provide substantial factors can also provide not. But these methods or microorganisms more is far removal effect hence the plaque plaque control health. important to periodontal Oral Irrigation devices: irrigate between and around the teeth. use water faucet to is steady and is controlled by turning The water pressure use an intermittent water jet. Oral the faucet handle. Others the bacteria and debris from irrigators clean non-adherent shown to disrupt and detoxify It has been oral cavity. and can be useful in delivering subgingival plaque pockets (subgingival antimicrobial agents into periodontal tips there are two types of irrigator irrigation). Currently, is the cannula type useful for subgingival irrigation. One use and other is a soft rubber tip recommended for office use at home. tip for patient’s —They are mainly useful to clean They are cone-shaped or cylindrical They Indicated in patients with low manual in patients with low Indicated Can be performed with a toothbrush, Wooden tips are either with or without handle. tips are either with Wooden They are inserted interproximally and are They are inserted interproximally tufted brushes. and can be used on the facial and lingual surfaces Single Small conical brushes adjacent to wide large, irregular concave tooth surfaces interdental spaces. Other Aids Gingival massage: rubber tip stimulator or interdental cleaning devices. It produces epithelial thickening, increased keratinization and increased mitotic activity in the epithelium and connective tissue. It is questionable whether the above mentioned Using floss holder: Using floss brushes: Interdental toothpicks can be attached to a handle. Example Wooden Perio-Aid throughout the mouth. again, this is repeated several times and the same is repeated times and the same is repeated several again, this other teeth. surfaces of on the proximal in and hospitalized patients dexterity and for handicapped floss holder should possess forks Ideally, cleaning their teeth. to hold the floss firmly and simple that are rigid enough but the disadvantages of floss holders mounting mechanism, and they must be rethreaded are more time consuming becomes soiled or frayed. whenever the floss types Two mounted on a handle. brushes made of bristles are available: a. tips: Wooden as Stim-U-Dent are Soft triangular wooden toothpicks such a way that the base placed in the interdental space in such the sides are in contact of the triangle rests on the gingiva and it is moved in and out with the proximal tooth surfaces and from the teeth and of the embrasure removing soft deposits also mechanically stimulating the papillary gingiva but its usefulness is limited to the facial surfaces in the anterior region of the mouth. activated with short back and forth strokes in between the activated with short back and forth strokes They are most useful in furcation areas, isolated teeth. of mandibular gingival recession and on the lingual surfaces molars and premolars. b. Technique: 298

4. Be safe to oral tissues at the recommended concentration. • Hypothiocynase 5. Significantly reduce plaque formation and gingivitis. • Mutanase 6. Inhibit calcification of plaque to calculus. C. Quaternary ammonium compounds 7. Not stain and alter taste. • Cetylpyridinium chloride 8. Not have adverse effects on teeth or dental materials. • Benzethonium chloride 9. Be easy to use. • Benzalkonium chloride 10. Be inexpensive. • Domiphen bromide D. Bisbiguanides Classification of Antimicrobial Agents

• Chlorhexidine PART IV PART Depending on antimicrobial efficacy and substantivity. • Alexidine First Generation Agents: Reduces plaque scores by 20 to • Octenidine/Bispyridines 50 percent, efficacy is limited by their poor retention in the E. Metallic salts oral cavity. Hence, used 4 to 6 times daily (poor sub- • Copper stantivity) •Tin Examples: Antibiotics, quaternary ammonium com- • Zinc pounds, phenols and sanguinarine. F. Herbal extracts Second Generation Agents: These are retained longer in Sanguinarine the oral cavity or tissues and slow release property provides G. Fluorides overall reduction in plaque score by 70 to 90 percent; used Strontium Fluoride

Periodontal Pathology Periodontal 1 to 2 times daily (higher substantivity). H. Oxygenating agents Example: Bisbiguanides. Hydrogen peroxide I. Phenolic compounds Third Generation Agents: It should be effective against specific periodontopathic organisms. Yet to be developed • Thymol clinically. • Menthol • Eucalyptol Chemicals Used for Supragingival Plaque Control J. Other antiseptics [Addy’s classification] • Iodine • Povidone iodine A. Antibiotics • Sodium hypochlorite • Penicillin • Hexetidine • Vancomycin • Triclosan • Kanamycin A chemical approach to therapy can be used for either • Erythromycin of the following purposes: • Spiramycin 1. Prevention or chemoprophylaxis • Metronidazole 2. Treatment or chemotherapy B. Enzymes • Mucinase Based on these purposes, antimicrobials are divided into • Protease two groups: • Lipase 1. Preventive agents—which affect development of • Amylase supragingival plaque. • Elastase 2. Therapeutic agents—which are directed against • Lactoperoxidase subgingival plaque. CHAPTER 37 Plaque Control 299 Offers following advantages: Offers (Discussed in detail elsewhere in ® It has a broad spectrum of antibacterial It has a broad Contains thymol, eucalyptol, menthol The cationic molecules of chlorhexidine bind readily to The cationic molecules solution is When 10 ml of 0.2 percent chlorhexidine Erythrosine dye: Erythrosine FDC No.3 dye: Two-tone • FDC No.3—Red • No.3—Green Mechanism of action: of Mechanism are more suscepti- bacteria In general, gram-positive activity. high bacteria. In relatively to gram-negative ble as compared is bactericidal but low concentrations, chlorhexidine be bacteriostatic to susceptible bacteria. concentrations may the cell wall and interfere with the oppositely charged initiating a leakage of low molecular membrane transport In high concentrations chlorhexidine weight substances. causes precipitation of the cytoplasm. penetrates the cell and in bactericidal action of Bisbiguanides This explains the general. 30 percent of the drug used as a mouthwash for one minute, of substantivity is retained in the mouth due to its property over a period of 8 to (i.e. the bound drug is released slowly have been reported following small 12 hours). No ill effects since it is poorly quantities of chlorhexidine being swallowed is excreted in feces. absorbed from gastrointestinal tract and that, 0.12 percent Long-term human trials have shown in plaque inhibition when chlorhexidine is equally effective chemical plaque used as a mouth rinse (twice daily) however; to scaling and root control cannot be used as a supplement in controlling planing (monotherapy) as it is not so effective available products total plaque inhibition. Commercially, Rexidine, Hexidine, in the concentration of 0.2 percent are Clohex; in 0.12 percent, as Periogard. Essential oil rinse: in and methylsalicylate. It has been proved to be effective reducing plaque and gingival scores. Commercially available as Listerine the book). Disclosing agents (Fig. 37.8): • Discloses plaque. • Permits patients to evaluate their performance at home. disclosing agents are: Various 1. 2. Affecting all plaque bacteria uniformly and bacteria uniformly all plaque Affecting Acting as a ‘Silver bullet’ to quantitatively as a ‘Silver bullet’ Acting removal, complete plaque control can be achieved removal, complete plaque control aids (which without extensive use of proximal cleaning are painful to use and may delay healing). of immediate and in the postoperative management denture construction. from a daily intermaxillary fixation devices will benefit solution (also rinse with a 0.2 percent chlorhexidine available in 0.12% concentration). gingival status are often very poor. over-growth. in patients with drug-induced gingival recurrent generalized oral infections. infections such as denture induced stomatitis, aphthous ulceration, dry socket and acute ulcerative gingivitis. prevention of post-extraction bacteremia, dry sockets and to reduce the bacterial content of the aerosol sprays during the ultrasonic scaling. be associated with burning sensation. of parotid duct. reduce only the periodontopathic plaque bacteria. reduce only the periodontopathic periodontal therapy. leading to a quantitative reduction in plaque. a quantitative reduction leading to Specific: Non-specific: 3. healing after routine oral surgical procedures Improves 4. Patients wearing fixed orthodontic appliances or 5. plaque control and For handicapped patients whose 6. plaque accumulation Chlorhexidine will help to control 7. from patients who suffer In medically-compromised 8. It can also be advised in patients with local, oral 9. it can be used as a prophylactic rinse in the Finally, Disadvantages/unwanted effects 1. stains. Extrinsic staining of teeth, i.e. Brown 2. Painful, desquamative lesions on the oral mucosa may 3. Impaired taste sensation. 4. Parotid swelling is rare—due to mechanical obstruction 5. Dryness and soreness of mucosa. 2. after pack. period—immediately postsurgical During Indications and uses 1. oral hygiene in initial Used as an adjunct to mechanical 2. Bisbiguanides (Chlorhexidine) The chemotherapeutic agents would be either: agents The chemotherapeutic 1. 300

Toothbrush bristles could be, hard or soft, natural or synthetic, multitufted or space tufted. The hardness of the bristles depend upon: a. Diameter of bristles — wider the diameter, stiffer are the bristles. b. Length of bristles — shorter bristles are stiffer. c. Number of filaments in a tuft — more tufts provide more support. d. Curvature of filament — curved filaments may be more

flexible and less stiff than straight filaments. PART IV PART Various Advantages of Powered Tooth Brushes • Increases patient motivation thereby resulting in better patient compliance. Fig. 37.8: Disclosing solution • Increased accessibility. • No specific brushing technique required. It can differentiate older to newer plaque; old plaque • Uses less brushing force. stains deep violet and new plaque pale violet. • If brushing timer is incorporated (as with some 3. Plaque-lite system: Available as wafers/tablets or brushes) the patient will brush for the required solutions which are swished around the mouth and duration. excess dye is removed by rinsing the mouth. Recent Development in Dentifrices • Toothpastes for children • Herbal (natural) toothpastes. Periodontal Pathology Periodontal • Whitening toothpastes (long-term use is not 1. Plaque control is defined as the removal of microbial plaque and the prevention of its accumulation on the recommended as it contains highly abrasive silica teeth and adjacent gingival surfaces. particles). 2. There are two basic approaches for plaque control, Factors Determining the Selection of Interdental Aids i. Mechanical by means of tooth brush, and interdental Type of gingival embrasures and others include: aids, ii. Chemical by means of various chemical agents like • Alignment of teeth. chlorhexidine, phenols, quaternary ammonium • Fixed prosthesis/orthodontic appliance. compounds. • Open furcation area. 3. The chemical agents are very effective when used along • Contact areas. with the mechanical means. However, the plaque inhibiting effect is not as striking when used as a Powered flossing devices are also available. monotherapy. Mechanism of Action of Chlorhexidine 4. To date, mechanical plaque control seems to be the Gluconate (0.2%) gold standard in preventing dental diseases. However, “Pin cushion effect” chemicals can be used as an adjunct to mechanical therapy. It could be explained as follows: One charged end of 5. For the treatment of gingivitis only two agents have been chlorhexidine (dicationic) molecule binds to the tooth accepted by ADA, chlorhexidine mouthwash and surface where as the other remains available to initiate essential oil mouthwash. the interaction with the bacterial membrane as the microorganism approaches the tooth surface — called as “pin-cushion effect…” KNOW MORE ... REVIEW QUESTIONS

Types of Toothbrushes 1. What are the ideal requirements of a toothbrush? Other than manual and powered toothbrushes, sonic and 2. Describe the various brushing techniques. ultrasonic and ionic toothbrushes are introduced. 3. What is the composition of a toothpaste? CHAPTER 37 Plaque Control 301 control; advantages and limitation. Proceedings of the European and limitation. control; advantages Control Chicago, on Mechanical Plaque Workshop Quintessence, 1998. Opin Periodontol 1993;11-128. periodontal disease. Curr 2002. ninth edition, WB Saunders, Oxford University Press Publication, and the Periodontium. 1992. Practice of the Dental Hygienist. 6th in: Clinical Toothbrushing edn, Philadelphia 1992. 4. plaque in effective role of manual toothbrushes Jepson S. The 5. in the prevention and treatment of Mouthrinses Baker. Karen 6. Carranza. Clinical Periodontology, A Fermin Newman, Takei, 7. Drugs, Diseases A. Heasman. Peter Seymour, A Robin 8. and Toothbrushes EM. Oral disease control: Wilkins Van der Veldenll, et al. Comparison Veldenll, der Van BIBLIOGRAPHY of different approaches of interdental oral hygiene: Interdental of different approaches Periodontol 1998;69:759. floss. J brushes versus dental of clinical trials. J Clin Periodontol 1999;26:407. edn, Blackwell Munksgaard Publication, 2003. note on its uses? 2. review A McCracken GI. Powered toothbrushes: Heasman PA, 3. 4th Jan Lindhe. Clinical Periodontology and Implant Dentistry, 1. MF, Timmerman Christon V, 7. properties of a mouthwash? What are the ideal 8. on chlorhexidine gluconate. in detail Write 4. its selection criteria? What are aids? What are interdental 5. control. used for plaque Classify the chemicals 6. agent and add a of disclosing What is the composition SECTION 2(B): Surgical Therapy

38 ChapterChapter

Principles of Periodontal Surgery

 INDICATIONS • Preparation of the Patient  CONTRAINDICATIONS • General Conditions  GENERAL PRINCIPLES  COMPLICATIONS DURING SURGERY  HOSPITAL PERIODONTAL SURGERY

INDICATIONS OF PERIODONTAL SURGERY 2. Patients with systemic diseases such as cardiovascular 1. Areas with irregular bony contours, deep craters and disease, malignancy, liver diseases, blood disorders, others requiring a surgical approach. uncontrolled-diabetes, consultation with the patient’s 2. Deep pockets where complete removal of root irritants physician is essential. is not possible, especially in inaccessible areas like 3. Where thorough subgingival scaling and good home care molars and premolar areas. will resolve or control the lesion. 3. In cases of Grade II and III furcation involvement, where 4. Where patient motivation is inadequate. apart from removing local irritants, necessary root 5. In the presence of infection. resection or hemisection can be considered. 6. Where the prognosis is so poor that tooth loss is 4. Infrabony pockets in non-accessible areas which are non- inevitable. responsive towards nonsurgical methods. 5. Persistent inflammation in areas with moderate and GENERAL PRINCIPLES OF SURGERY deep pockets. 6. Correction of mucogingival problems. a. Preparation of the patient b. The general conditions that are common to all CONTRAINDICATIONS OF PERIODONTAL periodontal surgical techniques, and SURGERY c. Complications that may occur during or after surgery. These may be oral or systemic. PREPARATION OF THE PATIENT 1. In patients of advanced age where teeth may last for life without resorting to radical treatment (Procedures Almost every patient has to undergo the initial or preparatory indicated in a person of 60 years of age may not be phase of therapy. (scaling + root planing and removal of justified in someone of 70 years of age). etiotropic elements) because it: CHAPTER 38 Principles of Periodontal Surgery 303 Dull instruments One of the cardinal In addition to being most In addition Have three components: Operate gently and carefully: and carefully: Operate gently should manipulation to the patient, tissue considerate it produces excessive tissue injury; be gentle because discomfort and delays healing. causes postoperative sharp: are Be certain the instruments trauma because of excess force will cause unnecessary for their ineffectiveness. usually applied to compensate with teflon. vicryl. unnecessary resorption. the “grasping area”. Tissue Management Tissue 1. 2. times. Observe the patient at all 3. Suturing nonabsorbable or Suturing materials are classified as either absorbable. Nonabsorbable • Natural: example—braided-silk • example—Dacron-coated and impregnated Synthetic: Absorbable • Natural: example—Surgical gut. • like Synthetic: example—Polyglycolic acid derivatives Goals of suturing 1. Maintains hemostasis 2. Permits healing by primary intention 3. pain Reduces postoperative 4. Permits proper flap position 5. Prevents bone exposure resulting in delayed healing and of surgical needles Parts 1. Eye. 2. point of the needle and is referred to as Widest Body: 3. Point: Point the tip can be conventional or reverse cutting. Knots and knot typing: 1. The loop created by the knot. 2. The knot itself. 3. Ears—cut ends of the suture. Suturing techniques and materials: rules in suturing is to avoid placing excessive tension on thus facilitating more accurate and delicate surgery more accurate thus facilitating and with the with the office Acquaints the patients thereby reducing the operator and assistants, The re-evaluation and fear. apprehension patient’s reprobing and re-examining all phase consists of indicated the need for the findings that previously procedure. Persistence of these findings the surgical The number for surgery. will confirm the indication and dates of the surgical the outcome procedures, needed are all and the postoperative care that is should decided before hand. Informed consent explaining the be taken from the patient after procedures, both verbally and in details of surgical writing. All the measures should be taken to prevent the All the measures should be taken I. lesions completely Eliminates some II.the tissues Renders more firm and consistent, III. Sedation and Anesthesia Sedation and the entire area In order to prevent pain during the surgery, to be treated should be thoroughly anesthetized by means of a regional block and local infiltration. Patients who are apprehensive and neurotic may require special management with agents like sedatives and anti-anxiety drugs. transmission of infections. These include the use of These transmission of infections. masks and protective eye wear. disposable gloves, surgical All surfaces that may be contaminated with blood or saliva and cannot be sterilized, must be covered with aluminium foil/plastic wrap. Ultrasonic scaling is contraindicated in patients with infectious diseases, as it generates aerosols and special care should be taken while using it (Pre- procedural mouth rinsing). For normal patients their use is not clearly demonstrated. For normal patients their use is not been advocated for The prophylactic use of antibiotics has as well as patients both medically-compromised patients procedures. Emergency bone-grafting undergoing at all the times. equipment should be readily available Premedication General Conditions that are Common to all Procedures 304

the tissues being sutured to the extent of inducing blanching. Such tension will result in necrosis of sutured area and subsequent loss of suture entirely.

Suturing Techniques (Figs 38.1 to 38.8) Interrupted Suture

a. Direct or loop suture b. Figure eight

PART IV c. Horizontal mattress d. Vertical mattress e. Distal wedge or Anchor suture f. Periosteal suturing (Fig. 38.6)

Continuous Suture a. Papillary sling b. Horizontal mattress c. Vertical mattress

Periodontal Dressing

Periodontal Pathology Periodontal Various commercially-available periodontal dressings are: a. Coe pak b. Kirkland periopak c. Peridress d. Periocare e. Periodontal pack f. Perio-putty g. Zone periodontal pak.

Advantages of Periodontal Packs/Dressings 1. It minimizes the likelihood of postoperative infection and hemorrhage. 2. Facilitates healing by preventing surface trauma during mastication. 3. Protects against pain induced by contact of the wound with food or with tongue during mastication. Types of Packs • Zinc oxide eugenol packs. • Non-eugenol packs.

Zinc oxide eugenol packs: Example—Wondre-pak Figs 38.1A to C: Direct or loop technique: (A) The needle penetrates from the outer surface of the first flap and engages developed by Ward. It is based on the reaction of zinc oxide the inner surface of the opposite flap. (B) The suture is brought and eugenol. back to the initial side. (C) Where the knot is tied CHAPTER 38 Principles of Periodontal Surgery 305 Vertical mattress: Interrupted. (A) The needle Vertical

Figs 38.3A to C: Figs 38.3A is inserted approximately 7 mm apical to the tip of the papilla, emerging again from the epithelialized surface of the flap 2 to 3 mm from the tip of the papilla. (B) The needle is brought back through the embrassure, where the technique is again repeated The knot is tied buccally (C) lingually or palatally. Interrupted figure—eight suture: (A) The Interrupted figure—eight suture: (A)

Apart from zinc oxide and eugenol, it has zinc needle penetrates the outer surface of the buccal flap. (B) And needle penetrates the outer surface of the buccal flap. (B) The suture is then the outer surface of the opposite flap. (C) brought to the first flap and the knot is tied Composition: used as a binder and filler, asbestos acetate as an accelerator, asbestos can induce lung disease and tannic acid. However, and tannic acid may lead to liver damage. Hence, both the substances have been eliminated. They are supplied in a liquid and powder form that is mixed prior to use. Eugenol Figs 38.2A to C: Figs 38.2A

306

PART IV Periodontal Pathology Periodontal

Figs 38.4A to C: Horizontal mattress—interrupted: (A) The Figs 38.5A to C: Distal wedge technique or anchor suture: needle is inserted 7 to 8 mm apical to one side of the midline of (A) The needle is placed at the line angle area of the facial the papilla, that is at the mesiobuccal line angle emerging again surface, suture is anchored around the tooth. (B) Passed 4 to 5 mm through the epithelialized surface on the distobuccal through the inner surface of the opposite flap. (C) The knot is line angle. (B) The needle is passed through the embrasure tied and the same maneuver is duplicated again on the lingual or palatal surface. (C) Then the knot is tied buccally CHAPTER 38 Principles of Periodontal Surgery 307 one-week, by the clinician. The pack is then rolled into two strips approximately to The pack is then rolled into two strips If calculus covered with a meshwork of new epithelium. red bead-like has not been removed completely, persist, which protuberances of granulation tissue will should be removed with a curette. epithelialized but may bleed readily when probed, hence pockets should not be probed. grayish-yellow or white granular layer of food debris that has seeped under the pack and can be easily removed with a moist cotton pellet. Instructions for the Patient after Surgery Instructions for the Patient after 1. take the advised medication. Patients should 2. The pack should remain in place until it is removed after static cyanoacrylates packs include agent. Other noneugenol obtained by of packs is gels. Retention and methacrylic and by the interdental spaces interlocking in mechanical facial portions of the pack. joining lingual and Application of and Preparation Dressing (Figs 38.9 to 38.11) Periodontal is prepared by mixing equal lengths Coe pak (Non-eugenol) tubes supplied, i.e. accelerator and base of pastes from the then placed in a The paste is color. until it has a uniform temperature for 2 to 3 minutes, when cup of water at room to be placed on the the pack loses its tackiness, it is ready site. surgical on buccal surface the length of the treated area and placed can be placed the from mesial-distal end and the remainder are The strips same way on the lingual/palatal surfaces. the distal most joined at the distal end by hooking it around gentle pressure tooth as well as interproximally by applying and lingual surfaces (with the help of a probe) to join facial area should Any overextension onto uninvolved of the pack. week after surgery. be avoided. It is usually kept on for 1 Findings at pack removal a. If gingivectomy has been performed, the cut surface is b. the incision areas are After a flap operation, c. The facial and lingual mucosa may be covered with a Example-Coe Pak. It is based on the Periosteal suturing involves five steps:

One of the tubes contains zinc oxide, oil for (1) Needle penetration where needle point is perpendicular to (1) Needle penetration where needle point of the needle point, (3) Glide, where needle bone. (2) Rotation out of the (5) Exits point glides against the bone, (4) Rotation, periosteum and bone plasticity, a gum for cohesiveness and lorothiodol—a plasticity, fatty acids The other tube contains liquid coconut fungicide. thickened with rosin and chlorothymol—a bacterio- Non-eugenol packs: Composition: may produce allergic reaction that may render the area may produce allergic erythematous combined with a burning sensation in some patients. reaction between a metallic oxide and fatty acids. It is supplied in two tubes. Figs 38.6A and B: and B: Figs 38.6A

308

PART IV Periodontal Pathology Periodontal

Figs 38.7A to E: Independent sling suture: (A) The needle is inserted on the facial papilla, a sling is placed on the palatal surface. (B) The facial papillae were sutured together. (C) When the last tooth is reached, the suture is anchored around it. (D) The palatal flaps are sutured together in a similar fashion. (E) Final knot is placed CHAPTER 38 Principles of Periodontal Surgery 309 Figs 38.8A to F

310 PART IV

Fig. 38.9: Periodontal pack Periodontal Pathology Periodontal

Fig. 38.10: Mixing

Figs 38.8G to I Figs 38.8A to I: Continuous vertical/horizontal mattress sutures: Technique is identical to independent papillary sling except that vertical or horizontal mattress sutures are substituted for the simple papillary sling Fig. 38.11: Application of Coe Pak CHAPTER 38 Principles of Periodontal Surgery 311 The pack is removed, The pack may be due to extension of may be due to extension Periodontal surgery performed Patients may experience a “washed Within the first two postoperative days patient Within junction. Persistent bleeding after surgery:Persistent are located and the bleeding is the bleeding points or sutures, electrosurgery stopped with pressure, the pack is After the bleeding is stopped, electrocautery. one. replaced by a fresh Sensitivity to percussion periodontal ligament. Gradual inflammation into The pack is a favorable sign. diminution of severity and the gingiva should be checked should be removed The particles for localized areas of infection or irritation. should be of calculus that may have been overlooked usually helpful. removed. Relieving the occlusion is caused by excess Sensitivity to percussion may also be of excess pack which interferes with occlusion. Removal should correct the condition. Swelling: cheek in the area reports a soft, painless swelling of the and may be lymph node enlargement There of operation. This type of temperature may be slightly elevated. reaction involvement is due to localized inflammatory persists and to operative procedures. If the swelling Antibiotics like associated with increased pain. 1 week should be amoxicillin, 500 mg every 8 hours for prescribed. weakness: Feeling of out”, weakened feeling for about 24 hours after the This represents a systemic reaction to a transient surgery. bacteremia-induced by operative procedure. It can be prevented by prescribing prophylactic antibiotics. Postoperative pain: following basic principles should produce only minor pain and discomfort. In a study the results revealed mucogingival procedures results in maximum discomfort plastic than any other and followed by osseous surgery gingival surgeries. Common sources of postoperative pain are: a. of pack beyond mucogingival Overextension Complications during the during Complications Week First Postoperative 1. 2. 3. 4. 5. Patient should be placed in

(a) Periodontal surgery produces profuse Periodontal surgery Pressure pack, cotton pellet dipped in ferric or transient loss of consciousness owing to a or transient loss of consciousness owing of previous syncopal attacks during dental of previous syncopal attacks during

reduction in cerebral blood flow. The most common The reduction in cerebral blood flow. It is usually preceded by a cause is fear and anxiety. by pallor, feeling of weakness which is followed dizziness and sweating, coldness of the extremities, slowing of the pulse. Management: Syncope foods to permit the pack to harden, try to chew on the harden, try to chew the pack to foods to permit and citrus juices Avoid side of the mouth. non-operated it causes pain and burning. spiced-food because of any type. beyond this for the first 4 to 5 hours after the operation, immediately. if there is bleeding, report to the doctor bleeding in its initial incisional steps. However, after bleeding in its initial incisional steps. However, the granulation tissue is removed, bleeding will disappear Excessive hemorrhage after the or reduce considerably. initial steps may be due to lacerated capillaries and arterioles or damage to larger vessels due to surgical invasion of anatomic areas. Treatment: (Trendelenburg position) a supine position with legs position) a supine (Trendelenburg clothes should be loosened and an Tight elevated. (b) Administration of oxygen is open airway ensured. (c) also helps. also useful. (d) Glucose administration History appointments should be explored before proceeding with the treatment. Hemorrhage: Thrombin, hastens the process of subsulphate powder. blood clotting, oxidized cellulose and Gel foam are most commonly used to control the hemorrhage. COMPLICATIONS DURING SURGERY COMPLICATIONS 1. 4.not smoke. Do 5. not brush over the pack. Do 6. During the first day apply ice. 7. exertion your daily activities, but avoid excessive Follow 8.is not unusual. Swelling 9. tinge of blood in the saliva There may be an occasional 3.avoid hot after the operation, first three hours For the 2. 312

b. Extensive and excessively prolonged exposure and Other procedures like iontophoresis, restorative resins dryness of bone can also induce severe pain. and dentin bonding agents have been used. c. When severe postoperative pain is present, the patient HOSPITAL PERIODONTAL SURGERY should be treated on an emergency basis. The wound should be examined (under local anesthesia). This Usually, periodontal surgery is performed in dental clinics, type of pain is related to infection accompanied by either sextant or quadrant wise at weekly or longer intervals. localized lymphadenopathy and a slight elevation in Under certain circumstances, the full mouth periodontal temperature. surgery may have to be done in a hospital operating room

Treatment: Antibiotics and analgesics should be under general anesthesia. Indications for this, include: PART IV prescribed. a. To control and manage the apprehensive patient. 6. Sensitive Roots/Root hypersensitivity: May occur b. Convenience for individuals who cannot endure multiple spontaneously when the root becomes exposed as a result visits to complete surgical treatment. of gingival recession or pocket formation or it may c. Patient protection—some patients who are suffering appear after scaling and root planing and surgical from systemic conditions that are not severe enough to procedures because the cementum at cementoenamel contraindicate surgery but at the same time require junction is extremely thin and is removed during the special precautions that best provided in a hospital above procedures. setting. Example: Patients with cardiovascular disease, abnormal bleeding tendencies, prolonged steroid therapy Mechanism: Transmission of stimuli from the surface and others. of dentin to the nerve endings is located in the dental pulp, One must clearly understand that the purpose of

Periodontal Pathology Periodontal which may occur through the odontoblastic process or owing hospitalization is to protect patients by anticipating their to a hydrodynamic mechanism. Example: By displacement special needs, but not to perform surgery when it is of fluid. Treatment for root sensitivity include, use of various contraindicated by the patient’s general condition. desensitizing agents like, strontium chloride, potassium nitrate and sodium citrate available in the form of pastes and are used by the patient. 1. Prior to any surgical procedure, every patient must Agents used in Dental Office are: undergo the initial phase of therapy including scaling • Cavity varnishes and root planing and re-evaluation phase. • Anti-inflammatory agents 2. Periodontal surgery must be performed painlessly, to achieve this; effective local anesthesia should be • Various agents are used to partially-obturate dentinal administered. tubules. 3. Proper tissue handling is most important, as it can cause postoperative patient discomfort and delayed wound Examples: healing. • Silver nitrate 4. Excessive hemorrhage following surgery should be of great concern to the operator and should be handled • Zinc chloride carefully. Hemostasis may be achieved with various • Formalin hemostatic agents such as gelatin sponge, oxidized cellulose and others. • Calcium compounds 5. The periodontal dressings that are placed on the surgical • Sodium fluoride area have no curative properties; but they help in • Stannous fluoride protecting the tissue and thereby assist in healing. 6. After the pack placement, written and verbal instructions • Strontium chloride, and should be given to the patient before he or she leaves • Potassium oxalate the operatory. CHAPTER 38 Principles of Periodontal Surgery 313 BIBLIOGR\APHY 34(3):403. of success volume 1, Quintessence approaches and evidence Publishing Co, Inc. 1998. Co., 2002. 9th edn, WB Saunders Dent Clin North in-office of tooth hypersensitivity. management Am 1990;34:583. packs. 1. 1990; Am Dent Clin North hypersensitivity. Tooth Curro FA. 2. Helloing. Periodontal therapy clinical T, Nevins, James 3. Carranza. Clinical Periodontology, A Fermin Newman, Takei, 4. review of current approaches to A HO, Silver DR. Trowbridge 3. periodontal and types of disadvantages Advantages, 4. hypersensitivity. for dentinal Treatment KNOW MORE ... MORE KNOW REVIEW QUESTIONS are safe to use. • packs. fracture strength than eugenol It has better • (e.g. Barricaid) A light curing dressing • Cyanoacrylate dressing. of Noneugenol Packs Advantages • they it does not contain asbestos or eugenol Since Types of Periodontal Dressings/Packs of Periodontal Types 1. Indications and contraindications of periodontal surgery. 2. Describe various suturing techniques in periodontics. 39 ChapterChapter

Gingival Curettage

 DEFINITION AND TYPES  PROCEDURE  HEALING AFTER SCALING AND CURETTAGE  RATIONALE  CLINICAL APPEARANCE AFTER SCALING AND  INDICATIONS CURETTAGE

DEFINITION lateral wall of the periodontal pocket. This tissue apart from having its usual components like fibroblastic and The term curettage is used in periodontics to mean the angioblastic proliferations, also contains areas of chronic scraping of gingival wall of a periodontal pocket to separate inflammation, pieces of dislodged calculus and bacterial diseased soft tissue. colonies (Justification to curettage is more so from the fact Whereas scaling refers to removal of deposits from tooth/ that this granulation tissue which is lined by epithelium may root surface and root planing means smoothening the root hamper or act as a barrier for the attachment of new fibers). to remove infected and necrotic tooth surface.

TYPES I. Gingival curettage: Consists of removal of inflamed soft tissue lateral to pocket wall (Fig. 39.1). a. Subgingival curettage: It is a procedure that is performed apical to epithelial attachment (Fig. 39.2). b. Inadvertent curettage: Curettage that is done unintentionally during scaling and root planing. II. Surgical curettage, chemical curettage, ultrasonic curettage.

RATIONALE

The main accomplishment of curettage is the removal of chronically-inflamed granulation tissue that forms in the Fig. 39.1: Gingival curettage with a curette CHAPTER 39 Gingival Curettage 315 incision is made from margin of free gingiva apically incision is made from margin below the base of pocket, it is carried all around the tooth surface, attempting to retain as much interdental tissue as possible. and the root surface is planed to a smooth hard consistency. Curettage as such does not eliminate local factors like Curettage as such attached between In subgingival curettage, the tissue inflammation and pocket depth, particularly where depth, particularly and pocket inflammation surgerypocket reduction been performed. has previously PROCEDURE Other Techniques Procedure (ENAP) Attachment Excisional New (Fig. 39.3) Naval Corps. It is a It was developed by United States definitive subgingival curettage procedure performed with a knife. The technique is: 1. After adequate local anesthesia, an internal bevel 2. The excised tissue is then removed with a curette • Basic technique. • Other techniques. therefore it should always be followed plaque and calculus, planing procedures. by scaling and root Basic Technique correct curette is After adequate local anesthesia, the the cutting edge is selected and adapted in such a way that is inserted so as to engage The instrument against the tissues. is carried along the the inner lining of the pocket wall and The pocket stroke. soft tissue wall usually in a horizontal pressure on external wall may be supported by gentle finger surface. crest is removed with the bottom of pocket and the alveolar The tooth surface. a scooping motion of the curette to the necessary sometimes area is flushed to remove debris. If sutures and a pack may be indicated. Subgingival curettage

Fig. 39.2: On the other hand, curettage may also eliminate all or On the other hand, curettage may also The dilemma now is that, is it justified to do curettage, The dilemma now is that, is it justified inflammation prior to pocket elimination procedures like flap surgeries. surgical procedures are contraindicated like aging, systemic complications, etc. where the treatment is compromised and prognosis is impaired. method of maintenance treatment for areas of recurrent moderately deep infrabony pockets located in accessible areas where a type of “closed surgery” is advised. INDICATIONS most of epithelium that lines the pocket wall and underlying most of epithelium that lines the pocket opinions differing junctional epithelium, though there are is still valid regarding this, the purpose of curettage phase where there is persistent particularly in presurgical scaling and root gingival inflammation even after repeated planing. just to eliminate the inflamed granulation tissue? Because just to eliminate the inflamed granulation the major source of when the root is thoroughly planed, changes in the bacteria disappears and the pathologic any need for periodontal pocket disappears without tissue also curettage. Due to this existing granulation destroyed by defence disappears, if any bacteria present, are mechanism due to their less number. 3. It can also be performed in patients where extensive 4. performed on recall visits as a Curettage is frequently 2. Can be done as a non-definite procedure to reduce 1. of new attachment in Can be performed as a part 316

epithelium is lifted off. It also alters the morphologic features of fibroblast nuclei. This method has proved to be as effective as the manual method but results in decreased inflammation and less removal of connective tissue.

Caustic Drugs

Drugs such as sodium sulfide, antiformin and phenol have been used to induce chemical curettage of the lateral wall

PART IV of the pocket. Disadvantage is the extent of tissue destruction with these drugs cannot be controlled.

HEALING AFTER SCALING AND CURETTAGE

Immediately after curettage, a blood clot fills the pocket area, hemorrhage is also present in tissues with dilated capillaries and increase in polymorphonuclear leukocytes appear on wound surface. Rapid proliferation of granulation Fig. 39.3: Excisional new attachment procedure (ENAP) tissue occurs shortly thereafter with a decrease in the number of blood vessel. Restoration and epithelialization of sulcus

Periodontal Pathology Periodontal 3. Approximate wound edges if necessary, place sutures takes place in 2 to 7 days. and a periodontal dressing. CLINICAL APPEARANCE AFTER SCALING Ultrasonic Curettage AND CURETTAGE (FIGS 39.4A AND B)

Ultrasonic scalers are used for ultrasonic curettage, here Immediately after curettage, the gingiva appears the ultrasonic vibrations disrupt tissue continuity, and the hemorrhagic and bright-red. After one week, the gingiva

Figs 39.4A and B: Clinical appearance before and after curettage CHAPTER 39 Gingival Curettage 317 BIBLIOGRAPHY REVIEW QUESTIONS REVIEW Library Cataloguing in Publication Data, 1995. Library Cataloguing in 1, Quintessence of Success Approaches and Evidence Vol Publishing Co, Inc, 1998. 2002. 9th edn, WB Saunders, 1. Outline of Periodontics. 3rd edn, British BM Eley. JD Manson, 2.Therapy Clinical Mellonig. Periodontal Myron Newins, James T 3. Carranza. Clinical Periodontology, A Fermin Takei, Newman, 1.gingival curettage? the indications of What are 2. What is ENAP? chemicals and ultrasonic scalers. chemicals and ultrasonic after scaling and root planing. scaling and root after which should be differentiated. periodontal pocket to separate the diseased soft tissue. soft the diseased separate periodontal pocket to 4.with the help of can also be performed Curettage 3. are very limited and can be used Indications for curettage 2. curettage There are gingival, subgingival and inadvertent 1. of the gingival wall of a Curettage is the scraping appears reduced in height with apical shift. The redness is apical shift. The in height with appears reduced proper oral hygiene two weeks, with After slightly reduced. comes back to normal. the gingiva 40 ChapterChapter

Gingivectomy

 DEFINITIONS  CONTRAINDICATIONS  PREREQUISITES  TYPES AND TECHNIQUES  INDICATIONS  ADVANTAGES AND DISADVANTAGES

INTRODUCTION 2. The underlying alveolar bone must be in normal or nearly normal form. If there is bone loss it should be of The term gingivectomy was coined by Pickerill in 1912 horizontal in nature. where in all the periodontal tissues including the bone should 3. There should be no infrabony defects or pockets. be removed to achieve healing. It was later modified by Kronfeld (1935) and Orban in about 1940 who introduced INDICATIONS modern uses of gingivectomy. If the above mentioned prerequisites are met, gingivectomy DEFINITIONS may be used to do the following: 1. Eliminate supra-alveolar pockets and abscesses. • Gingivectomy is the excision of the soft tissue wall of 2. Remove fibrous or edematous enlargements of the the pocket (Its objective is the elimination of pockets). gingiva. • Gingivoplasty is the recontouring of gingiva that has lost its physiologic form rather than elimination of 3. Transform rolled or blunted margins to physiologic form. pockets. 4. Create more esthetic form in cases in which exposure These two procedures are performed together although of the anatomic crown has not fully occurred. they may be considered separately for teaching purposes. 5. Create bilateral symmetry (where the gingival margin of one incisor has receded somewhat more than that of PREREQUISITES the adjacent incisor). The basic prerequisites for gingivectomy are as follows: 6. Expose additional clinical crown to gain added retention 1. There should be adequate zone of attached gingiva so for restorative procedures (access to subgingival areas, that excision of part of it will still leave a functionally etc.). adequate zone. 7. Correct gingival craters. CHAPTER 40 Gingivectomy 319 Steps in gingivectomy Steps Fig. 40.1: Carefully curette out the granulation tissue and Cover the area with surgical pack. Cover the area with surgical Remove the excised pocket wall. Clean the area and Periodontal knives are used for incisions on the facial Periodontal knives are used for incisions Discontinuous or continuous incisions may be used. The may be used. Discontinuous or continuous incisions remove any calculus and necrotic cementum so as to leave a clean and smooth root surface. 5: Step Step 2: Step Bard Parker and lingual surfaces as auxiliary instruments, The incision 12 and scissors are then used. and blades No. 11 the course of the is started apical to the points marking a point between the pockets and is directed coronally to bone. Exposure of base of the pocket and the crest of the healing may not bone is undesirable but if it occurs covered by the present a problem if the area is adequately periodontal pack. incision should be beveled at approximately 45 degrees to the tooth surface and should recreate as far as possible the normal festooned pattern of gingiva, failure to do this may lead to the formation of fibrous plateau that takes more time to heal and develop a physiologic contour than is ordinarily required. 3: Step closely examine the root surface for any deposits. 4: Step : The pockets on each surface are explored with a gingivectomy knives. scissors. or bizarre crestal bone form. or bizarre crestal bone patient mentally (requires considerable preparation of the and is not exactly a contraindication). anterior region. TYPES OF GINGIVECTOMY CONTRAINDICATIONS Step 1: Step Insert periodontal probe and marked with the pocket marker. the probing beak to the bottom of the pocket and mark the depth with the puncturing beak. Mark the bleeding points in all the areas with probing depth. Surgical Procedure Armamentarium 1. probe. Mouth mirror, 2. Pocket markers, Kirkland and Orban interdental 3. blade, Bard Parker handle. Surgical 4. forceps, curettes, Gracey curettes, tissue Surgical 5. Periodontal dressing. Surgical Gingivectomy (Figs 40.1 to 40.4) Surgical Gingivectomy (Figs 40.1 Technique 1. gingivectomy. Surgical 2. Gingivectomy by electrosurgery. 3. Laser gingivectomy. 4. Gingivectomy by chemosurgery. 2. infrabony pockets are present. When 3. junction. If pockets extends till/below the mucogingival 4. by the patients Inadequate oral hygiene maintenance 5. patients. Uncooperative 6.patients. Medically-compromised 7. procedure Dentinal hypersensitivity before the surgical in the maxillary 8. Esthetically challenging areas, especially Gingivectomy and gingivoplasty are not indicated in the are not indicated and gingivoplasty Gingivectomy following situations: 1. alveolar edges, interdental craters In the presence of thick

320 PART IV

Figs 40.2A to E: Case I clinical steps in gingivectomy. (A) Preoperative view, (B) Bleeding points, (C) External bevel incision, (D) Excision using blade, (E) Immediately after

gingivectomy. Periodontal Pathology Periodontal

Figs 40.2F and G: Clinical appearance before and after gingivectomy. CHAPTER 40 Gingivectomy 321 Case II gingivectomy. (A) Preoperative view. Case II gingivectomy. Procedure for Gingivoplasty Instruments used are periodontal knife, scalpel, diamond stones or electrodes. It consists of following steps: Figs 40.3A to G: Figs 40.3A of (B) Probing of pocket depth. (C) Pocket marking. (D) Strip (E) Gingival contouring gingivectomy. gingival tissue after view. healing—facial After gingivectomy). (F) (immediately after (G) Lingual view

322

PART IV Periodontal Pathology Periodontal

Figs 40.4A to E: Case III gingivectomy. (A) Preoperative view with probing of pocket depth. (B) Pocket marking (C) Strip of gingival tissue after gingivectomy. (D) Gingival contouring (immediately after gingivectomy) (E) After healing—Lingual view

a. Tapering the gingival margins. Healing after Surgical Gingivectomy b. Scalloped marginal outline. Basically healing is by secondary intention: c. Thinning of the attached gingiva and creating vertical a. The initial response is the formation of a protective interdental grooves. surface clot. d. Shaping the interdental papillae to provide sluice ways b. The clot is then replaced by granulation tissue. for the passage of food. CHAPTER 40 Gingivectomy 323 Loop Incisions can be made with the Needle electrodes and diamond- Ball electrode is used. electrode is used. For gingivoplasty: In all shaped electrodes are used for festooning. and moved reshaping procedures electrodes are activated and coagulating in a concise "Shaving" motion (Cutting current is used). For abscess drainage: needle electrode. For hemostasis: muscle attachment: and of frenum For relocation pacemaker. areas of cemental necrosis. abscess. a. b. c. d. Electrosurgery Healing after but Some investigators report no significant differences others however have reported delayed healing, greater reduction in gingival height and more bone injury after electrosurgery. Laser Gingivectomy Most commonly used lasers are carbon dioxide and They are used for excision of gingival lasers. Nd:YAG is not Their use in periodontal surgery over growth. supported by research. Disadvantages 1. cardiac with poorly shielded be used in patients Cannot 2. Causes unpleasant odor. 3. damage may result. If it touches the bone irreparable 4. this may cause tissue damage and Heat generated by Indications 1. of gingival enlargements. Removal 2. Gingivoplasty. 3. attachments. Relocation of frenum and muscle 4. abscesses and pericoronal Incision of periodontal Technique Used to prevent hemorrhage. Uses dehydrating current and least Uses high voltage current. It has Three procedures are performed incising, The highly vascular granulation tissues grow The highly vascular ligament migrate into the granulation tissue, and with in ligament migrate into with gingival vessels. two weeks they connect is generally complete after 5 Surface epithelialization Electrosection: excising and planing. Electrocoagulation: coronally, creating a new free gingival margin and sulcus. and margin creating a new free gingival coronally, tissue cells mainly angioblasts and by third day numerous mainly angioblasts tissue cells area. are located in this fibroblasts used, as it is a dangerous technique. Here the active electrode is inserted into the tissue and Electrofulguration: limited application in dentistry. Electrodesiccation: Permits adequate contouring of the tissues and controls hemorrhage. Gingivectomy by Electrosurgery Advantage to 14 days. Initially, keratinization is less than what it was to 14 days. Initially, epithelialization takes about 1 Complete prior to surgery. month. b. Electrosurgery (Surgical Diathermy) 7.5 million cycles per Uses high frequency current of 1.5 to second. used: There are three classes of electrodes 1. Single wire electrodes for incising and excising. 2. Loop electrodes for planing tissues. 3. electrodes for coagulation procedures. Heavy bulkier techniques are Four types of electrosurgical available: a. d. of periodontal Capillaries derived from blood vessels c. connective is an increase in new 24 hours, there Within the tissue surrounding the electrode is mass coagulated in in dermatological and This procedure is useful only situ. cancer surgeries. c. d. 324

Gingivectomy by Chemosurgery REVIEW QUESTIONS Chemicals used are 5 percent paraformaldehyde or 1. Define gingivectomy and describe the step by step potassium hydroxide to remove gingiva. procedure of surgical gingivectomy. 2. Describe various gingivectomy techniques. Disadvantages 3. Describe the indications and contraindications of 1. Their depth of action cannot be controlled hence it may gingivectomy. also injure normal tissues. 4. Describe healing after gingivectomy. 2. Gingival remodeling is not possible. 3. Healing is delayed. PART IV BIBLIOGRAPHY

1. Gottsegen R, Ammons WF Jr. Research in lasers in periodontics. Position paper. Chicago, American Academy of Periodontology, 1. Excision of soft tissue wall of the pocket is called May 1992. gingivectomy. 2. Gingivectomy may be performed by means of scalpels, 2. Jan Lindhe. Clinical Periodontology and Implant Dentistry, 4th electrodes, laser beams or chemicals. edn, Blackwell Munksgaard Publication, 2003. 3. In surgical gingivectomy, the incision should be beveled 3. Newman, Takei, Fermin A Carranza. Clinical Periodontology, at approximately 45 degrees to the tooth surface and 9th edn, WB Saunders and Co, 2002. should recreate normal festooned pattern of the gingiva. 4. Gingivectomy should be differentiated from gingivoplasty, in that, it is performed mainly to eliminate the pocket and also includes reshaping whereas the latter is performed for reshaping the gingiva to create normal Periodontal Pathology Periodontal physiological contour. 5. Basic healing after gingivectomy is by secondary intention. 6. The main advantage of laser and gingivectomy by electrosurgery is contouring of the tissue. 42 ChapterChapter

Osseous Surgery

 DEFINITION • Indications  RATIONALE • Contraindications • Examination Prior to Surgery  TERMINOLOGY • Methods  TYPES AND TECHNIQUES • Healing after Surgery  RESECTIVE OSSEOUS SURGERY  RECONSTRUCTIVE OSSEOUS SURGERY

DEFINITION TERMINOLOGY 1. Osteoplasty—It refers to reshaping the bone without Osseous surgery may be defined as the procedure by removing the bone supporting the tooth. which changes in the alveolar bone can be accomplished 2. Ostectomy—It refers to removal of bone supporting the to rid it of deformities induced by the periodontal disease tooth. or other related factors, such as exostosis and tooth 3. Osseous surgery—It is a periodontal surgery involving supraeruption. modification of the bony support of the teeth. According to the American Academy of Periodonto- RATIONALE logy; it is defined as “Procedures to modify bone support altered by periodontal disease, either by reshaping the It is based on the fact that the discrepancies in levels alveolar process to achieve physiologic form, without and shapes of the bone and gingiva predisposes patients the removal of the alveolar supporting bone, or by the to the recurrence of pocket depth post-surgically. Hence, removal of some alveolar bone, thus changing the the goal of osseous resective therapy is reshaping the position of crestal bone relative to the tooth root.” marginal bone to resemble the alveolar process 4. Osteoplasty—It is defined as reshaping of the alveolar undamaged by periodontal disease. The technique usually process to achieve a more physiologic form without involves apically-displaced flaps hence the procedure removal of supporting bones. not only eliminates periodontal pockets but also improves 5. Ostectomy—It is defined as the excision of bone or portion tissue contour to provide a more easily maintainable of a bone in periodontics, ostectomy is done to correct or environment. reduce deformities caused by periodontitis and includes removal of the supporting bone. 341

TYPES OF OSSEOUS SURGERY

Depending on the relative position of the interdental bone to radicular bone, osseous surgery is of following types

(Fig. 42.1): CHAPTER 42 1. Positive architecture—When the radicular bone is apical to the interdental bone. 2. Negative architecture—If the interdental bone is more apical than the radicular bone. 3. Flat architecture—It is the reduction of interdental bone to the same height as radicular bone.

