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Developmental disturbances of teeth

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This gives the overall detail of the various developmental disturbances of teeth.

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Developmental disturbances of teeth

  1. 1. DEVELOPMENTAL DISTURBANCES OF TEETH Presented by Melbia shiny First MDS
  2. 2. contents  Classification  Clinical features  Radiological features  Treatment
  3. 3. Development of tooth
  4. 4. amelogenesis  Formation of enamel matrix  Mineralisation of matrix  Maturation of enamel
  5. 5. dentinogenesis  Cusp tip  Predentin  Dentin till tooth eruption  Hydroxyapatite crystals  Crystal deposition radially from centre (spherulite)
  6. 6. classification 1)In number  Hypodontia  Anodontia  Hyperdontia 2)In size microdontia macrodontia
  7. 7. 3)in shape  Gemination  Fusion  Concrescence  Accessory cusp  Dens invaginatus  Ectopic enamel  Taurodontism  Hypercementosis  Acessory roots  dilaceration
  8. 8. In size of teeth 1)Microdontia – teeth physically smaller than usual. i)True generalised microdontia:  all teeth smaller than normal  uncommon  in downs syndrome , pituitary dwarfism ii)Relative generalised microdontia:  normal sized teeth in larger jaws.  hereditary
  9. 9. iii)Isolated microdontia common in max lateral incisors(peg shaped crown) third molars.
  10. 10. Macrodontia/megalodontia  Teeth are physically larger than usual. i)True generalised macrodontia/diffuse:  rare  all teeth larger than normal.  in pituitary gigantism ,otodental syndrome & pineal hyperplasia with hyperinsulinism. i
  11. 11. ii) Relative generalised macrodontia: – normal sized teeth crowed in small jaw. - hereditary. iii)Isolated macrodontia: uncommon in incisors, canine, second premolar & third molar.
  12. 12. HEMIFACIAL HYPERPLASIA
  13. 13. Treatment and prognosis  Done for aesthetic purpose  Peg laterals- full size porcelain crowns.
  14. 14. In number of teeth
  15. 15. Anodontia  Total lack of tooth development. i)True anodontia/congenital absence of teeth:  all teeth are missing.  affect both dentition.  rare  in hereditary hypohidrotic ectodermal dysplasia
  16. 16. Anhydrotic ectodermal dysplasia:
  17. 17. Hypodontia  Lack of development of 1/more teeth.  common in permanents.  Affect third molars, Second premolar,laterals.  Associated with microdontia,retained primary, Decrease alveolar development.  Non syndromic involment is due to gene mutation.
  18. 18.  Affected gene correlates to missing teeth: AXIN2 gene - second & third molar,second premolar, lower incisor. Associated with adenomatous polyp of colon & colorectal carcinoma.  PAX9 gene – second molar  MSX1 gene – second premolar & third molar  He-Zhao gene – third molar, second premolar,max laterals.
  19. 19. Syndromes associated with hypodontia
  20. 20. Book’s syndrome:(PHC syndrome) agenesis of premolars hypohidrosis canities white hair
  21. 21. Riegers syndrome: agenesis of incisors. congenital glaucoma.
  22. 22. Incontinentia pigmenti/bloch- sulzberger syndrome: peg/cone shaped baldness
  23. 23. Crouzon disease:  early closure of dysostosis  acanthosis nigricans  hypoplastic maxilla
  24. 24. Ellis van crevold syndrome: enamel hypoplasia middle upper lip fuse with max gingival margin. delayed tooth eruption
  25. 25. Apert syndrome Mid face hypoplasia Syndactyly Shovel shaped incisor
  26. 26. Down syndrome Enamel hypoplasia Hypo & hyperdontia macroglossia
  27. 27. Ehler danlos syndrome  Pulp stones  Enamel hypoplasia  both
  28. 28. Oligodontia  Lack of development of 6/more teeth. Radiology  Panoramic radiographs
  29. 29. Hyperdontia increase number of tooth  Supernumerary- additional teeth  Associated with macrodontia.  Develop from third tooth bud from dental lamina.  Splitting of permanent bud  Local , conditioned hyperactivity of dental lamina.
  30. 30. Classification of supernumerary  According to morphology : 1)Rudimentary abnormal shape & size.  Conical Peg shaped, common, as mesiodens  Tuberculate barrel shape anterior with> 1 cusp, less frequent , associated with delayed incisor eruption.  Molariform small molar/premolar like.
