Dental Plaque: a Host- Associated Biofilm
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DENTIN HYPERSENSITIVITY: Consensus-Based Recommendations for the Diagnosis & Management of Dentin Hypersensitivity
October 2008 | Volume 4, Number 9 (Special Issue) DENTIN HYPERSENSITIVITY: Consensus-Based Recommendations for the Diagnosis & Management of Dentin Hypersensitivity A Supplement to InsideDentistry® Published by AEGISPublications,LLC © 2008 PUBLISHER Inside Dentistry® and De ntin Hypersensitivity: Consensus-Based Recommendations AEGIS Publications, LLC for the Diagnosis & Management of Dentin Hypersensitivity are published by AEGIS Publications, LLC. EDITORS Lisa Neuman Copyright © 2008 by AEGIS Publications, LLC. Justin Romano All rights reserved under United States, International and Pan-American Copyright Conventions. No part of this publication may be reproduced, stored in a PRODUCTION/DESIGN Claire Novo retrieval system or transmitted in any form or by any means without prior written permission from the publisher. The views and opinions expressed in the articles appearing in this publication are those of the author(s) and do not necessarily reflect the views or opinions of the editors, the editorial board, or the publisher. As a matter of policy, the editors, the editorial board, the publisher, and the university affiliate do not endorse any prod- ucts, medical techniques, or diagnoses, and publication of any material in this jour- nal should not be construed as such an endorsement. PHOTOCOPY PERMISSIONS POLICY: This publication is registered with Copyright Clearance Center (CCC), Inc., 222 Rosewood Drive, Danvers, MA 01923. Permission is granted for photocopying of specified articles provided the base fee is paid directly to CCC. WARNING: Reading this supplement, Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis & Management of Dentin Hypersensitivity PRESIDENT / CEO does not necessarily qualify you to integrate new techniques or procedures into your practice. AEGIS Publications expects its readers to rely on their judgment Daniel W. -
Long-Term Uncontrolled Hereditary Gingival Fibromatosis: a Case Report
Long-term Uncontrolled Hereditary Gingival Fibromatosis: A Case Report Abstract Hereditary gingival fibromatosis (HGF) is a rare condition characterized by varying degrees of gingival hyperplasia. Gingival fibromatosis usually occurs as an isolated disorder or can be associated with a variety of other syndromes. A 33-year-old male patient who had a generalized severe gingival overgrowth covering two thirds of almost all maxillary and mandibular teeth is reported. A mucoperiosteal flap was performed using interdental and crevicular incisions to remove excess gingival tissues and an internal bevel incision to reflect flaps. The patient was treated 15 years ago in the same clinical facility using the same treatment strategy. There was no recurrence one year following the most recent surgery. Keywords: Gingival hyperplasia, hereditary gingival hyperplasia, HGF, hereditary disease, therapy, mucoperiostal flap Citation: S¸engün D, Hatipog˘lu H, Hatipog˘lu MG. Long-term Uncontrolled Hereditary Gingival Fibromatosis: A Case Report. J Contemp Dent Pract 2007 January;(8)1:090-096. © Seer Publishing 1 The Journal of Contemporary Dental Practice, Volume 8, No. 1, January 1, 2007 Introduction Hereditary gingival fibromatosis (HGF), also Ankara, Turkey with a complaint of recurrent known as elephantiasis gingiva, hereditary generalized gingival overgrowth. The patient gingival hyperplasia, idiopathic fibromatosis, had presented himself for examination at the and hypertrophied gingival, is a rare condition same clinic with the same complaint 15 years (1:750000)1 which can present as an isolated ago. At that time, he was treated with full-mouth disorder or more rarely as a syndrome periodontal surgery after the diagnosis of HGF component.2,3 This condition is characterized by had been made following clinical and histological a slow and progressive enlargement of both the examination (Figures 1 A-B). -
DENTAL CALCULUS: a STRATEGIC REVIEW Rajiv Saini1 1.Associate Professor,Department of Periodontology,Pravra Institute of Medical Sciences-Loni
