DOCSLIB.ORG

Dentin Dysplasia Type I with Hypomature Amelogenesis Imperfecta in an 18-Year-Old Girl

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Dentin Dysplasia Type I with Hypomature Amelogenesis Imperfecta in an 18-Year-Old Girl Dentin Dysplasia Type I with Hypomature Amelogenesis Imperfecta in an 18-year-old Girl Case Report Abstract 1 2 Ehsan Azma , Seyed Javad Kia , Introduction: Dentin dysplasia is a rare Somayeh Nemati3 autosomal dominant inheriting disturbance of dentin formation characterized by normal enamel formation, but atypical dentin with abnormal pulpal morphology. There are two major patterns: type I and type II. Amelogenesis imperfecta is an autosomal dominant. X-link 1,2Assistant Professor, Department of Oral Medicine, inherent disease that is classified by clinical Guilan University of Medical Sciences, Dental manifestation into hypoplastic, hypomature, School, Rasht, Iran hypocalcified. 3Assistant Professor, Department of Maxillofacial The simultaneous occurrence of dentin Radiology, Guilan University of Medical Sciences, dysplasia and amelogenesis imperfecta is quite Dental Faculty, Rasht, Iran rare. The purpose of this case report is to pre- sent a case of dentin dysplasia type I which is also associated with hypoplastic amelogenesis Received: Jun16, 2013 imperfecta in an 18 year old girl, without any Accepted: Nov11, 2013 syndromic signs. Key words:•Dentin dysplasia •Amelogenesis imperfecta •Dental anomalies Corresponding Author: Seyed Javad Kia, DDS, MS Address: Department of Oral Medicine, Guilan University of Medical Sciences, Dental School, Imam Street, Opposite Pardis Hotel, Rasht, Iran Telephone: +98-131-3263622 Fax: +98-131-3263623 E-mail: [email protected] Journal of Dentomaxillofacial Radiology, Pathology and Surgery Vol 2, No 3, Autumn 2013 Dentin dysplasia type I with hypomature amelogenesis imperfecta Introduction appropriately and radiographcally contrasts well with the underlying dentin.(4) Dentin dysplasia is presented as a rare The amelogenesis imperfecta may be a autosomal dominant inherent disorder of part of a syndrome, for example in dentin formation but with normal enamel Trichodento-osseous syndrome, the formation. It is categorized into type I or amelogenesis imperfecta accompany with radicular dysplasia and type II or coronal dysplastic nails, Taurodontism,curly dysplasia involving both primary and per- hair,osseous dysplastic defectsor Amelo- manent dentition and exhibiting an approxi- onycho-hypohidrotic syndrome, Morquio mate prevalence of 1:100,000. syndrome, Kohlschutter syndrome, Clinically, the teeth show a normal Epidermolysis bullos ahereditaria, AI morphologic character. Although, the enam- ,Nephrocalcinosis syndrome, and gingival el and coronal dentin are normal clinically calcification.(5,6,7,8) Butthe reported dentine and well formed, the radicular dentin loses dysplasia accompany with dentine dysplasia all organization and subsequently is short- inthe literature.(9) The purpose of this case ened dramatically.(1,2)The first sign of dentin report is to present a case of dentin dysplasia dysplasia type I may be the premature type I which accompanies with hypomature exfoliation of teeth, either spontaneously or amelogenesisimperfect in an 18 years old with minor trauma, but delay in dental girl. eruption has also been reported.(2)Partial or complete obliteration of pulp chambers, Case Report defective root formation, and tendency for This report describes the clinical and periapical radiolucency without obvious pathological findings of dentin dysplasia cause are radiographic signs of this disorder type I concomitant with amelogenesis in both deciduous and permanent teeth. Pri- imperfect in an 18 years old girl living in mary teeth show total pulpal obliteration, north of Iran (Rasht, Guilan). She referred to whereas permanent teeth show pre-eruptive the department of oral medicine, Guilan pulpal obliteration, resulting in crescent- University of medical sciences, dental shaped pulpal remnants parallel to the ce- school. Her chief complaints were dental mentoenamel junctions in radiographic (3,4) caries and mobility of teeth. In the past view. Amelogenesis imperfecta encom- medical history, having had a positive passes a complicated group of conditions history of grandma epilepsy from infancy, that demonstrate developmental alterations she has taken medication (60mg Phenobarbi- in the structure of the enamel in the absence tal tablet per day) to control it. There was of a systemic disorder. At least 14 different no prominent manifestation in the head and hereditary subtypes of amelogenesis imper- neck of the patient. fecta exist with numerous patterns of inher- In dental history, extraction of deciduous itance and a wide variety of clinical manifes- and permanent teeth was not found. In oral tations. There are three subdivisions of examination, the oral hygiene was poor and amelogenesis imperfecta: 1-hypoplastic, marginal gingivitis was seen. In dental 2-hypomature and 3-hypocalcified type. examination, the color of teeth was Both the deciduous and permanent denti- yellow-brown and hypodontia was tions are diffusely involved. In patients with detected. The teeth number 15, 16, 17, 24 hypoplastic amelogenesis imperfecta, the were lost due to significant mobility. basic alteration concentrates on inadequate Overall, the available teeth were loose deposition of enamel matrix. Insufficient without the periodontal pocket. The enamel available enamel matrix is mineralized was hypoplastic (Figure1). 35 E. Azma, S.J. Kia, S. Nemati abnormal and have short lengths, due to this malformation, teeth are loose without periodontal pockets around them. Radiographic examination is crucial for the identification of DD1. In this anomaly, roots have been found to be short, blunt, tapering, or absent in both dentitions. In radiographs, the primary teeth show total pulp obliteration; whereas, the permanent teeth show the obliteration of pulp Figure1. Clinical view Dentin Dysplasia Type I chambers, periapical radiolucent lesions are- with Hypomature Amelogenesis Imperfecta in an as that may represent granuloma, cyst, or 18-year-old Girl abscess associate with teeth that appears to In panoramic view, the bone structure be vital. Taurodontism, and short blunted and trabeculation were normal. The teeth roots with pre-eruptive pulpal obliteration numbers; 18, 28, 38, 37, 47 were impacted result in crescent-shaped pulpal remnants without adequate root development. The parallel to the cement-enamel (3,10,11,12) teeth number 27 and 48 were missed. The junctions. entire teeth had short roots and The pathogenesis of DD1 is still pulp oblitaration. The enamels of entire teeth unknown in the dental literature. Logan et al. were thin and on some surfaces of posterior proposed that dentinal papilla is responsible teeth were lost. The overall findings were for the abnormalities in root development. combination or concurrent dentin dysplasia They suggested that multiple degenerative type I and hypoplastic type of amelogenesis foci within the papilla become calcified, imperfecta. The alveolar bone loss exists in leading to reduced growth and final oblitera- (13) some areas (Figure 2). tion of the pulp chamber. Wesley et al. proposed that the condition is caused by an abnormal interaction of odontoblasts with ameloblasts leading to abnormal differentiation and /or function of these odontoblasts.(14,15) Some studies have localized dentin dysplasia to the interval of chromosome 4q21 containing the dentinogenesis imperfect locus.(12,15) It was proposed that dentin dysplasia and dentinogenesis imperfecta represent allelic mutations of a Figur2. Panoramic view Dentin Dysplasia Type I common gene. According to the study by with hypomature amelogenesis imperfecta in an kim et al., based on the radiographic views 18-year-old Girl. of their patients, the calcified pulp chambers, rootless teeth, periapical radiolu- Discussion cent and the nature of the periapical One of the causes of tooth exfoliation is lesion are characteristic findings for the the congenital disease DD1( dentin dysplasia diagnosis of DD type 1. DD1 is usually an type I).In this disorder, in spite of the normal autosomal dominant condition(13), but in the crown of teeth, the roots are completely case reported by Toomarian et al., there was 36 Dentin dysplasia type I with hypomature amelogenesis imperfecta no familial history of the disease. So, he was and gingival hyperplasia and nephrocalcino- considered to be the first generation sufferer. sis were found.(5,6,7) Teeth with radiographic or histologic The etiology of abnormal tooth eruption features of DD1 occur in a number of and coronal resorptionin amelogenesis disorders such as Calcinosis, Ehlers-Danlos imperfect hypoplastic type remains unclear, syndrome, and Brachio-skeleto-genital but appears to be the result of abnormal syndrome.