  31. 31. 2)supplemental: normal size & shape common in max laterals. 3)Odontome hamartomas ,included in odontogenic neoplasm.
  32. 32.  According to location: 1)Mesiodens  in max anterior incisors. .
  33. 33. 2)Distomolars  distal to third molar
  34. 34. 3)Paramolar lingual /buccal to molar.  Supernumerary in soft palate, max sinus ,nasal cavity, orbit, brain ,sphenomaxillary fissure.
  35. 35. Syndromes associated with hyperdontia
  36. 36. cleidocranial dysplasia
  37. 37. Gardner syndrome
  38. 38. Hallermann streiff syndrome  Dicephalia  Parrot/beaked nose  Mandibular hypoplasia  Dwarfism  Blue sclera  hypertrichosis
  39. 39.  Dental transposition- normal teeth erupt into inappropriate position Commonly involved max. canines , first premolars
  40. 40.  Natal teeth – accessory teeth present shortly after birth  Most common mad. Incisors
  41. 41.  Neonatal teeth Teeth arising with in first 30 days of life is  Arise from bud of accessory dental lamina.
  42. 42. Treatment & prognosis Hypodontia is associated with  Abnormal spacing of teeth  Delayed tooth formation  Delayed deciduous tooth exfoliation  Late permanent tooth eruption  Altered dimension of gnathic regions Single missing tooth – no treatment
  43. 43.  Multiple teeth – prosthetic replacement with RPD, FPD, osseointegrated implant & resin bonded bridge.  Children – FPD not indicated due to risk of pulp exposure & implant not recommended till completion of skeletal growth.  Orthodontic treatment eliminate need for restorative treatment follow up radiographs since associated with external root resorption.
  44. 44.  Radiology  Panaromic radiograph with occlusal & IOPA  Natal tooth - extracted if it is mobile & risk for aspiration.  Traumatic ulceration of adjacent soft tissue is Riga-Fede disease
  45. 45. In shape of teeth
  46. 46. Gemination/schizodontia  attempt of single tooth bud to divide with resultant formation of tooth with bifid crown,common root & canal .  single enlarged tooth or  joined tooth in which  tooth count is normal.
  47. 47. Types of gemination
  48. 48.  Both dentition  > in max anterior  Radiology  Enlarged notched crown  Two pulp chambers  Single root & pulp canal
  49. 49. Fusion/syndontia  union of two normally separated tooth bud with resultant formation of joined tooth with confluence of dentin  single enlargement of tooth /joined tooth tooth count reveals missing tooth.  > in mandible.
  50. 50.  Primary- thalidomide induced embropathy Radiology  Two pulp chambers & root canals
  51. 51. Concrescence  union of two teeth by cementum without confluence of dentine 
  52. 52.  True concrescence -developmental  Acquired concrescence –tooth completion postinflammatory (areas of damage repaired by cementum
  53. 53. Treatment & prognosis  Result in crowding , abnormal spacing & delayed /ectopic eruption of permanent  pronounced labial /lingual groove are caries prone so place fissure sealant or composite restoration.  Surgical division & endodontic treatment & full crown.
  54. 54.  Concrescence interferes with eruption – surgical removal done.  Extraction difficulties & surgical separation done.
  55. 55. Accessory cusps  Cusp of carabelli  Talon cusp  Dens evaginatus
  56. 56. Cusp of carabelli  Accessory cusp on palatal surface of mesio lingual cusp of max molar.  In both dentition
  57. 57.  Accessory cusp on mesiobuccal cusp of mad permanent /deciduous molar is protostylid  > in first molar
  58. 58. Talon cusp  Is a well delineated additional cusp that is located on anterior tooth extending from CEJ to incisal edge  > in permanent max incisors  Resemble eagle’s talon  Presence of deep developmental groove  .
  59. 59.  R/F - seen in central portion of crown include enamel & dentin
  60. 60. Syndroms associated  Rubinstein taybi syndrome  Mohr syndrome  Ellis van creveld  Incontinentia pigmenti achromias  Sturge weber angiomatosis
  61. 61. Dens evaginatus/leong premolar  Cusp like elevation of enamel located in central groove/lingual ridge of buccal cusp of premolar or molar.  Bilateral
  62. 62. •Consist of enamel , dentin, & mostly pulp. Due to proliferation & evagination of inner enamel epithelium & odontogenic mesenchyme into dental organ during tooth development
  63. 63.  R/F – tuberculated appearance & pulpal extension of occlusal surface.  Shovel shaped incisors - affected incisors have prominent lateral margins & hollowed lingual surface resembling scoop of shovel.