International Journal of Dental and Health Sciences Review Article Volume 01,Issue 05 DENTAL CALCULUS: A STRATEGIC REVIEW Rajiv Saini1 1.Associate Professor,Department of Periodontology,Pravra Institute of Medical Sciences-Loni ABSTRACT: Dental calculus or tartar is an adherent calcified mass that form on the surface of teeth and dental appliance through mineralization of bacterial dental plaque in aqueous environment. Dental calculus plays a vital role in aggravating the periodontal disease by acting as reservoir for the bacterial plaque and providing the protected-covered niche for bacteria to proliferate. Based upon the location of dental calculus in relation to marginal gingiva, it is classified into mainly two types: 1. Supragingival calculus and subgingival calculus. Calcium and phosphate are two salivary ions which are raw materials for dental calculus formation. The various techniques and equipments involved for calculus removal is Hand Instruments, Ultrasonic, Ultrasound Technology and Lasers. Chemotherapeutic agents have been used to supplement the mechanical removal of dental plaque, but a more potent oral rinse with anti-calculus properties to prevent mineralization will be the need of time to suppress calculus formation. Key Words: Periodontitis, Anti-calculus, Periogen. INTRODUCTION: biofilm is that it allows the micro-organisms to stick and to multiply on surfaces. [3] Periodontitis is a destructive inflammatory Mineralization of dental plaque leads to disease of the supporting tissues of the calculus formation. Dynamic state of tooth teeth and is caused either by specific surface is responsible for mineralization of microorganisms or by a group of specific plaque. A continuous exchange of ions is microorganisms, resulting in progressive always happening on the tooth surface with destruction of periodontal ligament and a constant exchange of calcium and alveolar bone with periodontal pocket phosphate ions. -
Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease
toxins Review Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease Rosalia Marcano 1, M. Ángeles Rojo 2 , Damián Cordoba-Diaz 3 and Manuel Garrosa 1,* 1 Department of Cell Biology, Histology and Pharmacology, Faculty of Medicine and INCYL, University of Valladolid, 47005 Valladolid, Spain; [email protected] 2 Area of Experimental Sciences, Miguel de Cervantes European University, 47012 Valladolid, Spain; [email protected] 3 Area of Pharmaceutics and Food Technology, Faculty of Pharmacy, and IUFI, Complutense University of Madrid, 28040 Madrid, Spain; [email protected] * Correspondence: [email protected] Abstract: It is widely recognized that periodontal disease is an inflammatory entity of infectious origin, in which the immune activation of the host leads to the destruction of the supporting tissues of the tooth. Periodontal pathogenic bacteria like Porphyromonas gingivalis, that belongs to the complex net of oral microflora, exhibits a toxicogenic potential by releasing endotoxins, which are the lipopolysaccharide component (LPS) available in the outer cell wall of Gram-negative bacteria. Endotoxins are released into the tissues causing damage after the cell is lysed. There are three well-defined regions in the LPS: one of them, the lipid A, has a lipidic nature, and the other two, the Core and the O-antigen, have a glycosidic nature, all of them with independent and synergistic functions. Lipid A is the “bioactive center” of LPS, responsible for its toxicity, and shows great variability along bacteria. In general, endotoxins have specific receptors at the cells, causing a wide immunoinflammatory response by inducing the release of pro-inflammatory cytokines and the production of matrix metalloproteinases. -
Dentinal Hypersensitivity: a Review
Dentinal Hypersensitivity: A Review Abstract Dentinal hypersensitivity is generally reported by the patient after experiencing a sharp pain caused by one of several different stimuli. The pain response varies substantially from one person to another. The condition generally involves the facial surfaces of teeth near the cervical aspect and is very common in premolars and canines. The most widely accepted theory of how the pain occurs is Brannstrom’s hydrodynamic theory, fluid movement within the dentinal tubules. The dental professional, using a variety of diagnostic techniques, will discern the condition from other conditions that may cause sensitive teeth. Treatment of the condition can be invasive or non-invasive in nature. The most inexpensive and efficacious first line of treatment for most patients is a dentifrice containing a desensitizing active ingredient such as potassium nitrate and/or stannous fluoride. This review will address the prevalence, diagnosis, and treatment of dentinal hypersensitivity. In addition the home care recommendations will focus on desensitizing dentifrices. Keywords: Dentinal hypersensitivity, hydrodynamic theory, stannous fluoride, potassium nitrate