(16) In the case studied by Tooma function of the enamel epithelium and rian et al.,the only permanent dentition was ameloblasts. Failure of eruption in patients affected and periapical radiolucencies were with this AI type may be the result of an seen and interpreted as periapical granuloma abnormality in the molecular control of the and cysts.(13) Scola and Watts proposed a eruption process that is known to be at least sub-classification of DD1 as total DD1, partially driven by the odontogenic characterized by the presence of teeth with epithelium.(19) significantly narrowed or obliterated pulp The researches indicates that all other spaces and permanent teeth with short forms of dentin dysplasia type I and dentine roots.(17) O’Carrol et al. presented another dysplasia, except dentin dysplasia type I, sub classification based on the radiographic appear to result from mutations in
Load more

Recommended publications
  • Glossary for Narrative Writing
    Periodontal Assessment and Treatment Planning Gingival description Color: o pink o erythematous o cyanotic o racial pigmentation o metallic pigmentation o uniformity Contour: o recession o clefts o enlarged papillae o cratered papillae o blunted papillae o highly rolled o bulbous o knife-edged o scalloped o stippled Consistency: o firm o edematous o hyperplastic o fibrotic Band of gingiva: o amount o quality o location o treatability Bleeding tendency: o sulcus base, lining o gingival margins Suppuration Sinus tract formation Pocket depths Pseudopockets Frena Pain Other pathology Dental Description Defective restorations: o overhangs o open contacts o poor contours Fractured cusps 1 ww.links2success.biz [email protected] 914-303-6464 Caries Deposits: o Type . plaque . calculus . stain . matera alba o Location . supragingival . subgingival o Severity . mild . moderate . severe Wear facets Percussion sensitivity Tooth vitality Attrition, erosion, abrasion Occlusal plane level Occlusion findings Furcations Mobility Fremitus Radiographic findings Film dates Crown:root ratio Amount of bone loss o horizontal; vertical o localized; generalized Root length and shape Overhangs Bulbous crowns Fenestrations Dehiscences Tooth resorption Retained root tips Impacted teeth Root proximities Tilted teeth Radiolucencies/opacities Etiologic factors Local: o plaque o calculus o overhangs 2 ww.links2success.biz [email protected] 914-303-6464 o orthodontic apparatus o open margins o open contacts o improper
    [Show full text]
  • Oral Health in Prevalent Types of Ehlers–Danlos Syndromes
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Ghent University Academic Bibliography J Oral Pathol Med (2005) 34: 298–307 ª Blackwell Munksgaard 2005 Æ All rights reserved www.blackwellmunksgaard.com/jopm Oral health in prevalent types of Ehlers–Danlos syndromes Peter J. De Coster1, Luc C. Martens1, Anne De Paepe2 1Department of Paediatric Dentistry, Centre for Special Care, Paecamed Research, Ghent University, Ghent; 2Centre for Medical Genetics, Ghent University Hospital, Ghent, Belgium BACKGROUND: The Ehlers–Danlos syndromes (EDS) Introduction comprise a heterogenous group of heritable disorders of connective tissue, characterized by joint hypermobility, The Ehlers–Danlos syndromes (EDS) comprise a het- skin hyperextensibility and tissue fragility. Most EDS erogenous group of heritable disorders of connective types are caused by mutations in genes encoding different tissue, largely characterized by joint hypermobility, skin types of collagen or enzymes, essential for normal pro- hyperextensibility and tissue fragility (1) (Fig. 1). The cessing of collagen. clinical features, modes of inheritance and molecular METHODS: Oral health was assessed in 31 subjects with bases differ according to the type. EDS are caused by a EDS (16 with hypermobility EDS, nine with classical EDS genetic defect causing an error in the synthesis or and six with vascular EDS), including signs and symptoms processing of collagen types I, III or V. The distribution of temporomandibular disorders (TMD), alterations of and function of these collagen types are displayed in dental hard tissues, oral mucosa and periodontium, and Table 1. At present, two classifications of EDS are was compared with matched controls.
