Development of Tooth

1. DEVELOPMENT
OF
TOOTH
DR RIPIKA SHARMA
1ST YEAR MDS
PUBLIC HEALTH
DENTISTRY

2. CONTENTS
• Introduction
• Formation of dental lamina
• Stages of tooth development
• Development of enamel,dentin,pulp,cementum and
periodontal ligament
• developmental anomalies & clinical considerations
• Recent research trends in tooth development
• Summary & conclusion
• References

3. INTRODUCTION

4. GROWTH (Meridith)
Entire series of sequential anatomic and physiologic
changes taking place from beginning of prenatal life
to senility.
DEVELOPMENT (Moyers)
All the naturally occurring unidirectional changes in the
life of an individual ,from its existence as a single cell
to its elaboration as a multifunctional unit,
terminating in death.

5. Why study growth &development of teeth?
Diagnose developmental anomalies of teeth
treat them successfully
restore function,esthetics and comfort of the patient

7. • Hard, inert, acellular ENAMEL
• Less mineralized
More resilient, vital DENTIN
Hard
• Soft tissue PULP
• Tooth supporting
connective tissues CEMENTUM
PERIODONTAL LIGAMENT
ALVEOLAR BONE

9. DEVELOPMENT OF THE TOOTH
 The primitive oral cavity or stomatodeum is lined by
stratified squamous epithelium called the oral
ectoderm.
 If we see under a light microscope, the newly formed
stomatodeum appears to be lined by 2-3 cell thick
layered epithelium covering an embryonic
connective tissue termed as ectomesenchyme,
these cells are thought to induce the overlying
ectoderm to start tooth development.

10. • Primary Epithelial Band :
 Oral ectoderm contacts the ectoderm of the
foregut to form the buccopharyngeal membrane.
 At about 27th day of gestation this membrane
ruptures and the primitive oral cavity establishes a
connection with the foregut.
 Most of the connective tissue cells underlying the
oral ectoderm are of neural crest or
ectomesenchyme in origin.

11.  When embryo is about 6 weeks old, certain area of
basal cells of oral ectoderm proliferate more rapidly
than do the cells of the adjacent areas.
leads to formation
of
PRIMARY EPITHELIAL BAND
 At about 7th week the primary epithelial band divided into
lingual process buccal process
DENTAL LAMINA VESTIBULAR LAMINA

12. Formation of the primary epithelial band
Thickening of ectodermal cells forms this band

13. Primary epithelial band

14. Not so much of proliferative activity at the
epithelium.....but change in orientation of mitotic
spindles at the region!*
*1970 Linde/Ruch

16. formation of dental and vestibular lamina
Distally gives
rise to
permanent
molars
Vestibular
lamina
(labially)
Dental lamina
(lingually)
Primary epithelial band
Its Lingual extension
(successional)
All permanents except
molars
primary
teeth

17. Vestibular Lamina :
 Labial and buccal to the dental lamina in each
dental arch ,another epithelial thickening develops
independently
 It is the vestibular lamina and also termed as Lip
Furrow band.
 It subsequently hollows and forms the oral
vestibule between the alveolar portions of the jaws
and the lips and cheeks.

18. Dental Lamina :
Within the dental lamina, continued and localised
proliferative activity leads to the formation of a series of
epithelial ingrowths into the ectomesenchyme at sites
corresponding to the positions of future deciduous tooth.
 So, the dental lamina serve as a primordium for the
ectodermal portion of the deciduous teeth .

19. Fate of Dental Lamina
• Activity of dental lamina extends
over a period of 5 years.
• Sometimes, it may be active in the
third molar area.
• As the teeth continuous to
develop they loose their
connection with the dental lamina
• Remnants of dental lamina persist
as epithelial pearls or islands –
Cell Rests of Serres

20. Clinical Significance :
•Any physical obstruction / disruptions of dental lamina may
result in the congenital absence of the teeth.
•Failure of the induction of underlying ectomesenchyme 
absence of dental lamina which may lead to absence of teeth.
•If there is an over proliferation of dental lamina leads to
macrodontia.
The distal proliferation of the dental lamina sometime is
responsible for the location of the germs of permanent
molars in the ramus of mandible and in the tuberosity of the
maxilla

22. Formation of enamel organ
10 small swellings develop in the region
of future primary teeth
They form enamel organ and give rise to
the enamel of the teeth

23. • Tooth germ consist of
Ectodermal Component Ectomescenchymal Component
ENAMEL ORGAN DENTAL PAPILLA
DENTAL FOLLICLE

24. Dental papilla and sac
Peripheral condensation
of ectomesenchymal
cells around enamel
organ forms dental
papilla
Surrounding dental
papilla and enamel
organ is dental follicle
or sac

25. Initiation of Tooth Development
Oral epithelial cells Mesenchymal cells
Enamel organ
Enamel
Dental Papilla
Dentin
Pulp
Dental Sac
Cementum
Perio lig.
Alveolar
socket

27. STAGES IN THE
DEVELOPMENT
OF TOOTH

28. • What initiates tooth development ?
• What determines tooth shape ?
• What determines tooth position ?