Citation: Walters PA. Dentinal Hypersensitivity: A Review. J Contemp Dent Pract 2005 May;(6)2:107-117. © Seer Publishing 1 The Journal of Contemporary Dental Practice, Volume 6, No. 2, May 15, 2005 Introduction The prevalence of dentinal hypersensitivity Dentifrices and mouth rinses are routinely used has been reported over the years in a variety as a delivery system for therapeutic agents of ways: as greater than 40 million people such as antimicrobials and anti-sensitivity in the U.S. annually1, 14.3% of all dental agents. Therapeutic oral care products are patients2, between 8% and 57% of adult dentate available to assist the patient in the control of population3, and up to 30% of adults at some time dental caries, calculus formation, and dentinal during their lifetime.4 hypersensitivity to name a few. -
Staining and Calculus Formation After 0.12% Chlorhexidine Rinses in Plaque-Free and Plaque Covered Surfaces: a Randomized Trial
www.scielo.br/jaos Staining and calculus formation after 0.12% chlorhexidine rinses in plaque-free and plaque covered surfaces: a randomized trial Fabrício Batistin Zanatta1,2, Raquel Pippi Antoniazzi1, Cassiano Kuchenbecker RÖSING2 1- DDS, School of Dentistry, Division of General Dentistry, Franciscan University Center (UNIFRA), Santa Maria, RS, Brazil. 2- PhD, Post-Graduate Program in Dentistry, Lutheran University of Brazil (ULBRA), Canoas, RS, Brazil. Corresponding address: Fabrício B. Zanatta - Rua Tiradentes, 76/801 - Bairro Centro - 97050730 - Santa Maria, RS - Brasil - Phone: +55 55 33078026 - Fax: +55 51 3338 4221 - e-mail: [email protected] Received: February 2, 2009 - Modification: September 5, 2009 - Accepted: September 28, 2009 ABSTRACT bjectives: Studies concerning side effects of chlorhexidine as related to the presence Oof plaque are scarce. The purpose of this study was to compare the side effects of 0.12% chlorhexidine gluconate (CHX) on previously plaque-free (control group) and plaque-covered surfaces (test group). Methods: This study had a single-blind, randomized, split-mouth, 21 days-experimental gingivitis design, including 20 individuals who abandoned all mechanical plaque control methods during 25 days. After 4 days of plaque accumulation, the individuals had 2 randomized quadrants cleaned, remaining 2 quadrants with plaque-covered dental surfaces. On the fourth day, the individuals started with 0.12% CHX rinsing lasting for 21 days. Stain index intensity and extent as well as calculus formation were evaluated during the experimental period. Results: Intergroup comparisons showed statistically higher (p<0.05) stain intensity and extent index as well as calculus formation over the study in test surfaces as compared to control surfaces. -
Desensitizing Agent Reduces Dentin Hypersensitivity During Ultrasonic Scaling: a Pilot Study Dentistry Section
Original Article DOI: 10.7860/JCDR/2015/13775.6495 Desensitizing Agent Reduces Dentin Hypersensitivity During Ultrasonic Scaling: A Pilot Study Dentistry Section TOMONARI SUDA1, HIROAKI KOBAYASHI2, TOSHIHARU AKIYAMA3, TAKUYA TAKANO4, MISA GOKYU5, TAKEAKI SUDO6, THATAWEE KHEMWONG7, YUICHI IZUMI8 ABSTRACT of the dentin hypersensitivity agent. Evaluation of effects on Background: Dentin hypersensitivity can interfere with optimal dentin hypersensitivity was determined by a questionnaire and periodontal care by dentists and patients. The pain associated visual analog scale (VAS) pain scores after ultrasonic scaling. with dentin hypersensitivity during ultrasonic scaling is intolerable The statistical analysis was performed using the paired Student for patient and interferes with the procedure, particularly during t-test and Spearman rank correlation coefficient. supportive periodontal therapy (SPT) for patients with gingival Results: The desensitizing agent reduced the mean VAS pain recession. score from 69.33 ± 16.02 at baseline to 26.08 ± 27.99 after Aim: This study proposed to evaluate the desensitizing effect of application. The questionnaire revealed that >80% patients the oxalic acid agent on pain caused by dentin hypersensitivity were satisfied and requested the application of the desensitizing during ultrasonic scaling. agent for future ultrasonic scaling sessions. Materials and Methods: This study involved 12 patients who Conclusion: This study shows that the application of the oxalic were incorporated in SPT program and complained of dentin acid agent considerably reduces pain associated with dentin hypersensitivity during ultrasonic scaling. We examined the hypersensitivity experienced during ultrasonic scaling. This availability of the oxalic acid agent to compare the degree of pain control treatment may improve patient participation and pain during ultrasonic scaling with or without the application treatment efficiency. -