    [Show full text]
  • Regional Odontodysplasia: Report of an Unusual Case Involving Mandibular Arch
    Regional odontodysplasia: Report of an unusual case involving mandibular arch N. S. Venkatesh Babu, R. Jha Smriti, D. Bang Pratima Abstract Regional odontodysplasia (RO) is a rare developmental anomaly involving both mesodermal and ectodermal components in primary or permanent dentition. It affects the maxilla and the mandible or both; however, maxilla is more commonly involved. This article reports the case of 33-month-old boy who came with the chief complaint of delayed eruption of mandibular teeth. Findings of clinical and radiographic examination were consistent with those of RO. Maxillary dentition was unaffected. Clinical and radiographic features and treatment options are discussed. Keywords: Mandibular arch, primary teeth, regional odontodysplasia Introduction cases of mandibular involvement have been reported so far.[5,8,9] Regional odontodysplasia (RO) is a rare developmental dental anomaly that involves ectoderm and mesoderm The teeth with RO often display a brownish or yellowish derived tissues.[1] It can affect either primary or permanent discoloration and most frequent clinical symptoms dentition.[2] This condition was first described by Hitchin accompanied by this anomaly are failure of eruption and in 1934. The prevalence of this condition is still not clear gingival enlargement. Radiologically, the affected teeth since the studies reported till date have mainly been based illustrate hypoplastic crowns and lack of contrast between on case reports. enamel and dentin is usually apparent. Enamel and the dentin are very thin,
    [Show full text]
  • Spectrum of Dentin Dysplasia in a Family
    CASE REPORT Spectrumof dentin dysplasia in a family: case report and literature review W. Kim Seow, BDS, MDSc, DDSc, PhD Stephen Shusterman, DMD Abstract The dentin dysplasias (DD),which maybe classified as type I (DD1)or type 2 (DD2),form a group of rare, inherited abnormalitiesthat are clinically distinct fromdentinogenesis imperfecta. Studies of affected families mayhelp to distinguish different types of DDand provide further insight into their etiology and clinical management.This report describes a family that showed characteristic dental features of DD1, including clinically normalcrowns in both primaryand permanentdentitions, and mobileteeth that maybe associated with prematureexfoliation. Radiographicfeatures included calcification of the pulp with crescent-shaped, radiolucent pulp remnants, short, tapering, taurodontic roots, and manyperiapical pathoses that maybe q¢sts or granulomas.A spectrumof dentin dysplasia wasnoted within the family. Strategies to prevent pulp and periapical infections and early exfoliation of the teeth include meticulousoral hygieneand effective caries-preventivemeasures. ( P ed iatr Dent16:437-42,1994) Introduction and literature review Histologically, in DD1, most of the coronal and Dentin dysplasias (DD) form a group of rare dentin mantle dentin of the root is usually reported to be abnormalities that are clinically distinct from normal, and the dentin defect is confined mainly to the dentinogenesis imperfecta. 1-3 Since its recognition in root2, s, 10 The dysplastic dentin has been reported to 19203 as "rootless teeth" and as "dentin dysplasia" by consist of numerous denticles, containing whorls of Rushton in 1933,4 the clinical features of DDhave been osteodentin that block the normal course of the den- tinal tubules,s, 10,11 well described.
    [Show full text]
  • Hereditary Disorders of Dentin: Dentinogenesis Imperfecta Type II
    CASE REPORT Hereditary Disorders of Dentin: Dentinogenesis Imperfecta Type II and Dentin Dysplasia Type II Sandhya Shanmugam1, Kuzhanchinathan Manigandan2, Angambakkam Rajasekaran PradeepKumar3 ABSTRACT Dentin is a mineralized tissue in tooth, produced from odontoblasts, that differentiates from the mesenchymal cells of dental papilla. Hereditary dentin defects are broadly classified into two types, namely, dentinogenesis imperfecta (DGI – type I and II) and dentin dysplasia (DD – type I and II). DGI is an autosomal dominant hereditary disorder, and DD is a rare hereditary disturbance of dentin formation that affects both the primary and the permanent dentition. The purpose of this report was to present a case of DGI–type II and a case of DD–type II to highlight the importance of diagnosing hereditary dentin disorders. Keywords: Dentin, Dentin discoloration, Dentin disorders, Dentin dysplasia, Dentinogensis imperfecta. Journal of Operative Dentistry and Endodontics (2020): 10.5005/jp-journals-10047-0091 INTRODUCTION 1,3Department of Conservative Dentistry and Endodontics, Thai Dentin is a mineralized tissue forming the the body of a tooth, which Moogambigai Dental College and Hospital, Dr M.G.R. Educational and serves as a protective covering for the pulp and supports overlying Research Institute, Chennai, Tamil Nadu, India enamel and cementum. Mature dentin is about 70% mineral, 20% 2Department of Conservative Dentistry and Endodontics, Faculty of organic matrix, and 10% water by weight. Dentin is the product of Dental Sciences, Sri Ramachandra Institute of Higher Education and specialized cells called odontoblasts.1 Research, Chennai, Tamil Nadu, India Hereditary developmental disorders affecting dentin are Corresponding Author: Angambakkam Rajasekaran PradeepKumar, rare anomalies occurring due to a genetic defect in structural Department of Conservative Dentistry and Endodontics, Thai or regulatory proteins in dentin.
