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Teeth abnormalities ii
 

Teeth abnormalities ii

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Oral Pathology I

Oral Pathology I
Third Year

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    Teeth abnormalities ii Teeth abnormalities ii Presentation Transcript

    • Oral Pathology I. Lab. BDS-231 .Aiman A. Ali DDS, PhD
    •  Slide preparation for histopathological examination Routine H & E Ground sections Decalcified sections
    • Macroscopic description
    • Old machine [Processing]
    • Computerized machine [Processing]
    • Paraffin bath
    • Microtome
    • Staining
    • Mounting
    • HP Diagnosis
    • Archiving
    • Ground sections
    • Decalcified sections
    • Periodic Acid Schiff (PAS)  This technique identifies a number of polysaccharides and carbohydrate-containing compounds
    • Masson Trichrome Stain  Collagen fibers stain an intense green
    • Aldehyde Fuchsin  Stains elastic fibers purple to black.
    • Verhoeff's Hematoxylin  This method stains elastic fibers black in addition to nuclei
    • Wright's/Giemsa Stain  Stains for blood and bone marrow smears
    • Immunohistochemical staining
    • February 19, 2005 Oral Pathology I Abnormalities of Teeth I & II
    • Alteration in Shape Taurodontism  It is a variation of tooth form.  Elongated crown  Apically displaced furcation  Increased height of pulp chamber  Associated with Down syndrome
    • Alteration in Shape Taurodontism  11% occurrence in middle east  It is of little clinical significance  No treatment is required
    • Alterations in Shape Supernumerary root  Accessory roots are most commonly seen in:  Mandibular canines  Premolars  Molars (thirds)  Recognition of extra-root numbers is important for extractions or endodontic treatment
    • Alterations in Shape Enamel pearls  Droplets of ectopic enamel, they occur most commonly on  The bi-or tri-furcation of teeth  Maxillary & mandibular molars  It may be detected on radiographic examinations  It is of significance when periodontal disease is present
    • Alterations in Shape Enamel pearls
    • Attrition, Abrasion & Erosion  Attrition: The loss of tooth structure from tooth to tooth contact  Abrasion: The loss of tooth structure due to repeated mechanical contact with objects other than teeth  Erosion: Non-carious loss of tooth structure due to chemical dissolution not related to acid produced by dental plaque
    • Attrition, Abrasion & Erosion
    • Alterations in Shape Attrition  It is a physiologic wearing of teeth as a result of mastication  It is an age related process & varies from one individual to another  Diet, dentition, musculature & chewing habits can influence the pattern of attrition
    • Alterations in Shape Abrasion  It is the pathologic wearing of teeth as a result of abnormal habit (abrasive substance)  Pipe smoking  Tobacco chewing  Aggressive toothbrushing  Abrasive dentifrices
    • Alterations in Shape Erosion  It is a loss of tooth structure from a non-bacterial chemical process  Acids  External: work environment or in the diet  Internal: regurgitation of gastric contents (chronic vomiting)  In many cases of tooth erosion, no cause is found
    • Alterations in Number Anodontia  It is an absence of teeth that is often associated with hereditary ectodermal dysplasia  It is caused by polygenic (enviromental & genetic factors)  The prevalence of hypodontia is 4.6% Complete anodontia: All teeth are missing
    • Alterations in Number
    • Alterations in Number Anodontia  Partial anodontia (hypodontia): one or several teeth are missing  Pseudoanodontia: when teeth are absent clinically  Most commonly seen in third molars, second premolars & maxillary lateral incisors
    • Alterations in Number Impaction  It is most commonly seen in mandibular third molars & maxillary cuspids, it occurs because of:  Crowding  Physical barrier  Abnormal eruption path  Ankylosis (fusion of tooth to alveolar bone)
    • Alterations in Number Supernumerary teeth  It results from continued proliferation of permanent or primary dental lamina  The tooth can be rudimentary & miniature  It can be an isolated event, familial or associated with syndromes
    • Alterations in Number Supernumerary teeth  Clinical significance:  Occupy space  Block eruption  Delay or mal-eruption  Natal teeth  Post-permanent dentition  Maxilla>mandible: 10:1  Anterior midline of maxilla (mesiodens)  Fourth molar
    • Defects of Enamel Environmental defects of enamel  Severe metabolic injury can cause:  Defects in the quantity & shape  Enamel hypoplasia  Defects in the quality and color  Enamel hypocalcification Enamel hypoplasia
    • Defects of Enamel Environmental defects of enamel  The extent of the defect is dependent on:  The intensity of the etiologic factor  The duration  The time of occurrence Enamel hypoplasia
    • Defects of Enamel Environmental defects of enamel  Etiologic factors can be  Local: (Turner’s tooth)    Trauma Abscess Clinical signs  Hypocalcification or hypoplasia
    • Defects of Enamel Environmental defects of enamel  Systemic  should occur after birth and before age 6  It commonly affect anterior teeth and first molars  Defects in primary teeth and possibly the tips of central incisors and first molars