  64. 64. Shovel shaped incisor syndrome  Interproximal caries  Lingual pit caries  Periapical & pulpal lesion  Shortened & tapered roots
  65. 65. Treatment & prognosis  Cusp of carabelli – no treatment.  Deep grooves are sealed to prevent caries.  Talon cusp – no therapy (mad teeth).  In max – interfere with occlusion hence removal  Periodic grinding for tertiary dentin deposition & pulpal recession , apply fluoride varnish (desensitizing).  After removal , dentin covered with Ca(OH)2 & enamel is etched & composite resin is placed.
  66. 66.  Dens evaginatus - occlusal interference eliminated with removal of minimum dentin & treatment with stannous fluoride.  Shovel shaped incisors – restoration of deep fissures to prevent caries.
  67. 67. Dens invaginatus/dens indente A deep surface invagination of crown/root lined by enamel. Due to invagination of surface of tooth crown before calcification occurred.
  68. 68.  > max laterals  i)coronal dens invaginatus:  Type I – invagination confined to crown.  Type II – extends below CEJ but not communicating with pulp.
  69. 69. Type III – extends through root & perforate apical / lateral radicular area.  Tooth with in tooth
  70. 70. ii) radicular dens invaginatus –  Arise secondary to proliferation of hertwig’s root sheath , with formation of enamel extending along surface of root.  Enamel deposition simillar to enamel pearl.
  71. 71.  R/F – enlargement of root  dilated invagination lined by enamel & opening of invagination along lateral aspect of root.  Mild form – pear shaped invagination of enamel & dentin
  72. 72. Treatment & prognosis  Type I – restoration of invagination to prevent caries.  If caries – endodontic treatment  Type III – temporary placement of Ca(OH)2 with endodontic treatment  Radicular - openings are closed before pulpal necrosis.
  73. 73. Palato gingival groove  Associated with periodontal defect
  74. 74. Ectopic enamel  Presence of enamel in unusual locations. i)Enamel pearl /enameloma: Hemispheric structures consist entirly of enamel/ contain dentin & pulp.
  75. 75.  Due to prolonged contact b/t hertwig’s root sheath & developing dentin inducing enamel formation.  1-4 epithelial pearls. > in root furcation /near CEJ.  R/F – well defined radiopaque nodules along root surface.(CEJ)
  76. 76. enamel pearl pulp stone
  77. 77. iii)cervical enamel extension :  Dipping of enamel from CEJ towards bifurcation of molar teeth.  Base of triangle is continuous with coronal enamel.
  78. 78. Buccal bifurcation cyst
  79. 79. Treatment & prognosis  Enamel pearl – area of weak point of periodontal attachment .  Oral hygiene maintained to prevent loss of periodontal support.  Flattening / removal of enamel & furcation plasty .
  80. 80. Taurodontism  Enlagement of body & pulp chamber of multirooted tooth , with apical displacement of pulpal floor & bifurcation of root.  Bull like tooth.  Unilateral/bilateral.  rectangular teeth with pulp chambers increased apico occlusal height & bifucation close to apex
  81. 81. etiology  Failure of hertwig’s epithelial sheath to invaginate  Mutation resulting from odontoblastic deficiency during dentinogenesis of root. Atavistic feature
  82. 82. Classification  According to degree of apical displacement of pulpal floor: i)Hypotaurodontism – mild ii)Mesotaurodontism - moderate iii)Hypertaurodontism - severe
  83. 83. Types
  84. 84. Hypertaurodont
  85. 85. Radiological features  Rectangular shape  Large pulp chambers with > apico occlusal height.  Lack of pulpal constriction ot cervical region.  Short roots  Bifurcation few mm above root apex.
  86. 86. Syndrome associated with taurodontism
  87. 87. Tricho dentoosseous syndrome  Kinky hair  Thin nail  Thickening of bones
  88. 88.  Klinfelter syndrome  Mohr syndrome  Down’s syndrome
  89. 89. Treatment & prognosis  No specific therapy  Significant periodontal destruction before furcation involvement occurs.