Peri-Implantitis: a Review of the Disease
DENTISTRY ISSN 2377-1623 http://dx.doi.org/10.17140/DOJ-2-117 Open Journal Review Peri-Implantitis: A Review of the Disease *Corresponding author and Report of a Case Treated with Zeeshan Sheikh, Dip.Dh, BDS, MSc, PhD Department of Dentistry Allograft to Achieve Bone Regeneration University of Toronto Room 222 Fitzgerald Building 150 College Street Toronto, ON M5S 3E2, Canada Haroon Rashid1#, Zeeshan Sheikh2#*, Fahim Vohra3, Ayesha Hanif1 and Michael Glogauer2 Tel. +1-416-890-2289 E-mail: [email protected]; [email protected] #These authors contributed equally Volume 2 : Issue 3 1Division of Prosthodontics, College of Dentistry, Ziauddin University, Karachi, Pakistan Article Ref. #: 1000DOJ2117 2Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Canada 3College of Dentistry, Division of Prosthodontic, King Saud University, Riyadh, Saudi Arabia Article History Received: September 20th, 2015 Accepted: October 1st, 2015 ABSTRACT Published: October 5th, 2015 Dental implants offer excellent tooth replacement options however; peri-implantitis can limit their clinical success by causing failure. Peri-implantitis is an inflammatory process Citation around dental implants resulting in bone loss in association with bleeding and suppuration. Rashid H, Sheikh Z, Vohra F, Hanif A, Glogauer M. Peri-implantitis: a review Dental plaque is at the center of its etiology, and in addition, systemic diseases, smoking, and of the disease and report of a case parafunctional habits are also implicated. The pathogenic species associated with peri-implan- treated with allograft to achieve bone titis include, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Tanner- regeneration. Dent Open J. 2015; ella forsythia. The goal in the management of peri-implantitis is the complete resolution of 2(3): 87-97. -
Intergeneric Communication in Dental Plaque Biofilms
JOURNAL OF BACTERIOLOGY, Dec. 2000, p. 7067–7069 Vol. 182, No. 24 0021-9193/00/$04.00ϩ0 Copyright © 2000, American Society for Microbiology. All Rights Reserved. NOTES Intergeneric Communication in Dental Plaque Biofilms HUA XIE,1* GUY S. COOK,2 J. WILLIAM COSTERTON,3 GREG BRUCE,4 4 5 TIMOTHY M. ROSE, AND RICHARD J. LAMONT School of Dentistry, Meharry Medical College, Nashville, Tennessee1; Bacterin Inc.,2 and Center for Biofilm Engineering, Montana State University,3 Bozeman, Montana; and Department of Pathobiology4 and Department of Oral Biology,5 University of Washington, Seattle, Washington Received 27 June 2000/Accepted 21 September 2000 Downloaded from Dental plaque is a complex biofilm that accretes in a series of discrete steps proceeding from a gram-positive streptococcus-rich biofilm to a structure rich in gram-negative anaerobes. This study investigated information flow between two unrelated plaque bacteria, Streptococcus cristatus and Porphyromonas gingivalis. A surface pro- tein of S. cristatus caused repression of the P. gingivalis fimbrial gene (fimA), as determined by a chromosomal fimA promoter-lacZ reporter construct and by reverse transcription-PCR. Signaling activity was associated jb.asm.org with a 59-kDa surface protein of S. cristatus and showed specificity for the fimA gene. Furthermore, P. gingivalis was unable to form biofilm microcolonies with S. cristatus. Thus, S. cristatus is capable of modulating virulence gene expression in P. gingivalis, consequently influencing the development of pathogenic plaque. at MONTANA STATE UNIV AT BOZEMAN on October 13, 2009 The study of the ability of bacterial cells to communicate which were grown in Trypticase Peptone broth supplemented with one another and coordinate behavior is a burgeoning field with yeast extract (5 mg/ml) and 0.5% glucose at 37°C aerobi- with relevance to a number of microbial ecosystems (5, 6, 11, cally; Treponema denticola GM-1, which was cultured for 5 12, 17). -
American Academy of Periodontology Task Force Report on the Update to the 1999 Classification of Periodontal Diseases and Conditions*