4. Ideal—When the bone is consistently more coronal on Surgery Osseous the interproximal surface than on the facial and lingual Fig. 42.1: Relative position of interdental bone to radicular bone surfaces. Depending on the thoroughness of the osseous reshaping techniques, osseous surgery is of following types: 1. Definitive osseous reshaping—Implies that further reshaping would not improve the overall result. 2. Compromise osseous reshaping—It indicates a bone pattern that cannot be improved without significant osseous removal, that would be detrimental to the overall result. Osseous surgery (Fig. 42.2) can also be: 1. Additive—Directed towards restoring the bone to original levels. 2. Subtractive—It is designed to restore the form of the pre-existing alveolar bone to the level existing at the time of surgery or slightly apical to this level.

RESECTIVE OSSEOUS SURGERY

Indications Fig. 42.2: Steps in osseous resective surgery 1. One-walled angular defects. 2. Thick, bony margins. 5. High caries index. 3. Shallow crater formations. 6. Extreme root sensitivity. 7. Advanced periodontitis. Contraindications 8. Unacceptable esthetic result. 1. Anatomic factors such as close proximity of the roots to Examination Prior to Surgery the maxillary antrum or the ramus. 2. Age. Clinical examination and probing determines the presence 3. Systemic health. and the depth of periodontal pockets and also gives a general 4. Improper oral hygiene. sense of the bony topography. Transgingival probing or 342

into the radicular surface. It is the first step of the resective process and is usually performed with rotary instruments such as, round, carbide or diamond burs. It is indicated in thick bony margins, shallow crater formation and is contraindicated in areas with close root proximity or thin alveolar housing.

Radicular Blending

PART IV PART It is the second step of the osseous reshaping technique. It is the continuation of the first step and it attempts to gradualize the bone over the entire radicular surface and Fig. 42.3: Resective osseous surgery instruments thereby provides a smooth, blended surface for good flap adaptation. sounding under local anesthesia confirms the extent and The indications are the same as in step one. Both step configuration of the infrabony component or furcation one and step two are purely osteoplastic procedures. Apart defects. from thick bony margins and craters, grade-I and grade II furcation involvements are treated with these two steps. Methods Instruments used —Combination of hand and rotary Flattening of the Interproximal Bone instruments are used (Fig. 42.3). Periodontal Pathology Periodontal It requires removal of very small amount of supporting bone. Hand instruments include: It is indicated when interproximal bone levels vary 1. Rongeurs-Friedman and Blumenthal. horizontally, e.g. one wall defects or hemiseptal defects. 2. Interproximal files—Schluger and Sugarman. This step is also best-utilized in areas where there are 3. Back action chisels. combined defects, i.e. coronally one-walled defect and 4. Oschsenbein chisels. apically three-walled defect, so that it is helpful in obtaining good flap closure and hence improved healing. But the main Rotary instruments include: limitation is that, it cannot be utilized in advanced defects 1. Carbide round burs. where removal of inordinate amounts of bone may be 2. Slow-speed handpiece. required. 3. Diamond burs. Gradualizing Marginal Bone TECHNIQUE The final step in the osseous resective technique, is also an The following steps are suggested: ostectomy procedure. Bone removal is minimal but 1. Vertical grooving. necessary to provide a sound regular base for the gingival 2. Radicular blending. tissue to follow. Failure to do so may result in ‘widow’s 3. Flattening of interproximal bone. peaks’, allows the tissue to rise to a higher level than the 4. Gradualizing marginal bone. base of the bone loss in the interdental area. This may result Not all the steps are necessary in each case. in selective recession and incomplete pocket reduction. This ostectomy procedure should be performed with great care Vertical Grooving so as to not damage the roots. Following the osseous It is indicated to reduce the thickness of alveolar housing resection, the flaps are positioned back to its original position and it provides continuity from the interproximal surface or apically and sutured with minimal tension. 343

Healing after Surgery measurements without standardized method may not be reliable.

Radiographic Methods

They also have the following drawbacks. Standardized CHAPTER 42 techniques for reproducible positioning of the film and tubing is very difficult. Even with standardization, the radiograph may not show the entire topography of the area before or after the treatment. Furthermore, thin bony trabeculae which was present before treatment may go undetected because minimal amount of mineralized tissue must be present to be seen or registered on the radiograph. Surgery Osseous The osteoblastic activity has been observed even after Only future studies with subtraction radiography will 1 year postoperatively in humans, hence the initial loss in enhance the usefulness of radiographic evaluation. bone height gets compensated to some extent by repair and remodeling. Surgical Re-entry

This can give the best view of the state of the bone crest RECONSTRUCTIVE OSSEOUS SURGERY that can be compared with the one taken during the initial Periodontal therapy for treatment of periodontitis involves surgical intervention and can also be subjected to the elimination of bacterial plaque. When periodontitis is measurements. Even models can be used to appreciate the resolved, an anatomic defect remains in the periodontium. results of the therapy (pretreatment and post-treatment). This This anatomic defect is characterized by reformation of method is very useful but has two shortcomings: gingival fibers, substantial reduction in inflammation, a. It requires a frequently unnecessary second operation. persistent loss of bone and ligament and the formation of b. It does not show the type of attachment that exists long junctional epithelium. (epithelial or connective tissue attachments). Thus, periodontal therapy involves two primary compo- nents: Elimination of bacterial plaque and elimination of Histological Methods the anatomic defects produced by periodontitis. There are The type of attachment can only be determined by the two primary approaches to eliminating these anatomic histologic analysis of the tissue block taken from the healed defects—resective and regenerative, both being surgical. area. Although this can give us the clear picture of regeneration of the attachment apparatus, it is not without Evaluation of New Attachment and problems. They are: Bone Regeneration a. The need to remove a tooth with its periodontium treated successfully limits the volunteers. Clinical Methods b. Animal models (monkey, dog, pigs) can be used to Consist of: clarify some aspects and but one must always remember 1. Probing depth measurements (pre- and post-treatment). the differences that exists when extrapolations to humans 2. Clinical gingival indices. are attempted. Mainly the exact nature of the periodontal 3. Determination of attachment level, care should be taken disease cannot be reproduced in animals and also bone to measure the defect by placing the probe at the exact defects have to be experimentally-induced which may same point before and after treatment and also with the lack their chronicity and self-sustaining features. Even same angulation. Pre- and postoperative probing if these defects are allowed to become chronically- 344

infected, they are never identical because all these types iv. Surgical methods— of lesions have different healing sequences and thereby • Excisional new attachment procedure with internal provides different types of information. bevel incision (ENAP). In addition, the exact location of epithelial attachment • Gingivectomy procedure. will be lost once you reflect the flap because it will be • Modified Widman flap. reflected beyond the normal periodontium. Hence, a notch • Coronal displacement of the flap. should be placed on the root surface either apical to the All these procedures are discussed elsewhere in this calculus (slightly coronal to the attachment) or crest of the book.

alveolar bone (slightly apical to the attachment). Base of PART IV PART the calculus is a better landmark (for which presence of Prevention of Epithelial Migration calculus is required). Eliminating junctional and pocket epithelium may not be The following reconstructive surgical techniques have sufficient because the epithelium from the excised margin been proposed. may rapidly proliferate apically to become interposed 1. Nongraft-associated new attachment. between the healing connective tissue and cementum. 2. Graft-associated new attachment . 3. Combination of both. Guided Tissue Regeneration (GTR)

Nongraft-associated New Attachment This concept is based on the assumption that periodontal ligament cells have the potential for regeneration of the New attachment can be achieved without the use of grafts attachment apparatus of the tooth.

in: Two types of membranes have been used: Periodontal Pathology Periodontal a. Meticulously treated three-walled defects (Infrabony a. Degradable—Collagen, Polylactic acid, Vicryl defect). (polyglactin 910) and Guidor membrane. b. Perioendodontal abscesses. b. Nondegradable—They must be removed in three to six c. When the destructive procedure has occurred very weeks time, e.g. Millipore, Teflon membrane, Goretex rapidly, for example, after treatment of pockets which periodontal material. had acute periodontal abscess. Surgical procedure (Figs 42.4 to 42.7) Various techniques of nongraft-associated new attach- Step 1: Raise a full thickness flap utilizing vertical incisions, ment are: extending a minimum of two teeth anteriorly and one tooth distally, to the tooth being treated. Removal of Junctional and Pocket Epithelium Step 2: Debride the osseous defect and plane the root The methods used to do so include: surfaces. i. Curettage—Only 50 percent of junctional epithelium Step 3: Trim the membrane according to the size of the area being treated. The membrane should extend and pocket epithelium can be removed. approximately beyond 2 to 3 mm on all the sides. ii. Chemical agents—Mostly used in conjunction with Step 4: Suture the membrane around the tooth with a sling curettage. The most commonly used drugs are sodium suture. sulfide, phenol, camphor, sodium hypochlorite and Step 5: The flap is positioned back to its original position antiformin. The main disadvantage is that the depth of or slightly coronal to it and is sutured using inter- action cannot be controlled. rupted sutures. Make sure the membrane is covered iii. Ultrasonic methods—It is again not very useful, completely. In case of non-resorbable membrane, because of lack of clinicians tactile sense while using after 5 weeks of the operation, it must be removed these methods. with a gentle tug. 345 CHAPTER 42

Fig. 42.7: Membrane barrier in place

Fig. 42.4: Guided tissue regeneration—adaptation of barrier create a space for undisturbed and stable maturation of the Surgery Osseous membrane on the defect clot. Hence, this hypothesis suggests that preservation of the root surface that is, a fibrin clot interface prevents apical migration of the gingival epithelium and allows for connective tissue attachment during the early wound healing period. A lot of research is required to explore this possibility, for example, it requires more postoperative care, root conditioning to enhance fibrin clot and connective tissue attachment.

Preparation of the Root Surface (Root Biomodification) (Fig. 42.8)

Several substances have been used to condition the

Fig. 42.5: Flap is positioned coronally and sutured root surface, for attachment of new connective, tissue fibers. These include citric acid, fibronectin and tetracycline. Citric acid: When used with pH1 for two to three minutes on root surface, after surgical debridement, it produces a surface demineralization, which inturn induces cementogenesis and attachment of collagen fibers. The following actions of citric acid have been reported by Register and Burdick in 1975. 1. It removes the smear layer and may open dentinal tubules, thus allowing cementum to form within these tubules creating the blunderbuss effect and produce Fig. 42.6: Membrane adaptation cementum pins. This could be associated with accelerated cementogenesis. Clot Stabilization, Wound Protection and 2. It has also been shown to expose collagen fibers on the Space Creation root surface, which may splice with the collagen fibers The successful results obtained with graft materials, barrier of a soft tissue graft or flap (called as collagen splicing) membranes and coronally-displaced flaps have been resulting in collagen adhesion without cementum attributed to the fact that all of these protect the wound and formation and accelerated healing. 346

during tooth development can induce acellular cementum formation which is believed to favor periodontal regene- ration, e.g. Emdogain approved by FDA.

Graft-associated New Attachment

Terminology 1. Graft: It is a viable tissue/organ that after removal from donor site is implanted/transplanted within the host PART IV PART tissue, which is then repaired, restored and remodelled. 2. Xenograft or heterograft: The donor of the graft is from a species different from the host. Fig. 42.8: Root biomodification using tetracycline solution 3. Allograft or homograft: A tissue transfer between individuals of the same species but with non-identical genes. 3. Epithelium does not migrate apically because of the 4. Autograft: A tissue transfer from one position to a new accelerated healing either by connective tissue position in the same individual. attachment or a collagen adhesion may occur before 5. Alloplastic graft: A graft of inert synthetic material which epithelium migrates. is sometimes called implant material. 4. Finally, citric acid, may demineralize small bits of 6. Osteoinduction: A process by which the graft material residual calculus, disinfect the root surface and aid in Periodontal Pathology Periodontal is capable of promoting cementogenesis, osteogenesis removing endotoxins. and new periodontal ligament. Steps involved: 7. Osteoconduction: The graft material acts as a passive a. Raise full thickness flap. matrix, like a trellis or scaffolding for new bone to cover. b. Perform thorough root planing. 8. Contact inhibition: The process by which the graft c. Apply cotton pellets soaked in citric acid pH1 for two material prevents apical proliferation of the epithelium. to three minutes. 9. Guided tissue regeneration: An epithelial exclusionary d. Remove and irrigate root surface profusely with water. technique that promotes new connective tissue e. Replace the flap and suture. attachment without the use of any implant material. Growth factors: They are polypeptide molecules released Ideal Requirements of a Bone Graft Material by the cells in the inflamed area, that regulates events in wound healing. These factors are primarily secreted by An ideal bone graft material should have biologic macrophages, endothelial cells, fibroblasts and platelets. acceptability, predictability, clinical feasibility, minimal They include platelet derived growth factor (PDGF), insulin- postoperative hazards, minimal postoperative sequelae and like growth factor (IGF), fibroblast growth factor (FGF) and good patient acceptance. TGF (transforming growth factor alpha and beta ). These To date there is a no single material that fulfills all the can all be used to control events during periodontal wound above criteria. Once the material is placed in the defect it healing, e.g. promoting proliferation of fibroblasts from may act in a number of ways. It may have no effect, act only periodontal ligament thereby favoring bone formation. as a scaffolding material for the host to lay down new bone, Enamel matrix proteins: This is based on the observations it may actively induce bone formation or through its own that amelogenin secreted by Hertwig’s epithelial root sheath validity it may deposit new bone in the defect. 347

All grafting techniques require presurgical scaling, Osseous coagulum: Rationale of this technique is that small occlusal adjustment as needed and exposure of defect with particles of donor bone are better resorbed and replaced full thickness flap, best-suited is papilla preservation flap than the larger particles. This technique uses small particles because it provides complete coverage of the interdental of donor bone and hence it provides additional surface area area after suturing. The use of antibiotics after the procedure for the interaction of cellular and vascular elements. Sources CHAPTER 42 is generally recommended. of the implant material include the lingual ridge on the Intraoral autograft: It is the tissue transfer from one area to mandible, exostosis, tori, edentulous ridges, the bone distal another in the same individual, sources of intraoral autografts to the terminal tooth. include healing extraction wound, bone from edentulous In this technique, a bur is used in the donor site to reduce ridges, immature bone removed during osteoplasty and it to small particles which when coated with blood becomes ostectomy, bone removed from a predetermined site like coagulum and is placed in the defect until there is tori and symphysis (Figs 42.9A to D). considerable excess and the flap is replaced. Surgery Osseous

Figs 42.9A to D: Autogenous . (A) Preoperative radiograph. (B) Harvesting of bone graft from symphysis region. (C) Harvested autogenous cancellous bone graft. (D) Postoperative radiographic view (after 3 months) 348

Disadvantages: Allografts: Allograft or homograft is the tissue transfer 1. Low predictability. between individuals of the same species, but of non-identical 2. Inability to procure adequate material. genetic composition. Since autografts induce surgical trauma 3. Inability to use aspiration for large defects which leads in another part of the patient’s body, it would be advanta- to poor surgical visibility. geous if a suitable substitute can be obtained commercially. Bone grafts are commercially available in tissue banks. Bone blend: To overcome the above-mentioned problems, They can be: bone blend technique has been proposed. It uses an 1. FDBA (Freeze dried bone allograft)—It is an autoclaved plastic capsule and pestle. Bone is removed from osteoconductive material, varying results have been PART IV PART the predetermined site with chisels or rongeur forceps, observed using this material. Average bone fill of placed in the capsule with a few drops of saline, and 50 percent has been reported. triturated for sixty seconds to a workable plastic-like mass 2. DFDBA (Demineralized freeze dried bone allo- and is packed into the bony defect. graft)—Demineralization process exposes the Intraoral cancellous bone marrow chips: It can be obtained components of bone matrix termed as bone morpho- from: genic protein, e.g. DemboneTM, which is a bone a. Maxillary tuberosity—It contains good amount of inductive protein isolated from the extracellular matrix cancellous bone with foci of red marrow and the bone is of human bones. Hence, this is an osteoinductive removed with a cutting rongeur. material (Fig. 42.10). b. Edentulous areas—The bone is removed with curette. Xenografts: They have been shown to cause severe c. Healing sockets—They are allowed to heal for eight to immunologic reactions because of molecular divergencies, Periodontal Pathology Periodontal twelve weeks and the apical portion is utilized as donor therefore it is not used any longer. Examples of xenograft material. are calf bone, kiel bone, anorganic bone. Bone swaging: This technique requires presence of an Alloplasts/non-bone graft material: Non-bone graft endentulous area adjacent to the defect from which the bone materials have also been used for restoration of the is pushed into contact with root surface without fracturing periodontium. Some of them are sclera, dura, cartilage, the bone at its base. plaster of Paris, ceramics, and coral derived materials. Disadvantages: i. It is technically difficult. ii. Its usefulness is limited. Bone from extraoral sites: Iliac autografts/extraoral hip marrow: The use of iliac cancellous bone marrow has shown good results in bony defects with varying number of walls and furcation defects. However, there are many disadvantages associated with it. i. Additional surgical trauma. ii. Postoperative morbidity infection, exfoliation, sequestration. iii. Root resorption. iv. Rapid recurrence of the defect. Hence, this technique is no longer used. Fig. 42.10: Dembone™ (Demineralized freeze dried bonegraft) 349

All alloplastic materials have shown more or less similar Bioactive glass: Consists of sodium and calcium salts, results because all of them are osteoconductive in nature. phosphates and silicon dioxide with particle size Lot of attention has been given to calcium phosphate ranging from 90 to 170 um (perioglas®) or 300 to 355 um ceramics which are of two types: (biogran®). a. Hydroxyapatite—nonresorbable (Figs 42.11A to C). CHAPTER 42 Coral-derived materials: Two types of materials are b. Tricalcium phosphate—partially-bioresorbable. available, natural coral and coral-derived porous hydroxy- apatite (both are proven to be biocompatible).

Combined techniques: A combination of both graft and non- graft associated methods have been proposed, e.g. combination of barrier techniques with bone grafts have been suggested by many authors. Surgery Osseous

1. Osseous surgery can be of resective type and regenerative types. 2. Under resective surgery the following techniques exist: a. Vertical grooving. b. Radicular blending. c. Flattening of interproximal bone and, d. Gradualizing marginal bone. 3. Reconstructive surgical techniques are subdivided into—Nongraft-associated and Graft-associated new attachment techniques. 4. Nongraft-associated new attachment procedures are: a. Removal of junctional and pocket epithelium. b. Prevention of epithelial migration. c. Clot stabilization, wound protection and space creation. d. Preparation of the root surface. 5. Graft-associated techniques include grafts like auto- genous bone grafts, allografts, xenografts and alloplasts which have been suggested and used successfully.

KNOW MORE ...

Specific Osseous Reshaping Procedures • Intrabony and hemiseptal osseous lesions. • Reverse osseous topography. Osteoplasty is Indicated in the Treatment of: a. Buccal and lingual bony ledges or tori. b. Shallow intrabony defects. Figs 42.11A to C: Reconstructive periodontics. (A) Preoperative view. (B) Defect is exposed after flap reflection and debridement. c. Thick interproximal areas. (C) The defect is filled with hydroxyapatite crystal d. Incipient furcation involvements. 350

Current Research is Exploring Various Possibilities REVIEW QUESTIONS of Promoting Periodontal Regeneration a. Biologic mediators. 1. Define osseous surgery, describe the steps in resective b. Enamel matrix proteins. osseous surgery. c. Platelet-rich plasma (PRP) in regeneration. 2. Define regeneration, repair, new attachment and d. Tissue engineering in regeneration. reattachment. Role of Biologic Mediators 3. What is GTR? These mediators are mostly physiologic molecules released by cells that can regulate events during wound 4. What is root biomodification?

healing. These molecules can function in either autocrine 5. What is osteoconduction and osteoinduction? PART IV PART or paracrine mechanisms. 6. Classify graft-associated new attachment procedures. These growth factors, mainly secreted by macrophages, fibroblasts and platelets include: • Platelet derived growth factor (PDGF). BIBLIOGRAPHY • Insulin like growth factor (IGF). • Fibroblast growth factor (FGF). 1. Alan M Polson. Periodontal Regeneration, Current Status and • Bone morphogenetic proteins (BMP). Directions. Quintessence Publishing Company, Inc., 1994. • Transforming growth factor (TGF). Their primary function is to stimulate periodontal 2. Edwin Rosenberg, Louis F Rose. Biologic and clinical wound healing thereby promoting migration and considerations for autografts and allografts in periodontal proliferation of fibroblasts → formation of bone. regeneration therapy. Dental Clin North Am 1998;42(3):467. b. Enamel Matrix Proteins: These proteins mainly 3. , Jack G Caton. Biodegradable barriers and amelogenin, are secreted by HRS (Hertwigs epithelial guided tissue regeneration. Periodontol 2000;1993;1:36. root sheath) during the development of tooth, which Periodontal Pathology Periodontal 4. Hessam Newzari. Aesthetic osseous surgery in the treatment of can induce formation of acellular cementum. Based periodontitis. Periodontol 2000;2001;27. on this, proteins are developed to promote periodontal 5. Mary E, Aichelmann Reidy, Raymond A Yukna. Bone regeneration, e.g. Emdogain (approved by US Food and Drug Administration (FDA). replacement grafts: The bone substitutes. Dent Clin North Am c. Platelet-rich Plasma (PRP): Is an autologous 1998;42(3):491. concentrate of platelets. Platelets release various 6. Michael A Brunsvold, James T Mellonig. Bone grafts and growth factors to initiate wound healing, e.g. PDGF, periodontal regeneration. Periodontol 2000;1993;1:80. TGF, vascular endothelial growth factors. 7. Newman, Takei, Fermin A Carranza. Clinical Periodontology, d. Tissue Engineering in Regeneration: Langer in 1993, 9th edn, WB Saunders Co., 2002. proposed tissue engineering as a possible technique 8. Raul G Caffess, Carlos R Quinomes. Polypeptide growth factors for regeneration. Various approaches for tissue and attachment proteins in periodontal wound healing and engineering could be protein based, cell based and gene based approaches. regeneration. Periodontol 2000;1993;1:69. These approaches aims at reconstructing the lost 9. Roxanne A. Lowenguth, Timothy M Blieden. Periodontal tissue by combining three elements, i.e. scaffold, regeneration: root surface demineralization. Periodontol 2000, signaling, cells (Tissue engineering triad). 1993;1:S4. Forum et al (2001) have proposed various factors that 10. Raymond A Yukna. Synthetic bone grafts in periodontics. can influence the outcome of clinical results: Periodontol 2000;1993;1:92. a. The dimension and morphology of the defect (deeper 11. Thorkild Karving, Sture Nyman, Jan Gottlow, Lars Laurell. lesions result in greater bone fill than shallower defects). Development of the biological concept of guided tissue regene- b. The number of bony walls (three-walled results in better bone fill than, two-walled and one-walled defects). ration—Animal and human studies. Periodontol 2000, c. Amount of root exposure. 1993;1:26. d. The angle of the defect to the long axis of the tooth (the smaller the angle, the better is the chance of success). 41 ChapterChapter

Periodontal Flap

 INDICATIONS • Modified Widman Flap

 DEFINITION • Undisplaced Flap • Palatal Flap  CLASSIFICATION • Apically-displaced Flap  INCISIONS • Distal Molar Surgery  FLAP TECHNIQUES FOR POCKET THERAPY  HEALING AFTER FLAP SURGERY

INTRODUCTION elimination of plaque, calculus and diseased cementum from the tooth surface. Whenever there is a pocket present, the Although in a strict sense all the instrumental therapy can plaque control becomes difficult and also deeper the pocket be considered surgical (as by Webster's definition of the more difficult is the access because, the surface area to surgery), those techniques mentioned here are considered be scaled is increased, presence of root surface irregularities as surgical procedures because it involves intentional and also furcation involvement also creates various problems. severing of tissues. Hence, the definition of surgery is, “the art, practice or All the above-mentioned problems can be reduced by work of treating diseases, injuries or deformities by manual either resecting or displacing the soft tissue wall of the operation or instrumental application”. pocket. Gingivectomy and the flap surgery are the treatment Periodontal surgery (open) is defined as intentional procedures to attain this result (Fig. 41.1). severing or incising of gingival tissue with the purpose of controlling or eliminating periodontal disease. Therefore, INDICATIONS/OBJECTIVES scaling and root planing (blind or closed) are not included. OF FLAP SURGERY 1. Gain access for root debridement. When should one consider for surgical 2. Reduction or elimination of pocket depth, so that patient pocket therapy? can maintain the root surfaces free of plaque. 1. For opening up the pocket area in order to remove all 3. Reshaping soft and hard tissues to attain a harmonious the irritants from the tooth surface. topography (physiologic architecture). 2. For elimination or reduction of the periodontal pocket. 4. Regeneration of alveolar bone, periodontal ligament and The successful periodontal therapy is based on total cementum.

326 PART IV PART

Fig. 41.2: Mucoperiosteal/full thickness flap Periodontal Pathology Periodontal

Fig. 41.1: Outcome of periodontal therapy Fig. 41.3: Partial/split thickness flap

Today the flap has become the basic surgical procedure underlying connective tissue, the bone is covered by a of periodontal therapy. It not only provides access to layer of connective tissue including periosteum underlying tissues, but also permits the surgeon to perform (Fig. 41.3). a variety of regenerative procedures. Indications DEFINITION I. Full thickness : If osseous surgery is A periodontal flap is a section of gingiva and/or mucosa contemplated. surgically-elevated from the underlying tissues to provide II. Partial thickness : For displacing flaps in the visibility of and access to the bone and root surface. presence of dehiscence and fenestrations. CLASSIFICATION According to the Placement of Flap According to the Thickness of the Flap/Bone Exposure after Surgery after Flap Reflection a. Nondisplaced flap: The flap is returned and sutured back The flaps are classified as: in its original position. a. Full thickness/mucoperiosteal flap: All the soft tissues b. Displaced flaps: The flap is repositioned coronal, apical including the periosteum is elevated (Fig. 41.2). or lateral to its original position. However, palatal flaps b. Partial thickness/mucosal flap/split thickness flap: cannot be displaced due to the absence of unattached Reflection of only the epithelium and a layer of gingiva. 327 CHAPTER 41

Fig. 41.4: Scallopings required for the different types of flaps Periodontal Flap Periodontal

Fig. 41.5: Location of the internal bevel incisions for the different types of flaps Figs 41.6A and B: Horizontal incisions

According to Design of the Flap/Management INCISIONS of the Papilla For Conventional Flap The flaps can be: 1. Horizontal Incision: a. Conventional flaps: Splitting the papilla into a facial half • Internal bevel incision (Fig. 41.5) and lingual/palatal half. For example, modified Widman • Crevicular incision flap, undisplaced flap, apically-displaced flap (Fig. 41.4). • Interdental incision 2. Vertical incision Indications: • Oblique releasing incision i. When the interdental areas are too narrow to permit the preservation of flap. For Papilla Preservation Flap ii. When there is a need for displacing flaps. Crevicular incision with no incisions across the interdental b. Papilla preservation flaps: Entire papilla is incorporated papilla is given. into one of the flaps. Horizontal Incisions (Figs 41.6A and B) Indications: Internal bevel incision: It starts at a distance (1 to 2 mm) i. Where esthetics is of concern. from the gingival margin and is aimed at the bone crest. It ii. Where bone regeneration techniques are attempted. is a basic incision to most of the flap procedures. 328

It accomplishes three important objectives: 1. Removes pocket lining. 2. Conserves relatively uninvolved outer surface of the gingiva. 3. It produces a sharp, thin flap margin for adaptation to tooth—bone junction. It is also known as first incision, reverse bevel incision. No. 15 and No. 11 surgical scalpels are most commonly

used. PART IV PART

Crevicular Incision It is also termed as the second incision, is made from the base of the pocket to the crest of the bone. The incision is carried around the entire tooth. No. 12B blade is used. This results in V-shaped wedge of tissue containing inflamed granulomatous tissue consisting of lateral wall of the pocket, junctional epithelium and connective tissue fibers between the base of the pocket and crest of the bone. After this, a periosteal elevator is used to separate the

Periodontal Pathology Periodontal flap from the bone. With this access, the surgeon is able to make the third or interdental incision, to separate the collar of the gingiva that is left around the tooth. The orban knife is usually utilized for this incision. A curette or a large scaler (U15/30) can be used to remove the gingiva around the tooth. If no vertical incisions are made, the flap is called an envelope flap.

Vertical Incision (Figs 41.7A and B) Figs 41.7A and B: (A) Vertical incisions without involving interdental papilla. (B) Location of vertical incision It can be done on one or both the ends of the horizontal incision. If the flap has to be displaced the incisions at both Papilla Preservation Flap (Figs 41.8 to 41.10) ends should be made. Another indication for vertical incision Step 1: Crevicular incision is made around each tooth. No is in the presence of isolated deep pockets. Vertical incisions should be made extending beyond mucogingival junction incisions through the interdental papilla. for easy displacement of flap. Step 2: Papilla is usually incorporated facially, hence a In general, vertical incisions are avoided: semilunar incision across the interdental papilla in a. In lingual or palatal areas. the palatal or lingual surface is made, which b. At the center of the interdental papilla or over the is at least 5 mm from the crest of the papilla radicular surface. (the deepest curve). They are made along the line angles of the tooth, avoid Step 3: The papilla is dissected from the lingual or palatal short flaps with long, apically directed incisions as it aspect using Orban knife and elevated intact with compromises blood supply to the flap. the facial flap. 329 CHAPTER 41

Fig. 41.8A: Facial view after sulcular incisions Periodontal Flap Periodontal have been made Fig. 41.8D: Flap is secured with sutures

Fig. 41.8B: Flap reflection Fig. 41.8E: The surgical site is covered with periodontal dressing

Figs 41.8A to E: Papilla preservation flap

After the desired incisions are made, the flap is elevated either by blunt dissection for a full thickness flap or sharp dissection for partial thickness flap or combination of both for various surgical procedures.

FLAP TECHNIQUES FOR POCKET THERAPY The periodontal flap is one of the most frequently employed procedure particularly for eliminating/reducing moderate to deep pockets in posterior areas. Considering the objectives it offers, there are three flap techniques available in current Fig. 41.8C: After curettage and root planing use (Table 41.1).

330

PART IV PART Periodontal Pathology Periodontal

Figs 41.9A to F: Case-2: Papilla preservation flap. (A) Probing depth. (B) Crevicular incision placed. (C) Intrasulcular and semilunar incisions. (D) Reflection and degranulation. (E) Bone graft placement, (F) Suturing of palatal and buccal flaps 331

CHAPTER 41 Periodontal Flap Periodontal

Fig. 41.10: Papilla preservation flap-incisions

Table 41.1: Differences between various flap techniques

Modified Widman flap Undisplaced flap Apically-displaced flap I. Purpose 1. To expose root surfaces for 1. Accessibility for instrumentation. 1. Improves accessibility. instrumentation. 2. For removal of pocket lining. 2. To remove the pocket wall to 2. It also eliminates the pocket by (It is not indicated to eliminate/ reduce or eliminate the pocket. transforming the previously reduce pocket depth, except for (An excisional procedure of the unattached keratinized pocket the reduction that occurs in gingiva). wall into attached tissues. healing by shrinkage). (offers dual function).

II. Variations in the design It does not intend to remove the Internal bevel incision is started at or The internal bevel incision should be pocket wall but eliminate pocket near a point just coronal to the placed as close to the tooth as possible lining. Therefore, internal bevel projection of the bottom of the pocket (0.5 to 1 mm) because the purpose of incision starts close (no more than on the outer surface of the gingiva. this technique is to preserve maximum 1 to 2 mm apical) to the gingival (Only performed when sufficient amount of keratinized tissue, displace margin. attached gingiva is to be left behind). it apically and transform it into attached The incision should be scalloped to gingiva. The flap is positioned approxi- preserve as much as interdental papilla. mately at the tooth bone junction.

They are: alveolar crest. Vertical releasing incisions are not i. Modified Widman flap. required (different from Widman flap). ii. Undisplaced flap. Step 2: Gingiva is reflected with a periosteal elevator iii. Apically-displaced flap. Step 3: A crevicular incision is made. Step 4: After the flap is reflected, third incision is made in Modified Widman Flap (Figs 41.11 to 41.13) the interdental spaces with Orban's knife and the gingival collar is removed. Presented in 1974 by Ramfjord and Nissle. Step 5: Tissue tags and granulation tissue are removed with Step 1: It is an initial, internal bevel incision 0.5 to 1 mm a curette. The root surfaces are examined and away from the gingival margin, directed to the scaled.

332

PART IV PART Periodontal Pathology Periodontal

Figs 41.11A to F: Periodontal flap technique (Modified Widman flap). (A) Persistent pockets 2-3 weeks after initial therapy, (B) Facial incisions (internal bevel, crevicular), (C) Interdental incisions performed, (D) Facial flaps are reflected, (E) Curettage and root planing performed, (F) Interrupted interdental sutures are placed

Step 6: Bone architecture is not corrected, good approxi- Undisplaced Flap (Figs 41.14 to 41.16) mation of flaps is necessary, hence sometimes flaps In this procedure the entire soft tissue pocket wall is removed may have to be thinned. with the initial incision. Thus, it may be considered as inter- nal bevel gingivectomy. To perform this enough attached Step 7: Interrupted direct sutures are placed. gingiva should remain after removal of the pocket wall. 333

CHAPTER 41 Periodontal Flap Periodontal

Figs 41.12A to E: Case-2: Modified Widman flap procedure. (A) Preoperative view with probing. (B) Internal bevel and crevicular incisions are placed. (C) Flap reflection and degranulation. (D) Suturing with direct loop sutures. (E) Pack placed

Step 1: The pockets are measured with the periodontal Step 2: The initial, internal bevel incision is made following probe and a bleeding point is produced on the outer the scalloping bleeding points made on the gingiva. surface of the gingiva to mark the base of the pocket. This incision is usually carried to a point apical to In this procedure, the final placement of the flap is the alveolar crest depending on the thickness of the determined by first incision. tissue. The thicker the tissue, the more apical will

334

PART IV PART Periodontal Pathology Periodontal

Fig. 41.13: Modified Widman flap—various steps

be the end point. The flap should be thinned with Palatal Flap (Figs 41.17 and 41.18) the initial incision only. The surgical approach is different here because of the Step 3: The second or crevicular incision is made from the nature of the palatal tissue which is attached, keratinized bottom of the pocket to the bone. tissue and has no elastic properties associated with other Step 4: The flap is then reflected with a periosteal elevator gingival tissues, hence no displacement and no partial (blunt dissection). thickness flaps. Step 5: Interdental incision is made with an Orban’s Variations in the Techniques interdental knife. Step 6: Triangular wedge of tissue is removed with a curette. 1. Usual internal bevel incision, followed by crevicular and interdental incisions, but if the tissue is thick horizontal Step 7: The area is debrided, removing tissue tags and gingivectomy incision is made, followed by an internal granulation tissue with sharp curettes. The roots are bevel incision. Thinning of the flap should be done prior scaled. to reflection of the flap. Step 8: The flap is then placed back to end at the root bone 2. The apical portion of the scalloping incision should be junction. narrower than the line angle area, because the palatal Step 9: The flaps are sutured together with continuous sling root tapers apically, rounded scallop will result in suture or interrupted sutures. improper adaptation of the flap around root. 335

CHAPTER 41 Periodontal Flap Periodontal

Figs 41.14A to G: Undisplaced flap. (A) Preoperative view. (B) Internal bevel incision. (C and D) Reflection and degranulation. (E) Suturing buccal and palatal flaps. (F) Palatal view after suturing. (G) Facial view after healing

336

PART IV PART Periodontal Pathology Periodontal

Figs 41.15A to D: Case-2: Undisplaced flap—step-by-step procedure. Clinical presentation. (A) Incisions placed at the base of the pocket. (B) Flap reflection. (C) After thorough debridement, sutures are placed. (D) Facial view after healing

Basically, one should make sure the flap fits around the elevated with a periosteal elevator (either split tooth snugly without exposing the bone, to achieve this thickness or full thickness). proper placement of the incision is very important. Step 4: Remove all the granulation tissue, root planing is done and flap is positioned apically at the tooth Apically-displaced Flap bone junction. Used for both pocket eradication and/widening the zone of Step 5: Flaps are sutured together. attached gingiva. Step 1 : Internal bevel incision is made, 1 mm from the Distal Molar Surgery crest of the gingiva and directed towards the crest • For maxillary molars of the bone. • For mandibular molars. Step 2 : Crevicular incisions are made followed by initial Technique for maxillary molars (Fig. 41.19): Two parallel elevation of flap and then interdental incision is incisions at the distal surface of terminal tooth are made. performed, the wedge of tissue containing the The deeper the pocket, the greater will be the distance pocket wall is removed. between the two parallel incisions. Followed by this a Step 3: Vertical releasing incisions are made extending transversal incision is made so that a long rectangular piece beyond the mucogingival junction and flap is of tissue is removed. This can be confirmed with the regular 337

CHAPTER 41 Periodontal Flap Periodontal

Fig. 41.16: Undisplaced flap technique—various steps flap in the quadrant being treated. These incisions can be by the blood clot, which consists of a fibrin reticulum with placed using No. 12 blade, after flap reflection and curetting many polymorphonuclear leukocytes, erythrocytes, debris the bone surface, the flaps are sutured together. from injured cells and capillaries at the edge of the wound. There are also bacteria and an exudate or transudate as a Technique for mandibular molars (Figs 41.20A and B): Two result of tissue injury. parallel incisions at the retromolar pad area are made. The incisions should follow the areas of greatest attached gingiva One to three days after flap surgery—space between the flap and the tooth or the bone is thinner and epithelial cells and underlying bone. After the reflection of the flap and migrate over the border of the flap, when the flap is closely- removal of tissue, osseous surgery may be performed (if adapted to the alveolar process there is only a minimal necessary) and flaps are sutured so as to approximate the inflammatory response. flap margins closely to each other. One week after flap surgery—an epithelial attachment to the root has been established by means of hemidesmosomes HEALING AFTER FLAP SURGERY and a basal lamina. The blood clot is replaced by granulation Immediately after suturing (0 to 24 hours), connection tissue derived from gingival connective tissue, bone marrow between the flap and the tooth or bone surface is established and the periodontal ligament.

338

PART IV PART Periodontal Pathology Periodontal

Fig. 41.18: Palatal flap—step-by-step procedure

Figs 41.17A to C: Palatal flap

Fig. 41.19: Distal molar surgery for maxillary molars Two weeks after surgery—collagen fibers begin to appear parallel to the tooth surface. Union of the flap and the tooth One month after surgery—a fully-epithelialized gingival is still weak (due to immature collagen fibers) but clinically crevice with a well-defined epithelial attachment is present. it appears almost normal. Supracrestal fibers begin to adapt a functional arrangement. 339

HEALING AFTER FULL THICKNESS FLAP Same as above but superficial bone necrosis takes place in one to three days followed by osteoclastic resorption at 4 to

6 days and declines thereafter. This results in bone loss of CHAPTER 41 about 1 mm and greater, if the bone is thin.

1. Periodontal flap is a section of gingiva and or mucosa surgically-elevated from the underlying tissues to provide visibility of and access to the bone and root surface. 2. Periodontal flaps are classified according to the

thickness as, full thickness and partial thickness flap; Flap Periodontal and according to the placement of flap as displaced and undisplaced flap; according to the design of the flap as conventional flap and papilla preservation flap. 3. In conventional flap, horizontal incisions and vertical incisions are given. 4. There are three types of horizontal incisions, internal bevel, crevicular and interdental incision. 5. Currently there are three types of periodontal flaps available, Modified Widman flap, Undisplaced flap and Apically-displaced flap. 6. Main objectives of periodontal flap surgery are gain access to root surface, reduction or elimination of pocket depth and attempt regeneration of periodontal ligament, alveolar bone and cementum.

REVIEW QUESTIONS 1. Define and classify the periodontal flaps. Describe the step-by-step procedure of modified Widman flap. 2. What are the indications of flap surgery? 3. Describe healing following flap surgery.

BIBLIOGRAPHY 1. Jan Lindhe. Clinical Periodontology and Implant Dentistry, 4th edn, Blackwell Munksguard Publication, 2003. Figs 41.20A and B: Distal molar surgery for 2. Myron Nevins, James T, Mellning. Periodontal Therapy and mandibular molars Clinical Approaches and Evidence of Success, Vol. 1, Quintessence Publishing Co. Inc., 1998. 3. Newman, Takei, Fermin A Carranza. Clinical Periodontology, 9th edn, WB Saunders Co., 2002. 43 ChapterChapter

Mucogingival Surgery

 DEFINITION • Apical Displacement  MUCOGINGIVAL PROBLEMS • Other Techniques  OBJECTIVES, INDICATIONS AND  TECHNIQUES FOR ROOT COVERAGE CONTRAINDICATIONS • Indications  TECHNIQUES TO INCREASE WIDTH OF • Modifications ATTACHED GINGIVA  OPERATIONS FOR REMOVAL OF FRENA • Gingival Extension Operation

DEFINITION MUCOGINGIVAL PROBLEMS Mucogingival surgery was first introduced in the 1950s. These are: According to the glossary of periodontal terms mucogingival i. Pockets extending up to or beyond mucogingival surgery refers to “Periodontal surgical procedures designed junction to correct defects in the morphology, position and/or amount ii. Recession causing denudation of root surfaces of gingiva surrounding the teeth. Recently, it has been iii. High frenum and muscle attachments suggested that “periodontal plastic surgery” may be more iv. Inadequate width of attached gingiva. appropriate and would be defined as “Surgical procedures performed to correct or eliminate anatomic, developmental OBJECTIVES, INDICATIONS AND or traumatic deformities of the gingiva or alveolar mucosa”. CONTRAINDICATIONS OF MUCOGINGIVAL Mucogingival surgery consists of “plastic surgical SURGERY procedures for the correction of gingiva, mucous membrane Objectives relationships that complicate periodontal diseases and may interfere with the success of periodontal treatment” 1. Widening the zone of attached gingiva (According to Glickman). 2. Coverage of denuded roots 352

3. Removal of aberrant frenum. Various gingival extension procedures are: 4. Creation of some vestibular depth when it is lacking. Gingival augmentation apical to the area of recession. 5. As an adjunct to routine pocket elimination procedures. Free Soft Tissue Autograft Indications Advantages

1. Augmentation of the edentulous ridge. • High degree of predictability—only with increasing 2. Prevention of ridge collapse associated with tooth width of keratinized gingiva extraction. • Simplicity

PART IV 3. Crown-lengthening. • Ability to treat multiple teeth at the same time 4. Loss of interdental papilla which presents as esthetic/or • This procedure can be performed where there is phonetic defect. inadequate keratinized gingiva adjacent to the involved area. Contraindications

They are the same as in any other periodontal surgery. Disadvantages The treatment procedures that may fall within the • Two operative sites definition of periodontal plastic surgery are: • Compromised blood supply • Gingival augmentation procedures for correction of • Greater discomfort mucosal defects (around implants) • Lack of predictability in attempting root coverage. • Root coverage procedures

Periodontal Pathology Periodontal Free soft tissue autografts are indicated in the presence of: • Gingival preservation at ectopic tooth eruption • An inadequate zone of attached gingiva • Removal of aberrant frenulum • Abnormal muscle attachment • Ridge augmentation • Shallow vestibular depth • Crown-lengthening procedures. • Gingival recession The most commonly performed mucogingival surgical • Deep pockets to prevent rapid initial down growth of procedures are discussed in this chapter. epithelium.

TECHNIQUES TO INCREASE THE WIDTH OF Procedure ATTACHED GINGIVA • Classic technique Gingival Extension Operation • Variant techniques. The width of attached gingiva varies in different individuals The Classic Technique and on different teeth in the same individual. Attached (Figs 43.1A to H and 43.2A to H) gingiva is different from the keratinized gingiva. The width of the attached gingiva is determined by subtracting the Step 1: Eliminate the pockets—If pockets are present resect depth of the sulcus or pocket from the total distance between them with a gingivectomy incision and scale and plane the the crest of the margin to the mucogingival junction. root surfaces. If there are no pockets present in the area, the Originally, it was thought that minimal width of attached gingival margin is left intact. gingiva is required for optimal gingival health to be Step 2: Preparation of the recipient site—It can be done by maintained. However, several studies have challenged this two techniques. and concluded that even in the presence of minimal amounts 1. First technique: By incising at the existing mucogingival of attached gingiva the tissues can be maintained in a normal junction with a #15 BP blade to a little more than the state. desired depth and then blending the incision on both CHAPTER 43 Mucogingival Surgery 353 Free soft tissue autograft. (A) Lack of attached gingiva in relation to lower right lateral incisor, (B) Classic gingiva in relation to lower right lateral incisor, (A) Lack of attached tissue autograft. Free soft Figs 43.1A to G: Figs 43.1A technique—Surgical bed preparation, (C) procured from the palate, (D) Donor tissue placed on the surgical (C) Free gingival graft technique—Surgical bed preparation, site, (G) Periodontal dressing is placed covering the graft Tinfoil is sutured with silk sutures, (F) The graft bed, (E)

354 PART IV

Fig. 43.1H: Various steps in classic technique

ends with the existing mucogingival line. Periosteum The graft should consist of epithelium and a thin layer should be left covering the bone. of underlying connective tissue. Place the template over 2. Another technique: Consists of outlining the recipient the donor site and make a shallow incision around it with a

Periodontal Pathology Periodontal site with two vertical incisions from the cut gingival # 15 blade. Insert the blade to the desired thickness at one margin into the alveolar mucosa. Extend the incisions edge of the graft and elevate it by holding with tissue forceps to approximately twice the desired width of the attached or placing sutures at the margins of the graft. gingiva, allowing for 50 percent contraction of the graft Proper thickness is important for the survival of the graft. when healing is complete. A # 15 blade is inserted along It should be thin enough to allow the ready diffusion of the cut gingival margin and is used to separate a flap nutritive fluid from the recipient site. If it is too thin the consisting of epithelium and connective tissue graft may shrivel and expose the recipient site. If the graft without disturbing the periosteum. Suture the flap is too thick, its peripheral layer is jeopardized because of where the apical portion of the free gingival graft the excessive tissue that separates it from new circulation will be located. and nutrients. Thick grafts may also leave a deeper wound Grafts can also be placed directly on the bone tissue. at the recipient site and may cause damage to the palatal The advantages of this variant includes, less postoperative arteries. The ideal thickness of a graft is between 1 to 1.5 mobility of the graft, less swelling, better hemostasis—1½ mm. After the graft is separated, remove loose tissue tags to 2 times less shrinkage, however a healing lag is observed from the under surface. for the first two weeks. Next make a tinfoil template of the Step 4: Transfer and immobilization of the graft—Remove recipient site, to be used as a pattern for the graft. the excess clot from the recipient site because thick clot Step 3:Obtaining the graft from the donor site. interferes with vascularization of the graft. Position the graft For classic technique: A partial thickness graft is used, the and adapt it firmly to the recipient site. Dead space will sites from which it can be obtained are in order of preference: retard the vascularization and jeopardize the graft. Suture • Attached gingiva the graft at the lateral borders and to the periosteum to secure • Masticatory mucosa from an edentulous ridge it in position. Be sure that the graft is immobilized because • Palatal mucosa. movement interferes with healing. CHAPTER 43 Mucogingival Surgery 355 fter Case-2: Free soft tissue autograft. (A) Gingival recession with lack of attached gingiva. (B) Surgical bed preparation. tissue autograft. Case-2: Free soft

harvesting. (G) Graft tissue sutured with graft stretching and vertical sutures. (H) Facial view after healing tissue sutured with graft stretching and vertical sutures. (H) Facial view after harvesting. (G) Graft (C) Tinfoil template placed on palatal donor site. (D) Harvesting of graft tissue. (E) Harvested donor tissue. (F) Donor site a template placed on palatal Tinfoil (C) Figs 43.2A to H: Figs 43.2A 356

Step 5: Protection of the donor site—Cover the donor site The process of accepting a graft: with a periodontal pack for one week and repeat if necessary. I. Plasmatic circulation stage (2-3 Days): Direct joining A modified Hawley retainer is useful to cover the pack on of capillaries between the graft and the recipient bed the palate and over the edentulous ridges. is seen and capillaries of the recipient bed invade the Variant techniques graft. Four variants to the classic technique are described: II. Capillary circulation stage (4-5 Days): Capillaries a. Accordion technique start functional circulation again. The epithelium at b. Strip technique this stage is almost desquamated and sparse. III. Organization stage (10-14 Days): Organization is PART IV c. The connective tissue technique d. Combination of strip and connective tissue techniques. completed by growth of fibroblasts in the graft and in the recipient bed. The network of capillaries become Accordion technique (Figs 43.3A to F) dense and regeneration of epithelium becomes active Accordian technique has been described by Rateitschak and to complete the epithelialization (wound healing is colleagues. Expansion can be achieved by giving alternate by secondary intention). incisions on the opposite sides of the graft. Strip technique (Fig. 43.4) Apically-Displaced Flap (Fig. 43.6) The strip technique by Han and associates consists of 2 or This technique can be used for the combined purposes of 3 strips of tissue about 1 mm wide and long enough to cover eliminating pockets and widening the zone of attached the entire length of the recipient site. These strips are placed gingiva. Depending on the purpose it can be a full thickness at the center and base of the recipient site and sutured from Periodontal Pathology Periodontal (or) split thickness flap. The partial (split) thickness flap is the oral mucosa. The area is then covered with tinfoil and a generally used to avoid exposure of bone and the surgical pack. accompanying risks of bone resorption and aggravation of Connective tissue technique bone dehiscences and fenestrations. The full thickness flap The connective tissue technique was originally described is indicated when access to bone is desired for recontouring by Edel. The advantages of this technique include: purposes. a. Donor site—Healing by primary intention is achieved because the donor material can be obtained from Procedure connective tissue that is present beneath the palatal flap. b. Color matching is better. Step I : Internal bevel incision 0.5-1 mm from the crest of the marginal gingiva is given. Combination techniques Step II : Crevicular incision and interdental incisions are It can be performed as follows: placed. Remove a strip of tissue about 3 to 4 mm thick from the Step III : Vertical incisions extending beyond the palate, place it between two wet tongue depressors, and slice mucogingival junction are made so that the flap it longitudinally with a sharp BP blade. Use a superficial can be displaced easily. Reflect the flap portion that contains epithelium and connective tissue, and depending on the purpose (split thickness or the deeper portion that only consists of connective tissue. full thickness). Healing of the graft (Figs 43.5A and B) Step IV : Debride the area and place the flap apical to The full thickness graft consists of fat, glandular tissue as its original position and suture. well as the epithelium. It is not easily accepted and not The edge of the flap can be located in any of the three required in periodontal surgery. following positions: CHAPTER 43 Mucogingival Surgery 357 sferred Free soft tissue autograft (Accordion technique): (A) Lack of attached gingiva, (B) Recipient bed preparation, (Accordion technique): tissue autograft Free soft

Figs 43.3A to F: Figs 43.3A (C) tran the removal of tissue for grafting, (D) Donor tissue (with alternate incisions), (E) Graft Donor site immediately after to recipient site and sutured in place, (F) Various steps in Accordion technique. steps in to recipient site and sutured in place, (F) Various 358

1. Slightly coronal to the crest of the bone—This may create the risk of recurrent pockets with thick gingival margins. 2. At the level of the crest—This results in satisfactory gingival contour. 3. 2 mm short of the crest—This produces the most desired gingival contour because new tissue will cover the crest of the bone to produce a firm, tapered gingival margin. But it also increases the risk of a slight reduction in bone height. PART IV Fig. 43.4: Various steps in strip technique

Other Techniques for Widening the Zone of Attached Gingiva

Fenestration Operation/Periosteal Separation

It utilizes a partial thickness flap, except in a rectangular area at the base of the operative field where the periosteum is removed, exposing the bone. This is the area of fenestration and its purpose is to create a scar that is firmly bound to the bone.

