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Dentinogenesis imperfecta
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Dentinogenesis imperfecta

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Hi friends, this is my presentation on Dentinogenesis Im

Hi friends, this is my presentation on Dentinogenesis Im


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  • Teeth are not sensitive even if most of the surface enamel is lost as dentinal tubules are haphazardly arranged and most of them are devoid of odontoblastic processes
    little scope for microorganism entry due to obliterated dentinal tubules
  • Transcript

    • 1. Presented by: Anupama Mukundan
    • 2.  What is dentinogenesis  Introduction to dentinogenesis  Classification  Etiology  Clinical features  Radiographic features  Histopathologic features  Treatment imperfecta
    • 3.  Dentinogenesis is the formation of dentin, which starts before amelogenesis.  Dentin is formed by odontoblast cells. Dentinogenesis takes place in two phases: 1. formation of organic collagen matrix 2. deposition of hydroxyapetite crystals 
    • 4.  Is an inherited disorder of dentin formation  Autosomal dominant condition  Affects deciduous and permanent teeth
    • 5. SHIELDS CLASSIFICATION 1. TYPE - I 2. TYPE - II 3. TYPE- III 1. REVISED CLASSIFICATION DENTINOGENESIS IMPERFECTA 1 DENTINOGENESIS IMPERFECTA 2 WITKOP CLASSIFICATION 1. DENTINOGENESIS IMPERFECTA 2. HEREDITARY OPALASCENT DENTIN 3. BRANDYWINE ISOLATE
    • 6.  TYPE I: Occurs in patients affected with osteogenesis imperfecta  TYPE II : Is not associated with osteogenesis imperfecta  TYPE III: “Brandywine type” rare condition, seen in racial isolate of Maryland, exhibits multiple pulp exposures and periapical lesions in deciduous dentition.
    • 7. DENTINOGENESIS IMPERFECTA 1  Without osteogenesis imperfecta  Corresponds to type II of shields classification DENTINOGENESIS IMPERFECTA 2  Corresponds to type III of shields classification  THERE IS NO SUBSTITUTE IN THE PRESENT CLASSIFICATION FOR THE CATEGORY DESIGNATED AS TYPE I IN THE SHIELDS CLASSIFICATION
    • 8. SYNONYMS  OPALESCENT DENTIN  DENTINOGENESIS IMPERFECTA WITHOUT OSTEOGENESIS IMPERFECTA  OPALESCENT TEETH WITHOUT OSTEOGENESIS IMPERFECTA   SHIELDS TYPE II CAPDEPONT TEETH
    • 9.  MUTATION IN THE DENTIN SIALO PHOSPHO PROTEIN (DSPP) gene ENCODING DENTIN PHOSPHOPROTEIN AND DENTIN SIALOPROTEIN
    • 10.  Clearly distinct from osteogenesis imperfecta with opalescent teeth & affects only the teeth  No increased frequency of bone fracture is seen  Frequency: 1 in 6000-8000
    • 11. Synonyms  SHIELDS TYPE III  BRANDYWINE TYPE DENTINOGENESIS IMPERFECTA
    • 12.  Some researchers say it is a separate mutation from DGI 1  Shield et al 1973 stated that markedly enlarged pulp chambers and pulp exposures occurs in deciduous teeth do not occur in DGI 1  Witkop 1975 suggested both are same  Recent studies suggests both are result of mutation in two tightly linked genes  MacDougall et al 1999 stated DGI 2 differ from DGI 1 by the presence of multiple pulp exposures normal non mineralized pulp chambers ,and general appearance of shell teeth
    • 13.    Affects males and females equally Teeth are blue gray or amber brown and opalescent Few days after eruption teeth may achieve a normal color, following which they become translucent
    • 14.  Finally become gray or brown with bluish reflection from enamel  Enamel may split readily from dentin when subjected to occlusal stress  Severe attrition of teeth  Obliterated pulp chamber  Sauk et al (1976)increase in glycosaminoglycans in edta soluble dentin in teeth from patients with this disorder as compared to controls and less gag in edta insoluble residue
    • 15.  Teeth are not sensitive  Dentin is soft and easily penetrable but not caries prone because of structural change in dentin  In some case there may be hypomineralised area on the enamel
    • 16.  Bulb shaped or bell shaped crowns of teeth with constricted cervical areas  Roots - thin and spiked  Obliteration of coronal and radicular pulp chamber depending on age  Cementum, alveolar bone and PDL appears normal  Type 2large pulp chambers with thin shell of dentin and enamel “shell teeth”
    • 17.  Enamelnormal  Mantle dentin (narrow zone of dentin below enamel)normal  Remaining dentin severely dysplastic with vast areas of amorphous matrix with globular or interglobular foci of mineralization  Reduced number of dentinal tubules
    • 18.  Tubules distorted, irregular in shape, widely spaced ,larger in size  Absence of odontoblastic processes and presence of degenerating cellular debris instead  Large area of atubular dentin  Pulp chamber and root canal obliterated by abnormal dentin deposition  DEJ smooth or flattened instead of scalloped (responsible for early chipping of enamel)
    • 19.  Increased water content (60 % than normal)  Decreased mineral content  Density, x-ray absorption and hardness are low  Micro hardness near to cementum
    • 20. AIMED AT PREVENTING LOSS OF ENAMEL AND DENTIN THROUGH ATTRITION Mild –moderate cases (no enamel loss or rapid wear of teeth) 1. Routine restorative techniques Eg:amalgam, composite 2. Bonding of veneers for esthetics as they mask opalescence of anterior teeth 3. Bleaching to an extend lightens the color
    • 21. Severe cases: (significant enamel loss and rapid wear) 1. Full coverage crown restoration  2. Primary teeth  stainless steel in posteriors  stainless steel with open face anterior teeth 3. Permanent composite for teeth porcelain fused metal crowns
    • 22.  Shafer’s text book of oral pathology (6 th edition)  Oral and maxillofacial pathology-Neville (3rd edition)
    • 23. THANK YOU

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