  90. 90. Roots  i) dilaceration  Abnormal angulation /bend in root.  Mostly idiopathic , but can occur due to injury , due to cyst /tumour.  Mostly in mad third molar, then max secon premolar, then mad second molar.  Deciduous involvement - inappropriate resorption & delayed eruption of permanent
  91. 91. Treatment & prognosis  Extraction of deciduous teeth  Endodontic treatment done carefully to avoid root perforation.  Splinting of dilacerated tooth done to overcome stress related problems , when used as abutment for prosthetic problems
  92. 92. Supernumerary root  Development of increase number of root in tooth.  Both dentition.  > in molars than cuspid & premolar  Radix entomolaris  R/F – some are seen , others superimposed
  93. 93. radix entomolaris
  94. 94. Hypercementosis/cemental hyperplasia  Non neoplastic deposition of excessive cementum continuous with normal radicular cementum  Generalised - paget’s Disease  isolated
  95. 95. radiology thickening/ blunting of root root outline is enlarged & delineated by PDL space & lamina dura
  96. 96.  hypercementosis   condensing osteitis 
  97. 97. Bulbous root  Increased dentin  Widened root apex
  98. 98. Treatment & prognosis  Detection of accessory root – decrease failure of endodontic treatment  Significance in exodontia.
  99. 99. Screw driver incisors/hutchinson’s teeth
  100. 100. Mulberry molars/fournier molar
  101. 101. Structure of teeth a)Amelogenesis imperfecta/hereditary enamel dysplasia: Developmental alteration in structure of enamel in absence of systemic disorders Classification according toWit kop (based on phenotype & pedigree.
  102. 102.  Type I -HYPOPLASTIC  Generalised pitted  Localised pitted  Localised pitted  Diffuse smooth  Diffuse smooth  Diffuse rough  Enamel agenesis
  103. 103.  Type II – HYPOMATURATION  Diffuse pigmented  Diffuse  Snow capped  Snow capped
  104. 104.  Type III- HYPOCALCIFIED  Diffuse  Diffuse  Type IV A– HYPOMATURATION- HYPOPLASTIC  Type IV B –HYPOPLASTIC - HYPOMATURATION
  105. 105. Mutated genes 1)AMELX gene amelogenin(protein for enamel formation). 2)ENAM gene enamelin 3)MMP-20 gene enamelysin(proteinase) 4)KLK4 gene kallikrein -4 (proteinase)
  106. 106. 5)DLX3 gene code for proteins for craniofacial, tooth , hair , brain & neural development. 6)AMBN gene ameloblastin
  107. 107. Hypoplastic amelogenesis imperfecta  Inadequate deposition of enamel matrix.
  108. 108. Generalised pattern:  Pin point to pinhead sized pits  Affect buccal surface  Staining of pit
  109. 109. Localised pattern  Both dentition  Incisal,middle & buccal surface. Autosomal dominant smooth pattern:  Enamel is thin hard & glossy  Open contact points  Opaque white to translucent brown.
  110. 110. Rough pattern:  Thin , hard ,rough surfaced enamel.  Colour – white to yellowish white  Anterior open bite
  111. 111. X linked smooth pattern:  Males - diffuse,thin, smooth, & shiny  Females – vertical furrows  Open bite  Brown – yellow brown.
  112. 112.  . Enamel agenesis  Total lack of enamel formation  Yellow brown hue  Open contact points
  113. 113. Hypomaturation  defect in maturation of enamel crystals  Normal shape  Mottled, opaque, white brown yellow discoloratioN
  114. 114. Pigmented pattern:  Agar brown & mottled enamel  Enamel fracture from dentin. X linked pattern :  Lyonization seen  Focal areas of brown discolouration  Males – opaque with translucent mottling  Females – vertical bands of white opaque enamel.
  115. 115.  Snow capped pattern:  White opaque enamel on incisal/occlusal one third of crown.  Both dentition.  Anterior & posterior distribution.
  116. 116. Snow capped
  117. 117. Hypocalcified  Enamel matrix is laid down appropriately but no mineralization.  Enamel is soft & easily lost.  Yellow – brown / orange but exhibit stained brown- black.  Coronal enamel is removed with cervical portion calcified
  118. 118. Amelogenesis imperfecta with taurodontia  hypomaturation/hypoplastic :  Both dentition  Enamel – mottled yellow- white to yellow- brown.  Buccal side – pits  R/F – enamel & dentine same density  - large pulp chambers.