    [Show full text]
  • Pediatric Periodontal Disease: a Review of Cases
    Pediatric Periodontal Disease: A Review of Cases Dental Acid Erosion: Identification and Management Martha Ann Keels, DDS PhD [email protected] or [email protected] www.dukesmiles.com California Society of Pediatric Dentistry Silverado Resort & Spa Napa, California April 23, 2016 Pediatric Periodontal Matrix Copyright Keels & Quinonez 2003 Healthy Diseased Bone Bone (no alveolar bone loss) (alveolar bone loss) Healthy Gingiva Box 1 Box 2 (pink, firm, stippled) Diseased Gingiva Box 3 Box 4 (erythematous, hemorrhagic) Box 1 – healthy gingiva and no bone loss Box 2 – healthy gingiva and bone loss Hypophosphatasia ** Inconclusive Pediatric Periodontal Disease (LJP) * Dentin Dysplasia Type I Post Avulsion / extraction Box 3 – unhealthy gingiva and no bone loss Gingivitis Eruption related gingivitis Mouthbreating Gingivitis Minimally attached gingival Gingival Fibromatotis Herpetic gingivostomatitis ANUG Thrombocytopenia Leukemia (AML / ALL) Aplastic anemia HIV Acrodynia Vitamin C deficiency Vitamin K deficiency Box 4 – unhealthy gingival and bone loss Neutrophil quantitative defect: (agranulocytosis, cyclic neutropenia, chronic idiopathic neutropenia)* Neutrophil qualitative defect: (Leukocyte adhesion deficiency)* Inconclusive pediatric periodontal disease (LJP) * Langerhan cell histiocytosis X *** Papillon-Lefevre disease * Diabetes mellitus * Down Syndrome * Chediak-Higashi disease * Chronic Granulomatous Disease * Tuberculosis * Ehlers-Danlos (Type VIII) * Osteomyelitis * * bacteriological culture and sensitivity needed ** tooth biopsy
    [Show full text]
  • Molarization of Premolar with Dentin Dysplasia Type Ia - a Rare Unilateral Entity Vidhi Mathur1, Rishi Thukral2, Ami Desai1, Rinky Ahuja1
    Journal of Medicine, Radiology, Pathology & Surgery (2018), 5, 5–8 CASE REPORT Molarization of premolar with dentin dysplasia Type Ia - A rare unilateral entity Vidhi Mathur1, Rishi Thukral2, Ami Desai1, Rinky Ahuja1 1Department of Oral and Maxillofacial Pathology, People’s College of Dental Sciences and Research Centre, Bhopal, Madhya Pradesh, India, 2Department of Oral and Maxillofacial Surgery, Government Medical College and Hospital, Vidisha, Madhya Pradesh, India Keywords: Abstract Dentin dysplasia, faciolingual, mandibular Human dentition exhibits variations in anatomic features. When the size and morphology second premolar, mesiodistal, of teeth are analyzed, a range exists within which a particular tooth should be probably tooth shape deviations placed, but some teeth show variance from this range. Mandibular premolars (MnP) Correspondence: are among such teeth. This paper presents a rare case of unilateral megadontia with Dr. Vidhi Mathur, Department of Oral dentin dysplasia, showing the presence of molariform appearance of second MnP and Maxillofacial Pathology, People’s which appeared radiographically as rootless tooth with deformative pulpal morphology. College of Dental Sciences and Research Clinically, the patient suffered from temporomandibular joint disorder which may be Centre, Karond-Bhanpur Bypass, Bhopal because of the occlusal instability caused by the lingually placed molarized premolar and - 462 042, Madhya Pradesh, India. so appropriate preventive therapy was recommended. Phone: +91-9340766592/9977701543. E-mail: [email protected] Received: 22 January 2018; Accepted: 25 February 2018 Doi: 15713/ins.jmrps.124 Introduction what can be called variation and what can be described as anomaly.[6] The anatomy of mandibular second premolar is Tooth anomaly affects both permanent and deciduous dentition particularly unpredictable and shows an elevated variability in and anterior and posterior teeth including maxillary and morphology.
