BDS10001 Disorders Of Hard Tissues 1 PDF
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Newgiza University
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This document is a lecture on "Disorders of Hard Tissue (1)" from New Giza University. It discusses various aspects related to hard tissue abnormalities in the mouth and aims to detail the histopathological aspects of common non-caries related abnormalities. It covers topics like tooth development, abnormalities in tooth number and size, and different types of dental disorders.
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BDS10001 Disorders of Hard Tissue (1) Date : Aims: The aim of this lecture is to detail the histopathological aspects of common non-caries related hard tissue abnormalities of the mouth Objectives: On completion of this lecture, the student should be able to: Understand the key histopathological...
BDS10001 Disorders of Hard Tissue (1) Date : Aims: The aim of this lecture is to detail the histopathological aspects of common non-caries related hard tissue abnormalities of the mouth Objectives: On completion of this lecture, the student should be able to: Understand the key histopathological features and clinical significance of hard tissue defects, involving number, size and shape of teeth Initiation stage proliferation stage Eruption stage Histo & morphodifferentiation stage Number Size Apposition & calcification stage Eruption Shape Structure Normal Tooth development 1. Developmental disturbances in number of teeth Decrease (anodontia or hypodontia) Increase or hyperdontia (additional teeth) Total Anodontia Absence of all teeth [usually associated with a syndrome such as hereditary ectodermal dysplasia or Streeter’s syndrome] Partial Absence of single tooth or group of teeth The most frequently reported missing teeth are third molar 8, upper lateral 2 and lower second premolar 5 Anodontia True [failure of tooth to develop] 3 1 1 3 False due to tooth loss by extraction or trauma Psuedo clinically absent tooth that developed but fail to erupt] Hereditary Ectodermal Dysplasia Oral manifestations Total or partial anodontia. Teeth are often conical in shape & retarded in eruption. Alveolar process has a reduced height Hereditary Ectodermal Dysplasia Oral manifestations Palate is frequently high and may be clefted. Salivary glands hypoplasia (Xerostomia) Lips are protuberant Increase in number of teeth (hyperdontia) Pre-deciduous dentition Supernumerary teeth Post-permanent dentition It is formed after the permanent dentition either: due to development of their extra enamel organs after giving those of the permanent series. The majority of cases are believed to be due to delayed eruption of embedded or impacted permanent teeth. Pre-deciduous Dentition Etiology A rare condition due to accessory buds before the formation of the enamel organ of the deciduous teeth. Clinical features It is present at birth or shortly after birth (natal & neonatal teeth) Rudimentary in size usually erupts in the mandibular incisor area Pre-deciduous teeth Clinical features Weakly attached to the gum. Should be distinguished from prematurely erupted deciduous teeth. Supernumerary teeth They are Extra teeth , morphologically don’t resemble normal dentition They are classified according to their site of eruption into: Mesiodens: Between the maxillary central incisors. Distomolar: Distal to third molar. Paramolar: On the buccal surface of upper 2nd or 3rd molars. Mesiodens Paramolar Distomolar Supplemental teeth Supernumerary teeth which morphologically resemble the normal. Their most common sites. 2, 5, 8 Cleidocranial Dysplasia It is a Hereditary rare disease Characterized by deficient growth of bones developed in membrane as cranial vault, maxilla and the clavicles which are usually hypoplastic or entirely absent. Cleidocranial Dysplasia Oral Manifestations The maxilla is narrow and V-shaped with high arched palate. Crown may be conical in shape. Some teeth may show gemination. Cleidocranial Dysplasia Oral Manifestations Delayed shedding of deciduous teeth (retained). Delayed eruption of permanent teeth. Presence of unerupted multiple supernumerary teeth. Cleidocranial Dysplasia Oral Manifestations Many teeth may exhibit enamel hypoplasia. Many unerupted teeth have hooked roots. Multiple dentigerous cysts may develop in relation to some of the unerupted teeth. Gardner’s syndrome It is characterized by variable abnormalities in bone, skin and teeth as well as colorectal polyps Multiple Fibromas & osteomas Multiple impacted Supernumerary teeth Multiple polyps in large intestine (premalignant) Gardner’s syndrome It is characterized by variable abnormalities in bone, skin and teeth as well as colorectal polyps Multiple Fibromas & osteomas Multiple impacted Supernumerary teeth Multiple polyps in large intestine (premalignant) The major problem for these patients is high risk for transformation of colorectal polyps into adenocarcinoma if untreated. Multiple osteomas are noted around puberty, leading to early diagnosis 2. Developmental disturbances in size of teeth Macrodontia Abnormal large teeth Microdontia Abnormal small teeth Macrodontia True generalized macrodontia. All teeth are larger than normal [gigantism]. ≠ Relative generalized macrodontia. Normal sized teeth in small jaws. Localized macrodontia [involving a single tooth] Maxillary central incisor– maxillary canine Macrodontia Localized macrodontia [involving a group of teeth usually associated with hereditary facial hemihypertrophy] Microdontia True generalized All teeth are smaller than normal. Occurs in pituitary dwarfism. Relative generalized Normal sized teeth appear small in large jaws. Heredity plays a role. Localized microdontia involving Single tooth Most commonly affected are maxillary lateral incisor “Peg Group of teeth as in unilateral facial hypoplasia 3. Developmental disturbances in shape of teeth 1. Gemination 2. Fusion 3. Concrescence 4. Dilaceration 5. Dens invaginatus 6. Dens evaginatus 7. Talon’s cusp 8. Taurodontism 9. Supernumerary roots 10. Enamel pearl 11. Syphilis 1. Gemination Partial division of a single tooth germ, tooth that exhibits two completely or incompletely separated crowns. Deciduous and permanent dentitions Most common in the maxillary incisor region. No. of teeth is normal. 