J Periodontol • July 2015 American Academy of Periodontology Task Force Report on the Update to the 1999 Classification of Periodontal Diseases and Conditions* The American Academy of Periodontology (AAP) peri- 4 mm CAL, and Severe =‡5 mm CAL.’’ Numerous odically publishes reports, statements, and guidelines important studies since 1999 have used similar pa- on a variety of topics relevant to periodontics. These rameters to define periodontitis. For example, the papers are developed by an appointed committee of recent epidemiologic studies outlining the prevalence experts, and the documents are reviewed and ap- of periodontitis in the United States used attachment proved by the AAP Board of Trustees. loss parameters to define various severities of peri- odontitis.2,3 It is recognized that CAL is of importance for the scientific advancement of the knowledge of n 2014, the American Academy of Periodontology periodontitis. However, in clinical practice, measure- Board of Trustees charged a Task Force to develop ment of CAL has proven to be challenging, and is time Ia clinical interpretation of the 1999 Classification consuming. Measuring the location of the cemento- of Periodontal Diseases and Conditions to address enamel junction (CEJ) when the gingival margin is concerns expressed by the education community, the located coronal to the CEJ is difficult and may involve American Board of Periodontology, and the practic- some guesswork when the CEJ is not readily evident ing community that the current Classification pres- via tactile sensation. These issues can result in ex- ents challenges for the education of dental students aminations being performed in which, rather than and implementation in clinical practice. -
Idiopathic Gingival Fibromatosis Associated with Generalized Aggressive Periodontitis: a Case Report
Clinical P RACTIC E Idiopathic Gingival Fibromatosis Associated with Generalized Aggressive Periodontitis: A Case Report Contact Author Rashi Chaturvedi, MDS, DNB Dr. Chaturvedi Email: rashichaturvedi@ yahoo.co.in ABSTRACT Idiopathic gingival fibromatosis, a benign, slow-growing proliferation of the gingival tissues, is genetically heterogeneous. This condition is usually part of a syndrome or, rarely, an isolated disorder. Aggressive periodontitis, another genetically transmitted disorder of the periodontium, typically results in severe, rapid destruction of the tooth- supporting apparatus. The increased susceptibility of the host population with aggressive periodontitis may be caused by the combined effects of multiple genes and their inter- action with various environmental factors. Functional abnormalities of neutrophils have also been implicated in the etiopathogenesis of aggressive periodontitis. We present a rare case of a nonsyndromic idiopathic gingival fibromatosis associated with general- ized aggressive periodontitis. We established the patient’s diagnosis through clinical and radiologic assessment, histopathologic findings and immunologic analysis of neutrophil function with a nitro-blue-tetrazolium reduction test. We describe an interdisciplinary approach to the treatment of the patient. For citation purposes, the electronic version is the definitive version of this article: www.cda-adc.ca/jcda/vol-75/issue-4/291.html diopathic gingival fibromatosis is a rare syndromic, have been genetically linked to hereditary condition -
Time to Quit Smoking
ToothTipsSM Time to Quit Smoking In conjunction with the Great American Smokeout, Dental Health Services wants to educate you about one specific threat to smokers—periodontal disease. How does smoking increase your risk? As a smoker, you are more likely than nonsmokers to have the following problems: ⇒ Calculus —plaque that hardens on your teeth and can only be removed during a professional cleaning ⇒ Deep pockets between your teeth and gums ⇒ Loss of the bone and tissue that support your teeth The bacteria in the calculus can destroy your gum tissue and cause your gums to pull away from your teeth. When this happens, periodontal pockets form and fill with disease-causing bacteria. Without treatment, your teeth may become loose, painful, and at risk to falling out. Save Your Smile Research shows that smokers lose more teeth than nonsmokers do. According to data from the Centers of Disease Control and Prevention, only about 20 percent of people over age 65 who have never smoked are toothless, while a whopping 41.3 percent of daily smokers over age 65 are toothless. Make an investment in your overall health now and for your future—you and your loved ones are worth it! Dental Your Personal Dental Plan Health 800.63.SMILE Services www.dentalhealthservices.com 12M028d © 2008 Dental Health Services 01/09 ToothTipsSM Time to Quit Smoking Not Just Cigarettes Other tobacco products are also harmful to your periodontal health. Smokeless tobacco can cause gums to recede and increase the chance of losing the bone and fibers that hold your teeth in place.