The results obtained are not as predictable as those Periodontal Pathology Periodontal obtained with the free gingival graft or apically-displaced flap (Fig. 43.7). Fig. 43.5A: Healing of a grafted site Vestibular Extension Operation

Originally described by Edlan and Mejchar, it produces statistically significant widening of attached non- keratinizing tissue. Currently this technique is of historical interest only. Procedure The operative field is outlined by two vertical incisions from the junction of the marginal and attached gingiva to approximately 12 mm from the alveolar margin into the vestibule. The vertical incisions are joined by horizontal incision. A mucosal flap is elevated exposing the periosteum on the bone. The periosteum is separated from the bone, starting from the line of attachment of the mucosal flap. The periosteum including muscle attachments is transported to bone and is sutured to the inner surface of the periosteum. The periosteum is then transported to the lip and is, sutured where the initial horizontal incision was made. Gingival Augmentation coronal to Recession(root Fig. 43.5B: Healing phases of the graft coverage) CHAPTER 43 Mucogingival Surgery 359 classified Sullivan and Atkins Sullivan and Several classifications have been removal and/or cervical abrasions. to altering abusive toothbrushing techniques and/ or plaque removal. i. Shallow-narrow. ii. Shallow-wide. iv. Deep-wide. iv.fail to respond Manage mucogingival defect which iii. Deep-narrow. iii.the defects resulting from root caries Manage Miller (1985) expanded this classification so as to help isolated gingival recession into four types: Classification— proposed in 1960s, the clinician to predict the outcome of the therapy. The the clinician to predict the outcome of the therapy. following four classes of recession have been proposed by Miller (Figs 43.8A to D). Recession can also be generalized and localized (Figs 43.9A and B). b. Various steps in apically-displaced flap steps Various Fig. 43.6: Periosteal separation/fenestration Fig. 43.7: i. root sensitivity. Reduces ii. Improves esthetics. Advantages for root coverage procedures are: coverage procedures Advantages for root Procedures for Root Coverage a.

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Fig. 43.8D: Class I, II, III and IV recession

Class II : Marginal tissue recession that extends to or beyond the mucogingival junction. There is no loss of bone and soft tissue in the interdental area. This type of recession may be wide or narrow. Class III : Marginal tissue recession that extends to or beyond the mucogingival junction. In addition, there is bone and/or soft tissue loss interdentally or tooth may be malposed. Class IV : Marginal tissue recession extends to or beyond the mucogingival junction. With severe bone and soft tissue loss interdentally and/or severe tooth Figs 43.8A to C: Miller’s classification of gingival recession (Class I, II and III) malposition. Type of recession Prognosis Class I: Marginal tissue recession that does not extend to Class I and II — good to excellent the mucogingival junction. There is no loss of Class III — only partial coverage can be bone or soft tissue in the interdental area. This expected type of recession can be narrow or wide. Class IV — very poor. CHAPTER 43 Mucogingival Surgery 361 (Figs 43.10A to C) (Figs 43.10A Make an incision, resecting gingival margin This band of marginal around the exposed roots. The gingiva is removed with a scaler or curette. exposed root surface is planed well. If granulation tissue is present along the incised edge of the gingiva, it should be removed carefully with curettes. a # 15 blade a vertical incision is made With gingiva into the extending from marginal adequate donor tissue laterally. gingiva. the adjacent teeth. The following is the step-by-step procedure for laterally- Regenerative procedures: Regenerative has been proposed. regeneration (GTR) Guided tissue Pedicle autografts: a. Laterally (Horizontally) displaced flap an original and unique developed Warren In 1956, Grupe and sliding flap operation. procedure called the flap: Advantages of laterally-displaced a. site One surgical b. flap. Good vascularity of the pedicle c. denuded roots that have Ability to cover isolated, flap: Disadvantages of laterally-displaced a. adjacent keratinized attached Limited by the amount of b. at the donor site. Possibility of recession c. Dehiscence or fenestration at the donor site. d. recession. Limited to one or two teeth with gingival Indications: a. For covering the isolated denuded root. b. is sufficient width of interdental papilla in When there c. vestibular depth. Sufficient Contraindications: a. Presence of deep interproximal pockets. b. Excessive root prominence. c. root abrasion or erosion. Deep or extensive d. Significant loss of interproximal bone height. displaced flap: IStep : site of the recipient Preparation II : Step (A) Localized recession, (B) Generalized recession Figs 43.9A and B: i. Free soft tissue autograft. ii. connective tissue grafts are available. Subepithelial If the donor site is associated with inadequate width: Conventional procedures Depending on the width of the attached gingiva, i.e. if adequate width is present at the donor site the following procedures can be selected: a. Laterally (horizontally) displaced flap. b. flap. Double-papilla c. Coronally-positioned flap Procedures for root coverage can be divided into: for root Procedures 1. Conventional procedures. 2. Regenerative procedures.

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Figs 43.10A to C: Laterally-displaced flap. (A) Preoperative view, (B) Postoperative view (after 2 month), (C) Various steps in laterally position flap mucogingival junction. A crevicular incision is recipient site. This will enable us to slide the then made from the vertical incision to the defect. flap laterally without excess tension at the base. A flap is then raised utilizing either partial Step III : Transfer the flap thickness or full thickness reflection. Each of After the flap is transferred onto the adjacent these has its own advantages and limitations, root, the flap is sutured to the adjacent gingiva e.g. partial thickness flap offers advantages like and alveolar mucosa with interrupted sutures. rapid healing at the donor site and reduced risk Step IV : Protect the flap and donor site of facial bone loss. However, if the gingiva is Cover the surgical site with a periodontal pack thin, flap survival becomes difficult. It may and after one week the pack and sutures can sometimes be necessary to give a short oblique be removed. Postoperatively, antibiotics are not incision into the alveolar mucosa at the distal always necessary in the normal course of corner of the flap, pointing more towards the treatment, but analgesics are prescribed to CHAPTER 43 Mucogingival Surgery 363 incisions, extending from a point coronal to the incisions, extending from a point coronal and distal cementoenamel junction at the mesial into the line angles of the tooth and apically lining mucosa. and is dissection at the mesial and distal ends incision. connected with an intracrevicular apical to the recession, a full thickness Facially, flap is raised. Some authors have debrided thoroughly. a pH 1.0 suggested the use of citric acid with for conditioning the root surface. the bone approximately 3 mm apical to dehiscense, a horizontal incision is made through the periosteum, followed by a blunt dissection into the lining mucosa to release muscle tension. Now the mucosal graft can be easily positioned coronally at the level of cementoenamel junction. interrupted sutures and additional sling sutures can be placed to maintain the flap in place. Periodontal dressing is placed to protect the wound during initial healing. Make two apically-divergent vertical releasing vertical Make two apically-divergent by sharp A split thickness flap is prepared are Once the flap is reflected the root surfaces the flap, At the base of the inner surface of The flap is secured firmly with the help of the existing problem. be performed utilizing two techniques. This procedure can Advantages: • root exposure. areas of of multiple Treatment • of adjacent teeth. No need for involvement • High degree of success. • work, it does not increase Even if the procedure does not Disadvantage: procedures if the zone of two surgical There is a need for is inadequate. keratinized gingiva First Technique 1Step : 2Step : 3Step : 4Step : 5Step : Modifications: One of the limitations of this procedure is, it cannot be width of attached performed when there is insufficient (Figs 43.11A to G) (Figs 43.11A Having to join together the small flap control pain. The flap may heal by connective The flap may control pain. tissue attachment or connective tissue adhesion, Some of the epithelium. or long junctional better results with citric acid studies have shown root conditioning. (Figs 43.12 and 43.13) the interdental bone is more resistant to loss than is radicular bone. gingiva than from the radicular surface of a tooth. mucogingival problem are sufficiently wide. mucogingival problem are sufficiently to allow for a Lateral Pedicle Flap. is insufficient a vertical or oblique incision at the distal end of the a vertical or oblique flap which is being transposed is donor site so that the wider at its base. of recession undisturbed in order to reduce the likelihood and bone resorption. Disadvantage: sensitive— Technique Indications: • Esthetic coverage of exposed roots. •sensitivity owing to gingival recession. For tooth 2. The papillae usually supply a greater width of attached 3.fairly good. The clinical predictability of this procedure is c. Coronally-repositioned flap or coronally-positioned flap Advantages: 1. The risk of loss of alveolar bone is minimized because in such a way so that they act as a single flap. Indications: 1. to the When the interproximal papillae adjacent 2. tooth When the attached gingiva on an approximating 3. pockets are not present. When periodontal b. Double papilla flap Lateral as the Double Wainberg First described by Cohen and Ross as Repositioned Flap and was refined by the Double Papilla Flap. b. is left periodontium site, the marginal In the donor Modifications: drawbacks of the procedure many Considering the sliding flap have been proposed. modifications of lateral a. the recipient site and oblique incisions over Converging

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Figs 43.11A to F: Double papilla flap. (A) Recipient site preparation, (B) Two vertical or oblique incisions at mesial and distal end of the defect, (C) Flaps are reflected (partial thickness), (D) The transposed flaps are sutured to obtain a single flap, (E) Final suturing, (F) The area covered with periodontal dressing

gingiva. To solve this problem, a two stage surgical Second Technique procedure has been proposed. First, a gingival extension Semilunar flap (Figs 43.14A to C) operation with a free gingival graft is performed. Two months later a second stage surgery is performed by Indication: coronally repositioning the flap which may include free soft • Areas where gingival recession is only 2 to 3 mm. tissue graft. CHAPTER 43 Mucogingival Surgery 365 Various steps in double papilla flap (Refer the text for explanation) Various

Various steps in coronally-positioned flap (Refer the text for explanation) Various

releasing incisions are placed, (C) Flap positioned coronally and sutured Fig. 43.11G: Fig. 43.12D: Coronally-positioned flap. (A) Measure the width and length of gingival recession (class I), (B) Two vertical Two (class I), (B) Coronally-positioned flap. (A) Measure the width and length of gingival recession

Figs 43.12A to C: Figs 43.12A

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Figs 43.13A to H: Case 2: Coronally repositioned flap procedure. (A) Preoperative view showing class I Miller’s recession. (B) Incision, (C) Reflection of flap, (D) Coronally displaced flap, (E) Root conditioning with tetracycline soaked cotton pellet, (F) Suturing of coronally displaced flap, (G) Tin foil placed prior to pack placement, (H) Facial view after healing CHAPTER 43 Mucogingival Surgery 367 A horizontal right angled incision is made in the vertical incision interdental papillae, followed by, at the proximal line angles of the adjacent teeth. The periosteum The retracted tissue is excised. graft A should be left intact in the apical areas. is obtained from the donor site, transferred to the recipient site and immobilized. Donor site is protected as described earlier. The tissue will now collapse freely, covering the The tissue will now collapse freely, The flap is then held in place with denuded root. is not a moist gauze for a few minutes. Suturing may be generally required. Periodontal dressing placed. Free Gingival Autograft Free Gingival The classic technique proposed for creating a widened zone of attached gingiva was described in the earlier section of this Miller in 1985, applied this with few modifications to chapter. The procedure is as follows: cover the denuded roots. 1Step : Step 3 : Step Various steps in semilunar flap (Refer the text for explanation) Various (B) Semilunar incision and coronal displacement of flap (B) Semilunar incision and coronal displacement Semilunar flap: (A) Class I gingival recession in relation to 21-preoperative view, Semilunar flap: (A) Class I gingival recession

Fig. 43.14C: Figs 43.14A and B: and Figs 43.14A A semilunar incision is placed, following the curvature of the gingival recession, make sure that the incision ends about 2 to 3 mm short of as This is very important, the tip of the papillae. the flap derives all of its blood supply from the adjacent papillary areas. Split thickness dissection is performed coronally and this is connected to an intracrevicular incision. dehiscence or fenestration. positioned flap. Step 2Step : Step 1Step : Disadvantages: • of gingival recession. areas Inability to treat large • The need for a free gingival graft if there is an underlying Advantages: •coronally- No vestibular shortening, as occurs with the • No esthetic compromise of interproximal papillae. • No need for sutures. 368

Subepithelial Connective Tissue Graft the gingival margin, perpendicular to the long axis of (Figs 43.15A to F) the teeth. The second incision is made parallel to the long axis of the teeth, 1 to 2 mm apical to the first Proposed by Langer and Langer in 1985. In 1994, Bruno incision. A small periosteal elevator is used to raise a described modification of the original Langer and Langer full thickness periosteal connective tissue graft. technique. Vertical incisions may be necessary at the mesial and Indications: distal extent of the graft to facilitate easy removal of • Where esthetics is of prime concern the connective tissue.

• For covering multiple denuded roots Once the graft is removed, the area is sutured with PART IV • In the absence of sufficient width of attached gingiva in 4-0 silk suture material. the adjacent areas. III. Grafting to the recipient site: The donor connective Advantages: tissue is secured to the papillae with interrupted sutures • High degree of cosmetic enhancement and the overlying partial thickness flap is then replaced • Incurs no additional cost for autogenous donor tissue over the donor tissue and interrupted sutures are placed • One step procedure in the mesial and distal papillae. No attempt is made • Minimal palatal trauma to cover the donor tissue completely. A periodontal • Increased graft vascularity. dressing is placed to cover the surgical site. The routine postoperative care is followed. The dressing and Disadvantages: sutures are removed after seven days postoperatively. • High degree of technical skills required. Periodontal Pathology Periodontal • Complicated suturing. Modifications: The technique is as follows: In the recipient site preparation: I. Preparation of recipient site: The initial horizontal a. Envelope technique (Fig. 43.17): In this technique, first right angle incision is made into the adjacent eliminate the sulcular epithelium by an internal bevel interdental papillae at, or slightly coronal to the incision. Secondly, an ‘envelope’ is prepared apically cementoenamel junction of the tooth with an exposed and laterally to the recession by split incision. root surface. A butt joint is provided. It is made sure b. Langer’s technique (Figs 43.18A to D): In addition to that the papillary incisions are not more than 1 mm the horizontal incision, two vertical releasing incisions deep, this is done to preserve the papillary blood 1 to 2 mm away from the gingival margin, extending supply. A partial thickness flap is raised without one-half to one tooth wider mesiodistally than the area vertical incisions. The exposed root is meticulously of gingival recession, is given. planed with curettes. At times, it may be desirable to c. Pouch and tunnel technique (Figs 43.19 and 43.20): In use finishing burs to reduce the root convexity. case of multiple adjacent recessions “envelopes” are Following root planing, the root is treated with either prepared on each tooth for receiving connective tissue citric acid pH 1.0 or tetracycline HCl in a concentration graft. of 250 mg mixed in 5 ml of sterile water. The solution is applied to the root surface for 2 to 3 minutes with Procuring the Graft from the Donor Site cotton pellets. Once the root is treated, the approximate In the palate, a partial thickness flap is raised with two mesiodistal width necessary for the graft is measured vertical releasing incisions, followed by this, the connective with a periodontal probe. tissue is harvested by placing two horizontal and two vertical II. Excision of the donor tissue (Fig. 43.16): The first incisions to the bone. After the graft removal, the flap is incision is made approximately 2 to 3 mm apical to positioned back and sutured. CHAPTER 43 Mucogingival Surgery 369 Subepithelial connective tissue graft.

Various steps in free connective tissue graft— Various Recipient site preparation (Refer the text for explanation) Fig. 43.15F: (A) A recession defect at a maxillary right canine, (B) Recipient A (A) from the connective tissue graft (C) Procuring site preparation, is placed in the recipient site and secured (D) The graft palate, in position with interrupted sutures, (E) Shows 3 months healing result Figs 43.15 A to E: A Figs 43.15

370 PART IV

Fig. 43.16: Various steps in free connective tissue graft— Fig. 43.17: Various steps in free connective tissue graft—

Donor site preparation Envelope technique Periodontal Pathology Periodontal

Figs 43.18A to D: Subepithelial connective tissue graft (Langer’s technique). (A) A gingival flap is reflected with two vertical incisions, (B) A large connective tissue graft is sutured in place, (C) Two weeks postoperative view, (D) Various steps in Langer’s technique CHAPTER 43 Mucogingival Surgery 371 Various steps in tunnel procedure Various Figs 43.20A to F: Figs 43.20A Various steps in pouch and tunnel technique steps Various Fig. 43.19: 372

• For areas of root sensitivity where oral hygiene is impaired. • For repair of recessions associated with failing or unesthetic class V restorations. Advantages: • Techniques does not require a secondary donor surgical site reducing postoperative discomfort. • New tissue blends evenly with the adjacent tissue, providing highly esthetic results.

PART IV Disadvantages: • It is sensitive technique. • Insurance of additional cost of . The technique consists of the following steps: Step 1 : A full thickness flap is raised up to the mucogingival junction, beyond it, atleast 8 mm apical to the mucogingival junction a partial thickness flap is raised. Step 2 : The root surface is meticulously planed, and a Goretex membrane is trimmed according to the

size of the defect and tied to the tooth. Make Periodontal Pathology Periodontal sure that it covers at least 2 mm of marginal periosteum. In order to prevent the membrane from collapsing in the defect, some authors have suggested to pass a suture through the membrane, that covers the bone and this suture is knotted on the exterior and tied to bend the membrane, so that a space is created between the root and the membrane. Step 3 : The flap is then positioned coronally and sutured. Four weeks later, the membrane is carefully removed without disturbing the growing tissue.

Modifications a. Titanium–reinforced membranes are used to create the space below the membrane. Figs 43.20G to I: Various steps in tunnel procedure b. Resorbable membranes have been used to prevent a second surgery. GUIDED TISSUE REGENERATION TECHNIQUE FOR ROOT COVERAGE OPERATIONS FOR REMOVAL OF FRENA Indications A frenum is a fold of mucous membrane usually with • Esthetic demand. enclosed muscle fibers, that attaches the lips and cheeks to • Indicated for single tooth with wide, deep localized the alveolar mucosa and/or gingiva and underlying recessions. periosteum. CHAPTER 43 Mucogingival Surgery 373 Where the frenum is Where the frenum Where the frenum is attached in the Where the frenum It is the incision and relocation of the incision and relocation It is the Where the frenum is inserted into the Where the frenum Where the frenum is in the attached gingiva. After anesthetizing the area, engage the frenum After anesthetizing the area, engage with a hemostat. hemostat, Incise along the upper surface of the along the simultaneously make a similar incision under surface of the hemostat. of the Remove the triangular resected portion frenum along with hemostat. This exposes the to the bone. fibrous connective tissue attachment and separate Make a horizontal incision to dissect the fibers attached to the bone. sutures. Close the wound by placing interrupted Frenotomy: Frenotomy: Frenal attachment may be of four types (Figs 43.21A Frenal attachment Papillary: interdental papilla. Mucosal type: alveolar mucosa. Papillary penetrating types: to palatal papilla. inserted from the facial Gingival: Step 1Step : 2Step : 3Step : 4Step : 5Step : Techniques for the Removal of the Techniques Frenum (Figs 43.22A to I) frenum to create a zone of attached gingiva between the attached gingiva create a zone of frenum to for periodontal and the frenum (Suffices gingival margin problems). to D). a. b. c. d. the frenum with a hemostat Types of frenal attachments Types Frenectomy procedure. (A) A case of high frenal attachment with tension test being positive, (B) Engage A Frenectomy procedure. (A)

It is the complete removal of frenum Figs 43.21A to D: Figs 43.21A may aggravate its severity. Frenectomy: Figs 43.22A and B: Figs 43.22A To prevent: To 1. The accumulation of irritants. 2. which The deflection of the wall of periodontal pocket 3. interference with post-treatment healing. Its 4. formation. Pocket 5. while brushing. Injury Indications It is indicated for, including its attachment to the bone. correction of abnormal diastema.

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Figs 43.22C to H: (C) After removal of triangular resected portion of the frenum, (D) The wound is closed with interrupted sutures, (E) A case of frenectomy, (F) Frenum relieved, (G) Sutures placed, (H) Clinical appearance parmediately after suture removal CHAPTER 43 Mucogingival Surgery 375 physiologic hyperpigmen- →

KNOW MORE ... treatment. (GTR) using various barrier membranes have been used (GTR) using various barrier membranes successfully to cover the denuded roots. to the bone. Whereas frenotomy is the its attachment create a zone of incision and relocation of the frenum to margin and the attached gingiva between the gingival frenum. 1. vestibular depth. Lack of sufficient 2. crown length for restorative procedures. Inadequate 3. Denuded root surface. 4. Alveolar defects. 5. Open gingival embrasures. 6. Excessive gingival pigmentation. 7. frenum. Aberrant 8. gingiva. Inadequate attached 9. teeth requiring orthodontic Impacted/unerupted 9. tissue regeneration Regenerative procedures like guided tation can be managed by mucosal excision, cryosurgery tation or laser surgery. 10. Excessive gingival display and gingival asymmetry. Gingival depigmentation 1996 World Workshop in Clinical Periodontics 1996 World as Periodontal Renamed Mucogingival Surgery Plastic Surgery The following problems are included: 10. Frenectomy is the complete removal of frenum including Various steps in frenectomy (Refer the text for explanation) Various Fig. 43.22I: autograft. techniques like fenestration operation and vestibular extension operation. shallow-narrow, shallow-wide, deep-narrow and deep- shallow-wide, deep-narrow and shallow-narrow, wide, PD Miller has modified this into Class-I, Class-II, Class-III and Class-IV gingival recession. • Conventional, e.g. pedicle autografts. • Regenerative procedures. donor site the following conventional procedures can be selected: • Laterally displaced flap • flap Double papilla • Coronally-positioned flap and semilunar flap. • and Free soft tissue autograft, •available. are Subepithelial connective tissue grafts procedures for the correction of gingiva mucous procedures for the correction of gingiva that complicate periodontal membrane relationships success of diseases and may interfere with the treatment. periodontal surgery”. procedures are: • of attached gingiva to increase width Techniques • Root coverage procedures • Operations for removal of frena. are: • tissue Gingival extension operation by free soft • Apical displacement of the pocket wall and other 6. Procedures for root coverage are divided into: 7. of the attached gingiva is adequate in the If the width 8. If the donor site is associated with the inadequate width: 5.Atkins have classified gingival recession into, Sullivan and 2. plastic been renamed as “Periodontal it has Recently, 3. Most commonly performed mucogingival surgical 4. gingiva of attached for increasing width Techniques 1. of plastic surgical consists Mucogingival surgery 376

Surgical → ideally, crown Surgical Techniques for Reconstruction lengthening procedure should endure ostectomy along of Missing Papilla with apically repositioned flap. Hence excising the gingiva Beagle (1992) proposed a pedicle graft procedure utilizing alone to increase the crown length would be inadequate. a split thickness flap which is dissected from the palatal Interdental papilla reconstruction → the most common aspect of the interdental area. The flap is elevated labially, cause of “black triangles” between the teeth is loss of folded and sutured to create the new facial papilla. papilla height as a result of loss of periodontal support Han and Takei (1996) proposed a surgical approach due to plaque-associated lesions. semilunar coronally repositioned flap based on the use of a free connective tissue graft. Nordland and Tarnow (1998) proposed a classification Many other techniques have also been proposed, system regarding papillary height based on three PART IV some of them utilizes microsurgery but none of them have anatomical landmarks (Fig. 43.23): exhibited any predictable results. a. The interdental contact point. b. The apical extent of CEJ (facial cementoenamel junction). REVIEW QUESTIONS c. The coronal extent of the proximal CEJ. Normal: The interdental papilla occupies the entire space 1. Enumerate various mucogingival problems. apical to the interdental contact point/area. 2. Describe the techniques to increase width of attached Class I: The tip of the interdental papilla is located between gingiva. the interdental contact point and the level of the proximal 3. Define gingival recession. Write about the etiology, CEJ. Class II: The tip of the interdental papilla is located at or classification and procedures for covering the denuded apical to the level of the proximal CEJ but coronal to the root surfaces. facial CEJ. 4. Differences between frenectomy and frenotomy.

Periodontal Pathology Periodontal Class III: The tip of the interdental papilla is located at or apical to the level of facial CEJ. Treatment of “Black Triangles” include: BIBLIOGRAPHY • Orthodontic treatment. • Modification of crowns. 1. American Academy of Periodontology. Proceedings of the World • Esthetic restoration. Workshop in Clinical Periodontics. Annals of Periodontology, • Combination therapy. Chicago 1996, The Academy.

Fig. 43.23: Illustration of classification system for papilla height CHAPTER 43 Mucogingival Surgery 377 9th edition, WB Saunders. 9th edition, coverage revisited. Periodontol 2000, making in aesthetics: Root 2001;27. surgery in the treatment of regeneration versus mucogingival 1992;63:919. Periodontol recession. J human buccal gingival Periodontol 1993;111-4. 6. Clinical Periodontology, A. Caranza. Fermin Newman, Takei, 7. Decision Alain Borghetti. Jacques Marlot, Philippe Bouchard, 8. et al. Guided tissue Vincenzi-G, Tinti-C, Pini-Prato G, 9. Curr Opin Jr Periodontal plastic surgery. Preston D Miller, new attachment following the treatment of a human buccal treatment of a human following the new attachment tissue regeneration procedure. means of a guided recession by 387. J Periodontol 1993; 64: successful and predictable A following citric acid application. wide recession. Int J Periodont Restor procedure in areas of deep Dent 1985;5:15. Periodontol 2000. 1996;2-7. plastic surgery. Quintessence Volume-1, of success, approaches and evidence Publishing Co. Inc. (1998). 2.of assessment Histologic C, Pini-Prato GP. Clauser P, Cortellini 3. a free soft tissue autograft Root coverage using Miller PD Jr. 4.of the periodontal The development EP. Allen Miller PD Jr, 5. clinical Mellonig. Periodontal therapy T Myron Nevins, James

44 ChapterChapter

Furcation Involvement and its Management

 DEFINITION  PROGNOSIS  ETIOLOGY  TREATMENT  CLASSIFICATION  INDICATIONS AND CONTRAINDICATIONS ROOT  CLINICAL FEATURES RESECTION AND SEPARATION

DEFINITION 2. Root separation—It is the portion of the tooth where adjacent roots forming the furcation are not in contact Furcation involvement refers to commonly occurring with each other and are separated by alveolar bone. conditions in which the bifurcations and trifurcations of 3. The surface of the tooth just coronal to the root multi-rooted teeth are invaded by the disease process. separation. This area is usually concave, grooved or According to American Academy of Periodontology fluted. (2001), “It is defined as pathologic resorption of bone within 4. The roof of furcation which contains furcation ridges. the furcation”. These ridges run mesiodistally in lower and buccolingually in upper molars. ETIOLOGY The roof of the furcation is concave in about 50 percent of maxillary first molars and is located 4.5 mm apical to the Primary Etiologic Factor cementoenamel junction. The roof is 0.5 to 1 mm coronal It is bacterial plaque and long-standing inflammation of to the root separation. Access to this area is extremely periodontal tissues. difficult for instrumentation of deep pockets. The extent of attachment loss in the is Anatomic and clinical characteristics of tooth, bone and related to: gingiva are of importance for the clinical management of furcation lesions.

Anatomic Considerations (Fig. 44.1) Tooth 1. Root trunk length—It is the portion of the root between The following features should be considered: cementoenamel junction and the separation of the roots a. Root trunk length—When the root trunk is short, the (Fig. 44.2). furcation will become involved early in the disease

382 PART V

Fig. 44.1: Anatomic considerations

mesiobuccal root of maxillary first molar and mesial root of mandibular first molar. c. Degree of separation of roots/inter-radicular dimension—Wide separation of roots improves access, thereby facilitating instrumentation. d. Cervical enamel projections—They occur approximately

Treatment of Periodontal Diseases Periodontal of Treatment in 15 percent of molars. They favor plaque accumulation and must be removed to facilitate scaling and root planing. It was classified by Masters and Hoskins in 1964 as: Grade I: The enamel projection extends from the Fig. 44.2: Relationship between disease involvement and trunk length cementoenamel junction of the tooth toward the furcation entrance. process. When the root trunk is long the furcation will Grade II: The enamel projection approaches the entrance be invaded later, but will be more difficult for to the furcation but does not enter the furcation and hence instrumentation. has no horizontal component. b. Concavity of the inner surface of exposed roots—All Grade III: The enamel projection extends horizontally the root surfaces facing the furcation exhibit some degree into the furcation. of concavity or depression in an occlusoapical direction. e. Anatomy of the furcation—Presence of bifurcation This may make instrumentation for plaque removal and ridges, presence of accessory canals can complicate the root planing almost impossible. But these concavities furcation treatment. increases the attachment area of a tooth and produce a f. Presence of accessory pulpal canals—It is believed that root shape that is resistant to torque. It is common in once the pulp is infected through the accessory canal, 383

endoperiocommunication may result, which in turn can CLASSIFICATION cause either destruction of interradicular periodontium or interfere with the healing response of either Glickman in 1953 (Figs 44.3A to D) had classified periodontal or endodontic procedures. furcation involvement into: Grade I: It is the incipient or early lesion. The pocket is 44 CHAPTER Bone suprabony, involving soft tissue. There is slight bone loss Bone shape in the exposed furcation area has a horizontal in the furcation area. No radiographic changes. component that determines the grades (I, II and III) of the Grade II: In grade II cases bone is destroyed on one or involvement and a vertical component that most often more aspects of the furcation, but a portion of alveolar bone creates a depression in the center of the remaining bone and periodontal ligament remains intact, permitting only similar to a crater in an interdental area. The vertical compo-

partial penetration of the probe into the furcation. The lesion Management Its and Involvement Furcation nent can also appear as a vertical or angular loss toward is essentially a cul-de-sac. The radiograph may or may not one of the roots. The latter defect can have one, two or three reveal the grade II involvement. osseous walls or can be funnel-shaped around one root. Grade III: In this type of furcation involvement, the inter- Gingiva radicular bone is completely lost but the facial or lingual The presence of sufficient attached keratinized gingival surfaces are occluded by gingival tissues. Therefore, the tissue and adequate vestibular depth will facilitate the furcation opening cannot be seen clinically, but it is gingival management of the furcation area. essentially a through and through tunnel. If the radiographs

Figs 44.3A to D: Glickman’s classification of furcation involvement: (A) Grade I, (B) Grade II, (C) Grade III, (D) Grade IV 384

are taken with proper angulation and the roots are divergent, facilitate visualization and radiographs also help detect the the lesion will appear as a radiolucent area between the roots. furcation invasions.

Grade IV: As in grade III lesions, the inter-radicular bone is Other classifications include: completely lost but in grade IV involvement the gingival According to Goldman (1958): tissues recede apically so that the furcation opening is seen Grade I : Incipient. clinically. The radiographic changes are essentially the same Grade II : Cul-de-sac. as that of grade III lesion. Grade III : Through and through.

Based on vertical component (Tarnow and Fletcher in According to Ramfjord and Ash (1979): PART V 1984) (Fig. 44.4) Class I : Beginning involvement. Tissue destruction Depending on the distance from the base of the defect to less than 2 mm (i.e less than 1/3rd tooth the roof of the furcation, furcations can be classified as: width) Class II : Cul-de-sac. Tissue destruction more than Subgroup A: Vertical destruction of bone upto one-third of 2 mm (i.e. more than 1/3rd tooth width) the inter-radicular height (0-3 mm). but not through and through. Subgroup B: Vertical destruction of bone upto two-third of Class III : Through and through involvement. the inter-radicular height (4-7 mm). Subgroup C: Vertical destruction beyond the apical-third (7 mm or more). Based on horizontal component (Hamp and Coworkers in 1975) (Fig. 44.5) Furcations can be classified as: Degree I : Horizontal bone loss of less than 3 mm. Degree II : Horizontal bone loss of more than 3 mm.

Treatment of Periodontal Diseases Periodontal of Treatment Degree III : Through and through horizontal lesion. Furcation can be clinically-detected by using Naber’s probe along with a simultaneous blast of warm air to Fig. 44.4: Vertical classification of furcation involvement

Fig. 44.5: Horizontal classification of furcation involvement (Hamp and coworkers) 385

According to Fedi (1985): pockets. Plaque, calculus and bacterial debris occupy the Its a combination of Glickman’s and Hamp’s classification. denuded furcation space. Grade I : It is the incipient or early lesion. The pocket is suprabony, involving soft tissue. There PROGNOSIS HPE 44 CHAPTER is slight bone loss in the furcation area. No Maxillary first premolars and maxillary as well as radiographic changes. mandibular molars are the teeth with multiple roots. Grade II : In grade II cases bone is destroyed on one Furcation involvement will be likely to occur in these or more aspects of the furcation, but a multirooted teeth. Maxillary first premolar often shows portion of alveolar bone and periodontal fusion of the roots and the furcation area may be located ligament remains intact, permitting only very much apically and also the roots of the maxillary first partial penetration of the probe into the

premolars are placed buccally and palatally with furcation Management Its and Involvement Furcation furcation. The lesion is essentially a cul- opening in a mesiodistal direction. For these reasons, furcation de-sac. The radiograph may or may not involvement in maxillary first premolar has poor prognosis. reveal the grade II involvement. In the case of maxillary molars furcations may open Grade II : Can be further divided into: bucally, mesially and distally because of the presence of Degree I : Interradicular bone loss less than 3 mm. the three roots. Since access from proximal areas is difficult Degree II : Interradicular bone loss more than 3 mm. for plaque control, prognosis of furcation involvement in Grade III and Grade IV are same as Glickman’s maxillary molars is not good. classifications. Mandibular molars have two roots, placed mesially and distally and the furcation opens buccolingually. The roots CLINICAL FEATURES are usually divergent especially in mandibular first molars. Clinically As a result prognosis of furcation involvement in mandibular molar (especially the first molar) is considered good. 1. The mandibular first molars are the most common sites and maxillary premolars are the least common. TREATMENT 2. The denuded furcation may be visible clinically or covered by the wall of the pocket. It is aimed to prevent further attachment loss and improve 3. Associated with suprabony and infrabony pockets. the maintenance of furcation area. Two treatment modalities 4. Periodontal abscess. have been proposed: 5. Root caries and tooth mobility are common. 1. Traditional treatment procedures. 2. Reconstructive or regenerative treatment.

Microscopically Factors to be considered when deciding on a mode of therapy It is simply a phase in the rootward extension of the are as follows: periodontal pocket. In its early stages, there is a widening 1. Degree of involvement. of the periodontal space with cellular and inflammatory fluid 2. Crown root ratio. exudation, followed by epithelial proliferation into the 3. Length of roots. furcation area from an adjoining periodontal pocket. 4. Degree of root separation. Extension of the inflammation into the bone leads to 5. Strategic value of the tooth or teeth in question. resorption and reduction in bone height. The bone 6. Root anatomy of the involved tooth. destructive pattern may produce horizontal loss, or there 7. Residual tooth mobility. may be angular osseous defects associated with infrabony 8. Endodontic therapy and complications. 386

9. Ability to eliminate the defect. Reconstructive and Regenerative Treatment 10. Periodontal condition of the adjacent teeth. Procedures

Grade I: Traditional treatment will do. Traditional Treatment Procedures Grade II: Various regenerative techniques include: They are those which are directed to maintain the state of a. Autogenous bone grafting, e.g. osseous coagulum, bone the health but do not attempt to regenerate the lost blend. periodontium. The goal is to prevent the further progression b. Allografts, e.g. freeze, dried bone allografts,

of the disease and provide an environment which will help demine-ralized freeze-dried bone allografts (FDBA, PART V in adequate plaque control. DFDBA). The procedures are: c. Alloplasts—hydroxyapatite, tricalcium phosphate. Grade I: They are usually associated with suprabony d. Citric acid root conditioning with coronally positioned pockets, hence, flap. a. Initial preparation or scaling and root planing. e. Guided tissue regeneration and combination techniques. b. Curettage or gingivectomy to expose the furcation area. For grade III and grade IV furcation involvements the c. Odontoplasty—to reshape the facial groove in order to success rate is limited. prevent plaque accumulation.

Grade II: In shallow grade II invasions, Definition of Root Resection, Hemisection and a. Osteoplasty with limited ostectomy may be helpful. Root Separation (Figs 44.6 to 44.8) b. Odontoplasty can be performed. (According to 1986 glossary of periodontal terms). In severe grades II to IV invasions elimination of Root resection: It is the surgical removal of all or a portion furcation by: of the root before or after endodontic treatment. a. Root resection or amputation: After periodontal flap

reflection, surgical removal of the root portion of the Hemisection: It is the surgical removal of a root with the Treatment of Periodontal Diseases Periodontal of Treatment affected tooth is most commonly performed in maxillary associated part of the crown. It is frequently used with first molars. reference to lower molars. b. Hemisection or root separation: It is the surgical removal Root separation/bicuspidization: It is the sectioning of the of the root along with the crown. Most commonly done root complex and the maintenance of all roots. in mandibular molars. c. Bicuspidization/root separation: Splitting of a two- rooted tooth into two separate portions. Frequently performed in mandibular molars. d. Tunnel preparation: It is by transforming the grade II lesion to grades III and IV for better access, but it is not performed anymore because of increased incidence of root caries. Grade III and grade IV can be treated with root resection and root separation. Fig. 44.6: Root separation/resection 387 HPE 44 CHAPTER

Fig. 44.7: Hemisection Furcation Involvement and Its Management Its and Involvement Furcation

Figs 44.8A and B: Root separation and resection

INDICATIONS AND CONTRAINDICATIONS FOR • Better bone recontouring during surgery. ROOT RESECTION AND SEPARATION • Allows precise flap closure. • Easy adaptation for temporary prosthesis. Indications b. Restorative phase—Construction of a provisional restoration. a. Severe bone loss affecting one or more roots untreatable c. Surgical phase—Most commonly distobuccal root of the with regenerative procedures. maxillary first molar is resected. b. Class II or III furcation invasions or involvement. c. Severe recession or dehiscence of a root. The procedure is as follows: (Figs 44.9A to G) 1. After appropriate local anesthesia a full thickness Contraindications mucoperiosteal flap is raised. 2. After debridement, resection of the root with advanced a. General contraindications like systemic diseases and bone loss is carried out. First an oblique cut/incision is poor oral hygiene. made directed from apical to the contact point through b. Fused roots, unfavorable tissue architecture. the tooth to the facial and distal orifices of the tooth. In c. Roots that are endodontically-untreatable. case of vital resection, it is advised to perform a Three phases of treatment is suggested for root separation horizontal incision through the root because an oblique and resection. incision can expose a large surface area of the radicular a. Endodontic phase—If possible it should be performed pulp or pulp chamber which inturn can lead to more prior to surgery. It offers the following advantages: postoperative pain.

388

PART V Treatment of Periodontal Diseases Periodontal of Treatment

Figs 44.9A to G: Furcation involvement. (A) Preoperative, (B) Incision placement, (C) Reflection of flap, (D) Bone graft placement, (E) Membrane placement, (F) Suturing, (G) Facial view after healing 389

3. After sectioning, the root is elevated from its socket and Divergence: It is the distance between two roots which is removed. If necessary odontoplasty is performed to normally increases in apical direction. remove any furcation deformities .If any bony defects Coefficient of separation: The length of the root cones in are present in the adjacent teeth, then resective or relation to the length of the root complex. regenerative procedures are performed. 44 CHAPTER 4. The flaps are then approximated and sutured to maintain Diagnosis of Furcation Defects the position. a. Clinical probing — using a curved graduated periodontal probe (Naber’s probe), an explorer or a small curette, furcations can be identified. 1. Furcation involvement refers to commonly occurring Maxillary molars — mesial furcation entrance is conditions in which the bifurcation and trifurcation of located closer to palatal than to the buccal surface, multirooted teeth are invaded by the disease process. hence, the mesial furcation should be probed from

2. Primary etiologic factor is bacterial plaque, predisposing the palatal aspect of the tooth. Whereas the distal Management Its and Involvement Furcation or anatomic factors include, aberrant root morphology, furcation is in the midway between buccal and palatal cervical enamel projections or pearls and presence of surfaces, hence, this furcation can be probed either accessory canals. from the buccal or palatal surface. The distal maxillary 3. Furcation involvement can be classified according to furcation is most frequently involved. Glickman as Grade I, Grade II, Grade III and Grade IV. 4. Depending on the distance from the base of the defect b. Radiographs — can only be used to confirm the to the roof of the furcation (vertical component). Tarnow findings made during probing of a furcation in and Fletcher classified furcation involvement into— individual tooth. subgroup A, subgroup B, subgroup C. 5. Furcation involvement can be diagnosed by Naber’s probe and radiographs. 6. Treatment of furcation involvement is divided into: REVIEW QUESTIONS a. Traditional treatment procedures. b. Reconstructive or regenerative treatment. 1. Define and classify furcation involvement. Describe the treatment for Grade II furcation involvement. 2. What are the indications and contraindications for root KNOW MORE ... resection/separation?

Furcation Anatomy BIBLIOGRAPHY Terminology: (Root complex): It is the portion of a tooth that is located apical to the CEJ (cementoenamel 1. Alan M. Polson. Periodontal Regeneration, Current Status and junction). Direction. Quitessence Publishing Company, Inc. The root complex may be divided into two parts: 2. Al-Shammari KF, Kazor CE, Wang HL. Molaroot anatomy and • The root trunk. management of furiation defects. J clin Periodontol 2001;28: • The root cones. 730-40. Root trunk: Represents the undivided region of the root, 3. Jan Lindhe. Clinical Periodontology and Implant Dentistry. which is the distance between the CEJ and the separation Fourth edition (2003), Blackwell Munksgaard Publication. line between the roots. 4. Myron Neyin, James T. Mellonig. Periodontal Therapy, Clinical Root cone: Present within the divided region of the root Appraoches and Evidence of Success. Vol 1, Quintessence complex. Two or more root cones make up the furcation Publishing Co, Inc (1998). region. 5. Massimode Sanctis, Giovan Paolo Piniprato. Root resection and Furcation: It is the area located between individual root root amputation. Curr Opin Periodontol 1993;105. cones. 6. Steven Garette, Gary Bogle. Periodontal regeneration with bone Furcation fornix: It is the roof of the furcation. grafts. Curr Opin Periodontol 1994;187-93. 45 ChapterChapter

Pulpoperiodontal Problems

 PATHWAYS OF COMMUNICATION BETWEEN  EFFECTS OF PERIODONTITIS ON THE DENTAL PULP PULP AND PERIODONTIUM  ENDODONTIC-PERIODONTAL LESIONS  EFFECTS OF PULPAL DISEASE ON • Classification PERIODONTIUM • Microbiological Findings • Diagnosis and Treatments

INTRODUCTION • Idiopathic resorption can be: a. Internal: From the pulp to the surface of the tooth. Normally, periodontitis is caused by extension of b. External: From the external surface of the inflammation from the gingiva into deeper periodontal root to the pulp. tissues. However, periodontitis can also be caused by pulpal Both internal and external resorption produces communication. infections that have entered the periodontal ligament either • Loss of cementum due to external irritants. through the apical foramen or through the lateral canals. 3. Pathways of iatrogenic origin Such a periodontal lesion is termed as “retrograde • Exposure of dentinal tubules following root planing. periodontitis.” Similarly, “retrograde pulpitis” can also occur • Accidental lateral perforation during endodontic as a result of periodontal disease and periodontal treatment. procedure. PATHWAYS OF COMMUNICATION BETWEEN • Root fracture due to endodontic procedure. PULP AND PERIODONTIUM (FIG. 45.1) EFFECTS OF PULPAL DISEASE ON It can be classified into three categories: 1. Pathways of developmental origin. THE PERIODONTIUM • Apical foramen The three major causes of pulpal inflammation are: • Accessory canals and lateral canals. 1. Instrumentation during periodontal, restorative or • Developmental grooves. • Enamel projections and pearls at the cervical portion. prosthetic procedures. 2. Pathways of pathologic origin 2. Progression of dental caries. • Tooth fracture (vertical). 3. Tooth fractures. 391

HPE 45 CHAPTER Pulpoperiodontal Problems Pulpoperiodontal

Fig. 45.1: Possible pathways for spread of infection between pulp and periodontal tissues

Of these dental caries is the most common cause of EFFECTS OF PERIODONTITIS ON pulpal disease. As long as the pulp remains vital, the THE DENTAL PULP inflamed pulpal tissue is unlikely to cause any change in Bender and Seltzer (1972) in their studies have reported the periodontium. But acute inflammation of the pulp that teeth with caries or restorations also suffering from increases the intrapulpal pressure and the inflammatory fluid periodontal disease have more atrophic pulps than teeth with may be pushed out through the apical foramen or accessory caries or restorations, but no periodontal disease. The cause canals. This results in periapical abscess which may drain of these atrophic changes (which is observed through the periodontal ligament into the gingival sulcus radiographically as narrowed canal space) is the disruption and a periodontal pocket may form in due course of the of blood flow through the lateral canals, which leads to localized areas of coagulation necrosis in the pulp. time. Similar lesions may develop adjacent to accessory or Subgingival scaling and root planing may also produce lateral canals. changes in the pulp, one possible explanation for this is Accessory canals branch off and run parallel to the main that blood vessels leading into lateral canals are severed root canal and are seen in the apical-third of the roots causing localized areas of pulpal necrosis (Fig. 45.2). and furcation areas of multirooted teeth, whereas lateral canals run perpendicular to the root canal and are seen in ENDOPERIOLESIONS greater number in the middle-third of the root. Passage Classification of infection from the pulp into the furcation area Pulpoperiodontal lesions have been classified by many through the accessory canals has been reported by many authors based on different criteria. Classification proposed authors. by Simon et al (1972) is most commonly employed.

392 PART V

Fig. 45.2: Schematic diagram showing possible pathways for spread of infection between pulp and periodontal tissue

Based on the etiology, diagnosis, prognosis and treatment, endoperiolesions can be classified into five groups (Table 45.1). 1. Primary endodontic lesion. 2. Primary endodontic with secondary periodontal lesion (Fig. 45.3). 3. Primary periodontal lesion. 4. Primary periodontal lesion with secondary endodontic

Treatment of Periodontal Diseases Periodontal of Treatment involvement. 5. True combined lesions.

Microbiological Findings Bacteria play an important role in the pathogenesis of both pulpal and periodontal disease. There seems to be significant Fig. 45.3: Radiograph of endoperiolession similarity between the microbiological findings of root canals and pockets with advanced periodontitis. B. forsythus, P. gingivalis and T. denticola, Fusobacteria, Spirochetes, probing, fiberoptic illumination to rule out whether a fracture Wolinella and Peptostreptococcus have been found in endo- exists, more importantly vitality test, percussion tests should perio lesions. be carried out. Numerous studies have demonstrated the inaccuracy of vitality testing. Probably because pulp testing Diagnosis and Treatment only indicates the neural response and gives little When one suspects the possible endodontic periodontal information about the vascularity or true vitality of the pulp. lesion, the first task is to assess endodontic status of the Research is currently under way to improve diagnostic tooth in question. Traditional diagnostic aids including, testing through the use of Doppler devices, pulse oximetry radiographic analysis with gutta percha tracing, periodontal and even magnetic resonance imaging. 393

Table 45.1: Classification of endoperiolesions

Type of lesion Sequelae Diagnosis Treatment Prognosis Primary It is characterized by Pulp vitality tests Conventional root canal It is excellent. endodontic necrotic pulp with a chronic are negative. therapy should be per- Healing is usually complete lesion apical periodontitis and a formed with multiple within 3 to 6 months. 45 CHAPTER draining sinus tract through appointments. the periodontal ligament No root planing and gingival sulcus. should be done when There may not be any the sinus tract is along periodontal involvement the periodontal ligament, in the other areas. The because these fibers are sinus tract can be probed, important for re-attach- with gutta percha and ment to occur. silver points.