1. Gemination It has a single root and root canal. 2. Fusion Results from the union of two adjacent tooth germs. Cause is uncertain – heredity, trauma, and crowding. The root canals may be either fused or separated. No. of teeth is reduced by one, except in cases where one of the fused tooth germ was that of a supernumerary tooth. 3. Concrescence A type of fusion that occurs after root formation is complete. The teeth are joined along their roots by cementum. Trauma or crowding of teeth can cause concrescence. 3. Concrescence Radiographic features Histopathology 4.Dilaceration The presence of angulation or a sharp bend along the long axis of a tooth. Trauma during root development. The curve or bend may occur anywhere along the length of the tooth, depending upon the amount of root formed when the injury occurred. 4.Dilaceration 5. Dens Invaginatus (Dens in Dente) Pathogenesis: Invagination of all layers of enamel organ into the dental papilla forming an enamel-lined cavity 5. Dens Invaginatus (Dens in Dente) Clinical features Normally shaped tooth OR malformed crown with a deep pit in the area of cingulum. Food debris tend to lodge in the pit causing caries, pulp infection and periapical disease. 5. Dens Invaginatus (Dens in Dente) Radiographic features tooth-like structure appears within the pulp of the involved tooth "dens in dente” 6. Dens evaginatus An accessory cusp on the occlusal surface between the buccal and lingual cusps of the premolar It may rarely occur on molars, canines and incisors. A pulp horn may extend into this extra cusp. 6. Dens evaginatus Pathogenesis: due to proliferation and evagination of enamel epithelium and subjacent mesenchyme during tooth development. Clinical significance: The "extra" cusp may contribute to displacement of the teeth and/or pulp exposure with subsequent infection following occlusal wear. 7. Talon’s cusp It is an extra cusp resembling an eagle's talon. It projects lingually from the cingulum area of a maxillary or mandibular permanent incisor and extends to the incisal edge. 8. Taurodontism Literally means "bull-like" teeth. Similar to the teeth of the ungulate animals. Enlargement of the tooth trunk at the expense of the roots; The bifurcation or trifurcation is located more apical than its normal position. 8. Taurodontism Classification: 1. Hypotaurodontism. 2. Meso-taurodontism. 3. Hypertaurodontism 8. Taurodontism Classification: 1. Hypotaurodontism. 2. Meso-taurodontism. 3. Hypertaurodontism 8. Taurodontism Pathogenesis: Failure of Hertwig's epithelial root sheath to invaginate at the proper horizontal level to form the furcation area. 8. Taurodontism Radiographic Features 1. 2. 3. 4. 5. Teeth rectangular in shape. Pulp chamber is extremely large. A greater apico-occlusal height than normal. Root lacks the usual cervical constriction. Bifurcation or trifurcation are apically displaced , roots are exceedingly short. 9. Supernumerary roots Supernumerary or extra roots are most commonly seen in mandibular premolars, canines, maxillary and mandibular third molars. They are diagnosed radiographically. 9. Supernumerary roots Supernumerary or extra roots are most commonly seen in mandibular premolars, canines, maxillary and mandibular third molars. They are diagnosed radiographically. 10- Enamel pearl Small, spherical enamel projection located on the root surface near the bifurcation or trifurcation area and is usually found on maxillary molars. Ectopi a 11. Congenital Syphilis A contagious venereal disease caused by the spirochete "treponema pallidum". Prenatal syphilis is transmitted from an infected mother to her fetus via the placenta. Children born to syphilitic mothers show abnormalities in the size, shape, structure and number of some of their permanent teeth because this infection results in distortion of the ameloblastic layer in tooth germ. The deciduous dentition is normal because it develops at an early stage of intra-uterine development. If the fetus becomes infected at such an early stage, abortion will take place. 11. Congenital Syphilis The most commonly affected teeth are Upper first permanent incisors Hutchinson's Teeth First molars in both jaws Moon's and Mulberry Molars 11. Congenital Syphilis Hutchinson's Teeth The permanent incisors barrel-shaped mesial and distal surfaces taper toward the incisal edge rather than toward the cervical margin giving a "screw-driver" appearance. The incisal edges have a central notch. The mesial and distal incisal angles are rounded. The incisors may show enamel hypoplasia. 11. Congenital Syphilis Moon's and Mulberry Molars Moon's molars: The first Mulberry molars: Occlusal surfaces may be rough, pitted and permanent molars shows a exhibit multiple, irregular tubercles constricted occlusal surface and replacing their normal cuspal rounded angles and is dome-shaped pattern Key points Abnormalities in number of teeth will result in either hypodontia or hyperdontia Abnormalities in size of teeth will result in either macrodontia or micrdontia Some abnormalities in shape of teeth will result in difficulty in tooth extraction and endodontic treatment such as dilaceration, taurodontism and supernumerary root Some abnormalities in shape of teeth will result in poor esthetics such as gemination, fusion and congenital syphilis Some abnormalities in shape of teeth will result in pulp involvement such as dens evaginatus and dens invaginatus Aims: The aim of this lecture is to detail the histopathological aspects of common non-caries related hard tissue abnormalities of the mouth Objectives: On completion of this lecture, the student should be able to: Understand the key histopathological features and clinical significance of hard tissue defects, involving number, size and shape of teeth Reading material: Students are advised to review any relevant teaching provided in the first year. In addition they are advised to read relevant sections of the following texts: Regezi et al. Oral Pathology: Clinical Pathologic Correlations. 7th Edition. Elsevier, 2017 pp 373-380 Neville et al. Oral and Maxillofacial Pathology. 4th Edition. Elsevier, 2016 pp 66-92 Thank you