Teeth abnormalities ii

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Oral Pathology I …

Oral Pathology I
Third Year

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  • 1. Oral Pathology I. Lab. BDS-231 .Aiman A. Ali DDS, PhD
  • 2.  Slide preparation for histopathological examination Routine H & E Ground sections Decalcified sections
  • 3. Macroscopic description
  • 4. Old machine [Processing]
  • 5. Computerized machine [Processing]
  • 6. Paraffin bath
  • 7. Microtome
  • 8. Staining
  • 9. Mounting
  • 10. HP Diagnosis
  • 11. Archiving
  • 12. Ground sections
  • 13. Decalcified sections
  • 14. Periodic Acid Schiff (PAS)  This technique identifies a number of polysaccharides and carbohydrate-containing compounds
  • 15. Masson Trichrome Stain  Collagen fibers stain an intense green
  • 16. Aldehyde Fuchsin  Stains elastic fibers purple to black.
  • 17. Verhoeff's Hematoxylin  This method stains elastic fibers black in addition to nuclei
  • 18. Wright's/Giemsa Stain  Stains for blood and bone marrow smears
  • 19. Immunohistochemical staining
  • 20. February 19, 2005 Oral Pathology I Abnormalities of Teeth I & II
  • 21. 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
  • 22. Alteration in Shape Taurodontism  11% occurrence in middle east  It is of little clinical significance  No treatment is required
  • 23. 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
  • 24. 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
  • 25. Alterations in Shape Enamel pearls
  • 26. 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
  • 27. Attrition, Abrasion & Erosion
  • 28. 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
  • 29. 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
  • 30. 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
  • 31. 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
  • 32. Alterations in Number
  • 33. 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
  • 34. 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)
  • 35. 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
  • 36. 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
  • 37. 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
  • 38. 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
  • 39. Defects of Enamel Environmental defects of enamel  Etiologic factors can be  Local: (Turner’s tooth)    Trauma Abscess Clinical signs  Hypocalcification or hypoplasia
  • 40. 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
  • 41. 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
  • 42. 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)
  • 43. Amelogenesis Imperfecta  The color varies from white opaque to yellow to brown  Dentin & pulp chamber appear normal  Cosmetic problem
  • 44. 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
  • 45. Defects in Dentin Dentinogenesis imperfecta  Type III: Only dental defects occur  Pulp exposures  Periapical radiolucencies  Variable radiographic appearance
  • 46. 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
  • 47. 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)
  • 48. 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
  • 49. 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
  • 50. 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
  • 51. 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
  • 52. 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
  • 53. 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)
  • 54. Defects of Enamel & Dentin Regional odontodysplasia  Permanent teeth>primary teeth  Maxillary anterior teeth are more affected  Eruption is delayed or does not occur
  • 55. 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
  • 56. 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
  • 57. Abnormalities of the Dental Pulp
  • 58. 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
  • 59. Internal Resorption  The root or crown can be perforated  In advanced cases teeth may appear pink  Treatment is root canal therapy before perforation
  • 60. External Resorption  It may be a result of an adjacent pathologic process  Chronic inflammatory lesion  Cysts  Benign tumors  Malignant neoplasms
  • 61. External Resorption  The cause has been related to:  Release of chemical mediators  Increased vascularity  Pressure
  • 62. 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
  • 63. Alterations in Color Exogenous stain  It is the stain that can be removed by abrasives  Dietary substances  Colored by-products of chromogenic bacteria
  • 64. 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
  • 65. 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