Radiographically, no Problems Pulpoperiodontal crestal bone loss. Primary If primary endodontic Pulp vitality tests First endodontic therapy Endodontic component is endodontic lesion is not diagnosed are negative. Perio- including root canal thera- excellent but regeneration lesion with and treated early, secon- dontal probing will py. Periodontal therapy in of attachment apparatus secondary dary periodontal problem reveal deep perio- the form of root planing. is limited by the perio- periodontal may result due to accu- dontal pocket in dontal prognosis. involvement mulation of plaque and this area. calculus in the drianage fistulous tract. Radiographically, bone loss may be evident. Primary Periodontal pocket which Pulp is vital, perio- Periodontal therapy to It is entirely dependent periodontal extends upto the apex of dontal probing, may eliminate the pocket is on the periodontal lesion the tooth. reach the apex of indicated. therapy. Spread of infection from the involved teeth. Root canal therapy is not the pocket into the pulp The periodontal usually indicated unless may occur in these cases. problems are seen pulp vitality test results In the pulp fibrosis on the other teeth change. Periodic reevalu- and calcification is noticed also. tion is necessary. but not necrosis. Minimal/no pain is experienced by the patient. Primary Primary periodontal Similar to those Both endodontic and It is dependent on the periodontal lesion may involve used in primary periodontal therapy. periodontal therapy, lesion with necrosis and patient may endodontic and healing response of peri- endodontic experience severe pain. secondary perio- apical lesion is not predi- involvement Pulpal necrosis could be dontal lesions. ctable. as a result of periodontal Generalized therapy where the blood perioodontal vessels to the pulp are problem. severed during perio- Pulp vitality test dontal instrumentation. results can be mixed. True These are those lesions Pulp testing is Both endodontic and Questionable prognosis combined that are formed when negative. The tooth periodontal therapy lesion pulpal and periodontal in question will including root resec- pathoses develop inde- have probing tion and hemisection pendently and unite. depths upto the is proposed. These lesions are usually apex of the tooth. of periodontal origin. Teeth with vertical root fractures also belong to this category. 394

Treatment 2. Lesion that require periodontal treatment procedures only. Some controversy seems to exist, as to whether endodontic 3. Lesions that require combined endodontic- therapy or periodontal therapy has to be performed first, in periodontic treatment procedures. the management of endoperiolesions. Considering many • According to Weine (1972): facts it was advised to perform endodontic therapy prior to 1. Class I: Tooth in which symptoms clinically and radiographically simulate periodontal disease but periodontal therapy. are infact due to pulpal inflammation and/or necrosis. 2. Class II: Tooth that has both pulpal or periapical

PART V 1. When inflammation from pulp extends into the disease and periodontal disease concomitantly. periodontium either through the apical foramen or through 3. Class III: Tooth that has no pulpal problem but the lateral canals destruction of periodontal tissues may requires endodontic therapy plus root amputation occur. This is termed as ‘retrograde periodontitis’. to gain periodontal healing. 2. Pathways of communication between pulp and 4. Class IV: Tooth that clinically and radiographically periodontium could be of : simulates pulpal or periapical disease but infact • Developmental origin. has periodontal disease. • Pathologic origin • Iatrogenic origin. 3. Endoperiolesions are classified into: REVIEW QUESTIONS • Primary endodontic lesions • Primary endodontic with secondary periodontal lesions 1. Enumerate various pulpoperiodontal problems. • Primary periodontal lesions 2. What is retrograde periodontitis? • Primary periodontal lesion with secondary endodontic 3. What are the effects of periodontitis on the dental pulps? involvement. • True combined lesions. BIBLIOGRAPHY

1. Brian F Paul, Jeffrey W Hutler. The endodontic periodontal continuum revisited: New-insights into etiology, diagnosis and

KNOW MORE ... treatment. JADA, November, 1997;128. Treatment of Periodontal Diseases Periodontal of Treatment 2. Gerald W Harrington, David R Steiner, William F Ammon Jr. Other Classifications of Endodontic-Periodontal The periodontal endodontic controvery. Periodontol 2000, Lesions 2002;30. • According to Oliet and Pallock (1968): Based on 3. Jan Lindhe. Clinical Periodontology and Implant Dentistry, 4th treatment procedure: edn, Blackwell Munksgard Publication, 2003. 1. Lesion that require endodontic treatment 4. Zehnder M, Gold SI, Hasselgren G. Pathologic interactions in pulpal procedures only. and periodontal tissues. J Clin Periodontol 2002; 29: 663-71. 46 ChapterChapter

Splints in Periodontal Therapy

 DEFINITION  PRINCIPLES  OBJECTIVES  INDICATIONS AND CONTRAINDICATIONS  CLASSIFICATION AND TYPES  ADVANTAGES AND DISADVANTAGES

DEFINITION OBJECTIVES OF SPLINTING

Dental splinting: It is defined as the joining of two or more 1. Provides rest. teeth into a rigid unit by means of a fixed or removable 2. For redirection of forces—the forces of occlusion are restorations/devices. Splint by definition is an appliance redirected in a more axial direction over all the teeth used for immobilization of injured or diseased parts. included in the splint. A periodontal splint: It is an appliance used for maintaining 3. For redistribution of forces—redistribution ensures that or stabilizing mobile teeth in their functional position. forces do not exceed the adaptive capacity of the The main objective of splinting is to promote periodontium. healing and to increase the patients comfort and function. 4. To preserve arch integrity—splinting restores proximal There are two schools of thought regarding the use of splinting. contacts, reducing food impaction and consequent Harmful Aspects breakdown of the periodontium. 5. Restoration of functional stability—restores a functional • It creates an environment for plaque accumulation. occlusion, stabilizes mobile abutment teeth and increases • Since functional movement of the tooth within the socket masticatory efficiency. is not possible it may lead to ankylosis. 6. Psychologic well-being—gives the patient freedom from Beneficial Aspects mobile teeth thereby giving him a sense of wellbeing. • Since they are splinted to the neighboring healthy teeth, 7. To stabilize mobile teeth during surgical, especially mobility during mastication is prevented. regenerative therapy. • Non-mobile teeth heal faster than mobile teeth. 8. To prevent the eruption of teeth without an antagonist. 396

CLASSIFICATION OF SPLINTS PRINCIPLES OF SPLINTING

According to the Period of Stabilization 1. Inclusion of sufficient number of healthy teeth: It is suggested that the healthy teeth included in the splint a. Temporary stabilization—to be worn for less than 6 should have double the root surface area of the mobile months, e.g. removable/fixed teeth to be splinted. Since the posterior teeth are multi- b. Provisional stabilization—to be worn for months or rooted the number of healthy teeth to be included in the several years, e.g. acrylic splints, metal bands. splint in the posterior segment will be less as compared c. Permanent splints—used indefinitely, e.g. removal/ to the anterior. fixed, intracoronal/extracoronal. PART V 2. Splint around the arch: Muscles of the lips, cheek and According to the Type of Material tongue exert some forces on the teeth. Based on the direction of such forces applied on the teeth, the dental i. Bonded, composite resin button splint. arch can be divided into two posterior sextants and an ii. Braided wire splint. anterior sextant. In the posterior sextant the tongue iii. A-splints. pushes the teeth buccally and the muscles of the cheek counter act it by pushing them lingually. When the splint According to the Location on the Tooth is confined to any one sextant, the splinted teeth tend to Intracoronal tilt lingually or outwards depending on the muscular forces. Such a collapse of the splinted sextant • Composite resin with wire can be prevented by including few teeth from the • Inlays adjacent sextant. This is termed splinting around the • Nylon wire arch. 3. Coronoplasty may be performed to relieve traumatic Extracoronal occlusion. • Tooth-bonded plastic 4. The splint should be fabricated in such a way as to

Treatment of Periodontal Diseases Periodontal of Treatment • Night guard facilitate proper plaque control. • Welded-bands 5. Splint should be aesthetically-acceptable and should not interfere with occlusion. VARIOUS COMMONLY USED SPLINTS 1. Splints for Anterior Teeth INDICATIONS AND CONTRAINDICATIONS a. Direct bonding system using acid etch techniques OF SPLINTING and a light cured resin. Indications b. Intracoronal wire and acrylic wire resin splint—It involves the teeth with stainless steel wire placed in 1. It stabilizes moderate to advanced tooth mobility that the slots thus stabilizing the teeth. can not be reduced by other means and which has not 2. Splints for Posterior Teeth responded to occlusal adjustment and periodontal a. Intracoronal amalgam wire splints—It uses resin therapy. restoration with wire on the proximal amalgam 2. When it interferes with normal masticatory function. restored areas of the tooth. 3. Facilitates scaling and surgical procedures. b. Bite-guard. 4. Stabilizes teeth after orthodontic movement. c. Rigid occlusal splint. 5. Stabilizes teeth after acute dental trauma, e.g. d. Composite splint. subluxation, avulsion, etc. 397

6. In order to prevent tipping and drifting of teeth. in traumatic occlusion, it can injure the periodontium 7. Prevent extrusion of unopposed teeth. of all the teeth within the splint. 4. Development of caries is an unavoidable risk. Thus, it Contraindications obviates the need of excellent oral hygiene in the patient. HPE 46 CHAPTER 1. Moderate to severe tooth mobility in the presence of In conclusion splinting decreases mobility thereby periodontal inflammation and/ primary occlusal trauma. improving the health of the tooth. It is important to note 2. Insufficient number of firm/sufficiently firm teeth to that if used incorrectly or not managed properly it may fail stabilize mobile teeth. to achieve the desired results. 3. Prior occlusal adjustment has not been done on teeth with occlusal trauma or occlusal interference. 4. Patient not maintaining oral hygiene. KNOW MORE ... Therapy Periodontal in Splints

ADVANTAGES Characteristics of an Ideal Splint • Should be easily available. 1. May establish final stability and comfort for patient with • Economical and stable. occlusal trauma. • Easily maintainable. • Rigid and durable. 2. Helpful to decrease mobility and accelerate healing • Compatible with the adjacent tissues. following acute trauma to the teeth. 3. Allows remodelling of alveolar bone and periodontal ligament for orthodontically, splinted teeth. REVIEW QUESTIONS 4. Helpful in decreasing mobility thereby favoring 1. Define and classify periodontal splints. regenerative therapy. 2. What are the advantages and disadvantages of 5. Distributes occlusal forces over a wider area. periodontal splints?

DISADVANTAGES BIBLIOGRAPHY 1. All the splints hamper patient’s self care. Accumulation of plaque at the splinted margins can lead to further 1. Ericsson I, Giargia M, Lindhe J, et al. Progression of periodontal periodontal breakdown in a patient with already tissue destruction at splinted /non-splinted teeth. An experimental study in the dog. J Clin Periodontol 1993; 10: 693. compromised periodontal support. 2. Saul Schluger. Periodontal Disease: Basic Phenomena, Clinical 2. Number of studies have shown that splinting does not Management and Occlusal and Restorative Interrelationships, actually reduce tooth mobility (once the splint is Second Edition, Lea and Febiger Publication. removed). 3. Sture R Nyman, Niklous P Lang. Tooth mobility and the 3. The splint being rigid acts as a lever with uneven biological rationale for splinting teeth. Periodontol 2000, distribution of forces, even if one tooth of the splint is 1994; 4. 47 ChapterChapter

Dental Implants: Periodontal Considerations

 TERMINOLOGY  CLASSIFICATION OF IMPLANTS  HISTORICAL BACKGROUND  CLASSIFICATION OF IMPLANT SYSTEMS  BIOLOGICAL CONSIDERATIONS  TREATMENT PLANNING • Soft Tissue Implant Interface • Bone Implant Interface  HEALING FOLLOWING IMPLANT SURGERY  BIOMATERIALS USED FOR IMPLANTS  PERI-IMPLANT COMPLICATIONS AND DISEASES

INTRODUCTION keratinized and mucosal oral soft tissues and prosthetic suprastructure. The concept of replacing missing teeth for esthetics and A dental implant is a permucosal device that is function has been an elusive goal for more than 1500 years. biocompatible and biofunctional and is placed on or within This has led to the evolution of many materials and the bone associated with the oral cavity to provide support techniques including complete dentures, removable and for fixed or removable prosthesis. fixed partial dentures. To overcome the limitations of these materials and techniques, dentistry has long sought a Oral implantology is the science and discipline concerned superior method of artificial tooth replacement through with the diagnosis, design, insertion, restoration and for dental implants with a goal of restoring the normal contour, management of alloplastic or autogenous oral structures to comfort, esthetics, health and the most traditional dental restore the loss of contour, comfort, function, esthetics, disciplines, which include the bone and soft tissue speech and/or health of the partially or completely edentulous patient. reconstruction. Implant surgery is that part of reconstructive surgery that TERMINOLOGY is concerned with the placement of endosseous, Dental implant is an integral component of the oral implant subperiosteal and transosseous implants for the restoration complex, which also consists of supportive bone, interposed and maintenance of mastication and speech. Such surgery 399

may also eliminate chronic pain related to nerve dehiscence, The Modern Era (1910 to 1978 AD) preserving remaining bone structure and prevent the Implant designs were carried out with the aim of finding a possibility of a pathologic fracture. superior metal which was biocompatible to the periodontal

Osseointegration: Direct structural and functional structures. By developing screw type implants using 47 CHAPTER connection between ordered living bone and the surface of vitallium, subperiosteal implants and extending their the load carrying implant. framework to external oblique region and introduction of the use of an endosseous implant with a central post and HISTORICAL BACKGROUND circumferential extensions, a step was taken in that direction. The need to replace missing teeth has haunted for time immemorial. The Contemporary Era (1978 Till Date)

According to Marshall (1987) there are five distinct eras Implants developed during this era are core-vent implant, Considerations Periodontal Implants: Dental of implant dentistry. screw-vent implant, swede-vent implant, a hydroxyapatite- coated bio-vent implant; microvent implant, starvent The Ancient Era (Before 1000 AD) implant; sterioss, root form endoosseous implant, step root The discovery of 2,000 years old cranium with a cast iron form design. dental implant in France demonstrated that dental Constant research is being conducted in the development implantology was one of the oldest existing forms of of newer implant systems with the aim of developing a dentistry. Ancient Egyptians attempted intraosseous perfect implant which will function well without any failure. transplantation of animal teeth. A fine dark flint stone- shaped like a tooth implanted in a Mayan Skull in Central BIOLOGICAL CONSIDERATIONS America during back to 600 AD. OF IMPLANTS I. Soft tissue implant interface. The Medieval Era (1000 to 1799 AD) II. Bone implant interface. The medieval period of implant dentistry was primarily concerned with transplantation of teeth with implants made Soft Tissue Implant Interface up of ivory, shells and bone or transplantation of teeth from The mucosal tissues around intraosseous implants form a one human to other or removing the teeth from the tightly-adherent band consisting of a dense collagenous impoverished people and transplanting them into the mouths lamina propria covered by keratinized stratified squamous of the affluent. epithelia. The implant epithelium junction is analogous to the The Foundation Era (1800 to 1910 AD) junctional epithelium around natural teeth; in that, the During this period newer materials and methods were epithelial cells attach to the titanium implant by means of developed like fabricating and inserting gold roots into hemidesmosomes and basal lamina. freshly extracted socket which were soldered together, use This evidence supports the concept that a viable biologic of gold plate in the treatment of cleft palate, using teeth seal can exist between the epithelial cells and the implants. made up of porcelain which had lead coated platinum post A sulcus forms around the implant lined with a sulcular fixed as an implant. Payne (1898) gave the first clinical epithelium that is continuous apically with the junctional demonstration on implants. epithelium. 400

Collagen fibers are nonattached and run parallel to the Vanadium Aluminum 6 percent, implant surface, owing to the lack of cementum. Since Vanadium 4 percent endosseous implants are permucosal, the soft tissue-implant c. Cobalt-Chromium Cobalt 66 percent + interface should be considered in their placement and Chromium 27 percent + maintenance. This suggests that epithelium adheres to Molybdenum 7 percent implant surfaces and has similar biological features of the d. Stainless steel Iron 70 percent + epithelium tooth interface. Chromium 18 percent + Nickel 12 percent

Bone Implant Interface e. Tantalum 100 percent pure PART V The relationship between endosseous implants and bone f. Zirconium 100 percent pure involves mechanisms like: g. Gold 100 percent pure • Fibro-osseous integration h. Platinum 100 percent pure • Osseointegration and Inert Ceramics • Bioactive integration.

a. Aluminum oxide (Al2O3) Fibro-osseous Integration • Polycrystalline It is defined as “tissue to implant contact by interposition • Single crystal. of a healthy dense collagenous tissue between the implant b. Zirconium oxide zircona. and the bone interface”. Normally, fibro-osseous union c. Titanium oxide. between the implant surface and adjoining alveolar bone is Calcium Phosphate Ceramics not desirable because union formed is a weak union. The formation of fibro-osseous integration is attributed to Calcium phosphate. proliferation of connective tissue into the interface, which

hampers the osseous integration process. Bioactive and Biodegradable Ceramics Treatment of Periodontal Diseases Periodontal of Treatment a. Hydroxyapatite. Osseointegration b. Tricalcium phosphate. It is defined as a direct structural and functional connection c. Bioglass. between ordered living bone and the surface of the load d. Ceramic. carrying implant. e. Calcium aluminates. f. Carbon. Bioactive Integration g. Carbon silicon. It is defined as the integration which results by a h. Polycrystalline glassy carbon. physiochemical interaction between collagen of bone and Polymers hydroxyapatite crystals of the implants. a. Polymethyl methacrylate. BIOMATERIALS USED FOR IMPLANTS b. Polytetrafluoroethylene. Metals and Alloys c. Polyethylene. d. Polyethylene tetraphthalate. a. Titanium 100 percent pure Titanium e. Polypropylene. b. Titanium-Aluminum Titanium 90 percent f. Polyoxymethylene. 401 g. Silicone rubber. 3. Implant innovations systems. h. Polysulfone. 4. Astra-dental implant system. 5. IMZ implant system (Interpore IMZ). CLASSIFICATION OF IMPLANTS 6. Corevent system. HPE 47 CHAPTER Implants are classified based on: 7. Sterioss system. 1. Shape and form and 8. Stryker implant system. 2. Surface characteristics. 9. Endosteal hollow basket system.

TREATMENT PLANNING Based on the Shape and Form Clinical Assessment 1. Endosteal. Selection of cases for implants is based on the: 2. Subperiosteal. Considerations Periodontal Implants: Dental 3. Transosteal. I. Age limitations for case selection. 4. Intramucosal inserts/submucosal implants/subdermal II. Anatomic prerequisites: implants. 1. Resorptive process. 5. Endodontic stabilizer. 2. Soft tissue situation. 3. Available bone. With regard to shape, it is possible to distinguish between: 4. Mandibular canal. a. Post or root form implants—Exhibiting rotation 5. Height of bone. symmetry. 6. Width of bone. b. Blade implants—Extension implants. 7. Bone shape (contour). The post or root implant designs can be of the following 8. Length of bone. types: 9. Implant crown relationship. 1. Solid tapering types. 10. Maxillary sinuses. 2. Solid cylinder type. 3. Pin type. The Absolute Requirements for 4. Screw-shaped implant type. Treating Implant Patients 5. Basket design. 6. Hollow cylinder design. 1. Have an acceptable patient. 2. Implant made of biocompatible material. The blade implant designs can be of following types: 3. Be durable. 1. Conventional blade design. 4. Have proper surface quality. 2. Vented blade design. 5. Have acceptable socket created in bone. 6. Have surgical procedure properly done. Based on Surface Characteristics 7. Have healing completed with acceptable bone interface. 1. Titanium plasma—sprayed coating. 8. Have healing period without pathological stress. 2. Sand blasting—surface etching. 9. Have normal implant function without pathological 3. Laser induced surface roughening. stress. 4. Hydroxyapatite coating. Indications for Implant Therapy CLASSIFICATION OF IMPLANT SYSTEMS A. The edentulous patient: 1. Branemark implant system (Nobel Biocare System). • Edentulous mandible 2. International team for implantology (ITI) system. • Edentulous maxilla. 402

B. The partially-edentulous patient: 3. Lateral cephalometric radiograph. • Free end edentulous situation 4. Occlusal radiograph. • Multiple missing teeth. 5. Tomography C. Single tooth loss. 6. Computed tomography

Absolute Contraindications for Implant Treatment Surgical Procedures 1. Uncontrolled-diabetes mellitus. Most threaded endosseous implants can be placed either in 2. Long-term immunosuppressant drug therapy. one stage (or) two stages.

3. Diseases of connective tissue. PART V 4. Blood dyscrasias and coagulopathies. One-stage: Endosseous Implant Surgery 5. Regional malignancy. In this procedure the coronal portion stays exposed through 6. Metastatic disease. gingiva during the healing period. For example, ITI system, 7. Previous radiation to the jaws that might lead to TG Implant of 3i system and Life core single– stage system. postsurgical osteoradionecrosis. 8. Alcohol or drug addiction. One stage endosseous implant surgery: In this implant 9. Severe psychologic disorders. surgery, the implant (or) healing abutment protrudes about 2 to 3 mm from the bone crest and the flaps are adapted Intraoral Contraindications around the implant. In posterior areas of the mouth the flap This includes: is thinned and sometimes placed apically to increase the 1. Unfavorable interarch relationships. zone of keratinized attached gingiva. 2. Problematic occlusal and functional relationships. Surgical Technique (Figs 47.1A to F) 3. Pathologic considerations in alveolar bone, example, Flap design and incisons: The flap design is always a crestal fibro-osseous disease. incision bisecting the existing keratinized tissue. The soft 4. Pathologic alteration of the oral mucosa, example, cysts, tissue is not thinned in anterior or other esthetic areas of the infections. mouth to prevent the metal collar from showing, full- Treatment of Periodontal Diseases Periodontal of Treatment 5. Xerostomia. thickness flaps are elevated buccally and lingually. 6. Macroglossia. 7. Unrestored teeth—poor oral hygiene. Placement of the implant: The implant site preparation to place implants in one stage surgery is identical to principles Radiographs of two-stage except, implants or healing abutment is placed in such a way that head of implant protrudes about 2 to 3 Radiographs used in dental implants are panoramic mm from the bone crest. radiographs. However, this technique has certain inherent Closure of the flap: The keratinized edges of the flap are problems that have to be taken into consideration like tied with independent sutures around the implant, when distortion of spatial relationships. In order to eliminate the keratinized tissue is abundant, scalloping around the implant distortion problems panoramic radiographs and their use of provides better flap adaptation. templates with incorporated metal spheres have been demonstrated. Advantages and disadvantages of one stage implant surgery. Advantages: Other Radiographic Procedures Employed a. Mucogingival management around the implant is easier. These are: b. Patient comfort increases because less surgeries are 1. Periapical dental radiographs. involved. 2. Rast-O-Pan bite blocks. c. Esthetic management is easier in many cases. 403

HPE 47 CHAPTER Dental Implants: Periodontal Considerations Periodontal Implants: Dental

Figs 47.1(A to F): Surgical steps in implant placement. (A) Initial incision placed (B) Reflection of flap (C) Osteotomy procedure at implant site (D) Checking for parallelism of implant (E) Placement of implant (F) Repositioning of flap and placement of sutures

Disadvantage: Two-stage: Endosseous Implant Surgery If extensive bone loss occurs at the implant site. Vertical In the two-stage implant surgical approach, the first stage bone augmentation is necessary, and or bone quality is poor ends by suturing the soft tissues over the implant so that it then two-stage surgical approach is recommended. remains excluded from the oral cavity. 404

In the mandible, the implants are left undisturbed for 2 Different Phases of Healing to 3 months, whereas in the maxilla, they remain covered Osseous Healing—Early Phase for approximately 4 to 6 months because of slower healing Preceded by hemorrhage and formation of a blood clot, this due to less dense bone. During this period, the healing bone coagulum consists of fibrin and embedded blood cells and makes direct contact with the implant surface represents the scaffold for reparative (granulation) tissue, (osseointegration) and sometimes grows to its occlusal the coagulum begins to organize with ingrowth of capillaries surface, even covering it. and pre-osteoblasts (centripetal bone growth). In second-stage surgery, the buried implant is uncovered During this early stage, in addition to new bone and a titanium abutment is connected to allow access to the PART V formation, the macrophages as well as multinucleated giant implant from the oral cavity. The restorative dentist then cells appear and recognizes the implant as foreign body. As proceeds with the prosthodontic aspects of the implant bone formation is initiated at the implant surface, the number therapy. of multinucleated giant cells are reduced. HEALING FOLLOWING IMPLANT SURGERY Osseous Healing—Late Stage If the space between an implant and its osseous bed is narrow, bone formation is comparable to primary healing Depending upon the width of the gap between the implant after a bone fracture, because no callus is formed. Direct surface and the osseous bed, direct filling of the space can bridging via lamellar bone occurs, at a rate of about 1 m/day. occur about 0.2 mm by means of concentric bony apposition. Healing of implants with a wide space around them is Wider spaces will usually be filled within 14 days by a comparable to secondary healing of a bone fracture, as bone network of new woven bone, which will be remodeled in formation occurs via formation of a fibrous and bony callus, about 2 months into lamellar bone: remnants of the early at about 50 to 100 μm/day. The temporal sequence is woven woven bone may persist centrally. Direct bony contact with bone with subsequent remodeling into lamellar bone. implant surface ranges from 56 to 85 percent with screw- During preparation of the implant bed, periosteal type implants and 46 to 82 percent with linkow blade

intracortical and endosteal blood vessels are damaged. As a implants. Areas of the implant surface not covered with bone Treatment of Periodontal Diseases Periodontal of Treatment result blood accumulates in peri-implant space, with a loose will manifest adipose cells without an intervening fibrous attachment of fibrin on the surfaces of both bone and layer. implant. This hematoma will be remodeled by proliferating tissue with new capillaries and fibrous collagen connective PERI-IMPLANT COMPLICATIONS tissue in 7 to 14 days. New bone formation can occur directly Despite the long-term predictability of osseointegrated in the vicinity of the implant depending upon the degree of implants, biologic, biomechanical, and esthetic compli- its stability. Implant instability influences cell differentiation cations can occur in a small percentage of cases. and therefore also bone formation. So the implant stability is an absolute requirement for all types of implants with PERI-IMPLANT DISEASES adequate blood supply. Bony remodeling of the callus is completed after 4 to Pathologic alterations in the tissues that contact a dental 6 weeks, thorough activation of the Haversian system, implant can be placed in the above category. numerous resorption canals are formed, and the Types of Peri-implant Diseases remodeling process into lamellar bone begins. These mineralization processes, which transforms the osteoid 1. Peri-implant mucositis: Inflammatory changes, which into calcified osseous substance, proceed at about are confined to soft tissue surrounding an implant is 1 micrometer per day. termed as peri-implant mucositis. 405

2. Peri-implantitis: It is a progressive peri-implant bone Microbial Monitoring loss in conjunction with soft tissue inflammatory lesion. It is useful in evaluating the peri-implant health condition Peri-implantitis begins at the coronal portion of the and microbial composition of a peri-implantitis site. implant, while the more apical portion of implant HPE 47 CHAPTER remains osseointegrated. This means that the implant is Management and Maintenance not clinically-mobile until late stages when bone loss had progressed to involve the complete implant surface. Management Occlusal therapy: When excessive forces are considered Clinical Features the main etiologic factor for peri-implant bone loss treatment • Color changes, bleeding upon gentle probing. involves an analysis of fit of the prosthesis

• Pocket formation and radiographic bone destruction. • The number and position of implants. Dental Implants: Periodontal Considerations Periodontal Implants: Dental • Suppuration, calculus build-up and swelling. • Occlusal evaluation. • Mobility has been extensively described to detect early Change in prosthesis design, improvement of implant and late failures. number, position and occlusal equilibration can contribute to arrest the progression of peri-implant tissue Diagnosis breakdown. A number of clinical parameters used to evaluate periodontal Anti-infective therapy: The nonsurgical treatment of peri- conditions have also been used to assess peri-implant implantitis involves: conditions. These parameters include evaluation of oral • Local removal of plaque deposits with plastic instruments hygiene, peri-implant marginal tissues, and bone implant and polishing of all accessible surface with pumice. interface. • Subgingival irrigation of all peri-implant pockets with 0.12 percent chlorhexidine Probing • Systemic antimicrobial therapy for 10 consecutive days A successful implant generally allows probe penetration of • Improved patient compliances with oral hygiene until a approximately 3 to 4 mm and the location of peri-implant healthy peri-implant site is established. bone level can be expected to be about 1 mm apical to the • Conventional hand and ultrasonic instruments are not position of the probe tip. suitable for the preparation and detoxification of the implant surface. Radiographs • Irradiation with soft lasers for elimination of bacteria associated with peri-implantitis has also shown Reveal the peri-implant bone status as well as the marginal promising results in the destruction of bacterial cells. bone level. Periapical intraoral radiographs are obtained instead of OPG (which have lower discrimination power). Surgical techniques for treatment of peri-implantitis: Once Direct imaging may have the potential to replace the inflammatory process in the peri-implant tissue is under conventional radiology. control, an attempt may be made to improve or re-establish To diagnose a compromised implant site, soft tissue osseointegration. measurements using manual or automated probes have been The surgical procedures are modified from techniques suggested; careful monitoring of probing depth and clinical used to treat bone defects around the teeth. attachment level seems useful in detecting changes of the Re-osseointegration: It can be defined as the growth of new peri-implant tissue. bone in direct contact to the previously contaminated 406

implant surface without an intervening band of organized 7. Surgical procedure involves: connective tissue. a. One-stage endosseous implant surgery. b. Two-stage endosseous implant surgery. 8. Healing involves two phases: Maintenance a. Osseous healing—Early phase. b. Late stage. After surgical intervention, all patients are placed on a close 9. Pathologic alterations in the tissues that contact a dental recall schedule. It is advised to schedule maintenance visits implant are peri-implant diseases, which are peri-implant mucositis and peri-implantitis at least every 3 months. This allows for monitoring of plaque levels, soft tissue inflammation, and changes in the levels

PART V of bone.

Oral Hygiene Aids KNOW MORE ...

• Toothbrushes with soft, rounded bristles should be used Implant Failure because the surfaces of the implants are easily damaged. Failures in implant therapy can happen sometimes and • Toothpaste should be only minimally-abrasive; the tooth- this could be due to: cleaning procedures should be conducted by rinsing or a. Complications that arise during the early phase brushing with chlorhexidine. following implant insertion—Early implant failures. • Gauze strips or superfloss are effective for cleaning b. Complications that arise after the reconstruction of interproximally. the implant—late implant failures. • Irrigators can also be used as adjunctive aids. Causes for Early Implant Failures 1. Improper preparation of the implant site. 2. Bacterial contamination. 1. A dental implant is a biologic or alloplastic biomaterial 3. Improper mechanical stability following implant inserted into soft or hard tissues of the mouth for functional insertion. or cosmetic purposes. 4. Premature loading of the implant.

Treatment of Periodontal Diseases Periodontal of Treatment 2. Osseointegration is a direct structural and functional connection between ordered living bone and the surface of the load carrying implant. Causes for Late Implant Failures 3. Soft tissue interface of the implant consists of mucosal According to proceedings of the 3rd European Workshop tissues around intraosseous implants which form a tightly on Periodontology the late implant failures could be as a adherent band consisting of dense collagenous lamina propria covered by stratified squamous keratinizing result of: epithelium. 1. Excessive load. 4. Bone implant interface is the relationship between 2. Infection, e.g. periimplant mucositis, periimplantitis. endosseous implants and bone which involves mechanisms like fibro-osseous integration, osseo- integration and bioactive integration. REVIEW QUESTIONS 5. Based on shape and form implants are classified into— Endosteal, subperiosteal, transosteal, submucosal 1. Describe the biological considerations of implant implants and endodontic stabilizer. therapy. 6. Based on surface characteristics implants are classified into titanium plasma sprayed coating, sandblasting- 2. Enumerate various types of implants and implant surface etching, laser-induced surface roughening and systems. hydroxyapatite coating. 3. What is peri-implantitis? 407

BIBLIOGRAPHY 5. Ericsson I, Lindhe J. Probing depths at implants and teeth. J Clin Periodontol 1993; 20: 263. 1. Belser UC, Buser D, Hess D et al. Aesthetic implant restorations 6. Jan Lindhe. Clinical Periodontology and Implant Dentistry, in partially edentulous patients—a critical appraisal. 4th edn, Munksgaard, 2003.

Periodontology 2000, 1998; 17: 132. 7. Michael Norton. Dental implants, Quintessence 1995. 47 CHAPTER 2. Berglundh T, Lindhe J et al. The topography of the vascular 8. Newman, Takei, Carranza. Clinical Periodontology. 9th edn, WB system in the periodontal and peri-implant tissues in the dog. Saunders 2002. J Clin Periodontol 1994; 4: 189. 9. Van Steinberghe D, et al. Survival and success rates with oral 3. Berman CL. Osseointegration, complications, prevention, endosseous implants. In Lang NP, Karring T, Lindhe J: recognition, treatment. Dent Clin North Am 1989; 33: 635. International implant dentistry. Proceedings of 3rd European 4. Buser D, Weber HP, Donath K, et al. Soft tissue reactions to Workshop in Periodontology. Berlin, Quintessence

non-submerged implants. J Periodontol 1990; 61: 597. 1999. Dental Implants: Periodontal Considerations Periodontal Implants: Dental 48 ChapterChapter Maintenance Phase (Supportive Periodontal Treatment)

 IMPORTANCE OF MAINTENANCE PHASE  OBJECTIVES OF MAINTENANCE PHASE  RATIONALE FOR SUPPORTIVE PERIODONTAL  PARTS OF MAINTENANCE PHASE TREATMENT  DETERMINATION OF MAINTENANCE RECALL  CAUSES FOR RECURRENCE OF PERIODONTAL INTERVALS DISEASE

IMPORTANCE OF MAINTENANCE PHASE healthy and functional, natural dentition for life. It is only Chronic periodontitis, like most other chronic infections with proper maintenance, including early detection and require supervision and maintenance overtime. Maintenance treatment of recurrent periodontal diseases that such an therapy after active treatment includes not only the care objective can be achieved. that patients receive through personal oral hygiene but also by the recall visits and re-evaluations done by the dental CAUSES FOR RECURRENCE OF team. Maintenance therapy is often supportive in nature PERIODONTAL DISEASE hence, it is also known as supportive periodontal treatment 1. Incomplete subgingival plaque removal. (SPT). In this phase, patients must be made to understand 2. Nature of dentogingival unit. the purpose of a maintenance program, and the dentist must 3. Improper restorations placed after the periodontal emphasize on the fact that the preservation of the teeth in treatment was completed. question are dependent on it. 4. Failure of the patient to return for periodic recall visits. RATIONALE FOR SUPPORTIVE 5. Presence of some systemic diseases that may affect host PERIODONTAL THERAPY resistance to previously acceptable levels of plaque. Rationale for maintenance phase is to prevent or minimize GOALS OF SUPPORTIVE the recurrence of periodontal diseases by controlling factors PERIODONTAL TREATMENT known to contribute to the disease process. The main aim of long-term therapy is to provide 1. To prevent or minimize the recurrence and progression supervised control for the patient in order to maintain a of periodontal disease in patients who have been CHAPTER 48 Maintenance Phase (Supportive Periodontal Treatment) 409 Correct sequence of periodontal Incorrect sequence of periodontal treatment phases treatment phases Flow chart 48.2: Flow chart 48.1: formation, faulty restoration, deteriorating or poorly designed formation, faulty restoration, diseases modifying host response to plaque. prosthesis, systemic pull, orthodontic therapy. prosthesis. attachment procedures, cracked teeth, dentures, failure of new diseases. new periodontal modifying host response. Symptoms and causes of recurrent diseases and causes of recurrent Symptoms graphically). care. ment. previously treated for gingivitis, periodontitis and for previously treated for gingivitis, periodontitis peri-implantitis. any prosthetic monitoring the dentition and by replacement of the natural teeth. in the oral found other diseases or conditions manner, cavity. PARTS OF MAINTENANCE PHASE OBJECTIVES OF MAINTENANCE PHASE OBJECTIVES OF MAINTENANCE Increased pocket depth with increased radiographicIncreased pocket depth with increased bone loss. restoration, Poor oral hygiene, subgingival calculus, deteriorating diseases surgical treatment, cracked teeth, systemic inadequate Increased pocket depth with no radiographic change.Increased pocket depth calculus, ill fitting partial Poor oral hygiene, subgingival Recession no change in pocket depthIncreased mobility with and no radiographic change. due to lateral occlusal interference, Bruxism, high Trauma designed or worn out restoration, poor crown root ratio, poorly abrasion, inadequate keratinized gingiva, frenum Toothbrush Symptomsmobilityin Increase Poor oral hygiene causing increase in inflammation and calculus cause Probable • changes Medical history • pathological examination Oral • Oral hygiene status • Gingival changes Part–I: Examination (Approximate Time –7 Min) 2. stable, clinical attachment level. Maintenance of 3. home Reinforcement and re-evaluation of proper 4. of a healthy and functional oral environ- Maintenance 1. of alveolar bone support (radio- Preservation 2. or reduce the incidence of tooth loss by prevent To 3. in a timely increase the probability and treating To 410 Treatment of Periodontal Diseases PART V to thepatient’s needs. can beextendedto3months, butmaybevariedaccording tional procedures). After 3or4suchsessionstheinterval recall treatment2to4weeks followingtreatment(fortransi- recommended thatthepatientbeseeninitially for Based onstudiesofhumanperiodontaltreatment,it is 4. 3. 2. 1. categories ofperiodontalmaintenancetherapy. Theyare: Correctsequenceofperiodontaltreatmentphases(Flow 2. Incorrectsequenceofperiodontaltreatmentphases 1. Sequence ofMaintenanceVisits Scheduleorrefertorestorativeprosthetictreatment. • Schedulefurtherperiodontaltreatment • Schedulenextrecallvisit • Part–III: ScheduleNextProcedure Chemicalirrigation. • Scalingandpolishing • Oralhygienereinforcement • (Approximate Time–35Min) Part–II: Treatment Restorativeandprostheticchanges. • Occlusalchanges • Mobilitychanges • Pocketdepthchanges • RECALL INTERVALS DETERMINATION OFMAINTENANCE prevention ofrecurrencedisease. Post-maintenance treatment therapy possible. compromised patientswhereactivetherapyisnot Compromised maintenancetherapy dontitis. Trial maintenancetherapy individuals. Preventive maintenancetherapy Schallhorn andSnider(1981)proposedfourseparate chart 48.2). (Flow chart48.1). —mild-to-moderate perio- —periodontally-healthy —maintenance for —medically- Procedures tobePerformedatRecall .Thepatientswho hasbeenfullyandsuccessfullytreated 4. Thepatientwhohasbeenhospitalizedforseveralweeks: 3. Thepatientwhohasrefused surgical treatment: The 2. Thepatientswhowillnotcooperateinoralhygienebut 1. Recall Patients Management ofParticularType of 3. 2. 1. recall intervals: .Treatment 5. By Assessmentof 4. Assessment of 3. Radiographically Allfindingsrecordedatthebase 2. At clinical 1. general healthreview, ifthisisfavorable, retreatment yet nowshowsdistinctbreakdown inlocalizedareas: A performed inhospital. review oforalhygienebythehygienistshouldbe If thepatientsconditionpermits,periodicscalingand to performproperly. instrumentation phaseinvolvesmoretimeandisdifficult therapy.who havereceivedsurgical The root recall mustbeshorterforthispatientthanpatients includes frequent,thoroughrootinstrumentation. will payforofficecare:Inthiscasepatientmanagement regain thetotalhealth,frequencydecreases. Degree ofcontrol ofinflammation achieved the frequencyofrecall. Effectiveness ofhomecare more frequentlythepatientisrecalled. Severity ofdisease Following factorsmaybeconsideredindeterminingthe ies atbaseline. patients oralhygiene disease linearecompared. Evaluationsof Evaluation examination Procedure : : The moreseverethedisease, dontal therapy. Appointments forfutureperio- antimicrobial agents ifindicated. occlusal therapy, applicationof Removal ofanyfreshdeposits, sary. Behavioral modificationifneces- Comparison withbaselinedata. additional findingsarerecorded. Assessment ofbonelevels. Any appliances, etc. status, occlusalandprosthetic complete oralandperiodontal comparing thefindingsobtained : Goodhomecaredecreases : As thetissue CHAPTER 48 Maintenance Phase (Supportive Periodontal Treatment) 411 BIBLIOGRAPHY REVIEW QUESTIONS – surgical procedures. Includes small – Local drug delivery. – Local intensive debridement. — visits of future SPT and determination 10 minutes may be reserved. approximately 5 to supportive treatment. Periodontol 2000, 2001; 25. supportive treatment. Periodontol 2000, 2001; J Periodontol 1991;62-731. supportive periodontal therapy. 9th edn, WB Saunder Co., 2002. in the first periodontal therapy part 1: Risk of non-compliance 5 year period. J Periodontol 1999; 670-79. This section may require additional appointments. This section may require therapy? periodontics. 1. Brady Hancock, Donald H Newell. Preventive strategies and 2. Compliance with AR, NewComb GM, Nixon KC. Mendoza 3. periodontology, Carranza. Clinical A Fermin Newman, Takei, 4.AB. Compliance with supportive Novacs Novaesab Jr, 3. sites (TRS). of reinfected Treatment 4. dentition, application of fluorides Polishing of the entire 1. of supportive periodontal What are the objectives 2. What is the sequence of maintenance visits? 3. Describe the importance of maintenance therapy in KNOW MORE ... it is also called supportive periodontal treatment (SPT). treatment periodontal it is also called supportive the recurrence of periodontal to prevent or minimize factors known to contribute to diseases by controlling the disease process. home care and degree of patients disease, effectiveness achieved. of control of inflammation The patient has been recommended. tenance visits at 2 to 4 weeks should be seen initially for recall treatment 3 or 4 such sessions the interval After following treatment. according can be extended to 3 months (can be varied to patient needs). 10-15 minutes. 30-40 minutes. of involved areas is done. Flap curettage and antibiotic areas is done. Flap of involved are Recall appointments be given. therapy should every 3 months. for at least once in scheduled SPT in Daily Practice of: The SPT recall hour is generally composed 1. and diagnosis (ERD) for Examination, re-evaluation 2. (MRI) for Motivation, reinstruction and instrumentation 1. in nature hence supportive Maintenance therapy is often 2. therapy is objective of supportive periodontal The main 3.is determined by severity of The interval of recall visits 4. Based on many long-term studies, the interval for main- 49 ChapterChapter

Occlusal Evaluation and Therapy in the Management of Periodontal Disease

 TERMINOLOGY  MANAGEMENT OF TRAUMA FROM OCCLUSION  CLINICAL EVALUATION OF OCCLUSION  POSSIBLE REQUIREMENTS FOR OCCLUSAL • TMD Screening Examination STABILITY • Intraoral Evaluation  OCCLUSAL THERAPY

TERMINOLOGY CLINICAL EVALUATION OF OCCLUSION

Occlusion: It is defined as the functional relationship Temporomandibular Disorders (TMDs) between the components of the masticatory system including the teeth, supporting tissues, neuromuscular system, Screening Examination temporomandibular joints and craniofacial skeleton. Screening for temporomandibular disorders (TMDs) should Intercuspal position (ICP): The position of the mandible be included in all routine dental examinations. when there is maximal intercuspation between the maxillary The accepted components of this examination are: and mandibular teeth. 1. Maximal intercuspal opening—recorded in Excursive movement: Any movement of the mandible millimeters. away from ICP. 2. Opening—closing pathway—deviations if any are Protrusion: Movement of the mandible anteriorly from ICP. recorded. Retrusion: Movement of the mandible posteriorly from ICP. 3. Auscultation for TMJ sounds—joint sounds can be, A physiologic occlusion: It is when no signs of dysfunction discrete clicks or diffuse grating sounds (crepitus). or disease are present and no treatment is indicated. 4. Palpation for TMJ tenderness—could be mild, A non-physiologic (or traumatic) occlusion: It is moderate or severe tenderness, recorded with light associated with dysfunction or disease due to tissue injury, bilateral palpation along the lateral aspects of and treatment may be indicated. condyles. A therapeutic occlusion: It is the result of specific 5. Palpation for muscle tenderness—the masseter and interventions designed to treat dysfunction or disease. temporalis muscles are examined bilaterally using CHAPTER 49 Occlusal Evaluation and Therapy in the Management of Periodontal Disease 413 b. posterior contacts Well-distributed c. teeth contacts between posterior Coupled d. Cross tooth stabilization e. axis of each tooth. Forces directed along long function. a. Interocclusal appliance therapy. b. Occlusal adjustment. c. Restorative procedures. d. surgery. Orthodontic movement and orthognathic tooth move- Restorative procedures and orthodontic is the selective Occlusal adjustment or coronoplasty Occlusal adjustment had once been the most commonly Coronoplasty is generally performed after gingival OCCLUSAL THERAPY 2. interference Smooth excessive movement without 3. occlusion No trauma from 4. and subjective response to occlusal form Favorable Occlusal therapy is performed to establish a stable functional Occlusal therapy is performed to establish of the patient, relationship, favorable to the oral health to achieve procedures Various including the periodontium. this objective are: patient is covered ments in the management of periodontal elsewhere, in this book. goal of establishing reshaping of occlusal surface with the This is achieved by a stable, non-traumatic occlusion. undesirable reshaping the crown surfaces and eliminating of a stable occlusal supracontacts and the creation mandibular position. employed procedure for treating occlusal trauma, temporomandibular joint problems and other associated problems. Since occlusal adjustment is an invasive, irreversible intervention, it should rarely be considered. It should never be undertaken as a preventive measure. inflammation and periodontal pockets have been elimi- The author recommends a reference book for nated. a detailed description on the procedure of occlusal adjust- ment. . . When the quantity of the . moderate finger pressure. The muscle pain may be The muscle pain finger pressure. moderate or severe type. mild, moderate secondary occlusal trauma a. Light or absent anterior contacts periodontitis. The treatment is simple and conservative. The treatment periodontitis. include plaque First, periodontal therapy is done which is progressive control, scaling and root planing. If there form of selective mobility then occlusal therapy in the be justified. grinding and the use of night guard may periodontitis, the treatment is often complicated. It often including root requires advanced periodontal therapy, resection, antimicrobial therapy and regenerative procedures along with adjunctive orthodontics, occlusal adjustment by selective grinding and splinting for periodontal stabilization is advocated. contact by placing mylar strips between the teeth and contact by placing to close and open. asking the patient POSSIBLE REQUIREMENTS FOR STABILITY OCCLUSAL MANAGEMENT OF TRAUMA MANAGEMENT FROM OCCLUSION 1. position Intercuspal b. In cases of secondary occlusal trauma and advanced a. with gingivitis or In cases of primary occlusal trauma remaining normal attachment apparatus has been remaining normal attachment apparatus and cannot withstand compromised by periodontal disease process is referred the normal forces of occlusion, the disease to as When an adequate quantity of periodontal support is present When an adequate quantity of periodontal yet excessive to withstand the normal forces of occlusion, capacity of the parafunctional forces exceed the adaptive is referred to as attachment apparatus, the disease process primary occlusal trauma Intraoral Evaluation of Occlusion Intraoral Evaluation 1. zones of of intercuspal position (ICP) Identification 2. excursive movements. Guidance in 3. mobility. Tooth 4. attrition should be noted. Attrition—excessive 414

BIBLIOGRAPHY

KNOW MORE ... 1. Burgett FG, Ramfjord Sp, Nissle RR, et al. A randomized trial of occlusal adjustment in the treatment of periodontitis patients. Occlusal Therapy J Clin Periodontol 1992;19:381. Guidelines to occlusal therapy in general are: 2. Gher ME. Changing concepts. The effect of occlusion on a. A sound biologic rationale should exist. periodontitis. Dent Clin North Am 1998;2:285. b. Should be considered an adjunct to periodontal 3. Robert S Rosenbaum. The possible effect of periodontal diseases therapy.

PART V PART on occlusal function: Editorial Review. Curr Opin Periodontol c. Be prepared for irreversible occlusal changes in the 1993;163. context of restorative care. 4. Sigurd P Ramfjord, Major M Ash. Periodontology and d. Thorough informed consent must be provided to the periodontics. Modern therapy and practice, Euro-America Inc. patient.