    [Show full text]
  • Guideline on Dental Management of Heritable Dental Developmental Anomalies Review Council Council on Clinical Affairs Revised 2013
    REFERENCE MANUAL V 38 / NO 6 16 / 17 Guideline on Dental Management of Heritable Dental Developmental Anomalies Review Council Council on Clinical Affairs Revised 2013 Purpose articles. Articles for review were chosen from this list and The American Academy of Pediatric Dentistry AAPD( ) recog- from references within selected articles. Thirty-nine articles nizes that pediatric dentists are uniquely qualified to manage each had full examination and analysis in order to revise this the oral health care needs of children with heritable dental guideline. When data did not appear sufficient or were incon- developmental anomalies. These children have multiple, com- clusive, recommendations were based upon expert and/or plex problems as their dental conditions affect both form and consensus opinion by experienced researchers and clinicians. function and can have significant psychological impact. These conditions may present early in life and require both immediate Background intervention and management of a protracted nature, including Anomalies of tooth development are relatively common and coordination of multi-disciplinary care. The AAPD’s Guideline may occur as an isolated condition or in association with other on Management of Dental Patients with Special Health Care anomalies. Developmental dental anomalies often exhibit Needs1 alludes to this patient population but does not make patterns that reflect the stage of development during which the specific treatment recommendations for the oral manifestations malformation occurs. For example, disruptions in tooth initi- of such diagnoses. This guideline is intended to address the ation result in hypodontia or supernumerary teeth, whereas diagnosis, principles of management, and objectives of therapy disruptions during morphodifferentiation lead to anomalies of of children with heritable dental developmental anomalies size and shape (e.g., macrodontia, microdontia, taurodontism, rather than provide specific treatment recommendations.
    [Show full text]
  • Oral Pathology Final Exam Review Table Tuanh Le & Enoch Ng, DDS
    Oral Pathology Final Exam Review Table TuAnh Le & Enoch Ng, DDS 2014 Bump under tongue: cementoblastoma (50% 1st molar) Ranula (remove lesion and feeding gland) dermoid cyst (neoplasm from 3 germ layers) (surgical removal) cystic teratoma, cyst of blandin nuhn (surgical removal down to muscle, recurrence likely) Multilocular radiolucency: mucoepidermoid carcinoma cherubism ameloblastoma Bump anterior of palate: KOT minor salivary gland tumor odontogenic myxoma nasopalatine duct cyst (surgical removal, rare recurrence) torus palatinus Mixed radiolucencies: 4 P’s (excise for biopsy; curette vigorously!) calcifying odontogenic (Gorlin) cyst o Pyogenic granuloma (vascular; granulation tissue) periapical cemento-osseous dysplasia (nothing) o Peripheral giant cell granuloma (purple-blue lesions) florid cemento-osseous dysplasia (nothing) o Peripheral ossifying fibroma (bone, cartilage/ ossifying material) focal cemento-osseous dysplasia (biopsy then do nothing) o Peripheral fibroma (fibrous ct) Kertocystic Odontogenic Tumor (KOT): unique histology of cyst lining! (see histo notes below); 3 important things: (1) high Multiple bumps on skin: recurrence rate (2) highly aggressive (3) related to Gorlin syndrome Nevoid basal cell carcinoma (Gorlin syndrome) Hyperparathyroidism: excess PTH found via lab test Neurofibromatosis (see notes below) (refer to derm MD, tell family members) mucoepidermoid carcinoma (mixture of mucus-producing and squamous epidermoid cells; most common minor salivary Nevus gland tumor) (get it out!)
    [Show full text]
  • El Paso Community College Syllabus Part II Official Course Description
    DHYG 1239; Revised Fall 2016/Spring 2017 El Paso Community College Syllabus Part II Official Course Description SUBJECT AREA Dental Hygiene COURSE RUBIC AND NUMBER DHYG 1239 COURSE TITLE General and Oral Pathology COURSE CREDIT HOURS 2 2 : 1 Credits Lec Lab I. Catalog Description Offers a general study of disturbances in human body development, diseases of the body, and disease prevention measures with emphasis on the oral cavity and associated structures. A grade of "C" or better is required in this course to take the next course. Prerequisites: BIOL 2401 and BIOL 2402 and CHEM 1306 and 1106. Corequisites: DHYG 1103 and DHYG 1201 and DHYG 1219 and DHYG 1304 and DHYG 1431. (2:1). Lab fee. II. Course Objectives Upon satisfactory completion of the course, the student will be able to: A. Introduction to Preliminary Diagnosis of Oral Lesions 1. Define each of the terms in the vocabulary list for this chapter. 2. List and define the eight diagnostic categories that contribute to the diagnostic process. 3. Name a diagnostic category and give an example of a lesion, anomaly, or condition for which this category contributes greatly to the diagnosis. 4. Describe the clinical appearance of Fordyce=s granules (spots), torus palatinus, mandibular tori, and lingual varicosities, and identify them on a slide. 5. Describe the radiographic picture and historical data (including the age, sex, and race of the patient) that are relevant to periapical cementl dysplasia (cementoma). 6. Define Avariant of normal@ and give three examples of such lesions involving the tongue. 7. List and describe the clinical characteristics and identify a clinical picture of fissured tongue, median rhomboid glossitis, geographic tongue, ectopic geographic tongue, and hairy tongue.
