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

1. DEVELOPMENTAL DISTURBANCES
OF TEETH
Presented by
Melbia shiny
First MDS

2. contents
 Classification
 Clinical features
 Radiological features
 Treatment

3. Development of tooth

5. amelogenesis
 Formation of enamel matrix
 Mineralisation of matrix
 Maturation of enamel

6. dentinogenesis
 Cusp tip
 Predentin
 Dentin till tooth eruption
 Hydroxyapatite crystals
 Crystal deposition radially from centre
(spherulite)

7. classification
1)In number
 Hypodontia
 Anodontia
 Hyperdontia
2)In size
microdontia
macrodontia

8. 3)in shape
 Gemination
 Fusion
 Concrescence
 Accessory cusp
 Dens invaginatus
 Ectopic enamel
 Taurodontism
 Hypercementosis
 Acessory roots
 dilaceration

9. 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

10. iii)Isolated microdontia
common in max lateral incisors(peg shaped
crown)
third molars.

11. 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

13. ii) Relative generalised macrodontia:
– normal sized teeth crowed in
small jaw.
- hereditary.
iii)Isolated macrodontia:
uncommon
in incisors, canine, second
premolar & third molar.

14. HEMIFACIAL HYPERPLASIA

15. Treatment and prognosis
 Done for aesthetic purpose
 Peg laterals- full size porcelain crowns.

16. In number of teeth

17. 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

18. Anhydrotic ectodermal
dysplasia:

19. 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.

21.  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.

22. Syndromes associated with
hypodontia

23. Book’s syndrome:(PHC
syndrome)
agenesis of premolars
hypohidrosis
canities
white hair

24. Riegers syndrome:
agenesis of incisors.
congenital glaucoma.

25. Incontinentia
pigmenti/bloch- sulzberger
syndrome:
peg/cone shaped
baldness

26. Crouzon disease:
 early closure of dysostosis
 acanthosis nigricans
 hypoplastic maxilla

27. Ellis van crevold syndrome:
enamel hypoplasia
middle upper lip fuse with max
gingival margin.
delayed tooth eruption

28. Apert syndrome
Mid face hypoplasia
Syndactyly
Shovel shaped incisor

29. Down syndrome
Enamel hypoplasia
Hypo & hyperdontia
macroglossia

30. Ehler danlos syndrome
 Pulp stones
 Enamel hypoplasia
 both

31. Oligodontia
 Lack of development of 6/more teeth.
Radiology
 Panoramic radiographs

32. 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.

33. 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.

35. 2)supplemental:
normal size & shape
common in max laterals.
3)Odontome
hamartomas ,included in odontogenic
neoplasm.

36.  According to location:
1)Mesiodens
 in max anterior incisors.
.

37. 2)Distomolars
 distal to third molar

38. 3)Paramolar
lingual /buccal to molar.
 Supernumerary in soft palate, max sinus
,nasal cavity, orbit, brain ,sphenomaxillary
fissure.

39. Syndromes associated with
hyperdontia

40. cleidocranial dysplasia

41. Gardner syndrome

42. Hallermann streiff syndrome
 Dicephalia
 Parrot/beaked nose
 Mandibular hypoplasia
 Dwarfism
 Blue sclera
 hypertrichosis

43.  Dental transposition- normal teeth erupt into
inappropriate position
Commonly involved max. canines , first
premolars

44.  Natal teeth – accessory teeth present shortly
after birth
 Most common mad. Incisors

45.  Neonatal teeth
Teeth arising with in first 30 days of life is
 Arise from bud of accessory dental lamina.

46. 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

47.  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.

48.  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

49. In shape of teeth

50. 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.

51. Types of gemination

52.  Both dentition
 > in max anterior
 Radiology
 Enlarged notched crown
 Two pulp chambers
 Single root & pulp canal

53. 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.

54.  Primary- thalidomide induced embropathy
Radiology
 Two pulp chambers & root canals

55. Concrescence
 union of two teeth by cementum without
confluence of dentine


56.  True concrescence -developmental
 Acquired concrescence –tooth completion
postinflammatory (areas of damage repaired
by cementum

58. 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.