USA, 1996. Treatment of Periodontal Diseases Periodontal of Treatment 50 ChapterChapter

The Role of Orthodontics as an Adjunct to Periodontal Therapy

 RATIONALE FOR ORTHODONTIC TREATMENT IN  TIMING OF ORTHODONTIC PROCEDURES IN PERIODONTAL THERAPY PERIODONTAL TREATMENT  USE OF ORTHODONTICS AS AN ADJUNCT TO  IATROGENIC EFFECTS ASSOCIATED WITH OVERALL TREATMENT ORTHODONTIC TREATMENT  INDICATIONS AND CONTRAINDICATIONS OF  MICROBIOLOGY AROUND ORTHODONTIC BANDS ORTHODONTIC THERAPY

INTRODUCTION accumulation sites that are difficult to clean. In addition, they open the distal contact creating an area of food The primary objective of periodontal therapy is to restore and maintain the health and integrity of the attachment impaction. Crowding also creates enlarged contact surfaces apparatus of teeth. In adults, the loss of teeth or periodontal and altered embrasure spaces that are displaced apically, support can result in pathologic tooth migration involving thereby becoming less accessible to use floss and other either a single tooth or a group of teeth. This may result in plaque removing devices. In these situations orthodontic the development of a median diastema or general spacing treatment can improve the health of the tissues. of the teeth, rotation or tipping of premolars and molars with the collapse of the posterior occlusion and decreasing Improving Gingival and Osseous Form vertical dimension. Adjunctive orthodontic therapy is There is an interrelation between the position of the tooth, necessary to resolve these problems. the shape of the gingiva and bone that surrounds it. For example, lower first or second molar tilted into an edentu- RATIONALE FOR ORTHODONTIC lous mesial space. In these cases there is a narrow space TREATMENT IN PERIODONTAL THERAPY between its crown and the bone that easily becomes inflamed and in which case a pocket may develop. Ortho- Reducing Plaque Retention dontic treatment may improve the shape of the Example: Crowded teeth (arch length deficiency), mesially- periodontium and reduces the indications for bone surgery tipped teeth, usually into an edentulous area creates plaque (Figs 50.1A to C). 416 Treatment of Periodontal Diseases PART V periodontal condition. for abettercontouredcrown andthiswillbenefitthe The uprightingoftiltedabutment teethmaybeimportant Facilitating ProstheticReplacements Figs 50.1AtoC: Crown lengtheningwithinternalbevel gingivectomy 0 Closureofdiastema. 10. Increasing/decreasingoverjet/overbite 9. Restoringlostverticaldimension 8. Repositioningteethforimplantplacement 7. Achievingadequateembrasurespaceandproperroot 6. Correctingcrowdingofteeth 5. Extrudingteeth/Intrudingteeth 4. Correctingcrossbites 3. Improvingfutureponticspaces(e.g.inadequatespaces) 2. Uprightingorrepositioningofteethtoimproveparallelism 1. other habits between anteriorteeth.Correctionoftongue-thrustingand Correction ofpathologictoothmigrationanddiastema Improving Esthetics by periodontaltherapybased onthebeliefthatorthodontics It isgenerallyrecommended thatorthodonticsbepreceded attachment lossandalteringthemorphologyofbone. of plaquesubgingivally, increasingtherateofperiodontal periodontal problem.Thiscanoccurbyshiftingtheposition of toothmovementoninflamedgingivamayexacerbate the in spiteofphase-Itherapyprocedures.Thesuperimposition The onlycontraindicationisthepersistenceofactivedisease Contraindications anterior diastema,mesialtiltingofmolarsandopencontacts. orthodontic therapysuchascrowdedteeth,closureof This includescommonproblemsthatcanbesolvedbyminor Indications TO OVERALL TREATMENT USE OFORTHODONTICS AS AN ADJUNCT IN PERIODONTAL TREATMENT TIMING OFORTHODONTICPROCEDURES OF ORTHODONTICTHERAPY INDICATIONSCONTRAINDICATIONS AND positioning of abutmentteeth(e.g.tippedteeth) CHAPTER 50 The Role of Orthodontics as an Adjunct to Periodontal Therapy 417 orthodontic forces Response of the periodontal ligament to

Fig. 50.2: movements failed to induce gingivitis, whereas in the movements failed to induce gingivitis, angular bone presence of plaque similar forces cause defects associated with attachment loss. the regions with cause gingival inflammation even in the non-inflam- reduced periodontal support, but is of matory type. Response of the Periodontal Ligament Response of the Periodontal to Orthodontic Forces (Fig. 50.2) Effects of Orthodontics on Dentition with on Dentition of Orthodontics Effects Apparatus Attachment Height of Normal that have demonstrated of experimental studies Number causes no damage to the supra-alveolar orthodontic forces orthodontic treatment will therefore connective tissue and tissue breakdown and pocket not result in periodontal formation. Reduced Height Dentition with Apparatus Attachment of have demonstrated that, The experimental studies a. orthodontic forces and tooth In the absence of plaque, b. limit failed to Orthodontic forces if kept within biologic Prevotella intermedia Prevotella count (Bloom and Brown, 1964) —Loss of attachment, root resorption —Gingivitis and gingival hyperplasia, Lactobacillus (Diamanti, Kipioti et al, Huser et al, 1990) anaerobes (Diamanti, Kipoti et al, Huser et al 1990). MICROBIOLOGY AROUND MICROBIOLOGY ORTHODONTIC BANDS IATROGENIC EFFECTS ASSOCIATED WITH ASSOCIATED EFFECTS IATROGENIC TREATMENT ORTHODONTIC a. Increased or no effects. Any of these three possibilities may be seen or no effects. in adult patients. b. Increased motile organisms (Leggott et al, 1984) c. Increased anaerobes like d. Decreased count of facultative microorganisms/ Short-term effects are mostly not associated with loss of attachment. Long-term effects are Effects of Orthodontic Bands on Effects of Orthodontic Bands the Periodontium Some amount of root resorption is unavoidable especially if Some amount of root resorption is unavoidable of the root, which it is seen at the marginal and middle thirds cementum. can be repaired by apposition of cellular Root Resorption Orthodontic treatment may cause injuries to the teeth and Orthodontic treatment are in most of the cases the changes periodontium but of the tooth structures reversible and regeneration and repair In some cases the changes and periodontal tissues can occur. All damage. may get out of control resulting in irreparable avoid this and radio- the precautions should be taken to intervals in order to graphy should be performed at regular the orthodontic disclose any iatrogenic effects during treatment. They are as follows: in the presence of inflammation can lead to rapid and can lead to of inflammation in the presence But any the periodontium. breakdown of irreversible reduction pocket or osseous procedures like elimination postponed until the end of orthodontic procedures may be movement may modify gingival and therapy because tooth osseous morphology. 418 Treatment of Periodontal Diseases PART V .Whenpressureisappliedtothetooth, thereisainitial 2. Resorptionoccurswherethereispressureandnewbone 1. responds inthefollowingmanner: When bonesurroundingthetoothissubjectedtoaforceit .Theonlycontraindicationfororthodontic treatmentis, 3. Basicrationalefororthodonticinterventionin 2. Adjunctiveorthodontic therapyisnecessarytoresolve 1. needs tobecontrolledbyperiodontaltreatment. is presentinperiodontaltissue.Hence,theinflammation periodontal ligamentdoesnotoccurwheninflammation tooth movementcanoccuragain.Regenerationof alveolar bone.Oncethehyalinizedzoneisremoved, adjacent areasofunaffected periodontal ligamentand by themarrowspaces(underminingresorption)and from thereorganization oftheareathroughresorption is eliminatedbyperiodontalregenerationthatoccurs moving (dependingontheforces). The hyalinizedzone zation avascular, cell-freezonebyaprocesstermed“ of theperiodontalligamentandthisproducesan ligament resultsinbloodsupplybeingcutoff toanarea ligament iscompressed.Compressionofperiodontal period ofmovementfor6to8daysastheperiodontal forms wherethereistension. persistent inflammationinspiteofphaseItherapy. In replacement andimproveesthetics. improve gingivalandosseousform,facilitateprosthetic periodontal therapyistoreduceplaqueaccumulation, decreasing verticaldimension. tipping ofteeth,collapsetheposteriorocclusionand problems likegeneralizedspacingofteeth,rotationor ”. When hyalinizationoccursthetoothstops hyalini- .Whataretheeffectsoforthodontictreatmenton 1. .Someofthecommoniatrogeniceffectsorthodontic 4. .Theimplantpatient—by repositioningtheadjacent c. Thepatientwith‘darktriangles’duetointerdental b. Thepatientwith aseverefractureofmaxillary a. osseous formandesthetics,italsobenefits: Apart fromreducingplaqueretention,improvinggingival, Rationale forOrthodonticTreatment .RobertGKein. Aesthetics inclinicalorthodonticperiodontic 3. JanLindhe.ClinicalPeriodontologyandImplantDentistry, 4th 2. Interrelationshipbetweenperiodonticsandadultorthodontics. 1. periodontium? interactions. Periodontol2000;27:2001. Edn, BlackwellMunkgardPublication2003. J ClinPeriodontol1998;25:271-7. teeth. papillary recession. adequate toothrestoration. anterior tooth,withforcederuptioncanpermit periodontal ligamentandothers. associated withorthodonticbands,changesin treatment are,rootresorption,gingivalinflammation movement canexacerbatetheperiodontalproblems. the presenceofactiveinfection,orthodontictooth REVIEW QUESTION BIBLIOGRAPHY KNOW MORE... 51 ChapterChapter

Periodontal-Restorative Inter-relationship

 MARGINS OF RESTORATIONS  CROWN CONTOUR  RULES FOR MARGIN PLACEMENT  HYPERSENSITIVITY TO DENTAL MATERIALS  RESTORATIVE MARGINS ENCROACHING ON  PROXIMAL CONTACT AND EMBRASURE THE BIOLOGIC WIDTH  PONTIC DESIGN

INTRODUCTION Supragingival margins have the least impact on the periodontium. The use of equigingival margins was thought It is a well-established fact that the periodontal health and to retain more plaque thereby interfering with gingival the restoration of teeth share an intimate and inseparable health, today these concerns are not valid. The greatest interrelationship. One must always remember that for biologic risk occurs when margins are placed subgingivally. restorations to survive, long-term restorative procedures must be performed on a periodontium free of inflammation Hence, from periodontal point of view, both supragingival and pockets without any mucogingival involvement, and and equigingival margins are well-tolerated. with the contour and shape of the periodontium corrected In view of the scientific evidence available, restorative for a good functional and esthetic restorative result. For the margins should be preferably placed supragingivally. periodontium to remain healthy, restorations must be However in certain situations, where subgingival margins critically prepared so that, they will remain in harmony with are unavoidable like carious tooth, tooth fracture or esthetic the surrounding periodontal tissues. concern, it should be placed not more than 0.5 mm into the sulcus so that, these margins could be accessible for finishing MARGINS OF THE RESTORATIONS procedures. In addition, if the margins are placed too far below the A clinician has three options for margin placement: gingival tissue crest, it violates the gingival attachment i. Supragingival ii. Equigingival (even with the tissue) apparatus. iii. Subgingival RULES FOR MARGIN PLACEMENT Restorations should be chosen not just by keeping esthetics in mind but for their favorable periodontal impact Rule 1: If the probing depth is 1.5 mm or less, the restoration as well. margin has to be placed below gingival tissue crest. 420 Treatment of Periodontal Diseases PART V provide: maintenance ofperiodontalhealth. An idealcontourmust Restoration contourplaysanimportantroleinthe 2. 1. ways: moving themargin awayfromthebone). margin) ororthodontically(bymovingthetoothandthus (removing boneawayfromproximitytotherestorative Biological widthviolationcanbecorrectedeithersurgically the the gingivalsulcusandcrestofalveolarboneiscalled The softtissueattachmenttothetoothbetweenbaseof margin placementisdoneinaccordancetoRule1. to reducethesulcusdepth1.5mm.Oncethisisachieved the toothhastobeevaluatedforgingivectomyprocedure Rule 3: depth belowthegingivalcrest. margin oftherestorationisplacedatonehalfprobing Rule 2: Connective tissueattachment(1.07mm)=2.04mm. inflammation. order topreventattachmentlossandpersistentgingival CROWN CONTOUR WIDTH VIOLATION METHODS TO CORRECTBIOLOGICAL ON THEBIOLOGICWIDTH(FIG. 51.1) RESTORATIVE MARGINSENCROACHING i.Esthetically-pleasing toothcontour. iii. i Fullnesstocreatethedesiredgingivalform. ii. .Accessfor hygiene. i. several weeks. extrusion tothedesiredamountiscarriedoutover forceBy rapidorthodontic extrusive with it. extruded slowlybringingtheboneandgingivaltissue By sloworthodontic extrusive force The orthodonticprocedurecanbeaccomplishedintwo Biologic width=Junctionalepithelium(0.97mm)+ Invasion intothisbiologicwidthshouldbeavoidedin biologic width Iftheprobingdepthismorethan1.5mm,then If thesulcusprobingdepthismorethan2mm,then . : : Where thetooth : The toothis considered ideal. inflammation, undercontouringofcrownsistherefore more plaqueaccumulationwithsubsequentgingival plaque removal,notitsretention.Overcontouringleadsto house thegingivalpapillawithout impingingonit.Proper It isbelievedthat,theidealinterproximal embrasureshould the toothsurface. has thepotentialtointerferewithadherenceofbacteria on acceptable becauseofitscapabilitytoreleasefluoridethat periodontal pointofviewglassionomerseemstobemore oral environment,itssurfacebecomesrough.From they donotlastverylongbecause,onceitisexposedto the composite resinshaveverysmoothsurfaceuponfinishing, glass ionomercementsandcompositeresins.Thoughthe materials. Today, themostcommonlyusedmaterialsare used subgingivally, asmoothsurfaceisessentialonall contribute toperiodontaldisease.Regardlessofthematerial Rough dentalsurfacesfavorplaqueaccumulationand PROXIMAL CONTACT AND EMBRASURE HYPERSENSITIVITY TO DENTAL MATERIALS v Protectionofthemarginal gingivafrommechanical iv. Hence, thecrowncontourshould,thereforehelpineasy protection theory. injury duringmastication—explainedingingival Fig. 51.1: Biologic width CHAPTER 51 Periodontal-Restorative Inter-relationship 421 biologic Ovate pontic Modified ridge lap pontic : This is the ideal pontic design. This is the ideal pontic : Fig. 51.5: Fig. 51.4: ’ which is 2.04 mm. which is 2.04 ’ periodontium free of inflammation and other signs of periodontal disease. equigingival or subgingival locations. Supragingival margin has the least impact on the periodontium. to the crest of the alveolar bone is called the ‘ width to create the desired gingival form and esthetically- pleasing tooth contour. ridge lap, modified ridge lap and ovate pontic sanitary, designs. It is created by forming a receptor site in the edentulous It is created by forming a receptor site ridge with either a diamond bur or electrosurgery. to replace missing Whenever fixed prosthesis is designed The ovate pontic 1. Restorative procedures should be performed on a 2. The restorative margins can be placed at supragingival, 3. between the base of the gingival sulcus tissue The soft 4. Ideal contour must provide, access for hygiene, fullness 5. Four types of pontic designs have been proposed: teeth, contact between the pontic and mucosa should be teeth, contact between the pontic and plaque control avoided or kept minimal so that meticulous can be advocated (Fig. 51.5). 4. : The tissue surface on the : Sanitary pontic Ridge lap pontic : Where the tissue surface of the pontic : : Where the tissue surface of the pontic Where : Fig. 51.2: Fig. 51.3: Sanitary pontic Sanitary The entire surface straddles the ridge much like a saddle. to clean (Fig. 51.3). is convex and is very difficult Modified ridge lap pontic the lingual saddle facial surface is concave, however, for oral hygiene has been removed to allow access (Fig. 51.4). is 3 mm from the underlying ridge (Fig. 51.2). is 3 mm from the underlying ridge (Fig. Ridge lap pontic PONTIC DESIGN Traditionally, four types of pontic designs have been four types of pontic Traditionally, lap and oviate ridge lap, modified ridge proposed—sanitary, pontic designs. 1. 3. 2. proximal contact is essential to prevent food impaction. The to prevent food impaction. contact is essential proximal facially to occlusally and should be placed contact point The ideal plaque control. access for interproximal facilitate to 3 mm coronal to the attachment, which contact should be 2 of the average interproximal sulcus. coincides with the depth 422 Treatment of Periodontal Diseases PART V 2. 1. It canbedividedintotwophases: for RestorativeDentistry Sequence ofTreatment inPreparingPeriodontium Crownlengthening procedure. – Ridgereconstructionandpreservation. – Treatment ofmucogingivaldeformities. – Preprosthetic surgery Adjunctiveorthodontictherapy. – Periodontal surgery. – Re-evaluation,anti-infectivetherapy. – Scaling,rootplaningandoralhygieneinstructions. – Extractionofhopelessteeth. – surgical andtreatment Control ofactiveperiodontal inflammationwithnon- KNOW MORE... .Whatisthebiologicwidth? 2. Whataretheeffects ofrestorativeprocedureonthe 1. .NiklausP. Lang,Sture RNyman.Implantandcrownbridge 3. MyronNevins.Periodontalconsiderationsinprosthetic 2. DanLundgren,LarsLaurell.Biomechanicalaspectsoffixed 1. periodontium? 2000;1994:4. therapy intheperiodontallycompromisedpatient.Periodontol treatment. CurrOpin.Periodontol1993;151-4. Periodontol 2000;1994:4. bridge worksupportedbynaturalteethandendosseousimplants. REVIEW QUESTIONS BIBLIOGRAPHY 52 ChapterChapter

Drugs Used in Periodontal Therapy

 CLASSIFICATION OF VARIOUS DRUGS USED  NON-STEROIDAL ANTI-INFLAMMATORY IN PERIODONTAL THERAPY DRUGS • Depending on Antimicrobial Efficacy and  LOCAL DRUG DELIVERY SYSTEMS Substantivity  LOCAL ADMINISTRATION OF ANTIBIOTICS • Chemicals Used for Supragingival AND ANTIMICROBIAL AGENTS Plaque Control  CURRENTLY AVAILABLE LOCAL DRUG  ANTIBIOTICS USED IN PERIODONTAL DELIVERY SYSTEMS IN PERIODONTAL THERAPY THERAPY

INTRODUCTION 1. Antiplaque and anticalculus agents. 2. Antibiotics in the management of periodontal disease. It is a well established fact that mechanical therapy is the 3. Anti-inflammatory drugs. foundation for periodontal therapy. In the past only necrotizing ulcerative gingivitis was treated with antibiotic Depending on Antimicrobial Efficacy therapy because it was considered as a fusospirochetal and Substantivity infection. With emerging evidence of bacterial specificity in relation to aggressive forms of periodontitis and also the Depending on antimicrobial efficacy and substantivity drugs difficulty in suppressing tissue invaded pathogens with can be classified as: conventional therapy in certain cases (like juvenile 1. First generation agents: They reduce plaque score by periodontitis) led to the development of antimicrobial 20 to 50 percent, efficacy is limited because of poor treatment strategies. But total elimination of the periodontal substantivity. pathogens with antibiotic therapy alone may not be possible, Examples: antibiotics, quaternary ammonium com- unless it is combined with scaling and root planing. pounds and sanguinarine. It should be used 4 to 6 times daily. CLASSIFICATION OF VARIOUS DRUGS 2. Second generation agents: They are retained longer in USED IN PERIODONTAL THERAPY the tissues and their slow release property provides Various drugs used in periodontal therapy can be divided overall reduction in plaque score by 70 to 90 percent into: (should be used twice daily). 424

Example: chlorhexidine, triclosan with either copolymer Quaternary Ammonium Compounds include: or zinc citrate. i. Benzathonium chloride. 3. Third generation agents: It should be effective against ii. Benzalkonium chloride. specific periodontopathic organisms. The most pro- iii. Cetyl pyridium chloride—CPC (ReachTM). mising agent seems to be Delmopinol which is a surface iv. Domiphen bromide (Cetrimide). active agent. Though it is a weak antimicrobial agent, it Mechanism of action: They have some similarities in their can exert its effect by binding to salivary proteins and mechanism of action to chlorhexidine, the molecules possess thereby alters the cohesive and adhesive properties of both hydrophobic, and hydrophilic groups allowing for ionic the films formed. PART V and hydrophobic interactions. It is assumed that the interaction with bacteria occurs with cationic binding, to Chemicals used for Supragingival the phosphate groups in the cell wall teichoic acid in the Plaque Control gram-positive bacteria and to the phosphate groups of the It is discussed elsewhere in this book. cell wall and in general to the membrane lipopolysaccharide of gram-negative bacteria. The membrane integrity may Phenols subsequently be disrupted by interaction with the lipophilic portion of the molecule, causing disturbance of membrane Mechanism of Action: Most phenols exert a nonspecific functions and leakage of cytoplasmic material. antibacterial action which is dependent upon the ability of the drug in its nonionized form to penetrate the lipid ANTIBIOTICS USED IN component of the cell walls of gram-negative organisms. PERIODONTAL THERAPY The resulting structural damage will affect the permeability which in turn affects the exchange of substances in addition Chemotherapeutic agents refers to the ability of an active to several metabolic processes that are dependent upon chemical substance to provide a therapeutic clinical benefit. enzymes contained within the cell membranes. Phenolic Antimicrobial agents are chemotherapeutic agents that

compounds have also been shown to exhibit anti- reduce the amount of bacteria present, either by specifically Treatment of Periodontal Diseases Periodontal of Treatment inflammatory properties, which may result from their ability targeting certain organisms or by nonspecifically reducing to inhibit neutrophil chemotaxis, the generation of neutrophil all bacteria. superoxide ion and the production of prostaglandin Antibiotics are a form of antimicrobial agents produced by synthetase. or obtained from microorganisms, that have the capacity to ListerineTM is an over the counter phenol precipitate that kill other microorganisms or inhibit their growth. contains thymol, eucalyptol, menthol, methyl salicylate, Chemotherapeutic agents may be administered either: benzoic acid and boric acid. i. Systemically, or ii. Locally. Quaternary Ammonium Compound Systemic Administration of Antibiotics Quaternary ammonium compounds are cationic antiseptics It may reduce or eliminate bacteria that cannot be removed and surface active agents. Quaternary ammonium by scaling or root planing, e.g. bacteria in the tissues/root compounds tend to be more effective against gram-positive surfaces. than gram-negative organisms. This may suggest that these Other uses of systemic administration of antibiotics compounds are most effective as anti plaque agents when include: used against early developing plaque, which predominantly • Decrease in plaque and gingivitis. contains gram-positive bacteria. • Retards bone loss. 425

• Use of antibiotics in conjunction with nonsurgical Tetracyclines therapy reduces/eliminates the need for periodontal Antibacterial Actions surgery. • It is also useful in cases of aggressive periodontal Tetracyclines are a group of antibiotics that are derived HPE 52 CHAPTER diseases that may be resistant to traditional nonsurgical naturally from Streptomyces or derived semi-synthetically. or surgical therapies, e.g. localized juvenile periodontitis, These antibiotics are bacteriostatic and are generally more rapidly progressive periodontitis. effective against gram-positive bacteria than gram-negative bacteria. Tetracyclines are very effective in treating Advantages of Systemic Medication periodontal diseases mainly because of their concentration i. It ensures drug penetration till the base of the pocket. in gingival crevicular fluid (GCF) which is 2 to 10 times

ii. Affects tissue invasive organisms. more than that in serum. In addition, many studies have Drugs Used in Periodontal Therapy Periodontal in Used Drugs iii. Takes less time and is inexpensive. proved that tetracyclines even at low concentrations are very iv. Treats multiple sites simultaneously. effective against many periodontal pathogens. v. In acute conditions like necrotizing ulcerative gingivitis, Tetracycline hydrochloride is also a chelating agent and 2+ 2+ 3+ etc. it is used to decrease active inflammation. chelates Ca , Mg , Al in the gastrointestinal tract. These vi. As a premedication for patients with medical problems ions, especially calcium are present in a variety of food requiring prophylactic antibiotic coverage. substances. Since the chelate is present poorly absorbed, it is advisable to take tetracycline either half an hour before Local Administration of Antibiotics or after food. Other properties of tetracyclines which are of value in Many chemotherapeutic agents can be delivered locally. the management of periodontal diseases are: a. Tetracyclines and collagenase inhibition (Host-derived Advantages of Local Drug Administration collagenase): These enzymes are derived from a variety i. Greater concentrations are achieved with reduced drug of sources including fibroblasts, epithelial cells, doses. macrophages and neutrophils. Collagenase derived from ii. Systemic side effects are reduced. neutrophils are more susceptible to tetracycline induced iii. Slow releasing devices have the advantage of releasing inhibition. antibiotics gradually. b. Tetracyclines and bone resorption: The antiproteolytic iv. Their effect can be directed to specific target area. properties together with anticollagenase activity has resulted in the use of these drugs to stop/inhibit bone Disadvantages resorption. Tetracyclines also inhibit bone resorption It can induce superinfections or hypersensitivity reactions. induced by parathyroid hormone, prostaglandin E series According to Gibson and bacterial endotoxins. An ideal antibiotic for use in prevention and treatment of c. Anti-inflammatory actions of tetracyclines: Potential periodontal diseases should be: anti-inflammatory properties include the ability of • Specific to periodontal pathogens tetracyclines to suppress polymorphonuclear leukocyte • Allogenic activity, in particular, the scavenging action of reactive • Nontoxic, substantive oxygen metabolites. Alternatively, the drugs may block

• Not in general use for treatment of other diseases eicosanoid synthesis (PGE2) by inhibiting phospholipase

• Inexpensive. A2 activity. 426

d. Tetracycline and fibroblast attachment: Contraindications for the Use of Tetracyclines • Pretreatment of dentine with tetracyclines enhances a. Pregnancy—staining of deciduous teeth, impaired bone fibroblast attachment and colonization. Tetracycline growth. can both condition the root surface and influence b. Breastfeeding—staining of developing teeth and the attachment properties of fibroblasts gastrointestinal disturbance in children. • Tetracyclines can bind to demineralize and release c. Renal impairment—aggravates uremia. from dentine. The substantivity of tetracycline is d. Hepatic disease. proportional to the concentration of the drug rather e. Systemic lupus erythematosus—exacerbation of lesions.

than to the time of application PART V • The drug also enhances fibronectin binding. (Hence, Specific Agents and their Dosage their use as an adjunct in treating periodontitis is Tetracycline, minocycline and doxycycline are all semi- very well established and their effect is maximum in synthetic members of the tetracycline group that are patients with localized juvenile periodontitis and commonly used in periodontal therapy. refractory periodontitis). Tetracycline—Requires administration of 250 mg four times Adverse Effects of Tetracyclines a day. It is inexpensive but compliance may be reduced by a. Gastrointestinal disturbances taking 4 capsules a day. • Diarrhea Minocycline—Exhibits broad spectrum of antibacterial • Nausea and vomiting activity especially in patients with adult periodontitis. • Severe colitis (rare). Dosage—200 mg twice a day for 1 week, side effects include b. Overgrowth of resistant organisms reversible vertigo. • Stomatitis • Vaginitis Doxycycline—Same spectrum of activity as minocycline. • Staphylococcal enterocolitis. Absorption from gastrointestinal tract is not altered by

c. Photosensitivity calcium, metal ions or antacids. Treatment of Periodontal Diseases Periodontal of Treatment • Skin rashes Dosage—100 mg twice on the first day followed by 100 • Hypersensitivity reactions. mg once a day or 50 mg twice a day for 4 days.

Significant Drug Interactions Metronidazole Involving Tetracyclines It is bactericidal to anaerobes and it is believed to disrupt bacterial DNA synthesis. They are not very effective against Drug Possible sequelae A. actinomycetemcomitans infections but quite effective Penicillin Antagonism of bactericidal action. against obligate anaerobes such as Porphyromonas Antacids Impaired absorption of tetracycline. Insulin Enhanced hypoglycemic action of gingivalis and Prevotella intermedia. insulin. Contraceptive pill Pill failure. Clinically—It is used to treat necrotizing ulcerative Digoxin Increased serum digoxin concentra- gingivitis, adult periodontitis and rapidly progressive tion. periodontitis. Warfarin sodium Enhanced anticoagulant effect. Carbamezapine and Decreased serum concentration of Dosage—200 mg four times a day for 1 week/400 mg three phenytoin doxycycline and minocycline. times a day for 1 week. 427

Side effects pathogenic changes occurring in periodontium. Hence • It has antabuse effect when alcohol is ingested NSAID may be of therapeutic value in treating periodontal • The symptoms include severe cramps, nausea and disease because they interfere with arachidonic acid vomiting metabolism and thereby inhibit inflammatory process. HPE 52 CHAPTER • It inhibits warfarin metabolism Various drugs that are studied include flurbiprofen, • Patients on anticoagulant therapy should avoid this drug ibuprofen, mefenamic acid and naproxen. because it prolongs prothrombin time. Actions of Flurbiprofen Penicillins • Decreased PMNL migration Penicillins are bactericidal but induce allergic reactions. • Decreased vascular permeability

Most widely studied antibiotics are amoxicillin and • Decreased platelet aggregation. Drugs Used in Periodontal Therapy Periodontal in Used Drugs amoxicillin clavulanate potassium (Augmentin). Mechanism of Action of NSAID (Fig. 52.1) Amoxicillin—It exhibits broad spectrum activity and is useful in patients with refractory or juvenile periodontitis. After the activation of inflammatory cells in the periodontium by bacteria, phospholipids in the plasma Dosage—500 mg three times a day for 1 week. membranes of cells are activated by the enzyme

Augmentin—It is a combination of amoxicillin with phospholipase A2 and this leads to release of free arachidonic clavulanate potassium. It is useful in patients with refractory acid in the area. Arachidonic acid can then be metabolized or juvenile periodontitis. into prostaglandins, thromboxanes and prostacyclins by cyclooxygenase or into leukotrienes, HETE and SRS-A by Dosage lipoxygenase enzyme.

• Augmentin 375 mg — amoxicillin 250 mg + clavulanic LOCAL DRUG DELIVERY SYSTEMS acid 125 mg three times a day for 1 week. The limited efficacy of mouth rinsing and irrigation in deep • Augmentin 625 mg — amoxicillin 500 mg + clavulanic periodontal pockets led to the development of alternative acid 125 mg twice a day for 1 delivery systems. week. The main aim of the drug delivery system is to direct antimicrobials to the infection sites and maintaining effective Ciprofloxacin—It is active against gram-negative rods but has minimal effect on Streptococcus species. At present, ciprofloxacin is the only antibiotic effective against all the strains of A. actinomycetemcomitans. Clindamycin—It acts against anaerobic bacteria and is shown to be effective in patients with refractory periodontitis. It is associated with pseudomembranous colitis more often than other antibiotics.

NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)

Strong evidence suggests that products of cyclooxygenase pathway (e.g. PGE2) are may be important mediators of Fig. 52.1: Mechanism of action of NSAIDs 428

level of drugs for sufficient period of time without eliciting any major side effects.

Indications

1. As an adjunct in the treatment of few localized non- responding sites in an otherwise controlled patient. 2. In ailing and failing implant cases. 3. In medically compromised patients where surgical

PART V procedures are not recommended. 4. Periodontal abscess. 5. Periodontal maintenance therapy. 6. Patient with gastrointestinal intolerance to systemic drug medication.

Contraindications Fig. 52.2: Intrasulcular placement of tetracycline fibers 1. Patients with history of allergy to a particular antimicrobial agent. II. Methods of delivery of chemotherapeutic agents include: 2. In pregnancy and lactating periods. Root biomodification (direct professional application to 3. Children under the age of 12 years. the root surface during surgery), Keyes technique, 4. Patients with complete renal failure. irrigation methods include home and professional drug 5. Patients susceptible to infective endocarditis. delivery. Advantages Vehicles for Local Delivery 1. High concentration in subgingival sites. Dentifrices, mouth rinses and chewing gum are inefficient

Treatment of Periodontal Diseases Periodontal of Treatment 2. Independent of patient compliance. delivery systems in periodontics because they fail to direct 3. Does not harm the symbiotic useful microflora of drugs into the periodontal pocket. They can be useful in gastrointestinal tract. reducing inflammation associated with gingivitis but they 4. Systemic intolerance is bypassed. do not penetrate well into the periodontal pockets. Disadvantages Slow-release Devices/Controlled-Release 1. Difficulty in placing of therapeutic concentrations of the Delivery Systems antimicrobial agents in deeper sites. 2. Has to be professionally placed or if manually placed, They are designed to release chemotherapeutic agents into requires manual dexterity and patient compliance. the periodontal pocket over an extended period of time, 3. Complete drug penetration is not possible and extra hence, they can achieve high levels of concentration at sites pocket sites are unaffected. where they are precisely needed.

LOCAL ADMINISTRATION OF ANTIBIOTICS Classification of Controlled-Release Local AND ANTIMICROBIAL AGENTS (FIG. 52.2) Delivery Systems I. Vehicles for local delivery of chemotherapeutic agents i. Reservoirs without a rate-controlling system, e.g. hollow include: Dentifrices, mouth rinses, chewing gum and fibers, gels and dialysis tubing (effective only for 24 slow release devices. hours). 429

ii. Reservoirs with a rate-controlling system, e.g. polymeric Home Irrigation Devices matrices, polymer membranes, monolithic matrices and The advantage of home irrigation device is, it allows the coated particles (effective for more than 24 hours). patient to deliver medicaments into the periodontal pocket EVA system (Ethylene vinyl acetate) is based on polymer

at home on a more frequent basis than in practice with 52 CHAPTER technology with tetracycline dispersed within a solid professional subgingival irrigation. The limiting factors for (monolithic) polymer of EVA. A formulation of 25 percent these devices are inability to access the depth of periodontal tetracycline in EVA (Actisite) has been developed as 0.5 pocket and manual dexterity of the patient. mm nonbiodegradable fiber and has been approved by the i. Supragingival home irrigation devices: Results in greater Food and Drug Administration (FDA). access to periodontal pockets than mouth rinsing alone. The use of slow release devices placed in deep periodontal The depth of penetration of medicament is a maximum defects, in conjunction with scaling and root planing may penetration of 4 to 5 mm. Therefore, these devices may offer promising results in the management of such defects. Therapy Periodontal in Used Drugs be useful in delivering medicaments in cases of gingivitis with shallow pocket depths, but they are less useful in Methods of Delivery of delivering medicaments in periodontitis patients with Chemotherapeutic Agents deeper pockets. a. Keyes technique. ii. Subgingival home irrigation devices: Generally includes b. Root biomodification. a blunt ended metal cannula that the patient inserts into c. Irrigation devices. the periodontal pocket. It increases the depth of i. Home irrigation devices penetration of fluid, but largely depends on the manual • Supragingival home irrigation devices dexterity of the patient and has the potential for injury • Subgingival home irrigation devices owing to the metal tip. • Marginal home irrigation devices iii. Marginal home irrigation devices: These are a hybrid ii. Professional subgingival irrigation. of both supragingival and subgingival home irrigation. Keyes Technique It has a jet tip attachment that has been modified so that it can deliver fluids subgingivally. Home irrigation Involves application, by tooth brushing, of a slurry of sodium devices allow penetration of fluid up to 90 percent in bicarbonate and hydrogen peroxide for the control of plaque pockets of 6 mm depth and lesser penetration in pockets microorganisms. Various studies have proved that minimal with deeper depths. The irrigation is more effective clinical benefit can be expected from this technique simply (supra/subgingival) if it is pulsed rather than constant. because tooth brushing offers an ineffective means of delivering medicaments into the periodontal pocket. Professional Subgingival Irrigation Root Biomodification It includes the use of a wide array of powered and manually Application of various medicaments to root surfaces during operated irrigators. Irrigation using a syringe with a blunt surgical therapy has been evaluated. These agents include needle has been used. The most commonly used solutions tetracycline, doxycycline, citric acid and fibronectin. are chlorhexidine gluconate, stannous fluoride, tetracycline, Application of these agents on diseased root surfaces during metronidazole and hydrogen peroxide. Irrigation with surgery may enhance connective tissue attachment to the medicaments performed in conjunction with root planing roots, although available data are inconclusive (discussed provide little, if any, additional benefit over root planing elsewhere in this book). alone. 430

CURRENTLY AVAILABLE LOCAL DRUG aggressive forms of periodontitis, systemic antibiotic DELIVERY SYSTEMS IN PERIODONTAL therapy was thought to be a valuable adjunct to mechanical therapy. THERAPY 2. Best results can be obtained by antibiotic therapy combined with scaling and root planing. Antimicrobial Product Nature Dosage 3. Tetracyclines are bacteriostatic antibiotics which agent name form provides a broad spectrum of activity against both gram- positive and gram-negative organisms. They are most Doxycycline Atridox® Biodegradable Mixture in commonly used in the management of periodontal syringe disease because the GCF (gingival crevicular fluid) Tetracycline ActisiteTM Nonresorbable Fibers concentration can be 5 to 10 times more than the serum. Metronidazole Elyzol Biodegradable Mixture in 4. Apart from antimicrobial activity, it also has other PART V syringe important properties like collagenase inhibition, anti- Minocycline Arestin Biodegradable Mixture in inflammatory action, inhibition of bone resorption, etc. Dentamycin syringe Other drugs that are commonly used in periodontal Periocline therapy are metronidazole, penicillins and quinolones. Chlorhexidine Periochip Biodegradable Chip device 5. Prolonged antibiotic therapy can cause adverse effects like: Frequently used Local Antimicrobials with a. Development of resistant organisms. Dosage Specification b. Hypersensitivity reaction. c. Drug interactions. d. Superinfection. Drug Dosage Release period in days e. Dependency on patients compliance to take the drug ActisiteTM 12.7 mg/9 inch fiber 10 regularly. of diameter .5 mm f. Though periodontal disease involves only small area Atridox® 10% of the body, due to systemic administration of the Periochip 2.5 mg of chlorhexidine 7 drug the whole body gets unnecessarily loaded with gluconate in the drug. (4 × 5 ×.35 mm) chip. 6. In order to overcome all the adverse effects of systemic administration, local drug delivery system was introduced in periodontics. CONCLUSION

Considering various factors of cost effectiveness, efficacy, Treatment of Periodontal Diseases Periodontal of Treatment potential advantages and disadvantages it can be concluded that local drug delivery could serve as a potent weapon in KNOW MORE ... periodontal chemotherapy and at the same time a valuable adjunct to mechanotherapy, but its use as a monotherapy Biological Implications of Systemic Antibiotic Therapy agent is still a topic of debate. in the Treatment of Periodontal Diseases 1. The putative periodontal pathogens tend to reside in REVIEW QUESTIONS the inaccessible areas, which cannot be eliminated by the mechanical treatment. 1. Classify antimicrobial agents, write in detail on role of 2. They may also evade mechanical treatment due to tetracyclines in periodontal therapy. their ability to penetrate periodontal tissues or dentinal 2. What are the advantages and disadvantages of systemic tubules. 3. Treated sites may be recolonized by periodontal antibiotics? pathogens residing in nondental areas such as the 3. Classify local drug delivery systems. dorsum of tongue or tonsils. An Ideal Antimicrobial Agent should Fulfill a Number of Criteria/Conditions a. The drug must demonstrate (in vitro) high antibacterial 1. Mechanical removal of tooth deposits is the foundation activity against the prominent periodontopathic of periodontal therapy. Since there is a possibility of organisms. bacterial invasion of periodontal tissues in cases of 431

2. Lindhe Jan. Clinical Periodontology and Implant Dentistry, 4th b. It should demonstrate a sufficient drug dose in the edn, Blackwell Munkgard Publication, 2003. sub-gingival environment to kill target organisms. 3. Newman, Takei, Fermin A, Carranza. Clinical Periodontology, c. Drug should not elicit any major local or systemic side 9th edn, WB Saunders and Co., 2002. effects. 4. Rethman Micahel, Greenstein Gary. Oral irrigation in the d. It should be able to maintain the required 52 CHAPTER treatment of periodontal diseases. Curr Opin Periodontol concentration of the drug over a long enough period 1994:187-93. to cause sufficient damage to the microbiota 5. Robin A. Seymour, Peter A. Heasman. Drugs, Diseases and the responsible for periodontal infections. Periodontium. Oxford University Press Publication, 1992. e. Finally, it should have better outcome, less adverse 6. Slots J, Rams TE. Antibiotics and periodontal therapy: effects, simpler to perform, cheaper and faster. Advantages and disadvantages. J Clin Periodontol 1990; 17:479. 7. Slots Jorgen, Ting Miriam. Systemic antibiotics in the treatment BIBLIOGRAPHY of periodontal diseases. Periodontol 2000, 2002;28.

8. Walker CB. Selected antimicrobial agents: Mechanism of Drugs Used in Periodontal Therapy Periodontal in Used Drugs 1. Gibson W. Antibiotics and periodontal disease. A selective review action, side effects and drug interactions. Periodontol 2000, of the literature. J Am Dent Assoc 1982;104:213. 1996;10:12. 53 ChapterChapter

Questionnaire for Clinical Case Discussion

QUESTIONS 13. Describe size of gingiva in health and disease. Name some factors responsible for normal size and enlarged 1. What is the significance of recording chief complaint, gingiva. history of present illness, past dental history, family 14. How do you check for normal consistency of the history and medical history? gingiva? In disease condition what are the changes that 2. What are the effects of bruxism, mouth-breathing, take place in consistency of the gingiva? tongue-thrusting, and cigarette smoking on the 15. What is the significance of stippling? How is normal periodontium? How do you diagnose the above stippling manifested? conditions? 16. What is the normal position of the gingiva? 3. What are the various methods of plaque control? 17. Define gingival recession and describe its etiology, 4. What are the various brushing techniques and its classification, clinical significance and treatment. advantages and disadvantages? 18. What is the significance of bleeding on probing? How 5. What is the difference between Bass method and do you check for gingival bleeding? modified Bass method? 19. What are the etiological factors responsible for gingival 6. Describe and demonstrate the modified Bass method. bleeding? 7. What are the various interdental aids? Which is used 20. What are the microscopic changes associated with where? Discuss the criteria for its selection. gingival bleeding? 8. In which conditions do you see lymph node pathology? 21. What is the width of attached gingiva? How do you measure the width of attached gingiva? 9. What is the normal color of the gingiva and what are 22. What are the tests done to identify whether the width the factors responsible for maintaining the normal color of attached gingiva is adequate or inadequate? of gingiva? 23. What are the mucogingival problems? 10. What are the conditions and factors responsible for 24. How do you clinically differentiate between true, change in gingival color? pseudo, and combined pocket; supra bony and infra- 11. Describe normal contour and factors responsible for bony pocket? it. What changes in contour are seen in disease? 25. How do you treat pockets? 12. Name some diseases in which gingival contour are 26. Describe the sequelae following unreplaced first changed. molars. 433

27. Describe the sequelae following loss of proximal 53. What are the instruments used for root planing? contact form. 54. Define scaling and root planing. 28. How do you diagnose furcation involvement? 55. What are the principles of periodontal instrumentation? 29. Describe the etiology, classification and treatment of 56. What are finger rests and grasps? HPE 53 CHAPTER furcation involvement. 57. Different angulations needed for scaling procedures. 30. What are the causes for tooth mobility? Give the 58. Recent advances in periodontal instrumentation? classification of mobility. 31. What is pathological migration? How do you clinically QUESTIONS AND ANSWERS identify it? Q.1. What is the significance of recording chief 32. What are the causes for pathological migration? complaint, history of present illness, past dental history, 33. Define attrition, abrasion and erosion. family history and medical history? 34. When is a tooth tender on percussion. Discussion Case Clinical for Questionnaire 35. What is retrograde periodontitis? Answer 36. How do you diagnose a case of trauma form occlusion? Chief complaint: It is the patient’s description of the 37. What are the types, signs and symptoms of trauma from symptoms related to the disease for which treatment is being occlusion? sought (to be recorded in patient’s own words). It is often 38. What is the difference between mobility and fremitus? recorded as patient’s desire and when the patient is 39. What are the various indices used for accessing oral questioned about the principal reason for his/her dental visit, hygiene? his/her desire is frequently expressed in the form of cleaning, 40. What are the indices for gingival bleeding? filling, etc. This should not be recorded as chief complaint. 41. Effects of over-hanging restorations on periodontium. The dentist has to further derive into for the actual complaint 42. Importance of recording various lab investigations. from the patient with questions like why he/she desires that 43. Effects of improper orthodontic treatment on perio- particular treatment, because most of the times in dontium. periodontics we deal with chronic problems, hence they do 44. What are the things you look for in a radiograph? not actually have any complaint. 45. What are the advantages and disadvantages of intraoral History of present illness: It is the chronological account of periapical radiographs? the problem indicated by the chief complaint. It comprises 46. Justify your diagnosis of the case. If diagnosis is the onset, duration, any relieving or aggravating factors of gingivitis then why? Or if diagnosis is periodontitis the illness which best describe the disease present and helps then why? in determining the diagnosis and treatment plan. Taking the 47. Define prognosis. What are factors responsible for detailed history of the illness of the patient enables the individual and overall tooth prognosis? operator to be as confident as possible that the patient will 48. Discuss the treatment plan in a sequential order. not be endangered during treatment. Past dental history: It consists of patient’s previous QUESTIONS RELATED TO PERIODONTAL experience of oral diseases and his treatment for those INSTRUMENTS AND TREATMENT diseases. It should acquaint the dentist with the patient’s 49. Classify periodontal instruments. previous dental treatment, professional and home care 50. Give the characteristics of a scaler and curette with procedures, frequency and nature of periodontal care, reason differences. for prior extraction of teeth, history of prior dental and 51. Differences between Universal and Gracey curette. periodontal disease and bleeding and anesthetic problem, 52. Classify various supragingival and subgingival scalers. drug allergies during previous dental procedures. All these 434

data aid in the development of diagnosis and prognosis and Diagnosis may have a significant influence on the plan of treatment. It can be made by simple tests: Family history: Many diseases such as idiopathic gingival 1. Mirror test: A double side mirror is held between the fibromatosis, hemophilia are inherited. Thus family history nose and the mouth. Fogging on the nasal side of the should record details of condition existing in other members mirror indicates nasal-breathing while fogging towards of the family. the oral side indicates oral breathing. 2. Cotton test: A butterfly-shaped piece of cotton is placed Medical History over the upper lip below the nostrils. If the cotton flutters

PART V The objectives are: down it indicates nasal breathing. 1. To determine systemic factors or diseases that will 3. Water test: The patient is asked to fill his mouth with require special consideration prior to, during or after water and retain it for a period of time. While nasal periodontal therapy. breathers accomplish this with ease, mouth-breathers 2. It aids the clinician in the diagnosis of oral manifestation find the task difficult. of systemic disease and in the detection of systemic Tonguethrusting condition that may affect the periodontal tissue response to local factors or that require special precaution and It entails persistent, forceful wedging of the tongue against modification in treatment procedure. the teeth, particularly in the anterior region. It causes 3. To identify the patients who are taking drugs or excessive lateral pressure, which maybe traumatic to the medication that could adversely interact with drugs periodontium. It also causes spreading and tilting of the prescribed, that would complicate dental therapy or they anterior teeth with an open bite anteriorly, posteriorly or in may serve as a clue to an underlying systemic disease, the premolar area. It causes labial drifting of teeth, thereby the patient has failed to mention. the antagonism between forces that direct the tooth labially 4. To provide information for the dentist to modify the and inward pressure from lip may lead to tooth mobility. treatment plan for the patient in light of any systemic The altered inclination causes accumulation of food debris. diseases or potential drug interaction. There is loss of proximal contact, which leads to food Treatment of Periodontal Diseasesy Periodontal of Treatment 5. To help establish a good patient-doctor relationship. impaction. It is also an important contributing factor in pathologic tooth migration. Q.2. What are the effects of bruxism, mouthbreathing, Tongue-thrusting can be diagnosed by its position. tongue-thrusting, and cigarette-smoking on the Normally, it is placed against the palate with the tip behind periodontium? How do you diagnose the above the maxillary teeth during swallowing. During tongue- conditions? thrusting it is placed behind the mandibular teeth. It can be Answer diagnosed by altered inclination of the teeth, spacing between the teeth and marked open bite. Mouthbreathing

It leads to localized gingival inflammation that is usually Cigarette Smoking confined to the labial gingiva of the maxillary anterior teeth. Smoking has a detrimental effect on the progression of The tissue becomes reddened and swollen and it bleeds periodontal disease and healing after periodontal therapy. easily. The surface of the gingiva is shiny. Gingival changes The following are its effects: associated with mouthbreathing are: 1. Brownish, tar-like deposits and discoloration of tooth a. Localized gingival inflammation in the maxillary surface. anterior region. 2. Diffuse grayish discoloration and leukoplakia of the b. Crowding of teeth with gingivitis. gingiva may occur. 435

3. Smoker’s Palate characterized by prominent mucous Diagnosis glands due to inflammation of orifices of mucous glands History and clinical examination in most cases is sufficient and a wrinkled, cobblestone surface may occur. to diagnose bruxism. Occlusal prematurities can be diag- 4. Postsurgical healing is delayed.

nosed by use of articulating papers. Electromyographic 53 CHAPTER 5. Produces an immediate transient but marked increase examination can be carried out to check for hyperactivity in gingival fluid flow, as a result of blood changes of the muscles of mastication. induced by nicotine. 6. More severe gingivitis and periodontitis. More calculus Q.3. What are the various methods of plaque control? has been reported in smokers. Answer 7. Factors responsible for increased periodontal problems Plaque control is the removal of microbial plaque and

in smokers: prevention of its formation on teeth. Basically there are two Questionnaire for Clinical Case Discussion Case Clinical for Questionnaire a. Increased keratinized cells in gingiva. types of plaque control. b. Nicotine metabolites have been found. c. Oral polymorphonuclear leukocytes have reduced Mechanical Plaque Control phagocytosis. a. Toothbrushes d. Vascular reaction is suppressed in smokers. b. Powered toothbrushes Diagnosis can be made by the presence of excessive black c. Interdental cleansing aids or brown stains on the tooth surface, discoloration of the • Interdental brushes gingiva and heavy amount of calculus is also found. • Single tufted brushes • Dental floss Bruxism d. Wooden tips e. Gum stimulator Bruxism is clenching or grinding of the teeth when the f. Oral irrigation devices individual is not chewing or swallowing. It has been g. Dentifrices estimated that during clenching or grinding the individual might impose a load of over 20 kg on a tooth over a period Chemical Plaque Control of 2.5 seconds each time. This is far in excess of normal functional stresses and causes increased flow within the The following chemicals are available in varying concentrations: viscoelastic periodontal ligament and distortion of alveolar a. Chlorhexidine gluconate 0.2 percent (Hexidine®, bone. It also causes attrition of teeth. Clohex®) and 0.12 percent (Periogard®) b. Phenolic compounds (Listerine®) containing, Clinical Features • Thymol – 0.06 percent 1. Advanced attrition, presence of wear facets. • Eucalyptol – 0.09 percent 2. Increased tooth mobility patterns which do not commen- • Benzoic acid – 0.15 percent surate with the amount of attachment loss or degree of • Menthol – 0.04 percent gingival inflammation. • Acetyl salicylate 3. Widened periodontal ligament spaces are seen in c. Quaternary ammonium compounds (Cetyl pyridium radiographs. chloride) commercially available as Reach®. 4. Hypertonicity of the muscles of mastication. All the above mentioned chemicals are used only as 5. Temporomandibular joint discomfort. adjunct to mechanical plaque control. 436

Q.4. What are the various brushing techniques and its 2. Patient might miss the gingival sulcus and may place advantages and disadvantages? the brush on the attached gingiva. 3. It only dislodges the plaque in interproximal areas but Answer does not remove them. Many methods of toothbrushing have been described, but studies evaluating the effectiveness of the most common Modified Bass Method brushing techniques have shown that no one method is Advantages clearly superior. The best method is the one that suits the individual’s needs and abilities and the responsibility of the 1. The short back and forth motion is easy to master PART V dental professional is to instruct the patient as to how to because it requires the same simple movement familiar perform the task thoroughly. to most patients who were using the scrub techniques. Various techniques are: 2. It dislodges and removes plaque from cervical and interproximal portions of the teeth.