    • Defects of Enamel Environmental defects of enamel  Research have shown that causes are attributed to  infectious diseases  Nutritional defects (rickets)  Congenital syphilis  Birth trauma (neonatal line)  Fluoride (hypoplasia or hypocalcification)  Idiopathic factors
    • Amelogenesis Imperfecta  It is a hereditary disorders affects both primary and permanent dentitions  It can be hypocalcified or hypoplastic  Hypoplastic type   Insufficient amount of enamel (pits & grooves to aplasia) Hypocalcified type:  Soft & friable enamel (wears readily)
    • Amelogenesis Imperfecta  The color varies from white opaque to yellow to brown  Dentin & pulp chamber appear normal  Cosmetic problem
    • Defects in Dentin Dentinogenesis imperfecta  It is an autosomal dominant trait  It affects dentin in both primary and permanent dentitions  Type I: Occurs in pts. With osteogenesis imperfecta  Type II: Only dentin but no bone abnormalities
    • Defects in Dentin Dentinogenesis imperfecta  Type III: Only dental defects occur  Pulp exposures  Periapical radiolucencies  Variable radiographic appearance
    • Defects in Dentin Dentinogenesis imperfecta  Clinical features:  Both dentitions exhibit translucent appearance  Yellow-brown to gray  The enamel fractures easily  Excessive constriction at the cementoenamel junction  Roots are shortened and blunted
    • Defects in Dentin Dentinogenesis imperfecta  Radiographically, Type I & II exhibits identical changes:  Opacifications of dental pulps  Short roots and bell shaped crowns  Type III:  Dentin appears thin  Pulp chambers and root canals are extremely large (Shell teeth)
    • Defects in Dentin Dentinogenesis imperfecta  Microscopically:  The dentin contains fewer but larger and irregular dentinal tubules  Pulp replaced by irregular dentin  Enamel appears normal but dentinoenamel junction is smooth  Treatment is directed toward protecting tooth from wear and esthetic appearance
    • Defects in Dentin Dentin dysplasia  It is a hereditary rare condition that has been subdivided to:  Type I (radicular type)  The color of both dentition is normal  Periapical lesions are regular features  Premature tooth loss (short roots)  Pulps are completely obliterated
    • Defects in Dentin Dentin dysplasia  Type II (coronal type)  Primary dentition is opalescent and permanent dentition is normal  The coronal pulps are large and filled with globules of abnormal dentin  Periapical lesion are not regular features  Primary teeth appeared similar to type I but permanent teeth exhibit enlarged pulp chamber
    • Defects in Dentin Dentin Dysplasia  Microscopically:  Enamel and immediately subjacent dentin appear normal  Deeper layers of dentin shows atypical tubular patterns & amorphous, atubular areas and irregular organization  Treatment is directed toward retention of teeth but prognosis is poor
    • Defects of Enamel & Dentin Regional odontodysplasia  It is a dental abnormality that involves the hard tissues that are derived from both epithelial (enamel) and mesenchymal (dentin & cementum) components of the tooth forming apparatus
    • Defects of Enamel & Dentin Regional odontodysplasia  A region or quadrant of the maxilla or mandibule are affected  Short roots  Open apical foramina  Enlarged pulp chambers  Poor mineralization of enamel & dentin (ghost teeth)
    • Defects of Enamel & Dentin Regional odontodysplasia  Permanent teeth>primary teeth  Maxillary anterior teeth are more affected  Eruption is delayed or does not occur
    • Defects of Enamel & Dentin Regional odontodysplasia  Cause in unknown, however:  Trauma  Nutritional deficiencies  Infections  Metabolic abnormalities  Systemic diseases  Local vascular compromize  Genetic influences  Treatment: teeth removal because of poor quality
    • Abnormalities of the Dental Pulp Pulp calcification  Occurs with increasing age  No apparent reason  Microscopic size  Large  Linear (diffuse)  Nodular (pulp stones)  True denticle  False denticle  Not source of pain
    • Abnormalities of the Dental Pulp
    • Internal Resorption  It may be seen as  Inflammatory response to pulpal injury  No apparent trigger  It occurs as a result of osteoclasts activation on internal surfaces
    • Internal Resorption  The root or crown can be perforated  In advanced cases teeth may appear pink  Treatment is root canal therapy before perforation
    • External Resorption  It may be a result of an adjacent pathologic process  Chronic inflammatory lesion  Cysts  Benign tumors  Malignant neoplasms
    • External Resorption  The cause has been related to:  Release of chemical mediators  Increased vascularity  Pressure
    • External Resorption  It may be associated with:  Trauma  Reimplantation  Impactions  Idiopathic  The lesion can occur on root surfaces below the gingival epithelial attachment  It can occur at the apex
    • Alterations in Color Exogenous stain  It is the stain that can be removed by abrasives  Dietary substances  Colored by-products of chromogenic bacteria
    • Alterations in Color Endogenous stain  It results from deposits of systemically circulating substances during tooth development  Tetracycline  Bright yellow color  The color change with time due to oxidization  Minocycline  It stains the root of adult teeth  Skin & mucosa
    • Alterations in Color Endogenous stain  Congenital porphyria (hereditary)  Errors in porphyrin metabolism  Deposition of porphyrin in developing teeth which appear red to brown  Liver disease, biliary atresia & neonatal hepatitis  It may cause discoloration of the primary teeth