59.  Concrescence interferes with eruption –
surgical removal done.
 Extraction difficulties & surgical separation
done.

60. Accessory cusps
 Cusp of carabelli
 Talon cusp
 Dens evaginatus

61. Cusp of carabelli
 Accessory cusp on palatal surface of mesio
lingual cusp of max molar.
 In both dentition

62.  Accessory cusp on mesiobuccal cusp of mad
permanent /deciduous molar is protostylid
 > in first molar

63. 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
 .

64.  R/F - seen in central portion of crown include
enamel & dentin

65. Syndroms associated
 Rubinstein taybi syndrome
 Mohr syndrome
 Ellis van creveld
 Incontinentia pigmenti achromias
 Sturge weber angiomatosis

66. Dens evaginatus/leong
premolar
 Cusp like elevation of enamel located in
central groove/lingual ridge of buccal cusp of
premolar or molar.
 Bilateral

67. •Consist of enamel , dentin, &
mostly pulp.
Due to proliferation &
evagination of inner enamel
epithelium & odontogenic
mesenchyme into dental
organ during tooth
development

68.  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.

69. Shovel shaped incisor
syndrome
 Interproximal caries
 Lingual pit caries
 Periapical & pulpal lesion
 Shortened & tapered roots

71. 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.

72.  Dens evaginatus - occlusal interference
eliminated with removal of minimum dentin
& treatment with stannous fluoride.
 Shovel shaped incisors – restoration of deep
fissures to prevent caries.

73. 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.

74.  > max laterals
 i)coronal dens invaginatus:
 Type I – invagination confined to crown.
 Type II – extends below CEJ but not
communicating with pulp.

75. Type III – extends through root & perforate
apical / lateral radicular area.
 Tooth with in tooth

76. 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.

77.  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

79. 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.

80. Palato gingival groove
 Associated with periodontal defect

81. Ectopic enamel
 Presence of enamel in unusual locations.
i)Enamel pearl /enameloma:
Hemispheric structures consist entirly of
enamel/ contain dentin & pulp.

82.  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)

83. enamel pearl pulp stone

84. iii)cervical enamel extension :
 Dipping of enamel from CEJ towards
bifurcation of molar teeth.
 Base of triangle is continuous with coronal
enamel.

85. Buccal bifurcation cyst

86. 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 .

87. 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

88. etiology
 Failure of hertwig’s epithelial sheath to
invaginate
 Mutation resulting from odontoblastic
deficiency during dentinogenesis of root.
Atavistic feature

90. Classification
 According to degree of apical displacement of
pulpal floor:
i)Hypotaurodontism – mild
ii)Mesotaurodontism - moderate
iii)Hypertaurodontism - severe

91. Types

92. Hypertaurodont

93. 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.

94. Syndrome associated
with taurodontism

95. Tricho dentoosseous syndrome
 Kinky hair
 Thin nail
 Thickening of bones

96.  Klinfelter syndrome
 Mohr syndrome
 Down’s syndrome

97. Treatment & prognosis
 No specific therapy
 Significant periodontal destruction before
furcation involvement occurs.

98. 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

100. 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

101. 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

102. radix
entomolaris

103. Hypercementosis/cemental
hyperplasia
 Non neoplastic deposition of excessive
cementum continuous with normal
radicular cementum
 Generalised - paget’s
Disease
 isolated

104. radiology
thickening/
blunting of root
root outline is enlarged &
delineated by PDL
space & lamina
dura

105.  hypercementosis

 condensing osteitis


106. Bulbous root
 Increased dentin
 Widened root apex

107. Treatment & prognosis
 Detection of accessory root – decrease failure
of endodontic treatment
 Significance in exodontia.

108. Screw driver
incisors/hutchinson’s teeth

109. Mulberry molars/fournier
molar

110. 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.