Scrub Technique Disadvantage Advantage It is time consuming because different areas of teeth need Very easy to learn and master the technique. to be brushed.

Disadvantages Modified Stillman Method

1. Inefficient plaque removal Advantages 2. Causes gingival trauma and recession 1. The gingiva is mechanically stimulated. 3. Causes cervical abrasion. 2. The gingival third of the tooth is contacted with a short vibratory motion and plaque is removed between the Roll Technique gingival margin and the exposed area of tooth surface. Disadvantages Hence, advised only in areas of gingival recession. Treatment of Periodontal Diseasesy Periodontal of Treatment 3. The tips of the bristles tend to reach the interproximal 1. Difficult to learn and requires sufficient dexterity. areas to clean and stimulate the interdental papilla 2. Poor plaque removal from the sulcus area. without injury. 3. Poor plaque removal from the gingival one-third of posterior teeth because of the contour of the teeth. Disadvantages 1. Patient might miss the gingiva and cervical areas of the Bass Method teeth, thus, leaving behind plaque. Advantages 2. Patient might not apply sufficient pressure to produce blanching of tissue. 1. The short back and forth motion is easy to master because it requires the same simple movement, familiar Charter’s Technique to most patients who were using scrub technique. 2. It cleans the cervical and interproximal portions of teeth. Advantages 1. In this method plaque is removed gently, without much Disadvantages pressure. 1. It is time consuming because different areas of teeth 2. It massages the gingiva and encourages healing, hence have to be brushed. advised only during postsurgical period. 437

Disadvantage Advantages Poor plaque removal when indicated in routine patients with 1. It removes plaque from the sulcus and other areas of or without periodontal involvement. tooth.

2. It aids in gingival massage. 53 CHAPTER Q.5. What is the difference between Bass method and modified Bass method? Disadvantage Answer It is hard to master. Bass method Modified Bass method Q.7. What are the various interdental aids? Which is Technique: The bristles are directed The modification consists of used where? Discuss the criteria for its selection.

apically into the gingival sweeping the bristles towards Questionnaire for Clinical Case Discussion Case Clinical for Questionnaire sulcus at 45° to the long the occlusal surface after Answer axis of the tooth and are completing the vibratory Various interdental aids are: activated by applying gentle motion in gingival sulcus. pressure in an apical direc- • Dental floss tion and by making short • Interdental brushes vibratory strokes. • Gauze strips Efficiency: • Unitufted brushes It is efficient in removing It is efficient in removing dental plaque from the dental plaque from the gin- • Toothpicks gingival third of the tooth gival sulcus and interdental and from shallow gingival areas. Criteria for selection of these aids depends upon the type sulcus. of embrasure: Q.6. Describe and demonstrate the modified Bass Type I: Interdental papilla completely fills the embrasure method. space. Dental floss can be used. Answer Type II: Mild loss of interdental papilla due to slight spacing It is also known as intrasulcus cleansing or intrasulcular between the teeth. Miniature bottlebrushes can be advised, method. e.g. Proxabrushes. Technique: Here the patient is asked to place the head of a Type III: No proximal contact between the teeth, like soft brush parallel with the occlusal plane, beginning with the most distal tooth in the arch covering 3 to 4 teeth at a diastema where there is no interdental papilla. Unitufted time. The patient is then asked to place the bristles at the brushes are advised. gingival margin, creating an angle of 45 degree to the long Dental floss: It is used for cleaning in narrow gingival axis of the teeth and exerting gentle vibratory pressure, using embrasures that are occupied by intact papillae and bordered short back and forth motion, without dislodging the tips of by tight contact zones. It is the most effective dental hygiene the bristles. After completing such 20 strokes in the same aid. position, the head of the brush is tilted and moved occlusally. This is repeated for 4-5 times. Patient is instructed to Interdental brushes: It is used in areas of moderate papillary continue brushing around the arch, 3 teeth at a time, both recession, proximal tooth surfaces adjacent to open facially and lingually. The brush is inserted vertically to embrasures, orthodontic appliances, fixed prosthesis, dental reach the lingual surfaces of the anterior teeth. The pits and implant and other areas that are hard to reach with regular fissures of the occlusal surfaces are brushed with 20 short, tooth brush. It is also used in concave proximal areas and back and forth movements. exposed class IV furcation. 438

Gauze strip: It is used for proximal surface of widely spaced teeth, for surface of teeth next to edentulous spaces and fixed appliances. Unitufted brush: It is used for inaccessible areas such as lingual surface of the mandibular molars, abutment teeth, distal surface of the most posterior teeth, crowded teeth, open interproximal areas and isolated areas of deep

recession. It is also indicated in fixed dental prosthesis. PART V Toothpicks: It is used for plaque removal at or just under- neath gingival margin, for concave proximal tooth surface and for exposed furcation areas. Fig. 53.1: Color of the gingiva in health

Q.8. In which conditions do you see lymph node Q.9. What is the normal color of the gingiva and what pathology? are the factors responsible for maintaining the normal Answer color of gingiva? Various systemic diseases contribute for lymph node Answer enlargements, which are as follows: Normal color of gingiva is coral pink (Fig. 53.1) i. Syphilis Factors responsible are: ii. Tuberculosis • Vascular supply iii. Acute bacterial infections • Thickness and degree of keratinization of epithelium iv. Fungal/parasitic infections • Presence of pigment containing cells. v. Malignant tumor metastasis from nasopharynx, oral Q.10. What are the conditions and factors responsible cavity, pharynx, thyroid for change in gingival color (Fig. 53.2)? vi. Lymphatic diseases such as Hodgkin’s disease and Treatment of Periodontal Diseasesy Periodontal of Treatment No. Disease condition Color change/ Factors lymphatic lymphoma clinical change responsible vii. Leukemia’s such as chronic lymphatic, chronic 1. Chronic gingivitis Varying shades 1. Vascular pro- granulocytic leukemia of red, reddish- liferation (ery- viii. Endocrinal disorders such as hyperthyroidism, blue, deep-blue thematous) 2. Reduction of hypopituitarism. keratinization Common conditions of oral cavity, which cause cervical owing to epi- lymphadenopathy are: thelial com- pression by i. Acute inflammatory conditions such as periodontal/ inflamed tissue periapical abscess, acute necrotizing ulcerative gingi- 3. Venous stasis 4. Tissue necrosis vitis, acute herpetic gingivostomatitis, aphthous ulcers 2. Acute gingivitis Bright red Same as above and others. a. NUG/HV erythematous ii. Oral manifestations of systemic diseases. b. Herpetic gin- Shiny-slate gray givostomatitis Dull-whitish gray iii. Malignant conditions: Secondary carcinoma such as c. Chemical epithelioma of tongue, lip, cheek and face. irritation 439

3. Bismuth, arsenic, Black line follow- Perivascular pre- mercury pig- ing the contour cipitation of mentation of marginal metallic sulfides gingival in subepithelial connective tissue HPE 53 CHAPTER seen only in areas of inflammation due to increased permeability of blood vessels 4. Lead pigmen- Bluish-red or Perivascular pre- tation deep-blue linear cipitation of pigmentation metallic sulfides (Burtonian line)

5. Silver pigmen- Violet marginal Perivascular pre- Discussion Case Clinical for Questionnaire tation line cipitation of Fig. 53.2: Color of the gingiva in disease. metallic sulfides. (Note the marginal erythema)

Q.11. Describe the normal contour and factors responsible for it. What changes in contour are seen in disease? Answer The normal contour of the marginal gingiva is scalloped and knife edged, whereas the interdental papilla, in the anterior region is pyramidal in shape and posteriorly it is tent-shaped (Figs 53.3 and 53.4). The factors responsible for the contour of gingiva are: • Shape of teeth and their alignment in the arch. • Location and size of proximal contact. • Dimensions of facial and lingual gingival embrasures. Fig. 53.3: Contour of the gingiva in health During disease process: 1. The marginal gingiva becomes rolled or rounded and interdental papilla becomes blunt and flat, e.g. chronic gingivitis 2. Punched out crater-like depressions at the crest of interdental papilla extending to the marginal gingiva is seen in necrotizing ulcerative gingivitis (NUG). 3. Irregularly-shaped denuded appearance of the gingiva, seen in chronic desquamative gingivitis. 4. Exaggerated scalloping of the gingiva as seen in gingival recession. 5. Apostrophe shaped indentation extending from the gingival margin to varying depths on the facial gingival surfaces are called as Stillman’s clefts. Fig. 53.4: Contour of the gingiva in disease 440

6. Lifesaver like enlargement on the marginal gingival, most commonly on the canine and premolar facial surface called as McCall’s festoons.

Q.12. Name some diseases in which gingival contour is changed.

Answer Gingival contour is changed in conditions like:

PART V • Gingival recession • Gingival enlargement • Acute and chronic gingivitis • Stillman’s clefts and McCall’s festoons.

Q.13. Describe size of gingiva in health and disease. Name some factors responsible for normal size and enlarged Fig. 53.5: Size of the gingiva in health gingiva.

Answer Normal The size of gingiva corresponds to sum of total bulk of cellular and intercellular elements and their vascular supply. Alteration in size is a common feature of gingival disease (Figs 53.5 to 53.7). Change in disease: Size of gingiva is enlarged and is called as gingival enlargement. It maybe inflammatory or

noninflammatory. In inflammatory, there is increase in cells Treatment of Periodontal Diseasesy Periodontal of Treatment and decrease in fibers. In noninflammatory there is increase in fibers and decrease in cells. Fig. 53.6: Inflammatory gingival enlargement Hypertrophy constitutes an increase in size of cells and corresponding increase in the size of the organ. Hyperplasia constitutes increase in number of cells in an organ or tissue there by contributing to an overall increase in organ size. Types of gingival enlargement i. Inflammatory enlargement • Chronic • Acute ii. Fibrotic enlargement • Drug-induced • Idiopathic iii. Combined enlargement Fig. 53.7: Fibrotic gingival enlargement 441

iv. Enlargement associated with systemic diseases or conditions • Pregnancy • Puberty HPE 53 CHAPTER • Vitamin C deficiency • Plasma cell gingivitis • Nonspecific conditioned enlargement • Leukemia • Granulomatous disease v. Neoplastic enlargement • Benign • Malignant Discussion Case Clinical for Questionnaire vi. False enlargement Q.14. How do you check for normal consistency of gingiva? In disease what are the changes that take place in consistency?

Answer Clinical and histopathologic changes in gingival consistency in disease (Figs 53.8A and B).

Clinical changes Microscopic changes Chronic gingivitis Figs 53.8A and B: Clinical demonstration for checking. 1. Soggy puffiness that Infiltration by fluid and cells of (A) Normal consistency, (B) Blanched gingiva pits on pressure inflammatory exudates. 2. Marked softness and Degeneration of connective tissue friability with ready and epithelium, thinning of epi- Q.15. What is the significance of stippling? How is fragmentation and thelium, edema and leukocytic normal stippling manifested? pinpoint surface areas invasion. of redness and Answer desquamation 3. Firm, leathery consis- Fibrotic and epithelial proliferation Stippling is a form of adaptive specialization or reinforce- tency. associated with longstanding ment for function. It is a feature of healthy gingiva and chronic inflammation. reduction and loss of stippling is a common sign of gingival Acute gingivitis disease (Fig. 53.9). 1. Diffuse puffiness and Diffuse edema, fatty infiltration. softening Stippling is produced by alternate rounded protruberan- 2. Sloughing with grayish Necrosis with formation of a ces and depressions in the gingival surface. Papillary layer flake like particles of pseudomembrane and degenera- of the connective tissue projects into the elevations, and debris adhering to ted epithelial cells in a fibrous eroded surface mesh work. Inter and intracellular the elevated and depressed areas are covered by stratified 3. Vesicle formation edema with degeneration of squamous epithelium. Stippling is best viewed by drying nucleus and cytoplasm and rup- ture of cell wall. the gingiva. Q.16. What is the normal position of the gingiva? The normal consistency of the gingiva can be checked by palpation either with a blunt instrument or digital Answer pressure. Pitting on palpation indicates soft and edematous The normal position of gingiva is 1 millimeter above the gingiva. cementoenamel junction.

442 PART V

Fig. 53.9: Stippling in normal healthy gingiva Fig. 53.10: Gingival recession

Physiologic factors responsible for normal position of c. Iatrogenic factors: gingiva are: • Deleterious habits (Pressure of foreign objects like 1. Position of teeth in the arch. finger nails, pencils, hairpins). 2. Root bone angle • Clasps and mandibular oral denture bars or aprons 3. Mesiodistal curvature of tooth surface. in partial dentures. • Prolonged orthodontic treatment, improper resto- Pathologic factors responsible for change in gingival rations. position are: 1. Toothbrush trauma Classification 2. Gingival inflammation 3. High frenal attachment I. Sullivan and Atkins classified gingival recession as: 4. Tooth malposition a. Shallow narrow b. Shallow wide Treatment of Periodontal Diseasesy Periodontal of Treatment 5. Friction from soft tissue c. Deep narrow Q.17. Define gingival recession and describe the etiology, d. Deep wide classification, clinical significance and its treatment. II. Millers classification Answer Class I: Includes marginal tissue recession that does not Gingival recession is defined as apical shift of the gingival extend to the mucogingival junction. There is no loss of margin to a position apical to the CEJ, with exposure of bone or soft tissue in the interdental area. This type of root surface to the oral cavity (Fig. 53.10). recession can be narrow or wide (group a and b in Sullivan and Atkins classification). Etiology Class II: Marginal tissue recession that extends to or beyond Mainly three factors are responsible: the mucogingival junction. There is no loss of bone or soft a. Inflammatory: Plaque induced inflammatory periodontal tissue in the interdental area. This type of recession can be diseases, toothbrush injury, and surgical treatment of classified into wide and narrow (group c and d of Sullivan inflammatory periodontal disease. and Atkins classification). b. Anatomic factors: Developmental anatomic abnor- Class III: Marginal tissue recession that extends to or beyond malities, (dehiscences, thin bony plates, high frenum the mucogingival junction, in addition there is bone and or attachments) malocclusion. soft tissue loss interdentally or malpositioning of the tooth. 443

Class IV: Marginal tissue recession that extends to or beyond the mucogingival junction, with severe bone loss and soft tissue loss interdentally and or severe tooth-malpositioning.

Clinical Significance 53 CHAPTER

Exposed root surfaces are susceptible to caries. Wearing away of the cementum exposed by recession leaves an underlying dentinal surface that is extremely sensitive. Hyperemia of the pulp and associated symptoms may also result from exposure of the root surface. Interproximal

recession creates spaces in which, plaque and food debris Questionnaire for Clinical Case Discussion Case Clinical for Questionnaire can accumulate. Fig. 53.11: Gingival bleeding on probing

Treatment to disease progression is unclear. Histologically, bleeding on Denuded root surfaces are covered for two purposes: probing results from increased vascularity, thinning and 1. To solve esthetic problem (in anterior teeth) degeneration of the epithelium and the proximity of the 2. To widen zone of attached gingiva, thereby solving a engorged vessels to the inner surface (Fig. 53.11). possible mucogingival problem It can be checked by using a blunt periodontal probe, which is carefully introduced to the bottom of pocket using Several procedures are as follows: forces up to 0.75N and gently moved laterally along the I. Treatment based on width of attached gingiva pocket wall. Bleeding may occur spontaneously or delayed by 30 to 60 seconds. Adequate Inadequate 1. Pedicle graft 1. Free soft-tissue autograft. Q.19. What are the etiologic factors responsible for • Double papillae • Laterally-displaced gingival bleeding? 2. Coronally, repositioned 2. Subepithelial connective Local Factors flap with semilunar incision tissue graft. Chronic bleeding II. Treatment based on distribution of recession • Chronic inflammation

Localized Generalized (involving few teeth) Acute bleeding

i. Pedicle graft i. Free soft tissue graft. • Aggressive toothbrushing • Double papillae • Sharp pieces of hard food • Laterally-displaced ii. Coronally repositioned ii. Subepithelial connective • Gingival burns flap with semilunar incision tissue graft. • Acute gingival diseases, e.g. NUG iii. Guided tissue regeneration iii. Coronally-repositioned flap.

Q.18. What is the significance of bleeding on probing? Systemic Factors How do you check for gingival bleeding? • Vascular abnormality Answer – Vitamin C deficiency Bleeding on probing is important as it is one of the earliest – Allergy such as Schönlein-Henoch purpura signs of gingival inflammation and is also a very sensitive, • Platelet disorder, e.g. idiopathic thrombocytopenic objective clinical indicator. However, its relationship purpura. 444

• Hypoprothrombinemia, e.g. vitamin K deficiency from liver disease or sprue. • Coagulation defects, e.g. Hemophilia, Christmas disease • Malignancy, e.g. leukemia. • Deficient platelet thromboplastic factor, e.g. uremia, multiple myeloma, postrubella infection purpura. • Drugs, e.g. salicylates, dicoumarol, heparin.

Q.20. What are the microscopic changes associated with

PART V gingival bleeding?

Answer Changes in Epithelium Fig. 53.12: Measurement of width of attached gingiva

Thinning of epithelium and microulcerations along the Q.22. What are the tests done to identify whether the surface of the epithelium. width of attached gingiva is adequate or inadequate? Factors responsible for it are the widening of the inter- cellular junctions and destruction of epithelium by the Answer bacteria and their byproducts (e.g. collagenase, hyaluroni- There are four different methods used to find the width of dase, protease, chondroitin sulfate or endotoxin) gaining attached gingiva. access into the connective tissue. 1. Measurement approach: In this method first the pocket depth or the sulcus depth is measured, and then the total Changes in Connective Tissue width of gingiva is measured, i.e. from gingival margin Dilation of the capillaries and venules and engorgement of to mucogingival line. Thus by subtracting these two the blood vessels. measurements we get the width of attached gingiva. Factors responsible for it are that they are the manifesta- Total gingival width–pocket depth = width of attached

Treatment of Periodontal Diseasesy Periodontal of Treatment tions of the gingival inflammation resulting in diapedesis gingiva. and emigration of the polymorphonuclear leukocytes. 2. By using Schiller’s potassium iodide solution Because the capillaries are engorged and closer to the It is similar to measurement approach. Potassium iodide thinned and degenerated epithelium, which is less protective, solution only stains the keratinized epithelium, i.e. any ordinary stimulus causes rupture of the capillaries and marginal gingiva, attached gingiva and interdental papilla. gingival bleeding occurs. After application of this solution the total width of gingiva is measured that is from gingival margin to Q.21. What is the width of attached gingiva? How do mucogingival line, and later the sulcus depth or pocket you measure the width of attached gingiva? depth is measured. Then by subtracting the total gingival Answer width from pocket depth we get the width of attached It is the distance between the mucogingival junction and gingiva. the projection on the external surface of the bottom of the Stained total gingival width – pocket depth = width of gingival sulcus or the periodontal pocket. attached gingiva. The width of attached gingiva is determined by Here, KI solution is used to know the accurate width subtracting the sulcus or pocket depth from the total width of gingiva, i.e. from free marginal gingiva to muco- of the gingiva (Fig. 53.12). gingival line, which is keratinized. 445

3. Tension test: This is done by stretching the lip or cheek Q.23. What are the mucogingival problems? to demarcate the mucogingival line and to see for any Answer movement of the free gingival margin. And if the free Mucogingival problems are the disease conditions, which gingival margin moves during stretching of lips then extend to or beyond the mucogingival junction. 53 CHAPTER the attached gingiva is considered to be inadequate (Figs Various mucogingival problems are: 53.13 and 53.14). 1. Inadequate width of attached gingiva. 4. Roll test: It is done by pushing the adjacent mucosa 2. Gingival recession extending up to mucogingival coronally with a dull instrument. If the gingiva moves junction. with the instrument then the width of attached gingiva 3. Decreased vestibular depth. is considered inadequate. In adequate width, the gingiva 4. Abnormal frenal attachment. does not move because the attached gingiva is firmly

5. Pockets extending up to the mucogingival junction. Discussion Case Clinical for Questionnaire attached to the underlying bone. Q.24. How do you clinically differentiate between true, pseudo and combined pockets; suprabony and infrabony pockets?

Answer (Figs 53.15 to 53.17) Pseudopockets: It is associated with gingival enlargement and also while probing, there is increased sulcus depth, the probe tip does not seem to go beyond the cementoenamel junction because junctional epithelium is still attached at the CEJ.

True pockets: It is associated with apical migration of junctional epithelium (attachment loss). This is clinically assessed by probing measurement. Fig. 53.13: Tension test (for abnormal frenal attachment)

Fig. 53.14: Tension test (for lack of attached gingiva) Fig. 53.15: Detection of a pocket (probe placed parallel to the long axis of the tooth) 446

The probing method is as follows, since normally junctional epithelium is attached at the cementoenamel junction. First: Detect the CEJ by running the probe perpendicular to the root surface. Second: Once the CEJ is detected, bring the probe back to parallel position and observe whether probe can be probed

beyond this point. If it can, then it is understood that the PART V junctional epithelium is shifted apically, hence diagnosed as a true pocket.

Combined pocket: It is associated with both gingival enlargement and attachment loss.

Suprabony pocket: It is a true pocket with base of the pocket coronal to underlying alveolar bone crest. Clinically, it can be assessed by probing measurements. After the probe is inserted into the gingival sulcus and when lateral pressure is applied, if soft tissue resistance is felt, then it is diagnosed as suprabony pocket.

Infrabony pocket: It is a true pocket with base of pocket apical to level of adjacent alveolar bone. Clinically, probe Figs 53.16A and B: True and Pseudopocket. (A) Clinical detec- is inserted into the gingival sulcus and when lateral pressure tion of true/pseudopocket. (B) Detection of cementoenamel junction is applied, hard tissue resistance is felt.

Q.25. How do you treat pockets? Treatment of Periodontal Diseasesy Periodontal of Treatment Answer The various methods of pocket elimination are classified as follows: 1. New attachment techniques: These offer the ideal result, because they eliminate pocket depth by reuniting the gingiva to the tooth at a position coronal to the bottom of the pre-existing pocket. 2. Removal of the pocket wall is the most common method. It can be removed by: a. Retraction or shrinkage by scaling and root planing. b. Surgical removal by gingivectomy technique or by

Fig. 53.17: Suprabony/Infrabony pocket means of an undisplaced flap. (Probe in place with lateral pressure) c. Apical displacement with an apically displaced flap. 447

3. Removal of the tooth side of the pocket, which involves Q.28. How do you diagnose furcation involvement? either extraction of the tooth or hemisection of the tooth. Answer Q.26. Describe the sequelae following unreplaced missing Furcation involvement can be diagnosed by two methods: first molars. 1. Clinical examination 53 CHAPTER Answer 2. Radiographs A thorough clinical examination is the key to diagnosis It consists of the following: and treatment planning. Careful probing is performed by i. Second and third molars tilt mesially leading to distal using a Naber’s probe. Transgingival probing further helps cusp elevation thereby plunger cusp effect. In the to define the anatomy of the furcation defect (Fig. 53.18). mesial cusp, due to mesial tilt the distance between Radiographs can also be used as diagnostic aids in the mesial cusp tip and bone is reduced thereby

diagnosing furcation involvement: Discussion Case Clinical for Questionnaire progression of periodontal disease becomes rapid. ii. Supraeruption of opposing first molar may lead to: Grade I: Radiographic changes are not usually found ↓ Grade II: Radiographs may or may not depict the furcation Loss of proximal contact involvement ↓ Food impaction Grade III: Show a radiolucent area in the crotch of the tooth ↓ Grade IV: Seen as a radiolucent area. Plaque accumulation ↓ Gingivitis ↓ Periodontitis iii. Premolars move distally, mandibular incisors tilt or drift lingually. Anterior overbite is increased. The mandibular incisors strike the maxillary incisors near the gingiva and traumatizes the gingiva. iv. The maxillary incisors are pushed labially and laterally. v. Extrusion of anterior teeth leading to diastema. Fig. 53.18: Diagnosis of furcation involvement using Naber’s probe Q.27. Describe the sequelae following loss of proximal contact form. Q.29. Describe the etiology, classification and treatment Answer of furcation involvement.

The tightness of contact should be checked by means of Answer clinical observation and with a dental floss. Etiology Abnormal contact relation or loss of proximal contact can cause plaque retention and food impaction → gingivitis 1. Extension of inflammatory periodontal disease. and periodontitis → mobility and loss of tooth. 2. Trauma from occlusion. 448

3. Cervical enamel projections Treatment 4. Pulpoperiodontal diseases Traditional procedures Regenerative procedures 5. Iatrogenic cofactors Grade I Scaling, root planing, 6. Anatomical factors curettage, gingivectomy, odontoplasty. Classification of Furcation Involvement Grade II Scaling, root planing, Autogenous and curettage, odontoplasty, autologous osseous According to Glickman (1953): osteoplasty with limited grafting, synthetic ostectomy, in shallow grafting, GTR, root Grade I: Pocket formation into the flute of the furcation grade II invasions. In conditioning, coro- more severe furcation nally displaced flap PART V but inter-radicular bone is intact involvements, root resection/ and combination hemisection is done. procedures. Grade II: Loss of inter-radicular bone and pocket formation Grade III Tunneling, root sectioning, GTR and combina- of various depths into the furcation but not completely hemisection, extraction tion procedures Grade IV Maintenance probable to the opposite side of the tooth.

Grade III: Complete loss of inter-radicular bone with pocket Q.30. What are the causes for tooth mobility? Give the formation that is completely probable to the opposite side classification of mobility. of the tooth. Answer Grade IV: Loss of attachment and recession that has made Causes for mobility can be divided into local and systemic the entire furcation clinically visible. factors (Fig. 53.19): According to Goldman and Cohen, furcation involvement can be: Local Factors

Grade I: Incipient lesion a. Bone loss and loss of tooth support— Grade II: It is a cul de sac lesion 1. Bone destruction caused by extension of gingival Grade III: Through and through furcation involvement inflammation, which can be either due to plaque products or pharmacologically active substances. According to Hamp et al.

Treatment of Periodontal Diseasesy Periodontal of Treatment 2. Trauma from occlusion, either in absence or Degree I: Horizontal loss of periodontal tissue support less associated with inflammation. than 3 mm. Degree II: Horizontal loss of support exceeding 3 mm but not encompassing the total width of the furcation area. Degree III: Horizontal through and through destruction of the periodontal tissues in the furcation. According to Tarnow and Fletcher Subclass A: Vertical destruction to one-third of the total inter- radicular height (1-3 mm). Subclass B: Vertical destruction reaching two-thirds of the inter-radicular height. (4 to 6 mm). Subclass C: Inter-radicular osseous destruction into or beyond the apical third (more than 7 mm). Fig. 53.19: Clinical demonstration of mobility 449 b. Hypofunction The characteristic clinical features are as follows: c. Periapical pathology 1. It occurs most frequently in the anterior region. d. After periodontal therapy 2. It is usually accompanied by mobility rotation and e. Parafunctional habits like bruxism or clenching extrusion of teeth. HPE 53 CHAPTER f. Pathology of jaws like tumor, cyst, etc 3. Drifting of maxillary and mandibular anterior g. Traumatic injury to dentoalveolar unit incisors labially creating diastema between the teeth. h. Tooth morphology 4. Should be differentiated from physiological i. Overjet and overbite migration. j. Implant mobility Q.32. What are the causes for pathologic migration? 1. Weakened periodontal support

Systemic Factors 2. Changes in the forces exerted on the teeth Questionnaire for Clinical Case Discussion Case Clinical for Questionnaire a. Age • Unreplaced missing teeth b. Sex and Race : Slightly higher incidence seen in females • Failure to replace first molars. and Negros 3. Other causes like: c. Menstrual cycle • Pressure from tongue d. Oral contraceptives • Pressure from granulation tissue of periodontal e. Pregnancy pocket. f. Systemic diseases such as Papillon-Lefevre syndrome, Q.33. Define attrition, abrasion and erosion. Down’s syndrome, neutropenia, Chediak-Higashi syndrome, etc. Answer Attrition : It is the occlusal wear resulting from functional Grading of Mobility contact with opposing teeth or, it is the term used for dental wear caused by teeth against teeth. Degree I: Mobility of crown of the tooth 0.2-l mm in horizontal direction Abrasion : Refers to the loss of tooth substance induced by mechanical wear other than that of mastication. Degree II: Mobility of crown of the tooth exceeding 1 mm in horizontal direction Erosion: It is a sharply defined wedge-shaped depression in the cervical area of the facial tooth surface or wear to the Degree III: Mobility of crown of the tooth in vertical nonoccluding tooth surface and includes sharply defined, direction as well. wedge-shaped depressions in the facial cervical areas of Q.31. What is pathological migration ? How do you the tooth. clinically identify it? Q.34. When is tooth tender on percussion? Answer Answer Pathologic migration refers to tooth displacement that Various causes for tooth to be tender on percussion are: results when the balance among the factors that maintain A. Periodontal diseases (Tooth is tender on lateral physiological tooth position is disturbed by periodontal percussion) disease. It is relatively common and may be an early sign B. Irreversible pulpitis of disease, or it may occur in association with gingival C. Root fracture inflammation and pocket formation as the disease D. Crown fracture progresses. E. Periapical pathology 450

Q.35. What is retrograde periodontitis? b. With help of occlusion registration strips/articulating paper. Answer c. Auditory test for trauma from occlusion: In centric Normally, periodontitis is caused by extension of inflam- relation, there is a distinct ringing sound during tooth mation from the gingiva into deeper periodontal tissues. contact. But in the traumatic occlusion with deflection However, periodontitis can also be caused by pulpal present, sound is dull and imperceptible. infections that have entered periodontal ligament either through apical foramen or through the lateral canal. Such a Tactile Method periodontal lesion is termed as retrograde periodontitis.

PART V In centric relation and normal excursive movement, response Q.36. How do you diagnose a case of trauma from to finger is smooth but with deflection present as in trauma occlusion? from occlusion, a roughness can be detected. Answer Q.37. What are the types, signs and symptoms of trauma a. Fremitus test (Fig. 53.20): It is a measurement of the from occlusion? vibratory pattern of the teeth when the teeth are placed in the contacting positions and movements. To measure Answer fremitus, dampened index finger is placed along the The various types are: buccal and labial surfaces of the maxillary teeth and the 1. Primary and secondary occlusal trauma. patient is asked to tap the teeth together in the maximum 2. Acute and chronic. intercuspal position and then grind systematically in the Signs and Symptoms lateral, protrusive movements and positions. The teeth 1. Presence of gingival recession. that are displaced by the patient in these positions are 2. Presence of Stillman cleft and McCall’s festoons. identified and graded. The following classification 3. Presence of traumatic crescent. system is used: 4. Presence of infrabony pockets. Class I fremitus: Mild vibration or movements detected. 5. Food impaction.

Treatment of Periodontal Diseasesy Periodontal of Treatment Class II fremitus: Easily palpable vibration but no visible 6. Excessive wearing of tooth cusps and appearance of movements. Class III fremitus: Movements visible with naked eye. wear facets. 7. Hypersensitivity of the teeth. 8. Increased tooth mobility. 9. Tenderness of TMJ and muscles of mastication. 10. Widening of periodontal ligament and thickening of lamina dura. 11. Vertical bone loss. 12. Condensation of alveolar bone. 13. Root resorption. 14. Buttressing bone formation seen in an occlusal radiograph. 15. Smudging of articulating paper. 16. Dull percussion note of an affected tooth. Fig. 53.20: Fremitus test is performed placing wet finger on the labial surface of maxillary anterior teeth 17. Vibrations are felt on performing Fremitus test. 451

Q.38. What is the difference between mobility and 1. Ideal locations for the accumulation of plaque fremitus? 2. Changing the ecologic balance of the gingival sulcus, Answer i.e. favor the growth of gram-negative anaerobic species, which altogether leads to the pathogenesis of chronic Mobility: It is a measurement of horizontal and vertical tooth 53 CHAPTER inflammatory periodontal disease. displacement created by the examining force applied that should be roughly 100 g force. Q.42. What is the importance of recording various lab Fremitus: It is a measurement of the vibratory patterns of investigations? the teeth when the teeth are placed in contacting positions Answer and movements. Complete Blood Count • Fremitus differs from mobility, in that fremitus is tooth

displacement created by the patient’s own occlusal force The complete blood count will include: Discussion Case Clinical for Questionnaire • Therefore, the amount of force varies greatly from i. Hemoglobin (Hgb). patient to patient, unlike mobility, where in the force ii. Hematocrit (Hct). with which it is measured tends to be the same for each iii. Red blood cell count (RBC). examiner. iv. White blood cell count (WBC).

Q.39. What are the various indices used for assessing I. Hemoglobin oral hygiene? i. Hgb is the oxygen carrier of the blood. It is decrea- sed in hemorrhage and anemias. It is increased in Answer hemoconcentration and polycythemia. 1. Oral hygiene index. ii. The normal range is 14 to 18 g/dl of blood in men 2. Simplified oral hygiene index. and 12 to 16g/dl of blood in women. 3. Patient Hygiene performance index. II. Hematocrit: It reflects the relative volume of cells to 4. Plaque component of periodontal disease index. plasma in the blood. In anemias and after blood loss, 5. Shick and Ash modification of plaque criteria. the Hct is lowered. In polycythemia and dehydration 6. Turesky-Gilmore-Glickman modification of the Quigley it is raised. The normal Hct range is 40 to 54 percent Hein plaque index. for men and 37 to 47 percent for women. 7. Plaque index. III. RBC count: RBC contains HgB. An increase in RBCs 8. Calculus index. may indicate hemoconcentration or polycythemia. Q.40. What are the indices for gingival bleeding? Decrease in number of RBCs may be indicative of blood loss or anemia. Answer IV. WBC count: WBCs are important in defence against 1. Sulcular bleeding index. invading microorganisms. Normal count is 5000 to 2. Papillary bleeding index. 10,000/mm3. Increase in WBC is seen in leukemia, 3. Bleeding points index. bacterial infection, infectious mononucleosis and 4. Interdental bleeding index. certain parasitic infections. Decrease in WBC’s seen 5. Gingival bleeding index. in aplastic anemia, lupus erythematosus, acute viral infections, and drug and chemical toxicity. Q.41. Describe the effects of overhanging restorations a. Neutrophils (50 to 70%) on periodontium. • Increase in most bacterial infections Answer • An increase in number of immature neutrophils Overhanging restorations causes violation of biologic width, is frequently found in acute infections. This is which may lead to: called shift to the left. 452

b. Eosinophils (1 to 4%): Increase in allergic condi- d. Partial thromboplastin time: It is designed to help tions and parasitic infections. the clinician recognize mild to moderate deficiencies c. Basophils (0 to 1%): May be increased in blood of intrinsic clotting factors. dyscrasias. Q.43. Effects of improper orthodontic treatment on d. Lymphocyte (25 to 40%): It increases in measles periodontium. and in severe bacterial or chronic infections. e. Monocyte (4 to 8%): It may be increased during Answer recovery from severe infections and Hodgkin’s Orthodontic tooth movement is possible because the diseases. PART V periodontal tissues are responsive to externally applied V. Blood glucose: Basic tests of blood glucose are: forces. Orthodontic forces at optimum rate and direction a. Fasting blood sugar have no negative impact on the periodontium. Unlikely b. Two hour postprandial blood sugar test when these forces are abnormal, it results in deleterious c. Glucose tolerance test effects such as: d. Random blood sugar test • Moderate orthodontic forces ordinarily result in bone The normal range for blood glucose is 70 to 110 remodelling and repair, whereas excessive forces may mg/dl of serum. produce necrosis of the periodontal ligament and VI. Blood urea nitrogen: adjacent alveolar bone. • Normal value is 8 to 23 mg /dl of blood. • Excessive orthodontic forces also increase the risk of • Increased value seen in extensive kidney disease, apical root resorption. congestive heart failure, dehydration. • Use of elastics to close diastema may result in severe VII. Serology—For screening of syphilis. attachment loss with possible tooth loss as the elastics • All are nonspecific tests for syphilis and may give migrate apically along the root. both false positive and false negative results. • Surgical exposure of impacted teeth and orthodontic Interpretation of these results requires patient history assisted eruption has the potential to compromise the and clinical findings. Confirmation is by Fluorescent periodontal attachment on adjacent teeth. Treatment of Periodontal Diseasesy Periodontal of Treatment treponemal antibody-absorption test (FTA-abs) or • Dentoalveolar gingival fibers are stretched when teeth the microhemagglutination treponemal palladium are rotated during orthodontic therapy. test (MHA-tp). VIII. Screening test for hemorrhagic disorders: Q.44. What are the things you look for in a radiograph? a. Bleeding time: It is the time required for hemostasis Answer to occur in a standard wound of the capillary bed. It Radiographs help in diagnosis of periodontal disease, varies with vascular and platelet abnormalities. The determination of patient’s prognosis and the evaluation of normal range is 1 to 7 minutes. the outcome of treatment. But radiograph is an adjunct to b. Platelet count: It is decreased in thrombocytopenic the clinical examination, not a substitute for it. purpura. In myeloproliferative diseases, platelets are The normal anatomic landmarks to be seen in a increased. Normal platelet count is 150,000 to radiograph are (First identify the type of X-ray its side, i.e. 400,000/mm3. left or right and which arch it belongs to): c. Prothrombin time: It is an indirect test of the clotting ability of the blood. It gives an indication of pro- Maxillary arch thrombin deficiency arising from liver disease. 1. Nasopalatine foramen. Normal range is 12 to 17 sec. 2. Median palatal sutures. 453

3. Nasal fossa. Advantages of OPG 4. Nasal septum. 1. For visualizing the maxilla and mandible in one film. 5. Anterior nasal spine. 2. For patient education. 6. Maxillary sinus.

3. To evaluate impacted teeth. 53 CHAPTER 7. Maxillary tuberosity. 4. In the evaluation of multiple unerupted supernumerary Mandibular arch teeth. 1. Genial tubercles. 5. To evaluate eruption sequence and pattern, growth and 2. Lingual foramen. development. 3. Mental process. 6. For detecting any pathology involving the jaws. 4. Mental foramen. 7. For evaluating traumatic injuries.

5. Oblique ridge. 8. Radiographic examination of patients with limited Questionnaire for Clinical Case Discussion Case Clinical for Questionnaire 6. Mandibular canal and submandibular fossa. mouth opening. 9. To identify diseases of the temporomandibular joint. Lesions to be seen are: 10. Reduces the risk of multiple exposures to radiation. 1. Caries a. Interproximal caries Disadvantages b. Occlusal caries c. Root surface caries 1. Images are not as sharp as in an intraoral film. 2. Periodontal disease, i.e. periodontitis—Bone loss. 2. It cannot be used in the diagnosis of caries. a. Types of bone loss 3. It cannot be used in the evaluation of bone loss due to i. Vertical or angular periodontal disease. ii. Horizontal bone loss 4. It shows superimposition especially in the premolar iii. Crater-like loss region. iv. Arc-shaped bone loss. 5. Structures in the anterior region may not be well-defined. b. Contour or Architecture of bone i. Positive Advantages of IOPA ii. Negative 1. Better visibility of periapical region. c. Continuation of lamina dura 2. Helps in the diagnosis of periapical pathology. d. Trabecular pattern of bone 3. To study crown and root length and their morphology. e. Furcation involvement 4. Helps in evaluating root apex formation. f. Amount of bone loss. 5. Evaluation of endodontic treatment. 3. Tooth fractures 6. Helps in evaluation of fracture of teeth. a. Crown fracture b. Root fracture Disadvantages 4. Resorption a. Internal resorption 1. Cannot be taken in case of patients with limited mouth b. External resorption opening. 2. It cannot detect any pathology involving the jaws. Q.45. What are the advantages and disadvantages of 3. Multiple radiographs have to be taken for the exami- IOPA radiographs and OPG? nation of the entire arch thereby increasing the risk of Answer exposure to radiation. 454

Q.46. Justify your diagnosis, if diagnosis is gingivitis then • Presence and severity of furcation involvements. why? Or if it is periodontitis then why? • Mobility. • Crown-root ratio. Answer • Pulpal involvement. Gingivitis is detected when there is evidence of gingival • Tooth position and occlusal relationship. inflammation such as swelling, redness, bleeding on • Strategic value. probing, often the pocket depth less than or equal to 4 millimeter but by-definition there is no measurable loss of Factors for overall prognosis are: probing periodontal attachment associated with periodontal • Age PART V infection. Gingival recession maybe associated with gingival • Medical status abrasion or prominent radicular surface. Plaque is usually • Individual tooth prognosis (distribution and severity) present; calculus may or may not be present. Tooth mobility • Degree of involvement, duration and history of the is rarely present and radiographic changes do not suggest disease bone loss. • Patient cooperation Periodontitis can be classified as early, moderate, • Economic consideration advanced. According to AAP’s classification, in early • Knowledge and ability of the dentist periodontitis there are shallow pockets, minor to moderate • Etiologic factors. bone loss, satisfactory topography and generally no tooth Q.48. Discuss the treatment plan in a sequential order. mobility. Moderate periodontitis is characterized by moderate to deep pockets, moderate to severe bone loss, Answer unsatisfactory topography and slight tooth mobility. In The objectives of treatment are: advanced periodontitis, there are deep pockets, many areas a. Elimination of disease. of severe bone loss, advanced tooth mobility and often a b. Restoration of efficient function. need for prosthesis to replace missing teeth or splint the c. Production of satisfactory appearance. mobile teeth. Periodontitis is by definition diagnosed when Sequence of therapeutic procedures: there is measurable attachment loss (e.g. >2 mm) and often Treatment of Periodontal Diseasesy Periodontal of Treatment a. Preliminary phase/Emergency phase associated with probing depth more than 4 mm. Plaque and 1. Treatment of emergencies like dental or periapical calculus are usually present. Tooth mobility may also occur. and periodontal problems Radiographic changes seen include alveolar crestal 2. Extraction of hopeless teeth and provisional resorption of varying degree and in advanced cases, loss of replacement, if needed alveolar bone in furcation areas may be seen. b. Phase I therapy (Etiotrophic phase). Q.47. Define prognosis. What are the factors responsible 1. Plaque control for individual and overall tooth prognosis? 2. Diet control 3. Removal of calculus and root planing Answer 4. Correction of restorative and prosthetic irritational Prognosis is a prediction of the duration, course and factors termination of a disease and its response to treatment. 5. Excavation of caries and restoration Factors for individual tooth prognosis are: 6. Antimicrobial therapy (local/systemic) • Percentage of bone loss. 7. Occlusal therapy • Probing depth. 8. Minor orthodontic movement • Distribution and type of bone loss. 9. Provisional splinting. 455

Evaluation of response to Phase I therapy ii. Used for other purpose, example: Schwartz I. Rechecking periotrievers – used for retrieval of broken instruments. • Pocket depth and gingival inflammation EVA system - correcting overhanging restorations • Plaque and calculus, caries. HPE 53 CHAPTER c. Phase II therapy (Surgical phase) Surgical Instruments • Periodontal surgery, including placement of implants 1. Excisional and Incisional Instruments, examples: • Root canal therapy • Periodontal knives (Gingivectomy knives) d. Phase III therapy (Restorative phase). • Interdental knives No 1-2 a. Final restorations • Surgical blades. (Scalpel No. 11, 12 and 15) b. Fixed and removable prosthodontics • Electrosurgery

Evaluation of response to restorative procedures, 2. Surgical curettes and sickles. Questionnaire for Clinical Case Discussion Case Clinical for Questionnaire periodontal examination Examples: e. Phase IV therapy (Maintenance phase) • Kramer curettes No. 1, 2 and 3 Periodic recall visits, re-checking for: • Ball scaler • Plaque and calculus. 3. Periosteal elevators, examples: No. 24 G elevator and • Gingival condition (inflammation, pockets). Goldman fox No: 14 • Occlusion, tooth mobility. 4. Surgical chisels and Hoes, examples: chisel in • Other pathologic changes. Oschsenbein No. 1-2, Rhodes chisels Q.49. Classify periodontal instruments. 5. Surgical files example: Sugarman files 6. Scissors and Nippers, example: Goldman fox No: 16 Answer scissors They are classified into surgical and nonsurgical 7. Needle holders, example: Castroviejo needle holder. instruments. Q.50. Give the characteristics of a scaler and curette with Nonsurgical Instruments differences. 1. Hand instruments. Answer 2. Machine driven instruments. Characteristics of a Scaler

Hand Instruments i. Triangular in cross-section ii. Pointed tip not suited for subgingival use 1. Diagnostic instruments, examples: explorers and iii. Two cutting edges per working end. periodontal probes iv. Pointed tip and straight cutting edges do not adapt well 2. Scaling and root planing and curettage instruments, to rounded root surfaces and concavities. examples: sickle scaler, curettes, hoe, chisel and file v. Face perpendicular to the lower shank so that cutting 3. Cleaning and polishing instruments, examples: edges are in level with one another Dental tapes, rubber cups and bristle brushes. vi. Shank • Anterior sickles—Simple design Machine Driven Instruments • Posterior sickles—Complex design i. Scaling and curettage instruments, examples: vii. Functions: Removal of medium to large-sized supra- ultrasonic, and sonic instruments gingival calculus deposits. 456

Provides good access to the: Q.52. Classify various supragingival and subgingival 1. Proximal surfaces on anterior crowns scalers. 2. Enamel surfaces apical to contact areas of posterior Answer teeth viii. Examples: Anterior sickle scaler—OD-1, Jacquette-30 Supragingival scalers Jacquette-33, Towner-015, Goldman H6 and H7, 1. Sickle scaler Posterior sickle scalers—Jacquette 34/35, Jacquette 14/ 2. Surface scaler 15, Jacquette 31/32, Ball 2/3. 3. Cumine scaler

PART V 4. Morse scaler Characteristics of Curette

Universal Area-specific Subgingival scalers Cross-section Semicircular Semicircular 1. Chisel scaler Back Rounded Rounded 2. Hoe scaler

Cutting edges Two cutting edges One cutting edge 3. Periodontal file per working end per-working end 4. Islet scaler Toe Rounded Rounded Face Perpendicular to Tilted at a 60°-70° to the Q.53. What are the instruments used for root planing? the lower shank lower shank Application Used to instrument Limited to use on a Answer all Tooth surfaces specific area of specific in the dentition tooth surface Curette is the instrument of choice for removing deep Function Removal of light to Removal of light medium-sized calculus deposits subgingival calculus; root planing, altered cementum and calculus deposits removing the soft tissue lining the periodontal pocket. Examples Columbia 2R/2L, Gracey series Columbia 13/14, Kramer-Nevins series, These include: Rule 3/4, Turgeon series, a. Universal curettes Barnhart 1/2 Barnhart 5/6 After five b. Area-specific curettes Langer 1/2 Mini five Treatment of Periodontal Diseasesy Periodontal of Treatment In Gracey curettes: Langer 3/4 Vision curvette series Langer 5/6 • 1-2, 3-4—Anterior teeth Langer 17/18 • 5-6—Anterior teeth and premolars Q.51. Differences between Universal and Gracey curette. • 7-8, 9-10—Posterior teeth facial and lingual • 11-12—Posterior teeth (mesial) Answer • 13-14—Posterior teeth (distal) Gracey curette Universal curette Q.54. Define scaling and root planing. Area of use Set of many curettes One curette designed designed for specific for all areas and Answer areas and surfaces surfaces Cutting edge One cutting edge Both cutting edges used Scaling is defined as a process by which plaque and calculus use used; work with work with either outer are removed from both supragingival and subgingival tooth outer edge only or inner edge surfaces. Curvature Curved in two Curved in one plane; planes; Blade curves Blade curves up, not to Root planing: It is a process by which residual embedded up and to the side side calculus and portions of cementum are removed from the Blade angle Offset blade: face of Not offset; face of blade beveled at blade beveled at 90° to roots to produce a smooth hard, and clean surface. 60° to shank shank OR 457

It denotes a technique of instrumentation by which the softened cementum is removed and the root surface is made hard and smooth.

