This document discusses various developmental disturbances that can affect teeth, including abnormalities in number, size, and shape. It classifies and describes conditions like hypodontia (missing teeth), hyperdontia (extra teeth), microdontia, macrodontia, gemination, fusion, dens invaginatus, and others. For each type of disturbance, it covers clinical features, radiographic findings, associated syndromes, and recommendations for treatment and prognosis. Overall, the document provides a comprehensive overview of developmental disturbances that can impact odontogenesis.

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