111.  Type I -HYPOPLASTIC
 Generalised pitted
 Localised pitted
 Localised pitted
 Diffuse smooth
 Diffuse smooth
 Diffuse rough
 Enamel agenesis

112.  Type II – HYPOMATURATION
 Diffuse pigmented
 Diffuse
 Snow capped
 Snow capped

113.  Type III- HYPOCALCIFIED
 Diffuse
 Diffuse
 Type IV A– HYPOMATURATION-
HYPOPLASTIC
 Type IV B –HYPOPLASTIC -
HYPOMATURATION

114. 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)

115. 5)DLX3 gene
code for proteins for craniofacial, tooth ,
hair , brain & neural development.
6)AMBN gene
ameloblastin

116. Hypoplastic amelogenesis
imperfecta
 Inadequate deposition of enamel matrix.

117. Generalised pattern:
 Pin point to pinhead sized pits
 Affect buccal surface
 Staining of pit

118. 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.

120. Rough pattern:
 Thin , hard ,rough surfaced enamel.
 Colour – white to yellowish white
 Anterior open bite

122. X linked smooth pattern:
 Males - diffuse,thin, smooth, & shiny
 Females – vertical furrows
 Open bite
 Brown – yellow brown.

123.  .
Enamel agenesis
 Total lack of enamel formation
 Yellow brown hue
 Open contact points

124. Hypomaturation
 defect in maturation of enamel crystals
 Normal shape
 Mottled, opaque, white brown yellow
discoloratioN

125. 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.

127.  Snow capped pattern:
 White opaque enamel on incisal/occlusal one
third of crown.
 Both dentition.
 Anterior & posterior distribution.

128. Snow capped

129. 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

131. 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.

132.  Hypoplastic hypomaturation:
 Enamel – thin
 R/F - enamel & dentin same density.
 - large pulp chambers.
 In tricho -dento- osseous syndrome

133. CLINICAL FEATURES
 Hypoplastic - pitted surface
 Hypocalcified - soft enamel removed with
 Prophylaxis scaler
 Hypomaturation - can be pierced by
explorer, lost by chipping

134. radiology
 Hypoplastic - tapered crown
 lack of contact
 Hypocalcified - no contrast b/t enamel &
dentin
 Enamel moth eaten appearance
 Hypomaturation - enamel chips & abrades

135.  H/F – decalcification – enamel is lost.
 Ground section of non- decalcified specimens

136. Treatment & prognosis
 Placement of full crowns
 Severe case – full dentures (over dentures)

137. Turner’s tooth

138. Hypoplasia due to
antineoplastic therapy

139. Environmental enamel
hypoplasia

140. Dentinogenesis Imperfecta
 Hereditary developmental disturbance of
dentin in absence of systemic disorder.
 Mutation of DSPP(dentin
sialophosphoprotein) gene

141. 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

142. DI with out osteogenesis
imperfecta/opalescent dentin
 Blue brown discoloration

143. DI with osteogenesis
imperfecta
 Genes COL I A1, COL I A 2 code for type I
collagen.

144. radiology
.bulbous crown
.thin roots
.obliteration
of root canal & pulp
chamber.
.cervical constriction
.enamel hypoplasia.

145. Dentinogenesis imperfecta
III/brandy wine type/shell teeth
 Dentin is amber & smooth
 R/L - enamel normal
 Thin dentin
 Enlarged pulp (shell teeth)

146. Histology
 Dentin near enamel is normal, rest abnormal
 Atypical odontoblast lining pulp surface are
entrapped in defective dentin
 Enamel is normal

147. Treatment & prognosis
 Crown not recommended ( cervical
fracture) , so over lay dentures & teeth
covered with Fluorid releasing GIC

148. Dentin dysplasia
 Type I - radicular dentin dysplasia/ rootless
teeth
 Type II - coronal dentin dysplasia

149. Rootless tooth
 Short root - less root dentin
 Tooth mobility (premature exfoliation)
 Predispose to fracture

150. O’carroll’s classification
of Dentin dysplasia

151. Type I a
typeI d

152. Coronal dentin dysplasia
blue–amber-brown
R/L – thistle tube/
flamed shape

153. Pulpal dysplasia
 Normal clinically
 Both dentition thistle tube shaped / flamed
shaped
 Multiple pulp stones

154. 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

155. 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

156. Regional
odontodysplasia/ghost teeth
 Localised , non hereditary developmental
abnormality of teeth with extensive
adverse effect on formation of enamel
dentin & pulp

157. 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

158. Histology
 Enameloid conglomerates - focal collection
of basophilic enamel like calcification.

159. 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.

160. 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

161. Thank you