Q.55. What are the principles of instrumentation? 53 CHAPTER Answer General principles of instrumentation are: 1. Accessibility. 2. Visibility, illumination and retraction. 3. Condition of instruments.

4. Maintaining a clean field. Questionnaire for Clinical Case Discussion Case Clinical for Questionnaire 5. Instrument stabilization. Fig. 53.21: Extraoral fulcrums—Palm up 6. Instrument activation.

Q.56. What are finger rests and grasps? Answer Finger rests serve to stabilize the hand and the instrument by providing a firm fulcrum as movements are made to activate the instrument. A good finger rest prevents injury and laceration of the gingiva and surrounding tissues by poorly controlled instruments. Most clinicians for the finger rest prefer the fourth finger. Maximal control is achieved when the middle finger is kept between the instrument-shank and fourth finger. This “built-up fulcrum” is an integral part Fig. 53.22: Extraoral fulcrums—Palm down of the wrist-forearm action that activates the powerful working stroke for calculus removal (Figs 53.21 to 53.29).

Finger rest Extraoral finger rests: a. Palm up. b. Palm down.

Intraoral finger rests a. Conventional b. Cross-arch c. Opposite arch d. Finger on finger Fig. 53.23: Conventional—Intraoral finger rests Grasps: A proper grasp is essential for precise control of movements made during periodontal instrumentation. the middle finger is positioned so that the side of the pad The commonly used grasps are: next to the finger nail is resting on the instrument shank. a. Modified pen grasp: The thumb, index finger, and middle The index finger is bent at the second joint from the finger are used to hold the instruments as pen is held, but fingertip and is positioned well above the middle finger

458 PART V

Fig. 53.24: Intraoral finger rests—Cross-arch Fig. 53.27: Instrument grasps—Pen grasp

Fig. 53.25: Opposite arch (Intraoral finger rests) Fig. 53.28: Instrument grasps—Modified pen grasp Treatment of Periodontal Diseasesy Periodontal of Treatment

Fig. 53.26: Finger on finger (Intraoral finger rests) Fig. 53.29: Instrument grasps—Palm and thumb grasp

on the same side of the handle. The pad of the thumb is b. Palm and thumb grasp: It is used for stabilizing placed midway between the middle and index fingers on instruments during sharpening and for manipulating air the opposite side of the hand thereby creating tripod and water syringes, but it is not recommended for effect. periodontal instrumentation. 459

Q.57. Different angulations needed for scaling procedure. Vth Generation Probes: Ultrasound probes. They are still under research. Answer Angulation refers to the angle between the face of bladed Dental endoscope : Perioscopy system, which works on fiber instrument and tooth surface. It is also called tooth blade optic system. It is used for subgingival calculus detection, 53 CHAPTER relationship. caries, defective restoration, and fractures. a. For subgingival insertion of bladed instruments angulations should be close to 0 degrees as possible. ADVANCES IN ROOT PLANING b. For scaling and root planing, angulation should be INSTRUMENTS between 45 to 90°. 1. Gracey no 15-16: It is a modification of standard 11-12 c. For gingival curettage angulation>90° is established so and has an 11-12 blade with a 13-14 shank. It is useful

that the cutting edge will engage and remove the pocket for mesial surfaces of posterior teeth. Discussion Case Clinical for Questionnaire epithelium. 2. Gracey no 17-18: It is a modification of standard 13-14. It is a 13-14 Gracey curette with a terminal shank Q.58. Recent advances in periodontal instrumentation. elongated by 3 mm and a more accentuated angulation Answer of shank. Advances in Diagnostic Instruments 3. Extended shank curettes (after five curettes): Here shank is elongated by 3 mm and is used for deeper periodontal Probes: They are classified, based on the generation of pockets of 5 mm or more. development. 4. Mini-bladed curettes (mini five curettes): They are Ist Generation Probes: Conventional probes, e.g. Williams modifications of after five curettes with their blade probe reduced by half. It is used in furcation area, develop- IInd Generation Probes: Pressure sensitive probes, e.g. mental grooves, tight pockets, deep narrow pockets. Borodontic probes 5. Gracey curettes: Here the blade length is half of the conventional gracey curette and blade curves upwards. IIIrd Generation Probes: Computer aided probes, e.g. 6. Langer and mini-langer curettes: It is a combination of Florida probes universal and gracey curettes available in 5-6, 11-12 and IVth Generation Probes: Records sequential probe positions 13-14. It has similar shank design to a gracey curette along gingival sulcus. They are still under research. but blade angle is 90 degrees. Glossary

Abrasion Refers to the loss of tooth substance induced by mechanical wear other than that of mastication. —Carranza Abscess A localized collection of pus. Acellular Cementum/ Cementum lacking embedded cells. —Grant/Stern Primary Cementum Acellular Cementum/ Cementum that forms in conjunction with root formation and tooth eruption. Primary Cementum —Lindhe Acantholysis Hyperplasia of the prickle cell layer (stratum spinosum) of stratified squamous epithelia resulting in thickened rete redges and widening of this layer. Acquired Coatings It includes those exogenous origins such as saliva, bacteria, calculus and surface stains. Acquired Immunodeficiency It is characterized by profound impairment of the immune system. Syndrome (AIDS) Acquired Pellicle It is a homogeneous, membranous, acellular film that covers the tooth surfaces and frequently forms the interface between the surface of the dental plaque and calculus. —Saul Schluger Active Eruption Active eruption is the movement of the teeth in the direction of the occlusal plane. —Carranza Actual Position It is the level of the epithelial attachment on the tooth. —Carranza Acute Gingivitis Inflammation of gingiva which is of short duration, sudden onset and can be painful. Acute Trauma from Occlusion It results from abrupt occlusal impact such as that produced by biting on hard object. —Carranza Adaptation Refers to the manner in which the working end of the periodontal instrument is placed against the surface of the tooth. —Carranza Addison’s Disease It is caused by adrenal dysfunction and produces isolated patches of discoloration varying from bluish black to brown. —Carranza Additive Osseous Surgery Includes procedures directed at restoring the alveolar bone to its original level. Adjuvant A nonspecific stimulant of the immune response which enhances the response to antigen. Many bacterial cell wall components have this property. Adult Periodontitis A form of periodontitis that usually has an onset beyond the age of 35 years. Bone resorption usually progresses slowly and predominantly in the horizontal direction. Aerobe A microorganism which grows in the presence of oxygen. Ageing of Periodontium Ageing is a slowing of nature function, a disintegration of the balanced control and organization that characterize the young adult. —Carranza Aggressive Periodontitis It is a periodontal destruction that becomes clinically significant around adolescence or early adulthood. —Carranza 462

Aggressive Periodontitis It is characterized by the rapid loss of attachment and bone loss occurring in an otherwise clinically healthy patient with the amount of microbial deposits inconsistent with disease severity and familial aggregation of diseased individuals. Aggressive Periodontitis Was formerly classified as early onset periodontitis, i.e. localized juvenile periodontitis (LJP). Generalized aggressive periodontitis was previously classified as Generalized Juvenile Periodontitis (GJP) and Rapidly Progressive Periodontitis. Agranulocytosis Agranulocytosis is characterized by a reduction in the number of circulating granulocytes and results in severe infection including ulcerative necrotizing lesions of the oral mucosa, skin, gastrointestinal and genitourinary tracts. —Carranza Alleles Variations in the nucleotide sequence at a locus is termed as alleles. Allograft or Homograft A tissue transfer between individuals of the same species but with non-identical genes. GLOSSARY Allograft A graft between genetically dissimilar members of the same species. —Periodontal Literature Review Alloplast Graft A graft of inert synthetic material, which is sometimes called, implant material. Alveolar Bone Proper It is a plate of compact bone, the radiographic image of which is termed as Lamina dura. —Genco Alveolar Bone Proper It is the thin lamella of bone surrounding the root, seen as lamina dura in the radiographs (Opaque line). —Grant Alveolar Mucosa Mucosa covering the basal part of the alveolar process of continuing without demarcation into the vestibular fornix and the floor of the mouth. It is loosely attached to the periosteum and is movable. —Periodontal Literature Review Alveolar Process Alveolar process is defined as the parts of the maxilla and mandible that form and support the sockets of the teeth. —Lindhe Alveolar Process It is that part of the jawbone which supports the teeth. Alveolar Process It is that portion of the maxilla and the mandible that form and support the sockets of the teeth. —Carranza Alveolar Process It is the part of the maxilla or mandible that forms and supports the teeth. —Grant/ Stern /Listgarten Anaerobic Growth in absence of oxygen. Anemia It is a deficiency in the quantity or quality of blood as manifested by reduction in the number of erythrocytes and in the amount of hemoglobin. —Carranza Angular Chelitis The commissure appears erythematous with surface crusting and fissuring. Angular Defects They are classified on the basis of the number of the osseous walls it may have one, two or three walls. Angulation Refers to the angle between the face of the bladed instrument and the tooth surface. Also known as tooth-blade relationship. —Carranza Ankylosis Fusion of the cementum and the alveolar bone with the obliteration of the periodontal

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials ligament is termed as ankylosis. —Carranza Antibiotics Are a naturally occurring, semisynthetic or synthetic type of antimicrobial agent that destroys or inhibits the growth of selective microorganisms, generally at low concentrations. Antibody A class of serum proteins that are induced following interaction with an antigen, they bind specifically to the antigen that induced their formation. Antibody An immunoglobulin which binds to a specific antigen. Lymphocytes which have recognized an antigen may differentiate into plasma cells and secrete antibody against that antigen. Antigen Any following material that is specifically bound by antibody. Antigen A structure recognized as foreign by the immune system. The word is derived from antibody generator. 463

Antigenicity Capacity of the foreign agent to combine with or be recognized by metabolites or products of immune response. Antimicrobial Agent It is a chemotherapeutic agent that works by reduction in bacterial number. Antiseptic Are chemical antimicrobial agents that are applied topically or subgingivally to mucous membrane wounds, intact dermal surfaces to destroy microorganisms and inhibit their metabolism and reproduction. —Carranza GLOSSARY Apparent Position It is the level of the crest of the gingival margin. Attached Gingiva Width of the attached gingiva—it is the distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or the periodontal pocket. —Carranza Attached Gingiva The attached gingiva is continuous with the marginal gingiva. It is firm, resilient and tightly bound to the underlying periosteum of the alveolar bone. —Carranza Attrition Is occlusal wear resulting from functional contacts with opposite teeth. —Carranza Autograft Tissue transferred from one position to another within the same individual. Bacterial Succession The appearance and disappearance of species as mixed flora evolves. Biofilm It describes the relatively indefinable microbial community associated with a tooth surface or any hard non shedding material. —Wilderer and Charaklis [1989] Biofilm It is defined as matrix enclosed bacterial population adherent to each other and/or to surface or interfaces. —Costerton Biofilms Biofilms are natural communal aggregations of microorganisms that may form on wide range of surfaces. —Lindhe Bio-integration A bonding of the living bone to the surface of an implant which is independent of any mechanical interlocking mechanism. —Periodontal Literature Review Biologic Depth It is the distance between the gingival margin and the base of the pocket. (Coronal end of the junctional epithelium). —Carranza (it can be measured only in carefully prepared and adequately oriented histological section) Biologic Width It is defined as; the dimension of space that the healthy gingival tissues occupy above the alveolar bone. —Carranza Bruxism or occlusal necrosis It is defined as the clenching or grinding of the dentition during nonfunctional movements of the mastication system. —Periodontal Literature Review Bruxism It is the clenching /grinding of teeth when individual is not chewing or swallowing. Bulbous Bone Contours Bulbous bone contours are bony enlargements caused by exostosis, adaptation to function, or buttressing bone formation. Commonly found in maxilla. Bullous Pemphigoid It is a chronic autoimmune subepidermal, bullous disease with tense bullae that rupture and become flaccid in the skin. —Carranza Bundle Bone The layer of the alveolar bone into which the principal fibers (Sharpey’s fibers) are inserted. —Lindhe Buttressing Bone Formation/Lipping Bone formation occurring in an attempt to buttress bony trabeculae weakened by resorption. Buttressing Bone Formation If it occurs within jaw, it is termed central buttressing bone formation. Buttressing Bone Formation When it occurs on external surface, it is referred to as peripheral buttressing bone formation. Bystander damage Accidental damage to host tissues caused by complements, neutrophils and macrophages during inflammation. Calculus A hard concretion that forms on teeth or dental prosthesis through calcification of bacterial plaque —Periodontal Literature Review Calculus Calculus is a calcified plaque. —Manson and Eley Calculus Calculus is essentially mineralized plaque covered on its external surface by vital, tightly adherent, nonmineralized plaque. —Genco 464

Calculus Consists of mineralized bacterial plaque that forms on the surface of the natural teeth and dental prosthesis. —James E Hinrichs (Carranza) Calculus Is a calcified mass which forms on and adheres to the surface of teeth and other solid objects in the mouth, e.g. restoration and denture. Calculus It is defined as a hard deposit that forms by mineralization of dental plaque and is generally covered by a layer of unmineralized plaque. —Carranza Calculus When dental plaque calcifies the resulting deposit is called Dental calculus. These calcified deposits occur as hard, firmly adhering masses on the clinical crowns of the teeth. —Grant Capnophilic Organisms which require greater concentration of carbon dioxide. —Periodontal Literature Review. GLOSSARY Carrier Molecule Is a part of the antigen recognized by T-lymphocytes. —Grant Cell-mediated Immunity An immune reaction mediated by T-cells. Cell-mediated Immunity An immune reaction mediated by T-lymphocytes (activated lymphocytes release biologic response modifiers (lymphokines) on exposure to antigen. Cellular Cementum/ Cementum that contains cells in lacunae located within the mineralized matrix. Secondary Cementum —Grant/ Stern/Listgarten Cellular Cementum/ Cementum that forms after tooth eruption and in response to functional demand. Secondary Cementum —Lindhe Cementum Cementum is a calcified connective tissue which covers the root dentine and into which bundles are inserted. —JD Manson & BM Eley Cementum Cementum is a calcified mesenchymal tissue that forms the outer covering of the anatomic root. Cementum Cementum is a hard bone like tissue covering the anatomic roots of the teeth. —Genco Cementum Cementum is a hard bone like tissue covering the root surfaces and occasionally small portions of the crown of the teeth. —Lindhe Cementum Cementum is mineralized connective tissue that covers the roots of the teeth. —Grant/ Stern/Listgarten Chemotaxis Locomotion of cells which is directed along an increasing chemical gradient of a soluble substance. Chemotaxis The migration of cells along a concentration gradient of an attractant. Chemotherapeutic Agents General term used for a chemical substance that provide chemical therapeutic benefit. Chronic Gingivitis Is slow in onset and is of long duration, and is painless unless complicated by acute or subacute exacerbations. —Carranza Chronic Periodontitis An infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss and bone loss. —Carranza

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Chronic Trauma from Occlusion It results from gradual changes in occlusion produced by tooth wear, drifting movement, extrusion of teeth, etc. —Carranza Clenching It is the closure of the jaws under vertical pressure. Coatings of Developmental Origin Those normally formed as part of tooth development (reduced enamel epithelium, dental cuticle). —Carranza Coefficient of Separation The length of root cones in relation to the length of root complex. —Lindhe Combined Lesion Combined lesion occurs when pulpal necrosis and periapical lesion occurs on a tooth that also is periodontally involved. —Carranza Combined Osseous Defect The number of walls in the apical portion of the defect may be greater than that in its occlusal portion. 465

Complement A group of serum proteins involved in the control of inflammation, the activation of phagocytes and lytic attack on cell membranes. The system can be activated by interaction with antigen-antibody complexes or bacterial substances. —Periodontal Literature Review Complement It is an interacting network of about 30 membrane associated cell receptors and soluble serum glycoprotein. —Carranza GLOSSARY Compliance Action in accordance with recommendations. Compromise Osseous Reshaping It indicates a bone pattern that cannot be improved without significant osseous removal that would be detrimental to overall result. —Carranza Contact Inhibition Inhibition of movement and division caused by physical contact between cells of the same type. Contact Inhibition The process by which the graft material prevents apical proliferation of the epithelium. Coronal Cementum Cementum that is found over enamel. —Grant/ Stern/Listgarten Curettage It is used in Periodontics for scraping of the gingival walls of the periodontal pocket to separate the diseased soft tissue. Curettes Are manual instruments with cutting edge on both sides of the blade and rounded toe. Curtain procedure A procedure designed to retain the marginal portion of the facial and interproximal gingiva for esthetic purpose in surgical treatment of periodontal pockets usually in maxillary anterior region by means of a palatal approach. The facial gingiva will be coronal to the palatal margin, thus creating a curtain. Cuticle Thin, acellular structure with a homogenous matrix, sometimes enclosed within clearly demarcated, linear borders. —Carranza Cyst Cyst is a swelling consisting of fluid in a sac, which is lined by epithelium or endothelium. —Bailey and Love Cytokine A small protein messenger released by cells which affects the division, differentiation and function of other cells, which may be of the same or different types. Debridement The removal of inflamed, devitalized or contaminated tissue or foreign material from or adjacent to a lesion. Definitive Osseous Reshaping Implies that further osseous reshaping would not improve the overall result. Degree of Separation It is the angle of separation between two roots. —Lindhe Dehiscence Alveolar dehiscence is a dipping of the crestal bone margin exposing the root surface. —Grant/ Stern /Listgarten Dehiscence Denuded surfaces involving the marginal bone, the defect is called as dehiscence. —Carranza Dental Calculus It is a tightly adherent plaque that has undergone mineralization. Dental Calculus It is an adherent, calcified or calcifying mass that forms on the surfaces of teeth and dental appliances. Dental Epidemiology Is the study of pattern (distribution) and dynamics of dental diseases in a human population. —Carranza Dental Implant Dental implant is perimucosal devices that is biocompatible and bio-functional and is placed on or within the bone associated with the oral cavity to provide support for fixed or removable prosthesis. Dental Plaque Dental plaque comprises of complex microbial communities that form on virtually all surfaces of the teeth exposed to the bacteria-laden fluids of the mouth. —Robert Wirthilin and Gary C Armitage Dental Plaque Dental plaque is an adherent, intercellular matrix consisting primarily of proliferating microorganisms, along with a scattering of epithelial cells leukocytes and macrophages. 466

Dental Plaque Dental plaque is defined as a soft deposit that forms the biofilm adherent to the tooth surface or other hard surfaces in the oral cavity including removable and fixed restorations. —Carranza Dental Plaque It is a host associated biofilm. Dental Splint An appliance designed to immobilize and stabilize loose teeth. Dental Stain Pigmented deposits on tooth surface. —Carranza Dentifrices Agent that aids in cleaning and polishing tooth surfaces. Desmosome A specialized attachment between epithelial cells which impart strength to epithelium. Desquamative Gingivitis Coined in 1932 by Prinz, to describe a peculiar condition characterized by intense erythema, desquamation, and ulceration of the free and attached gingiva. —Carranza Diagnosis It may be defined as identifying disease from an evaluation of the history, signs and GLOSSARY symptoms, laboratory tests and procedures. Differentiation Differentiation involves the process of keratinization, which consists of sequence of biochemical and morphologic events that occur in the cell as it migrates from the basal layer. —Carranza Diffuse Gingivitis It affects gingival margin, the attached gingiva and the interdental papillae. —Carranza Disclosing Agents They are solutions or wafers capable of staining bacterial deposits on the surface of teeth, tongue and gingiva. Disease Atrophy Nonfunctional and hypofunction may be expressed as disease atrophy. The disease of the periodontal tissue is characterized by a rearrangement of fibers of the periodontal ligament and of the trabeculation of the alveolar bone without gingival recession. —Grant Disinfectant An antimicrobial agent that is generally applied to inanimate surfaces to destroy microorganisms. Displaced Flap It is placed apically, coronally or laterally to their original position. —Carranza Disuse or Functional Atrophy When occlusal forces are reduced, the number and thickness of the trabeculae are reduced, with atrophy of periodontal ligament appearing thinned, with reduction in number of fibers and density. —Carranza Divergence It is the distance between two roots (cones); this distance normally increases age in apical direction. —Lindhe Down’s Syndrome Is a congenital disease caused by a chromosomal abnormality and characterized by mental deficiency and growth retardation. Ecological Niche The functional position which bacterial species occupies within a complex ecosystem such as plaque. Electrocoagulation It provides a wide range of coagulation or hemorrhage control obtained by using electrocoagulation current. Electrosection Electrotomy or acusection is used for incision, excision and tissue planing.

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Electrodesiccation Uses dehydrating current and is least used. Electrofulguration A method of electrosurgery used to produce superficial desiccation of tissue, which employs a highly or moderately damped alternating current that is radiated through a monoterminal active electrode that is held close to the patient so that the sparks spray over the lesion being treated. Electrosurgery (Radiosurgery) It is currently used to identify surgical techniques performed on soft tissue using controlled high frequency electrical current in the range of 1.5-7.5 million cycles/sec or MHz. Electrosurgery Division of tissue by high frequency electrical current applied locally with a metal instrument or needle. Endodontic-periodontal Lesions Pulpal necrosis precedes periodontal changes. A periapical lesion originating in pulpal inflammation and necrosis may drain to the oral cavity through periodontal ligament and adjacent alveolar bone. —Carranza 467

Endotoxin A complex heat stable toxin which is a structural component of gram-negative bacterial cell wall. The active component is a lipopolysaccharide. Epidemiology The study of the distribution and determinants of health-related states or events in specified populations and the application of this study to control health problems. —Carranza Epithelial Adaptation It is the close apposition of the gingival epithelium to the tooth surface without obliteration GLOSSARY of the pocket. Epulis It is the generic term to designate all discrete tumor and tumor-like mass of gingiva. —Carranza Erosion (Cuneiform Defect) It is a sharply defined wedge shaped depression in the cervical area of the facial tooth surface. —Carranza Etiology The cause of disease, in the case of gingivitis and periodontal disease, microbial dental plaque. Evidence-based Therapy Current concept of evaluating health care requires a scientific basis for treatment. Excisional New Attachment It is a definitive subgingival curettage performed with a knife. Procedure Excursive Movement Any movement of the mandible away from intercuspal position. Exostosis Exostosis is outgrowths of the bone of varied size and shape. Exploratory Stroke It is a light “feeling” stroke that is used with probes and explorer to evaluate the dimensions of the pocket and to detect calculus and irregularities of the tooth surface. Exposure It is defined as a factor that may possibly lead to disease or may be protective against a disease. —Mauricio Ronderers Extrusion Pathologic migration in the occlusal or incisal direction is termed as extrusion. —Carranza Factitious Pertaining to a state or situation produced by other natural means; self-inflicted. Facultative Anaerobe Growth in either an aerobic or anaerobic environment. Fc The part of an immunoglobulin molecule which binds to specific receptors on neutrophils and macrophages, but which does not bind to antigen. Fenestration It is a circumscribed hole in the cortical plate over the root and does not communicate with the crestal margin. —Grant/ Stern /Listgarten Fenestration An isolated area in which the root is denuded of the bone and the root surface is covered only by the periosteum and the overlying gingiva are termed fenestration. Here the margin is intact. —Grant/ Stern /Listgarten Fibroma Arises from the gingival connective tissue or from the periodontal ligament. —Carranza Fibronectin A connective tissue protein which binds cells to the extracellular matrix. Fibro-osseous Integration In which soft tissue such as fibers and/ or cells, are interposed between the two surfaces. Fimbriae A fine filamentous surface appendage on a bacterium. These are important for attachment and adhesion and are important antigens on some species. Finger Rest The finger rest serves to stabilize the hand instrument by providing a firm fulcrum as movement is made to activate the instrument. Flap A loosened section of the tissue separated from the surrounding tissue except at its base. —Periodontal Literature Review Flat Architecture It is reduction of the interdental bone to the same height as radicular bone. —Carranza Food Impaction It is the forceful wedging of food into the periodontium by occlusal forces. —Carranza Food Impaction The forceful wedging of the food into the interproximal space by chewing pressure or the forcing of food interproximally by tongue or cheek pressure. 468

Fremitus A palpable or visible movement of teeth when subjected to occlusal forces. Fremitus It is the measurement of the vibratory patterns of the teeth when teeth are placed in contacting positions and movements. —Genco Frenectomy It is complete removal of the frenum, including its attachment to underlying bone and may be required in correction of an abnormal diastema between maxillary central incisors. Frenotomy It is the incision of frenum. —Carranza Frenum It is a fold of mucous membrane usually with enclosed muscle fibers that attaches the lip and cheeks to the alveolar mucosa and / or gingiva and underlying periosteum. Full Thickness Flap All the soft tissue, including the periosteum is reflected to expose the underlying bone. Furcational Entrance It is the transitional area between the divided and undivided part of the root. —Lindhe GLOSSARY Furcational Fornix The roof of the furcation. Furcation Invasion Pathologic resorption of bone within the furcation. —Periodontal Literature Review Furcation Involvement Furcation involvement refers to the invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease. —Carranza Furcation Furcation is defined as the area located between individual root cones. —Lindhe Furcation It is the anatomic area of a multirooted tooth where the roots diverge. —Periodontal Literature Review Generalized Aggressive Periodontitis Clinically characterized by “generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors”. —Carranza Generalized Diffuse Gingivitis Involves the entire gingiva of the entire mouth. Generalized Gingivitis Involves the entire mouth. Generalized Marginal Gingivitis Involves the gingival margins in relation to all the teeth. —Carranza Generalized Periodontitis It is considered generalized when >30% of the sites assessed in the mouth demonstrate attachment loss and bone loss. Genetic Marker Genetic marker refers to any gene or nucleotide sequence that can be mapped to a specific location or region on a chromosome. —Carranza Genotype The generic composition of an organism. Gingiva Gingiva is the part of the oral mucosa that covers the alveolar process of the jaws and surrounds the neck of the teeth. —Genco Gingiva The fibrous investing tissue covered by keratinized epithelium which immediately surrounds a tooth and is contiguous with its periodontal ligament and with the mucosal tissues of the mouth. —Periodontal Literature Review Gingiva The gingiva is the part of the masticatory mucosa, which covers the alveolar process and surrounds the cervical portion of the teeth. —Lindhe

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Gingiva The gingiva is the part of the oral mucosa that covers the alveolar processes of the jaws and surrounds the necks of the teeth. —Carranza Gingiva The gingiva is the part of the oral mucous membrane attached to the teeth and the alveolar processes of the jaws. —Grant/ Stern/Listgarten Gingiva The gingiva is that part of the oral mucosa which surrounds the tooth and covers the alveolar ridge. —Manson & Eley Gingival Abscess Gingival abscess is a localized, painful, rapidly expanding lesion, which is usually of sudden onset. It is generally limited to the marginal gingiva or interdental papilla. —Carranza Gingival Abscesses Gingival abscesses are those that are localized to the marginal gingiva or interdental papilla. —Gary C Armitage 469

Gingival Abscesses Localized in the gingiva, caused by injury to the outer surface of the gingiva and not involving the supporting structures. —Carranza Gingival Crevicular Fluid GCF is an altered serum transudate found in the gingival sulcus. —Genco Gingival Crevicular Fluid Tissue fluid that seeps through the crevicular epithelium. It is increased in the presence of inflammation. —Periodontal Literature Review Gingival Curettage It consists of the removal of inflamed soft tissue lateral to pocket wall. GLOSSARY Gingival Curettage It means the scraping of the gingival wall of the periodontal pocket to separate diseased soft tissue. Gingival Cyst Found within the gingiva, most commonly in the canine—premolar region. —Periodontal Literature Review Gingival Enlargement Increase in the size of the gingiva. Gingival Hyperplasia Defined as an enlargement of gingiva due to the increase in the number of cells. —Periodontal Literature Review Gingival Pocket (Pseudo Pocket) This type of pocket is formed by gingival enlargement without destruction of the underlying periodontal tissues. Gingival Recession Is the exposure of root surface due to apical shift in the marginal gingiva. —Grant Gingival Sulcus The gingival sulcus is the shallow crevice or space around the tooth bounded by the surface of the tooth on one side and the epithelia lining the free margin of the gingiva on the other. —Carranza Gingivectomy Excision of a portion of the gingiva. —Periodontal Literature Review Gingivectomy It means excision of gingiva. —Carranza Gingivitis Inflammation of the gingiva. Gingivoplasty Gingivoplasty is “a surgical reshaping of the gingiva”. Gingivoplasty It is the reshaping of the gingiva to create physiologic gingival contour, with the sole purpose of recontouring the gingiva in the absence of periodontal pocket. —Carranza Glycosaminoglycan A molecule of repeating sugar subunits which forms a major component of connective tissue ground substance. Gnotobiotic Animal A laboratory animal whose microbial flora is known. Specific microorganisms are introduced into germ-free animals to make them gnotobiotic. Gracey Curettes Set of many curettes designed for specific area and surfaces. Graft Any tissue or organ used for implantation or transplantation. Graft It is a viable tissue/ organ that after removal from donor site are implanted within the host tissue, which is then repaired, restored and remodeled. Guidance Pattern of opposing tooth contact during excursive movements of the mandible. The teeth making such contact cause separation of the other teeth. Guided Tissue Regeneration An epithelial exclusionary technique that promotes new connective tissue attachment without the use of any implant material. Guided Tissue Regeneration Procedures attempting to regenerate lost periodontal structures through differential tissue responses. Habit An act of repeated performance, almost automatic, such as bruxism or tongue thrusting. Halitosis Also termed as fetor ex ore and oral malodor, is foul or offensive odor, emnating from oral cavity. —Carranza Hapten Is a part of antigen recognized by B-lymphocytes. —Grant Hemidesmosome Structure which attaches epithelial cells to the basement membrane. It resembles half a desmosome, but has different structural components. Hemisection It is surgical removal of a root with the associated part of crown. 470

Hemisection It is the splitting of the two-rooted tooth into two separate portions. The process has been called Bicuspidization or Separation. Hemiseptum The one wall defect is also called as hemiseptum. Homeostasis The production of a stable equilibrium in a body system by means of feedback mechanisms. Horizontal Bone Loss Common pattern of bone loss in which bone is reduced in height, but the bone margins roughly perpendicular to the tooth surface. Hydrolytic Enzymes A class of enzymes which cleaves various types of bond, including peptide, ester and glycosidic bonds, with the addition of water. Many degradative and lysosomal enzymes fall into this category. Hypercementosis It refers to the prominent thickening of the cementum. It may be localized or generalized. —Carranza GLOSSARY Hyperfunction Is a functional adaptation in which additional structural elements are formed on cementum and in bone to withstand the added force expressed clinically and microscopically as a thickened lamina dura, buttressing bone formation, osteosclerosis and cemental spurs. —Grant Hypersensitivity Root surfaces exposed by gingival recession may be hypersensitive to thermal changes or tactile stimulation. Iatrogenic Factors Inadequate dental procedure that contribute to the deterioration of the periodontal tissues. —Carranza Immune Complex A complex of antigen and antibody molecules bound to one another and together. Immunogenicity It is the capacity to induce a detectable immune response such as the production of antibody or the stimulation of cellular immunity. Immunoglobulin A glycoprotein composed of heavy and light peptide chains; functions as antibody in serum and secretions. —Periodontal Literature Review Implant An alloplastic material or device that is surgically placed into the oral tissue beneath the mucosal or periosteal layer or within bone for functional, therapeutic and esthetic purposes. Implant To insert a graft or alloplastic device into the oral hard or soft tissue for replacement of missing or damaged anatomic parts or stabilization of periodontally compromised tooth or group of teeth. —Periodontal Literature Review Inadvertent Curettage Some degree of curettage is done unintentionally while scaling and root planing is performed. —Carranza Inflammation A cellular and vascular reaction of tissue to injury. —Periodontal Literature Review Inflammation A localized protective response elicited by injury or destruction of tissue, which serves to destroy, dilute or wall off both the injurious agent and injured tissue. —Periodontal Literature Review Inflammation Is an observable alteration in tissue associated with changes in vascular permeability and dilation, often with the infiltration of leukocytes into affected tissue.

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials —Periodontal Literature Review Intercuspal Position (ICP) The position of the mandible when there is maximum intercuspation between the maxillary and mandibular teeth. —Synonym-Centric occlusion Interdental Gingiva The interdental gingiva occupies the gingival embrasure, which is the interproximal space beneath the area of tooth contact. —Carranza Interference Any contact in ICP or excursion that prevents the remaining occlusal surfaces from achieving stable contact. —Synonym-Supra contact Interleukins Cytokine which mediate communication between leukocytes. Intermediate Cementum It is an ill-defined zone near cementodentinal junction of certain teeth that appear to contain cellular remnants of Hertwig’s sheath embedded in calcified ground substance. —Carranza 471

Intrabone/Intrabony/ Bottom of the pocket is apical to the level of the adjacent alveolar bone. Supracrestal Pocket —Carranza Intrabony Defects The three-wall vertical defect was originally called intrabony defect. Junctional Epithelium A single or multiple layer of non-keratinizing cells adhering to the tooth surface at the base of the gingival crevice. —Periodontal Literature Review Junctional Epithelium It denotes the tissue that joins to the tooth on one side and to the oral sulcular epithelium GLOSSARY and connective tissue on the other. Juvenile Periodontitis A disease of Periodontium occurring in an otherwise healthy adolescent which is characterized by a rapid loss of alveolar bone, about more than one tooth of the permanent dentition. Lamina Dura The compact bone (Alveolar bone proper), which lines the tooth socket, and in a radiograph appears as a dense opaque line is called as lamina dura. —Lindhe Lateral Pressure Refer to the pressure created when force is applied against the surface of a tooth with the cutting edge of a bladed instrument. —Carranza Laterotrusion Movement of the mandible laterally to the right or left from ICP. Laterotrusive Movement The side of either dental arch corresponding to the side of mandible moving away from the midline. —Synonym-Working side Ledges Ledges are plateau like bone margins caused by resorption of thickened bony plates. —Carranza Leukemia It is a malignant neoplasia of WBC precursors. —Carranza Leukoplakia A white patch or plaque that does not rub off and cannot be diagnosed as any other disease. —World Health Organization Lichen Planus It is a relatively common, chronic dermatosis characterized by the presence of cutaneous, violaceous papules that may coalesce to form plaques. Lichen Planus Is defined as unique cutaneous entity consisting of an eruption of papules distinct in color and configuration, in patterns and location of appearance and in microscopic and gross structure. —Fitz Patrick Lipopolysaccharide The active component of bacterial endotoxins. Localized Gingivitis It is confined to the gingiva of a single tooth or group of teeth. Localized Aggressive Is characterized as having localized first molar or incisor disease with proximal Periodontitis attachment loss on at least 2 permanent teeth, one of which is a first molar. —Carranza Localized Diffuse Gingivitis It extends from the gingival margin to the mucobuccal fold but is limited in area. Localized Marginal Gingivitis It is confined to one or more areas of the marginal gingiva. Localized Periodontitis It is considered localized when <30% of the sites assessed in the mouth demonstrate attachment loss and bone loss. Loci Loci are defined as the specific location on the chromosomes. Lymphokine Cytokine secreted by lymphocytes. Cytokine is now preferred term for this group of substances because they are secreted by other cell types as well. Malnutrition Any disorder of nutrition, it may be due to imbalance or insufficient diet or to defective assimilation or utilization of foods. —Dorland’s Marginal Gingiva The marginal or attached gingiva, is the terminal edge or border of the gingiva surrounding the teeth in a collar-like fashion. —Carranza Marginal Gingivitis Inflammation of the gingival margin and may include a portion of the contiguous attached gingiva. Marginal Plaque Plaque is in direct contact with the gingival margin and also referred to as marginal plaque. —Carranza Marginal Plaque It is the supragingival plaque that is in direct contact with the gingival margin. 472

Masticatory Mucosa The gingival and the mucosal covering of the hard palate. Materia Alba Is a yellowish or whitish, soft loose deposit found in neglected mouths comprising of a mass of microorganisms, desquamated epithelial cells, food debris, leukocytes plus salivary deposits. —J.D Manson and B.M Eley Materia Alba Is a deposit composed of aggregates of microorganisms, leukocytes, dead, exfoliated epithelial cells attached to surfaces of the teeth, plaque and gingiva. —Saul Schluger Materia Alba It refers to the soft accumulation of bacteria and tissue cells that lack the organized structure of dental plaque and are easily displaced with a water spray. —Carranza McCall’s Festooning Are life preserver-shaped enlargements of the marginal gingiva that occurs most frequently in the canine and premolar areas on the facial surface. GLOSSARY Mediotrusive Side The side of either dental arch corresponding to the side of mandible moving towards the midline. —Synonym-Balancing side, non-working side Metalloproteinases Enzymes which degrade protein in the presence of metal ions, usually calcium or magnesium. Micro-aerophilic Organisms which grow best in an atmosphere of reduced oxygen. Microbial Dental Plaque Is described as aggregations of bacteria that are tenaciously attached to the teeth and other surfaces. —Genco Mitogen A substance that causes DNA synthesis, blast transformation, and mitosis in lymphocytes. Mobility Is a measurement of horizontal and vertical tooth displacement created by examiner force. Moderate Periodontitis Periodontal destruction is generally considered moderate when 3 to 4 mm of clinical attachment loss has occurred. Modified Pen Grasp The thumb, index finger, and middle finger are used to hold the instrument as a pen is held, but the middle finger is positioned so that the side of the pad next to the finger nail is resting on the instrument shank. The index finger is bent at the second joint from the finger tip and is positioned well above the middle finger on the same side of the handle. —Carranza Modified Widman Flap A scalloped, replaced, mucoperiosteal flap, accomplished with an internal bevel incision that provides access for root planing. —Periodontal Literature Review Monocyte A large mononuclear phagocytic leukocyte, the circulating precursors of macrophages. Mucogingival Deformity It is defined as “a significant departure from the normal shape of gingiva and alveolar mucosa” and may involve the underlying alveolar bone. Mucogingival It is defined as “a generic term used to describe the mucogingival junction and its relationship to the gingiva, alveolar mucosa, frenula, muscle attachments, vestibular fornices and the floor of the mouth”. Mucogingival Surgery Is defined as periodontal surgical procedures designed to correct defects in the morphology, position, and/or amount of gingiva. —Carranza

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Mucogingival Surgery Periodontal surgical procedures used to correct defect in the morphology, position and or amount of gingiva. —Periodontal Literature Review Mucogingival Surgery Surgical procedure for the correction of relationships between the gingiva and oral mucous membrane with reference to three specific problems. Those associated with attached gingiva, shallow vestibule and a frenum interfering with the marginal gingiva. Mucosa A mucous membrane. Mucous Membrane Pemphigoid Also known as Cicatricial Pemphigoid, is a chronic, vesiculobullous autoimmune disorder of unknown cause that predominantly affects women in the fifth decade of life. —Carranza Multifactorial Diseases whose etiologies include both genetic and environmental factors. Muscular Contact Position (mcp) The position of the mandible when lifted into contact from resting position. 473

Necrotizing Ulcerative Periodontitis Is an extension of necrotizing ulcerative gingivitis (NUG) into the periodontal structures, leading to attachment and bone loss. Necrotizing Ulcerative Gingivitis It is an inflammatory destructive disease of gingiva, which presents characteristic signs and symptoms. —Carranza Necrotizing Ulcerative It is defined as severe and rapidly progressive disease that has a distinctive Periodontitis erythema of the free gingiva, attached gingiva and alveolar mucosa; extensive soft tissue GLOSSARY necrosis; severe loss of periodontal attachment; deep pocket formation is not evident. —Periodontal Literature Review Negative Architecture Refers to, if interdental bone is more apical than radicular bone. Neutrophil A phagocytic polymorphonuclear leukocyte. New Attachment It is the embedding of new periodontal ligament fibers into new cementum and the attachment of the gingival epithelium to the tooth surface previously denuded by disease. —Carranza New Attachment It is the union of the connective tissue or epithelium with a root surface that has been deprived of its original attachment apparatus. —Periodontal Literature Review Non-displaced Flap When the flap is returned and sutured in its original position. Non-thrombocytopenic Purpura It occurs as a result of either vascular wall fragility or thrombasthenia. Occlusal Trauma An injury to the attachment apparatus as a result of excessive occlusal force. —Lindhe Offset Blade To describe gracey curettes, because they are angled approximately 60-70 degree from the lower shank. Opsonin A substance capable of enhancing phagocytosis. —Periodontal Literature Review Opsonin A substance which facilitates phagocytosis when bound to the surface of a bacterium or other particle. Oral Candidiasis Infection of oral mucous membrane by a fungus of the genus Candida. Oral Epithelium Oral epithelium covers the crest and outer surface of the marginal gingiva and the surface of the attached gingiva. Oral Epithelium The oral or outer epithelium covers the crest and outer surface of the marginal gingiva and the surface of the attached gingiva. —Carranza Oral Mucosa The tissue lining the oral cavity. Oral or Outer Epithelium The outer or oral epithelium covers the crest and outer surface of the marginal gingiva and the surface of the attached gingiva. —Carranza Osseointegration A direct contact on the light microscopic level, between living bone tissue and an implant. Osseous Craters Osseous craters are concavities in the crest of the interdental bone, confined within the facial and lingual walls. Osseous Defects Different types of bone deformities can result from periodontal disease. Osseous Surgery It is defined as a procedure by which changes in the alveolar bone can be accomplished to rid it of deformities induced by the periodontal disease process or other related factors such as exostosis and tooth supraeruption. —Carranza Osseous Surgery Periodontal surgery involving modification of bony support of the teeth. —Periodontal Literature Review Ostectomy Includes removal of tooth supporting bone. —Carranza Ostectomy It is defined as the excision of bone or portion of bone in periodontics; Ostectomy is done to correct or reduce deformities caused by periodontitis and includes removal of the supporting bone. Osteoclast Activating Factor (OAF) A mixture of cytokines, including IL-1, TNF, TNF-β, and PDGF, which induces bone resorption and was previously thought to be a distinct cytokine. 474

Osteoconduction It is a physical effect by which the matrix of the graft forms scaffold that favors outside cells to penetrate the graft and form new bone. Osteoconduction The graft material acts as passive material, like a trellis or scaffolding for new bone to cover. Osteogenesis Development of the bone; Formation of bone. Osteogenesis Refers to formation or development of new bone by cells contained in the graft. Osteoinduction A process by which graft material is capable of promoting cementogenesis, osteogenesis and new periodontal ligament. Osteoinduction It is a chemical process by which molecules contained in the graft (BMPs) convert the neighboring cells into osteoblast, which in turn form bone. Osteoplasty Thinning of the buccal bone, using diamond burs, included as part of the surgical technique, GLOSSARY results in areas of bone necrosis with reduction in the bone height, which is later remodeled by new bone. Osteoplasty It is defined as the reshaping of the alveolar process to achieve a more physiologic form without removal of supporting bone. Osteoplasty Refers to reshaping the bone without removing tooth supporting bone. —Carranza Osteoplasty Reshaping the alveolar process to achieve a more physiologic form without removal of the supporting bone. —Periodontal Literature Review Papillary Gingivitis It involves interdental papillae and often extends into the adjacent portion of the gingival margin. Papillon-Lefévre Syndrome Is characterized by hyperkeratotic skin lesions, severe destruction of the periodontium and in some cases, calcification of the dura. Partial Thickness Flap Includes only the epithelium and a layer of the connective tissue. —Carranza Passive Eruption Passive eruption is the exposure of the teeth by apical migration of the gingiva. —Carranza Pathogenesis The mechanism by which a disease develops. Pathologic Migration Refers to tooth displacement that results when the balance among the factors that maintain physiologic tooth position is disturbed by periodontal disease. —Carranza Pellicle A thin biofilm. —Genco Pellicle An organic coating formed when the crown of the teeth emerges and is exposed to saliva, which is called dental pellicle. —Grant/ Listgarten Pellicle Pellicle is defined as tooth or mucosal adherent salivary protein. —Periodontal Literature Review Pellicle The earliest layer of plaque composed of salivary glycoprotein, which is later colonized by bacteria. Pemphigoid Applies to a number of cutaneous, immune-mediated, subepithelial bullous diseases that is characterized by a separation of the basement membrane zone. —Carranza

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Pemphigus Vulgaris Are a group of autoimmune bullous disorders that produce cutaneous and/ or mucous membrane blisters. —Carranza Peri-implant Mucositis Inflammatory changes confined to the soft tissue surrounding an implant. —Carranza Peri-implantitis A term used to describe inflammation around a dental implant and/ or its abutment. —Periodontal Literature Review Peri-implantitis Progressive peri-implant bone loss in conjunction with a soft tissue inflammatory lesion is termed as peri-implantitis. —Carranza Periodontal Abscess It is a localized accumulation of pus within gingival wall of a periodontal pocket. Periodontal Abscess Localized purulent inflammation in the periodontal tissues. —Carranza 475

Periodontal Abscess Periodontal abscess are acute lesions that may result in very rapid destruction of the periodontal tissues. —Carranza Periodontal Abscess Periodontal abscess are purulent infections localized to the gingival, periodontal or pericoronal regions. —Carranza Periodontal Cyst A small cyst of periodontal ligament found most often in the mandibular canine and premolar area; associated with a vital tooth and postulated to originate from the rests of mallassez, GLOSSARY the rests of the dental lamina or a supernumarary tooth bud. Periodontal Disease Comprises of a group of inflammatory conditions of the supportive tissues of the teeth that are caused by bacteria. —Carranza Periodontal Dressing/Pack A protective material applied over the wound created by periodontal surgical procedures. —Periodontal Literature Review Periodontal Flap Periodontal flap is a section of the gingiva and/or the mucosa surgically separated from the underlying tissues to provide visibility and access to the bone and the root surface. —Carranza Periodontal Healing/Regeneration Restoration of lost periodontium. Periodontal Instruments They are designed for specific purposes, such as removing calculus, planing root surfaces, curetting the gingiva, removing diseased tissue. Periodontal Ligament The periodontal ligament is a dense, fibrous connective tissue attaching the tooth to the alveolar bone. —Grant/ Stern /Listgarten Periodontal Ligament The periodontal ligament is the connective tissue that surrounds the root and connects it to the bone. —Carranza Periodontal Ligament The periodontal ligament is the soft, richly vascular and cellular connective tissue which surrounds the roots of the teeth and joins the root cementum with the lamina dura or the alveolar bone proper, or the socket wall. —Lindhe Periodontal Ligament The periodontal ligament is the tissue that surrounds the roots of the teeth and attaches it to the bony alveolus. Periodontal Plastic Surgery It is defined as the surgical procedures performed to correct or eliminate anatomic, developmental or traumatic deformities of the gingiva or alveolar mucosa. Periodontal Pocket Gingival sulcus deepening can occur by coronal movement of gingival margin, apical displacement of gingival attachment or combination of two processes. Periodontal Pocket Periodontal Pocket is defined as “a pathologically deepened gingival sulcus”. —Carranza Periodontal Pocket Pocket occurred with the destruction of the supporting periodontal tissues. Periodontal Splint It is an appliance used for maintaining or stabilizing mobile teeth in their functional position. Periodontal Surgery It is defined as intentional severing or incising of gingival tissue with the purpose of controlling or eliminating periodontal disease. Periodontal Trauma It is a morbid condition produced by repeated mechanical force exerted on the periodontium exceeding the physiologic limit of tissue tolerance and contributing to a breakdown of supporting tissues of tooth. —Genco Periodontal-Endodontic Lesion The bacterial infection with periodontal pocket associated with loss of attachment and root exposure may spread through accessory canals to the pulp, resulting in the pulpal necrosis. —Carranza Periodontics The clinical science that deals with the periodontium in health and disease, is called periodontology, the practice of which is periodontics. —Grant/ Stern/ Listgarten Periodontitis Inflammation of the supporting tissues of the teeth. An extension of the inflammation from gingiva into the adjacent bone and ligament. —Periodontal Literature Review Periodontitis It is the most common type of periodontal disease and results from extension of the inflammatory process initiated in the gingiva to the supporting periodontal tissues. 476

Periodontitis Periodontitis is defined as “an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession or both”. —Carranza Periodontitis Periodontitis is the inflammation combined with loss of attachment. —Mark U. Thomas, Brain L. Mealey Periodontium Periodontium is the functional unit of the tissues supporting the tooth. —Grant/ Stern/ Listgarten Periodontium The periodontium consists of the investing and supporting tissues of the tooth (gingiva, periodontal ligament, cementum, alveolar bone). —Micheal G. Newman Periodontium The periodontium consists of those tissues that surround and anchor the tooth in the GLOSSARY maxillary and mandibular alveolar process. —Mark I Ryder Periodontology The clinical science that deals with the periodontium in health and disease is called periodontology, the practice of which is periodontics. —Grant Periodontology The various diseases of the periodontium are collectively termed as periodontal diseases. Their treatment is referred to as periodontal therapy. Periodontology The various diseases of the periodontium are collectively termed as periodontal disease. The branch of dentistry concerned with prevention and treatment of periodontal disease is termed periodontics or periodontia. Phagocytosis Is the process by which cells ingest particles of a size visible by light microscopy. —Carranza Phase I Therapy To alter or eliminate the microbial etiology and contributing factor for gingival and periodontal disease. Phenotype Collection of traits or characteristics. Physiologic Mesial Migration With time and wear, the proximal contact areas of the teeth are flattened and the teeth tend to move mesially. This is referred to as physiologic mesial migration. Physiologic Occlusion It is one that has demonstrated the ability to survive despite anatomic obliterations from the hypothetical normal or preconceived ideal form of occlusion and function. —Genco Plaque Control It is the removal of dental plaque on a regular basis and prevention of its accumulation on teeth and adjacent gingival surfaces. Plaque An organized mass consisting mainly of microorganisms that adheres to teeth, prosthesis and oral surfaces and is found in the gingival crevice and periodontal pockets. —Periodontal Literature Review Plasma Cell A mature B lymphocyte which secretes antibody. Positive Architecture Refers to radicular bone being apical to interdental bone. Predictive Value Refers to the probability of the test results.