    [Show full text]
  • Dentin Dysplasia Type I A
    Folia Morphol. Vol. 78, No. 3, pp. 637–642 DOI: 10.5603/FM.a2019.0012 C A S E R E P O R T Copyright © 2019 Via Medica ISSN 0015–5659 journals.viamedica.pl Dentin dysplasia type I A. Kobus1, M. Świsłocka2, A. Kierklo1, J. Borys3, E. Domel3, J. Różycki4, S. Ławicki5, J. Bagińska1 1Department of Dentistry Propaedeutics, Medical University of Bialystok, Poland 2Resident in the Course of Specialisation in Conservative Dentistry with Endodontics, Karedent Sp. J., Bialystok, Poland 3Maxillofacial Surgery Clinic, Medical University of Bialystok, Poland 4Department of Radiology, Medical University of Bialystok, Poland 5Department of Population Medicine and Civilisation Disease Prevention, Medical University of Bialystok, Poland [Received: 13 November 2018; Accepted: 10 January 2019] This paper describes a rare case of genetically determined dentin dysplasia type I in 26-year-old male patient. The paper highlights anatomical and radiological aspects of dental abnormalities and emphasizes the significance of the education of both general practitioners and paediatricians as regards referring patients with diagnosed dentin dysplasia for a multi-specialty therapy. (Folia Morphol 2019; 78, 3: 637–642) Key words: dental abnormalities, dentin dysplasia, pulp obliteration, computed tomography INTRODUCTION acidic phosphoprotein gene and the dentin sialophos- Dentin dysplasia is a congenital disease entity phoprotein gene may occur [15, 17]. which may occur separately or as one of the symp- Dentin dysplasia is divided into dysplasia type I, toms of an underlying disease [7]. It is one of dental also referred to as root dysplasia, and dysplasia type II, hard tissue disorders of genetic origin apart from such i.e.
    [Show full text]
  • Orthodontic Movement of Teeth with Short Root Anomaly: Should It Be Avoided, Faced Or Ignored?
    original article Orthodontic movement of teeth with short root anomaly: Should it be avoided, faced or ignored? Jose Valladares Neto1, José Rino Neto2, João Batista de Paiva3 Introduction: Short Root Anomaly (SRA) is an uncommon disease and a challenge for orthodontic treatment as it tends to increase the risk of root resorption. Objective: Assess the current status of the diagnosis, etiology and orthodon- tic management of teeth with SRA, and present case reports. Method: A literature review was carried out in PubMed, SciELO, LILACS, Scopus and Web of Science databases. Results: A differential diagnosis of SRA should be conducted for teeth with incomplete root formation, external apical root resorption, dentin dysplasia type I and post dental trauma root hypoplasia. SRA is genetically determined and orthodontic movement requires changes in clinical and radiographic management in order to restrict damage. Conclusion: Orthodontic movement of teeth with SRA is contraindicated in extreme cases, only. Caution at all stages could minimize attachment loss and lead to long-term stability. Keywords: Tooth root. Tooth abnormalities. Root resorption. Orthodontics. Introdução: a anomalia de raiz curta (ARC) é uma patologia incomum e constitui um desafio para o tratamento ortodôn- tico, pois tende a elevar o risco de reabsorção radicular. Objetivo: revisar a literatura sobre o diagnóstico, a etiologia e a con- duta ortodôntica recomendada para esses casos, ilustrando esse tema com relatos de caso. Métodos: devido ao baixo nível de evidência sobre o tema, realizou-se a revisão narrativa da literatura com estratégia de busca nas bases de dados PubMed, SciELO, Lilacs, Scopus e Web of Science.
    [Show full text]