  119. 119.  Hypoplastic hypomaturation:  Enamel – thin  R/F - enamel & dentin same density.  - large pulp chambers.  In tricho -dento- osseous syndrome
  120. 120. CLINICAL FEATURES  Hypoplastic - pitted surface  Hypocalcified - soft enamel removed with  Prophylaxis scaler  Hypomaturation - can be pierced by explorer, lost by chipping
  121. 121. radiology  Hypoplastic - tapered crown  lack of contact  Hypocalcified - no contrast b/t enamel & dentin  Enamel moth eaten appearance  Hypomaturation - enamel chips & abrades
  122. 122.  H/F – decalcification – enamel is lost.  Ground section of non- decalcified specimens
  123. 123. Treatment & prognosis  Placement of full crowns  Severe case – full dentures (over dentures)
  124. 124. Turner’s tooth
  125. 125. Hypoplasia due to antineoplastic therapy
  126. 126. Environmental enamel hypoplasia
  127. 127. Dentinogenesis Imperfecta  Hereditary developmental disturbance of dentin in absence of systemic disorder.  Mutation of DSPP(dentin sialophosphoprotein) gene
  128. 128. Shield’s classification a)Dentinogenesis imperfecta I /capdepont teeth/shield’s type II/DI with out osteogenesis imperfecta. b)Dentinogenesis imperfecta II/ shield’s type I/DI with osteogenesis imperfecta. c)Dentinogenesis imperfecta III/brandy wine type/shell teeth
  129. 129. DI with out osteogenesis imperfecta/opalescent dentin  Blue brown discoloration
  130. 130. DI with osteogenesis imperfecta  Genes COL I A1, COL I A 2 code for type I collagen.
  131. 131. radiology .bulbous crown .thin roots .obliteration of root canal & pulp chamber. .cervical constriction .enamel hypoplasia.
  132. 132. Dentinogenesis imperfecta III/brandy wine type/shell teeth  Dentin is amber & smooth  R/L - enamel normal  Thin dentin  Enlarged pulp (shell teeth)
  133. 133. Histology  Dentin near enamel is normal, rest abnormal  Atypical odontoblast lining pulp surface are entrapped in defective dentin  Enamel is normal
  134. 134. Treatment & prognosis  Crown not recommended ( cervical fracture) , so over lay dentures & teeth covered with Fluorid releasing GIC
  135. 135. Dentin dysplasia  Type I - radicular dentin dysplasia/ rootless teeth  Type II - coronal dentin dysplasia
  136. 136. Rootless tooth  Short root - less root dentin  Tooth mobility (premature exfoliation)  Predispose to fracture
  137. 137. O’carroll’s classification of Dentin dysplasia
  138. 138. Type I a typeI d
  139. 139. Coronal dentin dysplasia blue–amber-brown R/L – thistle tube/ flamed shape
  140. 140. Pulpal dysplasia  Normal clinically  Both dentition thistle tube shaped / flamed shaped  Multiple pulp stones
  141. 141. Histology  Type I coronal enamel & dentin normal  Whorls of dentin & atypical osteodentin (stream flowing around boulders)  Type II numerous interglobular dentin near pulp Pulp stones
  142. 142. Treatment & prognosis  Type I - short root s (early loss from periodontitis)  Pulp channels close to DEJ ( restoratio n & endodontic treatment)  Type II - permanent - endodontic treatment
  143. 143. Regional odontodysplasia/ghost teeth  Localised , non hereditary developmental abnormality of teeth with extensive adverse effect on formation of enamel dentin & pulp
  144. 144. Clinical feature  Yellow to brown , rough surface  Dentinal cleft & long pulp horn  Max >  R/L - short root  open apex  Thin enamel & dentin  Widened pulp chamber  Ghost teeth
  145. 145. Histology  Enameloid conglomerates - focal collection of basophilic enamel like calcification.
  146. 146. Treatment & prognosis  Retension of altered teeth to pressure surrounding alveolar ridge  Unerupted teeth - left till skeletal growth completes  Erupted teeth - etched retained restoration/stainless steel crowns  Osseointegrated implant after pubertal growth.
  147. 147. references  Text book of oral pathology shafer, hine levy  Colour atlas of common oral diseases langlais miller  Human embryology inderber singh  Diagnostic imaging of jaws – langlais langland  Oral 7 maxillofacial pathology neville damm  Orbans oral histology & embrology
  148. 148. Thank you

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