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Primary Herpetic Gingivostomatitis It is an infection of the oral cavity caused by the herpes simplex virus type-1. Primary Trauma from Occlusion It is the injury resulting from excessive occlusal forces applied to a tooth or teeth with normal support. —Periodontal Literature Review Primary Trauma from Occlusion It includes a tissue reaction, which is elicited around a tooth with normal height of the periodontium. —Lindhe Primary Trauma from Occlusion When trauma from occlusion is the result of alteration in the occlusal forces; it is called primary trauma from occlusion. —Carranza Probing Depth It is a distance to which an ad hoc instrument (probe) penetrates into pocket. —Carranza Prognosis Prognosis is a prediction of the probable course, duration and outcome of the disease based on a general knowledge of the pathogenesis of the disease and the presence of the risk factors for the disease. —Carranza 477

Proliferation Proliferation of keratinocytes takes place by mitosis in the basal layer and less frequently in the suprabasal layers, where a small proportion of cells remain as a proliferative compartment while a larger number begins to migrate to the surface. Proteoglycan A protein with numerous glycosaminoglycan side chains. A component of connective tissue ground substance. Protrusion Movement of the mandible anteriorly from intercuspal position (ICP). GLOSSARY Provisional Prognosis It allows the clinician to initiate treatment of teeth that have a doubtful outlook in the hope that a favorable response may tip the balance and allow teeth to be retained. Psychosomatic Disorders Harmful effects that result from psychic influences on the organic control of the tissues. —Carranza Puberty Gingivitis A higher prevalence and severity of gingivitis and gingival enlargement is found in the circumpubertal period. —Carranza Puetz-Jegher’s Syndrome Produces intestinal polyposis, melanin pigmentation in the oral mucosa & lips. —Carranza Pyogenic Granuloma It is a tumor like gingival enlargement that is considered an exaggerated conditioned response to minor trauma. —Carranza Pyorrhea An archaic term for several periodontal diseases. Radicular Cementum Cementum that covers the root. Radius of Action Range of effectiveness of about 1.5-2.5 mm within which bacterial plaque can induce loss of bone. —Page and Schroeder Reattachment It is used to refer the repair in areas of the root not previously exposed to the pocket, such as after surgical detachment of the tissue or the following traumatic tear in the cementum, tooth fracture or treatment of periapical lesions. —Carranza Reattachment To attach again. The reunion of epithelial and connective tissue with root surfaces and bone such as occurs after an incision or injury. —Periodontal Literature Review Recession Refers to the location of gingiva, not its condition. Recurrent Gingivitis Reappears after having been eliminated by treatment or disappearing spontaneously. —Carranza Redox Potential A measure of the ease with which oxidation and reduction reactions will occur. Refractory Periodontitis According to American Academy of Periodontology, it has been defined as; those cases which do not respond to any treatment provided whatever the thoroughness or frequency. Refractory Periodontitis It includes patients who are unresponsive to any treatment provided whatever the thoroughness or frequency, as well as patients with recurrent disease at single or multiple sites. —Periodontal Literature Review Regeneration It is the growth and differentiation of new cells and intercellular substances to form new tissue and parts. —Carranza Regeneration Reproduction or reconstitution of a lost or injured part. Repair Healing of a wound by tissue that does not fully restore the architecture or function of the part. —Periodontal Literature Review Repair It simply restores the continuity of the diseased tissue. —Carranza Repair Simply restores the continuity of the diseased marginal gingiva and re-establishes a normal gingival sulcus at the same level on the root as the base of the pre-existing periodontal pocket. Healing by scar formation. —Carranza Reverse Architecture Reversed architecture defects are produced by loss of interdental bone, including the facial plates, lingual plates or both, without concomitant loss of the radicular bone, thereby reversing the normal architecture. Retrograde Periodontitis Periodontitis caused by pulpal infection that have entered the periodontal ligament either through the apical foramen or through the lateral canals. 478

Retrusion Movement of the mandible posteriorly from ICP. Risk Factor Is defined as an aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or inherited characteristic, that, on the basis of epidemiologic evidence, is known to be associated with health conditions considered important to prevent. —The Dictionary of Epidemiology Risk Factor May be environmental, behavioral or biologic factor that when present increases the likelihood that an individual will get the disease. —Carranza Risk Indicator A probable or putative risk factor that has been associated with the disease through cross- sectional studies. Risk Marker A factor that is associated with increased probability of future disease. Risk It is the probability that an individual will get a specific disease in a given period. GLOSSARY Root Amputation The removal of a root from mutirooted teeth. Root Planing Stroke It is a moderate to light pull stroke that is used for final smoothening and planing of the root surface. Root Planing It is the process by which residual embedded calculus and portion of cementum are removed from the roots to produce a smooth, hard and clean surface. —Carranza Root Resection/Hemisection It is the splitting of two rooted tooth into two separate portions. Root Resection It is the surgical removal of all or a portion of root before or after endodontic treatment. Root Resection Surgical removal of all or portion of a tooth root. Root Separation/Bicuspidisation It is the sectioning of the root complex and maintenance of all roots. Saccharolytic Bacteria which break down carbohydrates for energy are saccharolytic. Saliva Defined as the fluid secreted by the salivary glands that begins the digestion of food. —Genco Scaling Stroke It is short, powerful pull stroke that is used with bladed instruments for the removal of supragingival and subgingival calculus. Scaling Scaling is a process by which plaque and calculus are removed from both supragingival and subgingival tooth surface. Secondary Trauma from Occlusion Injury resulting from normal occlusal forces applied to tooth or teeth with inadequate support. —Periodontal Literature Review Secondary Trauma from Occlusion Tissue reaction elicited around a tooth by occlusal forces, with reduced height of periodontium. —Lindhe Secondary Trauma from Occlusion When the trauma results from reduced ability of the tissues to resist the occlusal forces, it is known as secondary trauma from occlusion. —Carranza Segregation Analyses Classic twin study—reared together monozygotic and dizygotic twins are compared to estimate the effects of shared genes. —Carranza Segregation Analyses The observed pattern of disease in families is compared with patterns expected under various models of inheritance. —Carranza

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Sensitivity Refers to ability of a test or observation to detect the disease whenever it is present. Serumal Calculus Calculus formed apical to gingival margin, often brown or black, hard and tenacious. —Periodontal Literature Review Severe Periodontitis Periodontal destruction is considered severe when 5 mm or more of clinical attachment loss has occurred. Sickle Scaler Sickle scalers have a flat surface and two cutting edges that converge in a sharply pointed tip. Slight (mild) Periodontitis Periodontal destruction generally considered slight when no more than 1 to 2 mm of clinical attachment loss has occurred. Slough Necrotic tissue in the process of separating from the viable portion of the body. 479

Specific Immune Response The ability of T-cells and B-cells to recognize specific oligomeric structures on a pathogen and generate progeny that also recognize the structure, enables the immune system to respond more rapidly and effectively when exposed to that pathogenic agent. Specificity Recognition of the structural features of an oligomer by receptors on immune cells. —Carranza Specificity Refers to the ability of a test or observation to clearly differentiate one disease from another. GLOSSARY Splint Any apparatus, appliance, or device employed to prevent motion or displacement of fractured or movable parts. Splint It is an appliance used for immobilization of injured or diseased parts. Stillman’s Clefts They are apostrophe shaped indentations extending from and into the gingival margin for varying distances on the facial surface. Stippling Stippling is a form of adaptive specialization or reinforcement to function. —Carranza Subgingival Calculus It is located below the crest of the marginal gingiva and not visible in routine clinical (Serumal Calculus) examination. —Carranza Subgingival Curettage Refers to the procedure that is performed apical to the epithelial attachment severing the connective tissue attachment down to the osseous crest. —Carranza Subgingival Plaque Can be defined as the community of microorganisms that develops on tooth surfaces that are apical to the gingival margin. —Lindhe Subgingival Plaque Subgingival plaque is found below the gingival margin, between the tooth and gingival sulcular tissue. —Carranza Subacute Less severe phase of acute condition. Subclinical Gingivitis The initial response of the gingiva to bacterial plaque is not apparent. —Carranza Subtraction Radiography It is a technique that facilitates both qualitative and quantitative visualization of even minor density changes in bone by removing the unchanged anatomic structures from the image. Subtractive Osseous Surgery Designed to restore the form of the pre-existing alveolar bone to the level existing at the time of surgery or slightly more apical to this level. Sulcular Epithelium The Sulcular epithelium lines the gingival sulcus, it is a thin, non-keratinized squamous epithelium without rete pegs and extends from the coronal limit of the junctional epithelium to the crest of the gingival margin. —Carranza Sulcular Epithelium The soft tissue wall of the gingival sulcus is lined coronally with sulcular epithelium, extending from the gingival margin to the junctional epithelium. Suprabony Pocket In which the bottom of the pocket is coronal to the underlying alveolar bone. Supragingival Calculus Calculus formed coronal to the gingival margin, usually formed more recently than subgingival calculus. —Periodontal Literature Review Supragingival Calculus Supragingival calculus is located coronal to the gingival margin and therefore visible in the oral cavity. It is usually white or yellowish in color, hard with clay like consistency and easily detachable from the tooth surface. —Carranza Supragingival Plaque Supragingival plaque is defined as the community of the microorganisms that develop on the tooth surfaces coronal to the gingival margin. —Lindhe Supragingival Plaque Supragingival plaque is formed at or above the gingival margin. Surgery It is the art practice or work of treating diseases, injuries or deformities by manual operation or instrumental application. Susceptibility Genes Genes involved in complex multifactorial diseases referred to as susceptibility genes. —Carranza Synergy An interaction which is cooperative. 480

Tetralogy of Fallot It is characterized by pulmonary stenosis, right ventricular enlargement, a defect in interventricular septum and the malposition of the aorta to the right. The oral changes include a purple red discoloration of the lip and gingiva and periodontal destruction. —Carranza Thrombocytopenic Purpura It is defined as a platelet count < 100000/mm3. Tissue Inhibitor of Metalloproteinases An enzyme inhibitor secreted by fibroblasts to control the activity of metalloproteinases (TIMP) in the turn over of connective tissue ground substance. Tooth Mobility The degree of looseness of a tooth beyond physiological movements. —Periodontal Literature Review Trauma from Occlusion A tooth subjected to excessive occlusal forces but otherwise exhibits health with intact periodontal support; no loss of gingival connective tissue attachment and no apical migration GLOSSARY of junctional or sulcular epithelium is described as ‘trauma from occlusion’. —Genco Trauma from Occlusion It is defined as “a condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position”. —Stillman (1917) Trauma from Occlusion It is defined as “damage in the periodontium caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaws”. Trauma from Occlusion It is defined as, “a condition occurring on a tooth having a major loss of support, which is displaced in the remaining alveolus by a force applied to it, even the force of the tongue, cheek or chewing soft food”. —Genco Trauma from Occlusion It is the term used to describe pathologic alteration or adaptive changes which develop in periodontium as a result of undue force produced by masticatory muscles. —Lindhe Trauma from Occlusion When occlusal forces exceed the adaptive capacity of the tissue, tissue injury results. The resultant injury is termed as “Trauma from Occlusion”. —Carranza Trauma Refers to the precise pathologic changes occurring in the tissues. Traumatic Occlusion An occlusion which produces such injury is called traumatic occlusion. —Carranza Treatment Plan It is the blueprint for case management. It includes all procedures required for the establishment and maintenance of oral health. —Carranza Tunnel Preparation A surgical procedure performed on a multirooted teeth, usually a mandibular molar, resulting in a completely opened furcation to provide access for hygiene. Ultrasonic Scaler An instrument vibrating in the ultrasonic range which, accompanied by the stream of water, can be used to remove adherent deposits from teeth. Universal Curette One curette designed for all area and surfaces. Vitalometer A device that measures the response of a tooth to an electric stimulus to aid in determining pulp vitality. Vertical or Angular Defects They occur in an oblique direction, leaving a hollowed-out trough in the bone alongside

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials the root. Vertical/Angular Defects Vertical/Angular defects are those that occur in an oblique direction, leaving out a hollowed- out trough in the bone alongside the root; the base of the defect is located apical to the surrounding bone. Vincent’s Angina It is a fusospirochetal infection of the oropharynx and throat. —Carranza Wasting Diseases of the Teeth Wasting is defined as any gradual loss of tooth substance characterized by the formation of smooth polished surfaces without regard to the possible mechanism of this loss. —Carranza Wegener’s Granulomatous It is a rare disease characterized by acute granulomatous necrotizing lesions of the respiratory tracts, including nasal and oral defects. —Carranza Xenograft or Heterograft The donor of the graft is from different species from the host. Index

A Adaptive remodeling of periodontium 96 Ancient era 399 Angular defects 216 Abscesses of periodontium 40, 64 Adult periodontitis 36, 64 Angulation 285 Absolute Advanced Ankylosis 27 contraindications for implant intraoral finger rests 284 Antibiotic therapy 228 treatment 402 radiographic techniques 259 Antibiotics used in periodontal therapy requirements for treating implant Advances in root planning instruments 424 patients 401 459 Antibody deficiency disorders 109 Absorbing paper strips 140 Advantages of Anti-inflammatory actions of Acatalasia 106 noneugenol packs 313 tetracyclines 425 Accordion technique 356 periodontal packs/dressings 304 Antimicrobial agents 424 Acellular sharpness 282 afibrillar cementum 24 systemic medication 425 Antiserum 262 extrinsic fiber cementum 25 ultrasonic and sonic instruments 289 Aphthous Acquired Adverse effects of tetracyclines 426 stomatitis 181 deformities 40 Aerosol production 289 ulceration 175 immunodeficiency syndrome 109, Age changes in periodontium 29, 31 Apically-displaced flap 336, 356 239, 255 Aggregatibacter actinomycetemcomitans Aplastic anemia 105 neutropenia 40 131 Arteriosclerosis 109 Actinobacillus actinomycetemcomitans Aggressive periodontitis 38, 225 Artificial crowns 73 64, 131, 190, 254 Agranulocytosis 178 Asynchronous multiple burst Actinomyces 63 Aids-associated ulcerative periodontitis model 222 viscosus 61 232 Atrophic lichen planus 197 Actions of flurbiprofen 427 Air powder polishing 277 Attached gingiva 9, 45 Acute Alexidine 298 Attachment to tooth surface 72 and subacute leukemia 192 Allografts 346, 348 Atypical ulcers 238 bleeding 153 Alloplastic graft 346 Auditory test for trauma from occlusion gingival infections 175 Alveolar 450 gingivitis 186, 441 bone 21, 26, 186 Auscultation for TMJ sounds 412 herpetic gingivostomatitis 179, 186 gingival fibers 14 Autograft 346 inflammatory enlargement 160 Alveolocrestal group 18 Autoimmune diseases 138 necrotizing ulcerative gingivitis 64, Amelogenin 5 Azurophilic granules 86 86, 187 Anaerobic chamber techniques 261 pericoronitis 182 Anaphylactic reactions 89 B phases of leukemia 170 Anatomic considerations in children 185 trauma from occlusion 95 Anatomy of gingival crevice or sulcus B. forsythus 128 ulceromembranous gingivitis 176 138 Bacillary angiomatosis 238 482

Bacterial in periodontal disease 219 CDC surveillance care classification 238 adherence 60 patterns in periodontal disease Cell-mediated 90 attachment via 216 response in periodontal diseases 88 electrostatic interaction 60 from extraoral sites 348 Cells of basal layer 11 hydrophobic interactions 60 implant interface 400 Cellular balance 137 loss 213 components 22 colonization 90 marrow 27 composition 16 infections 175 morphogenetic proteins 350 elements 141 invasion 90 resorption 425 intrinsic fiber cementum 25

INDEX plaque and immune response 30 swaging 348 mixed stratified cementum 25 zone 178 Booster mechanism 72 Cemental resorption and repair 25 Bacteriocin 190 Borodontic probe 264 Cementicles 19, 27 Bacteroides Bristle brushes 277 Cementoblasts 16, 17 capillus 64 Brown stain 80 Cementoenamel junction 25, 27 forsythus 64, 131, 254 Brushing techniques 293 Cementoid 5 Basal layer 10 Bruxism 78, 435 Cementum 24, 27, 186 Basic approaches for plaque control 291 Bulbous bony contours 217 Cervical enamel projections 249 Bass method 436 Bullous Cetylpyridinium chloride 298 B-cells 87 lichen planus 198 Changes in Beneficial aspects 395 pemphigoid 197 alveolar bone and cementum 30 Benign Bundle bone 21 connective tissue 444 familial neutropenia 103 consistency of gingiva 153 tumors 159 C epithelium 444 of gingiva 171 forces exerted on teeth 99 Benzalkonium chloride 298 Calcium gingiva 185 Bioactive compounds 312 gingival contour 158 and biodegradable ceramics 400 phosphate ceramics 400 plaque microflora 107 glass 349 Calculus 70, 79, 81 position of gingiva 156 integration 400 component of root surface wall 208 Biofilms 57 periodontal disease 51 size of gingiva 155 Biological considerations of implants simplified oral hygiene 51 soft tissue wall 207 399 index-simplified 49 Characteristics of Biology of periodontal tissues 8 surface index 52 ideal splint 397 Biomaterials used for implants metals Campylobacter rectus 64, 21 index 44 and alloys 400 Cancellous bone 21 scaler 455 Bisbiguanides 298, 299 Candidiasis 186, 188 synthetic cell 16 Bismuth intoxication 109 Canker sores 181 Charter’s

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Bispyridines 298 Capillary circulation stage 356 method 294 Black stain 80 Capnocytophaga 61, 4, 90, 21 technique 436 Bleeding points index 46 Cardiovascular diseases 109 Chédiak-Higashi syndrome 40, 86, 105, Blood Case history proforma 242 186, 192, 233 supply 15 Causes for Chemical supply to bone 24 early implant failures 406 irritation 78 vessels 19 late implant failures 406 plaque control 297, 435 B-lymphocytes 87 pathologic halitosis 112 Chemiluminescence 113 Bone 29 physiologic halitosis 112 Chemotactic inhibition factors 190 blend 348 recurrence of periodontal disease 408 Chemotaxis 84 destruction 214, 215 Causes of periodontal abscess 212 cellular activation 83 483

Chemotherapeutic agents 424 Clenching 78 Continuous paradigm 222 Chewing gum additives 38 Clindamycin 427 Contour of restorations 73 Chin-cup technique 284 Clinical Conventional Chisel scalers 276 evaluation of occlusion 412 flaps 327 Chlorhexidine 298, 299 features of procedures 361 stains 80 bruxism 78 Copper 298

Chronic gingivitis 151 Coral-derived materials 349 INDEX benign neutropenia of childhood 103 Closure of flap 402 Corncob formations 61 bleeding 153 Clot stabilization 345 Coronally-repositioned flap 363 candidiasis 189 Cohen syndrome 40 Cotton test 434 gingivitis 63, 441 Cohort study 43 Crevicular incision 328 granulomatous disease 105 Collagen fibers 16 Cribriform plate 21 idiopathic neutropenia 103 Collagenase 190, 263 Cross inflammatory enlargement 161 inhibition 425 sectional studies 43 leukemia 171 Colloidal proteins 72 syndrome 174 marginal gingivitis 186, 189 Color changes in gingiva 153 Crown contour 420 periodontitis 38, 220 Combination techniques 356 Crystal forms 71 toothbrush trauma 78 Combined Curettage instruments 272 trauma from occlusion 95 enlargement 165 Current classification systems of ulcerative stomatitis 195 osseous defect 217 periodontal disease 35 Cicatricial pemphigoid 197, 198 Community Curvature of filament 300 Cigarette smoking 434 acquired bacterial pneumonia 126 Cyclic neutropenia 86, 103 Ciprofloxacin 427 periodontal index of treatment 53 Cyclosporine 164 Circular fibers 14 Complete Cystein 112 Citric acid 345 blood count 451 Cytokines 118 Classic technique 352 periodontal examination 112 Cytolysis 83 Classical pathway 83 Complications during surgery 311 Cytotoxic reactions 89 Classification of Composition of antimicrobial agents 298 alveolar bone 22 D controlled-release local deliver 428 dental plaque 59 furcation involvement 448 desmosome 11 Debilitating diseases 178, 188 gingival gingival crevicular fluid 141 Debris index-simplified 49 diseases in childhood 192 toothpaste 295 Deep bite 76 recession 156 Compromise osseous reshaping 341 Deeper reticular layer 14 halitosis 111 Computer assisted densitometric Defence mechanisms of gingiva 137 implant systems 401 image analysis 260 Definition of plaque control 291 periodontal Computerized tomography 260 Degree of disease 36, 236 Condition of instruments 282 bone loss 248 instruments 272 Conditioned enlargement 167 gingival enlargement 160 splints 396 Congenital heart disease 109 Delayed stains 79 Connective tissue 153 healing 238 various associated plaque 59 hypersensitivity 90 acute gingival lesions 175 cells 16 Dental drugs used in periodontal 423 technique 356 endoscope 277 Classification systems of periodontal Consistency of diet 101 floss 296, 437 diseases 35 Contact inhibition 346 implants 398 Cleansing and polishing instruments 272, Containing genetic material 180 materials 74 277 Contemporary era 399 mirror 281 484

plaque 57 Drugs Endogenous 79 induced gingival disease 37, 251 allergy and contact hypersensitivity infections 64 restorative materials 38 175 sources 80 splinting 395 in gingival fluid 144 Endotoxin 117, 190 tape 277 induced agranulocytosis 86 Enlargement in Dentogingival fibers 14 used in periodontal therapy 423 pregnancy 167 Dentoperiosteal fibers 14 puberty 168 Dermatitis herpetiformis 198 E Enriched media 261 Dermatoses 194 Entire lingual gingival margin 45

INDEX Design of flap 327 Early development of cementum 4 Envelope technique 368 Desquamative gingivitis 178, 194 Edentulous areas 348 Enzyme Determination of Effect of and enzyme inhibitors 144 maintenance recall intervals 410 aging on progression of periodontal linked immunosorbent assay 262 pocket depth 209 30 reduction technique 261 prognosis 246 hematological disorders on Epidemiology 42, 43 Development and acquired anomalies of periodontium 103 of gingival and periodontal diseases cementum 27 insufficient occlusal force 97 42 Development of orthodontic Epidermal and perioral type 189 dental plaque 59 bands on periodontium 417 Epithelial junctional epithelium 6 on dentition 417 attachment 12 periodontium 4 periodontal infection 123 cell rests of malassez 16, 17 Diabetes mellitus 86, 106 periodontitis on dental pulp 391 Epithelium 153 associated gingivitis 38 pulpal disease on periodontium 390 associated subgingival plaque 59 Diagnosis of smoking cessation 129 connective tissue interface 13 furcation defects 389 treatment on aging individuals 30 Epstein-Barr virus 180 halitosis 112 Ehler-Danlos syndrome 40, 186, 191 Era of focal infection 121 osseous defects 219 Eikenella Erosive lesions 196 periodontal diseases 240 corrodens 64, 221 Erythema multiforme 38, 175, 181, 198 Diagnostic criteria for chronic nodatum 128 Erythromycin 298 periodontitis 220 Elastin fibers 15, 16 Etiotropic phase 266 Diameter of bristles 300 Electrocoagulation 323 Eubacterium brachy 64 Different Electrodesiccation 323 Eucalyptol 298 culture techniques 261 Electrofulguration 323 European workshop in periodontology phases of healing 404 Electrolytes 141 36 types of T-cells 87 Electrosection 323 Evaluation of Direct immunofluorescence 262 Eliminate amount of fluid collected 140 Discoid lupus erythematosus 197 gingival new attachment and bone

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Disorders of WBC function 105 bleeding 268 regeneration 343 Disposable probe 264 inflammation 268 scaling and root planning 287 Distal infection 268 Evasion of host responses 117 facial papillae 45 pain 268 Excellent prognosis 246 molar surgery 336 Enamel Excessive production of matrix Domiphen bromide 298 cuticle 6 metalloproteinases Double papilla flap 363 matrix proteins 346, 350 132 Down’s syndrome 40, 86, 191, 186, 233, pearls 27 Exogenous 234 projections 27 infection 65 Doxycycline 426 Enameloids 5 sources 80 485

Experimental epidemiology 43 Fones technique 294 Gingival Extent and severity index 44, 48 Food impaction 75 abscess 40, 175 Extracellular Foreign body reactions 38 bleeding components 17 Formalin 312 index 46 matrix 15 Formation of calculus 72 on probing 152 Extraction of impacted third molars 76 Formative and remodeling function 20 bone count index 48

Extraoral hip marrow 348 Foundation era 399 changes associated with menstrual INDEX Extrinsic stains 79, 80 Fourth generation probes 264 cycle 108 Free crevicular fluid 83 F gingiva 9 curettage 314 gingival depigmentation 375 Facial margin 45 autograft 367 disease 37, 38, 251 Facially-displaced teeth 76 groove 7 enlargement 159 Facilitating prosthetic replacements 416 soft tissue autograft 352 epithelium 83 Factitious gingivitis 186, 189 Fremitus test 450 fibromatosis 174 Factors determining Frenectomy 373 fluid bone morphology in periodontal 216 Frenotomy 373 flow and sex hormones 144 choice of dental floss 296 Functions of in diabetic patients 144 selection of interdental 300 immunoglobulins 92 index 45 Factors for determination of prognosis macrophages in gingiva 86 inflammation 147 247 neutrophils 84 lesions 186 Fair prognosis 246 periodontal ligament 20 manifestations of systemic conditions False enlargement 173 Fungal diseases 175 38 Fanconi’s anemia 106 Furcation massage 297 Faulty restorations 73 anatomy 389 periodontal index 52 Feeling of weakness 311 fornix 389 recession 158 Females involvements 218 status 243 during pregnancy 144 Fusobacterium nucleatum 61, 63, 64, sulcus 9 on birth control pills 144 128 tissues 191 Fenestration operation 358 tumor 159, 171 Fibers of secondary group 15 G washings 141 Fibroblast 14, 16, 17 Gingivectomy 318, 324 growth factor 350 Gas chromatography 112 Gingivitis 35, 36, 38, 47, 148 Fibro-osseous integration 400 Gastrointestinal Gingivitis artefacta 189 Fifth generation probes 264 disturbances 426 component of periodontal disease 45 Filter separation enzyme immunoassay tract 112 in puberty 108 263 Gauze strip 438 Glandular fever 175 Finger rest 283, 457 General Glickman’s Flap health and gingival fluid 144 concept 97 design and incisons 402 principles of surgery 302 index 50 techniques for pocket therapy 329 Generalized Glutathionine 112 Flat architecture 341 aggressive periodontitis 228 Glycogen storage disease 40 Flattening of interproximal bone 342 juvenile periodontitis 64 Gonads 107 Flezar’s index 54 periodontitis 221 Gonococcal stomatitis 178 Flow cytometry 263 prepubertal periodontitis 190 Gracey curettes 275, 276 Fluorides 298 Genetic disorders 40 Gradualizing marginal bone 342 Flushing action 288 Genuine halitosis 111 Graft 346 Focal infection 122 Gingiva 8, 26, 27, 29 Gram-negative organisms 63 486

Gram’s staining 261 gingivitis 109 Important cytokines 119 Granular layer 10 necrotizing gingivitis 236 Inadvertent curettage 314 Granuloma pyogenicum 159 opportunistic infections 236 Indications for implant therapy 401 Granulomatous diseases 159, 171 periodontitis 109 Indications of Green stain 80 Hoe scalers 276 flap surgery 325 Ground substance 17, 18 Home irrigation devices 429 periodontal surgery 302 Guided tissue regeneration 344, 346 Homograft 346 Indices of gingival bleeding 45 Horizontal Indices used to H bone loss 216 assess gingival inflammation 44, 45

INDEX incisions 327 Haemophilus influenzae 126 Hospital treatment needs 44 Halimeters 113 acquired 126 measure Halitophobia 112 bacterial pneumonia 126 calculus 44, 51 Head rest 281 periodontal surgery 312 periodontal destruction 44, 46 Healing after Host plaque accumulation 44, 48 flap surgery 337 modulating therapy 132 Indirect immunofluorescence 262 full thickness flap 339 modulation in periodontal therapy Individual tooth prognosis 250 periodontal therapy 269 131 Inert ceramics 400 scaling and curettage 316 modulators 134 Infantile genetic agranulocytosis 40 surgery 343 response 82 Inflammatory cells 14 Healing Human Inflammatory of graft 356 cytomegalovirus 64 enlargement 160 sockets 348 herpes virus 8 180 mediators 119 Helper inducer T-cells 87 Humoral response to plaque 87 reaction 138 Hemorrhage 311 Hunton probe 264 Influence of Herbal Hydrogen peroxide 298 host responses on periodontal disease extracts 298 Hyperplasia 440 90 toothpastes. 300 Hyperplastic type 189 mechanical stimuli 144 Herpangina 175 Hypersensitivity Infrequent dental visits 255 Herpes reactions 426 Inhibition theory 73 labialis 187 to dental materials 420 Inorganic components 71 simplex virus 180 Hypertrophy 440 Instructions for patient after surgery 307 varicella 175 Hypophosphatasia 40, 186, 233, 234 Instrument virus 64, 180 grasp 282 Herpetic gingivostomatitis 186 I stabilization 282 Herpetiform aphthae 182 Insulin like growth factor 350 Hertwig’s root 5 Iatrogenic factors 73 Intercircular fibers 15

Heterograft 346 Ideal requirements of bone graft material Interdental Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Hexetidine 298 346 bleeding index 46 Hill’s criteria 256 Idiopathic gingival fibromatosis 165 brushes 297, 437 Histiocytosis syndrome 40 Iliac autografts 348 cleaning aids 296 Histopathology of gingivitis in children Immune complex 89 gingiva 3, 9 186 Immunological mechanisms 88 papilla reconstruction 376 Histoplasmosis 38 Immunosuppressive factors 190 Intergingival fibers 15 HIV 255 Implant Intermediate cementum 5, 25 associated failure 406 Internal bevel incision 327 gingivitis 236 surgery 398 Interpapillary fibers 15 periodontitis 236 Importance of maintenance phase 408 Inter-radicular fibers 18 487

Intraoral Leukocyte adhesion deficiency 40, 186, Matrix metalloproteinases 119, 120 autograft 347 192, 233, 234 Maxillary cancellous bone marrow chips 348 Leukotoxin 190 stabilization appliance 78 evaluation of occlusion 413 Lichen planus 38, 196 tuberosity 348 examination 112 Light microscopy 261 Maximal intercuspal opening 412 signs 187 Linear Measles 175

and symptoms 176 gingival erythema 38 Measurement of INDEX Intrinsic stains 79, 80 gingivitis 237 disease 42 Iodine 298 IGA disease 197 oral malodor 112 Irregular alignment of teeth 76 Lipooligosaccharide 117 Mechanical plaque control 291, 435 Ischemic heart diseases 123 Lipoteichoic acid 60 Mechanism of Local action of J drug delivery systems 427 chlorhexidine gluconate 300 effects of nicotine 130 NSAID 427 Jar technique 261 predisposing factors 177 anaphylactic hypersensitivity 89 Junctional epithelium 6, 10, 12 Localized bone formation 214 Juvenile periodontitis 90, 190, 230 aggressive periodontitis 225 and bone destruction 214 gingival recession 186, 189 Medieval era 399 K juvenile periodontitis 64, 86 Menopausal gingivostomatitis 108 periodontitis 221 Menstrual cycle-associated gingivitis 38 Kanamycin 298 Location on tooth 396 Menthol 298 Kaposi’s sarcoma 180, 238 Loss of proximal contact 75 Mercury intoxication 110 Keratinized Lupus erythematosus 38 Mesial facial papillae 45 cell layer 10 Lymphatic vessels 19 Metabolic and epithelium 10 Lysozyme 83 bacterial products 144 Keratotic lesions 196 endocrine disorders 106 Keyes technique 429 M Metallic Knots and knot typing 303 pigmentation 158 Knuckle-rest technique 284 Macrophages 14, 17 salts 298 Magnitude 94 stains 80 Maintaining clean field 282 L Methods of delivery of chemotherapeutic Major aphthae 182 agents 429 Lactoferrin 83 Malignant Metronidazole 298, 426 Lamina dura 21 neoplasias 192 Microbial Laminar airflow system 289 tumors 159 monitoring 405 Langer and mini Langer curettes 276 of gingiva 171 shifts from health to disease 65 Langer’s technique 368 Management of specificity of periodontal diseases 62 Laser gingivectomy 323 particular type of recall patients 410 Microbiology and disease progression Later development of cementum 5 trauma from occlusion 413 260 Lateral Marginal Microbiology of food impaction 75 enlargement 167 LJP 190 pressure 285 gingiva 9, 45 periodontal diseases in children 186 Laterally displaced flap 361 line calculus index 52 Microtopography of gingival wall of Latex agglutination 262 Margins of restorations 419 pocket 208 Lazy leukocyte syndrome 105 Marquis color-coded probe 273 Mild gingivitis 47 Lead intoxication 110 Mast cells 14 Miller’s index 50 Length of bristles 300 and macrophages 16 Mini-bladed curettes 276 Leukemia 104, 159 Masticatory mucosa 3 Minocycline 426 488

Minor aphthae 182 Nifedipine 164 Opportunistic infection 65 Mirror test 434 Non-ambulatory patient 178 Opsonization 83 Miscellaneous habits 77 Non-bone graft material 348 Oral Moderate periodontitis 222 Nondisplaced flap 326 hairy leukoplakia 238 Modern era 399 Non-eugenol packs 307 hygiene methods 242 Modified Nongraft-associated new attachment 344 hyperpigmentation 238 bass method 293, 436 Noninflammatory gingival enlargement implantology 398 navy plaque index 44, 50 162 irrigation devices 297 Modified Stillman’s Nonkeratinized epithelium 10 malodor 111

INDEX method 436 Non-oxidative mechanisms 86 prophylaxis 145 technique 293 Non-physiologic occlusion 412 sulcular epithelium 12 Modified Widman flap 331 Nonplaque-induced gingival lesion 38, symptoms 176, 180 Mononuclear cells 215 251 ulceration 170 Mouthbreathing 77, 434 Nonselective media 261 Orange stain 80 Mucogingival Nonspecific Organic line 3 conditioned enlargement 159, 169 components 72 problems 351 protective mechanisms 137 compounds 144 surgery 351 Non-steroidal anti-inflammatory drugs Orofacial granulomatosis 195 Mucoperiosteal flap 326 427 Orthodontic tooth movement 21 Mucosal Nonsurgical instruments 455 Orthopantamograph 259 flap 326 Normal Osseointegration 399, 400 type 373 anatomy of alveolar bone 213 Osseous Murray-Puretic-Drescher syndrome 174 color of gingiva 438 coagulum 347 variation in alveolar bone 216 craters 217 N Nuclear medicine bone scan 260 surgery 340 Number of filaments in tuft 300 topography 22 Nature of disease progression 222 Nutritional Ostectomy 340 Necrotic zone 178 and sensory function 20 Osteoclasts 16, 17, 22, 215 Necrotizing deficiency 177, 188 Osteoconduction 346 periodontal disease 40, 252 Nyman’s index 54 Osteocytes 22 stomatitis 236, 238 Osteoinduction 346 ulcerative O Osteoplasty 340, 349 gingivitis 40, 176, 186, 237 Osteoporosis 255 periodontitis 40, 109, 176, 231, Objectives of Outer epithelium 10, 11 237 maintenance phase 409 Ovate pontic 421 Neisseria gonorrhoeae 38 periodontal therapy 268 Overall Neoplastic enlargement 159, 171 splinting 395 clinical factors 247 Nerve Oblique group 18 Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials prognosis 250 innervation 19 Occlusal Overgrowth of resistant organisms 426 supply 19 disharmony 76 Oxidative mechanism 85 Neurosis 76 evaluation and therapy in Oxygenating agents 298 Neutral seated position for clinician 280 management 412 Oxytalan fibers 15, 16 Neutropenia 103, 186, 233, 234 forces on pulp 97 Neutrophil 84 neurosis 78 P chemotaxis 84 therapy 413, 414 rich zone 178 Occupational habits 77 P. gingivalis 128, 132 New attachment techniques 211 Octenidine 298 P. intermedia 128 Newer generation probes 264 Open bite 76 Palatal flap 334 489

Palm and coronary heart disease 122 Phagocytosis 138 down technique 284 and diabetes mellitus 124 Pharmacological agents and bone up technique 284 in children 185 resorption 215 Palpation for in Down’s syndrome 191 Phenolic compounds 298 muscle tenderness 412 index 44, 45, 47 Phenols 424 TMJ tenderness 412 dressing 304 Phenytoin-induced gingival hyperplasia

Papilla preservation flaps 327, 328 endoscope 272 162 INDEX Papillary bleeding examination 245 Phosphatase 72 index 46 features of scurvy 102 Photodensitometric analysis 260 on probing 51 fibers 17 Physiologic adaptive capacity of Papillary flap 325 periodontium 94 gingiva 45 infection and stroke 124 Piggy-backed fulcrum 284 marginal attachment index 45 instruments 272 Pituitary gland 107 penetrating types 373 lesions 186 Placement of Papillon-Lefévre syndrome 40, 86, 186, ligament 16, 26, 27, 186 flap after surgery 326 implant 402 191, 233 manifestations 103-105 Plaque 57, 61 Parafunctional habits 78 medicine 121 component of periodontal disease Parathyroid glands 107 in clinical practice 126 index 48 Partial thickness 326 microbiology 57 control 248, 291, 435 Parts of pocket 203, 208 measures 291 alveolar bone 21 probes 257 record 51 maintenance phase 409 restorative inter-relationship 419 free score 51 surgical needles 303 scores 47 index 44, 50 Pathogenesis of screening and recording 258 induced gingival diseases 251 LJP 190 splint 395 lite system 300 periodontal diseases 116 structures in aging humans 29 weight 44, 51 Pathologic tooth migration 98 surgery 302 Plasma cell gingivitis 159, 168, 195 Patient hygiene performance index 50 therapy 3 Plastic instruments for implants 276 Patterns of bone destruction 213 and gingival fluid 145 Platelet Pemphigoid 38 vaccines 65 derived growth factor 350 Pemphigus vulgaris 38, 197, 198 Periodontia 3 rich plasma 350 Penicillins 298, 427 Periodontics 3 PMNL’s function 106 Peptostreptococcus micros 63, 64, 128 Periodontitis 35, 36 Pocket contents 208 Pericoronal abscess 40 associated with Polymerase chain reaction 263, 264 Pericoronitis 182 endodontic lesions 40 Polymers 400 Peri-implant syndromes 191 Pontic design 421 complications 404 systemic disease 186 Porphyromonas gingivalis 30, 61, 64, mucositis 404 severity index 48 131, 221, 254 Peri-implantitis 405 Periodontium 110 Positive architecture 341 Periodontal Periods of destruction 215 Possible requirements for occlusal abscess 40 Periosteal stability 413 considerations 398 elevators 278 Postoperative pain 311 cyst 209 separation 358 Potassium oxalate 312 diagnosis 240 Periosteogingival fibers 15 Pouch and tunnel technique 368 disease 3, 63, 102, 106, 255 Permeability of sulcular and junctional Povidone iodine 298 activity 209 epithelium 139 Powered toothbrushes 295 and acute respiratory infection Peroxidase 82 Preferred sequence of periodontal therapy 126 Persistent bleeding after surgery 311 267 490

Preparation of root surface 345 Q Risk indicators for periodontal disease Prepubertal periodontitis 86, 189 255 Pressure Quaternary ammonium compound 298, Role of 424 from tongue 99 bacteria 177 Quétin furcation curettes 277 probe 264 bacterial invasion 116 sensitive probe 264 biologic mediators 350 Prevention of epithelial migration 344 R cell constituents 117 Prevotella chronic gingival inflammation 214 intermedia 61, 63, 64, 221 Radicular blending 342 cytokines 119 nigrescens 128 Radiographic approaches to measure

INDEX enzymes 117 Prichard’s index 54 bone loss 44, 48 exotoxins 117 Primary Radius of action 215 MMPS in human periodontal diseases epithelial attachment 6 Ramon’s syndrome 174 132 etiologic factor 381 Random burst theory 222 orthodontics 415 gingivostomatitis 179 Rapidly progressive periodontitis 86 periodontitis in pregnancy outcome granules 86 Rate of bone loss 215 124 Principles of Rationale for saliva in host defence 82 intraoral translocation 65 orthodontic treatment 268, 418 Roll periodontal surgery 302 supportive periodontal therapy 408 method 294 scaling and root planing 286 Recent development in dentifrices 300 technique 436 splinting 396 Reconstructive osseous surgery 343 test 445 Pristine gingiva 150 Recrudescent oral HSV infection 180 Root Probe method of calculus assessment 52 Recurrent aphthous stomatitis 181 biomodification 429 Procedures for root coverage 359 Red blood cell disorders 105 complex 389 Procuring graft from donor site 368 Reduced enamel epithelium 4, 6 cone 389 Production of arachidonic acid Reducing plaque retention 415 hypersensitivity 312 metabolites 132 Refractory periodontitis 64, 86, 232 planing 286, 456 Professional subgingival irrigation 429 Regulation of Progenitor cells 16, 17 technique 287 bone metabolism 133 resorption 417 Prognosis for patients with immune and inflammatory responses gingival disease 251 trunk 389 131 periodontitis 251 Rubber cups 277 Removable partial dentures 74 Progression from health to periodontitis Rules for margin placement 419 Removal of junctional and pocket 149 Russell’s periodontal index 44, 46 epithelium 344 Prostaglandins 263 Rutherford’s syndrome 174 Resective osseous surgery 341 Prosthetic/restorative factors 250 Resorptive cells 16, 17 Protein deficiency 102 S Restorative procedures 74 Protrusion 412 Reticulate fibers 18 S. vincentii 128 Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials Proximal contact and embrasure 420 Reticulin fibers 16 Salivary peroxidase system 82 Pseudohalitosis 112 Retrograde Sanguinarine 298 Pseudomembranous type 188 Pseudopockets 445 periodontitis 390 Sanitary pontic 421 Psychosomatic pulpitis 390 Sarcoidosis 171 disorders 110 Reversed architecture 218 Scaling 272, 286 factors 178, 188 Reversibility of traumatic lesion 97 Schiller’s potassium iodide solution 444 Puberty 159 Ridge lap pontic 421 Schwartz periotrievers 276 associated gingivitis 38 Risk factors for Scoring criteria 47 Pulpoperiodontal problems 390 disease 222 Scrub technique 295, 436 Pyogenic granuloma 38 periodontal disease 254 Second generation probes 264 491

Secondary Standard Surface epithelial attachment 6 intraoral finger rest 283 integrity 137 fibers of periodontal ligament 18 periodontal therapy 228 texture 155 Selection of teeth and surfaces 50, 51 Stannous fluoride 312 Surgical Selective media 261 Staphylococcal enterocolitis 426 crown lengthening 376 Semicircular fibers 15 Stenson’s duct 70 gingivectomy 319

Semilunar flap 364 Stevens-Johnson syndrome 181 Suturing techniques 304 INDEX Sensitive roots 312 Stillman’s method 293 Synthetic cells 16 Stomatitis 426 Sequence of therapeutic procedures 266 Systemic Stratum Severe periodontitis 222 administration of antibiotics 424 basale 10 Sharpey’s fibers 5 diseases 109, 159, 248 corneum 10, 12 Sickle factors 153 germinativum 10 cell anemia 106 predisposing factors 177 granulosum 10, 11 scalers 274 spinosum 10, 11 T Significance of Streptococcus T-cells 87 gingival mutans 65 Techniques for bleeding on probing 152 sanguis 61 mandibular molars 337 sulcus and fluid 139 Strip technique 356 maxillary molars 336 vasculature and crevicula 139 Stroke direction 286 removal of frenum 373 pus formation 212 Strontium Significant immune findings in chloride 312 Temporomandibular disorders 412 periodontal disease 90 fluoride 298 Tencate 23 Tension test 445 Silver nitrate 312 Structures present in connective tissue 19 Tensional theory 20 Simplified oral hygiene index 48 Sturge-Weber’s syndrome 174 Terminology 412 Skin 29 Subepithelial connective tissue graft 368 Tertiary granules 86 Slight periodontitis 221 Subgingival Testing for HIV antibodies 239 Slow-release devices 428 calculus 70 Tetracyclines 425, 426 Small conical brushes 297 curettage 314 Theories of calculus formation 72 Smoking and periodontal diseases 128 plaque 58, 62 restorations 249 Therapeutic occlusion 412 Sodium scaling 287 Thickness of fluoride 312 Subjective organoleptic method 112 cementum 25 hypochlorite 298 Sulcular flap 326 Soft tissue implant interface 399 bleeding index 45 Thiol 112 Speciation techniques 262 epithelium 10 Thrombocytopenic purpura 104 Specific fluid 138 Thrombogenesis 123 aspects of disease pathogenesis 131 Sulcus bleeding index 44 Thymol 298 granules 86 Superficial papillary layer 14 Thyroid gland 107 osseous reshaping procedures 349 Supportive Tin 298 plaque hypothesis 62 media 261 Tissue protective mechanism 138 periodontal treatment 408 destruction 90 Spinous layer 10 Suppressor-cytotoxic T-cells 87 engineering in regeneration 350 Spiramycin 298 Supra-alveolar connective tissue 14 T-lymphocytes 87 Spirochetes 61 Supragingival Tobacco stain 80 Splints for calculus 70 Tongue thrusting 77, 434 anterior teeth 396 plaque 58, 61 Tooth mobility 250 posterior teeth 396 control 424 indices 50, 54 Splints in periodontal therapy 395 scaling technique 287 Tooth-associated subgingival plaque 58 492

Toothbrush trauma 78 material 396 Vestibular extension operation 358 Toothpastes for children 300 osseous surgery 341 Vincent’s Toothpicks 438 packs 304 angina 178 Tooth-supporting structures 16, 26 peri-implant diseases 404 infection 176 Traditional treatment procedures 386 periodontal Viral infections 175 Transforming growth factor 350 dressings 313 Viscoelastic theory 20 Transgingival fibers 15 probes 273 Vitamin Trans-septal periodontitis 189 A 103 fibers 14 toothbrushes 300 B-complex 103

INDEX group 18 Tzanck smear 181 C 102 Traumatic lesions of gingiva 175 deficiency 159, 167, 167 Treatment and management of oral U D deficiency 102 malodor 113 E 103 Treatment for Ultrasonic Volatile sulfur compounds 112 ambulatory patients 179 and sonic instruments 277 Volume of gingival fluid 141 non-ambulatory patients 178 curettage 316 Treatment of instruments 287 W aggressive periodontitis 230 Underlying bruxism 78 dental tissues 173 Waerhaug’s concept 98 desquamative gingivitis 199 osseous lesions 173 Wasserman’s index 54 drug-associated gingival enlargement Undisplaced flap 332 Water test 434 164 Unitufted brush 438 Wegener’s granulomatosis 171 gingival abscess 161 Universal curettes 276 White blood cell disorders 103 linear gingival erythema 238 Unreplaced missing teeth 75, 99 Whitening toothpastes 300 necrotizing Use of Wolinella recta 64 stomatitis 239 orthodontics 416 Wooden toothpicks 297 ulcerative periodontitis 235, 238 tobacco 77 World workshop inclinical periodontics periodontal pocket 210 35 pocket depends on type of pocket V Wound protection 345 210 Treatment plan 245, 266 Vaginitis 426 Trench mouth 176 Vancomycin 298 X Treponema pallidum 38 Variant techniques 356 Xenografts 35, 348 Triclosan 298 Varicella zoster virus 180 Xeroradiography 259 True pockets 445 Various Tuberous sclerosis 174 treatment considerations in chronic Tumor-like gingival enlargement or period 223 Y

Essentials of Clinical Periodontology and Periodontics and Periodontology Clinical of Essentials pregnancy tumor 167 types of Two types of gingival responses 229 mirror surfaces 281 Yeaple probe 264 Types of occlusal forces 100 bony defect 248 uses of dental mirror 281 Z conventional periodontal probes 258 Vascular changes 106 dental plaque 58 Vehicles for local delivery 428 Zimmerman-Laband syndrome 174 epidemiologic research 42 Veillonella parvula 63 Zinc 298 gingival enlargement 440 Vertical chloride 312 gingivectomy 319 component 384 oxide eugenol packs 304 gingivitis 151 grooving 342 Zone of spirochetal infiltration 178 infection 64 incision 328 Zoster virus infections 175