29. What initiates tooth development ?

30. Oral epithelium of first arch
Produces signalling molecules*
Expression of Lhx-6/7(lim-
homeobox) genes in the
mesenchyme
Initiation of tooth development
*Thesleff et al.1995

31. TOOTH TYPE/SHAPE DETERMINATION
(PATTERNING)
 Determination of specific tooth types at their correct position
in jaw is patterning.
 Mammals are heterdont.(tooth come under 3 families
incisor,canine and molars)
 Two hypothetical models explains patterning,

32. What determines tooth shape ?
Determination of specific tooth types at their
correct positions in jaws
Patterning of dentition
2 hypothetical models
field model clone theory

33. Field model* *(McCollum/Sharpe)2001
 Factors responsible for tooth shape reside in the
ectomesenchyme in distinct but graded fields for each
tooth family
Ex: - each of the field expresses differing
combinations of patterning Homeobox genes

34. Homeo box genes support this theory.
This model is based on observation of spatially restricted
expression of several homeobox genes in ectomesenchyme
cells of that particular field
Group of homeo box genes expressed in incisor field will
influence formation of incisor teeth in that region ;where
as group of homeo box genes expressed in molar field will
influence the formation of molar teeth in that region .

35.  FGF8,BMP4,are also expressed here & induce many
expression genes in mesenchyme as overlapping domain and
provide spatial information needed for patterning.
 Molar region- domains of Barx-1, Dlx-1/-2
 Incisor region- domains of Msx1,Msx2,Alx-3
 Canine & premolars- Dlx-1/-2, Msx1

36. Homeo Box Code Model

37. Premolar—Msx-1,Dlx-1,Dlx-2

38. Clone model* *(Osborne/Tencate)1983
Each tooth crown is derived from a clone of
ectomesenchymal cells programmed by the
epithelium to produce teeth of a given pattern
Proposes that each tooth class is derived from a
clone of E-M cells programmed by epithelium to
produce teeth of a given pattern
Ex: - isolated presumptive first molar tissues
continue to develop to form third molar teeth in their
normal positional sequence.

40. What determines tooth position ?
Pax-9 Gene *: Earliest mesenchymal gene
that defines location of tooth germ
Co-localizes with the exact sites where tooth
germs appear
*Tencate2000

41. 3 morphological stages in tooth development are seen------
Stages named after the shape of the enamel organ and are
called as………………….
BUD STAGE
CAP STAGE
BELL STAGE
early
advanced

42. Stages of Tooth Development
Morphologic
Stages
Dental lamina
Bud stage
Cap stage
Bell stage- early
Bell stage- advanced
Form of enamel and
dentin matrix
Physiologic process
Proliferation
Initiation
Histodifferentiation
Morphodifferentiation
Apposition

43. BUD STAGE (8th week of IUL)
• First morphological stage in tooth development
• Physiologic process involved-proliferation.
• Derives its name from shape of developing enamel
organ
• Enamel organ  small ovoid epithelial mass
• Peripheral low columnar cells; centrally polygonal
cells
• Epithelial cells have RNA and enzymes
• Underlying ectomesenchymal cells closely packed,
also shows proliferation and condensation, with
basement membrane still intact.

44. Oral ectoderm
Dental lamina
Central Polyhedral cells
Ectomesenchymal cells
Peripheral cuboidal cells
BUD STAGE

45. Bud stage

46. Bud stage and its relation to adjacent structures

47. CAP STAGE 9th to 10th week IUL
PHYSIOLOGIC PROCESS INVOLVED –proliferation,
differentiation, morphogenesis.
• Named so,Due to nonuniform expansion of
enamel organ
• Shallow invagination on deep surface of bud
• Dental papilla cells seem to be contained in the
invagination ; hence the name
• Distinct histologic structures seen now

48. Histology of cap stage
1) Inner and outer enamel epithelia:
Peripheral low cuboidal in shape
columnar cells------> (cap stage)
(bud stage) OUTER ENAMEL
EPITHELIUM
Cells in concavity of cap--->tall columnar
INNER ENAMEL
EPITHELIUM

49. • STELLATE RETICULUM
• Cells in centre of enamel organ b/w OEE & IEE are
polygonal / star shaped called Stellate Reticulum they
synthesise glycosaminoglycan which is hydrophillic, pull
water from surrounding ectomesenchyme by osmotic
force .
• As a result polygonal cells force apart become star shaped
but retain contact with each other by cytoplasmic process.

50. Mucoid fluid b/w star shaped cells are rich in albumin
gives cushion like consistency act as shock absorber &
protect ,support enamel forming cells.
*Pannese E (1960)

51. Cap stage
Oral ectoderm
Oral ectoderm
Outer enamel epithelium
Stellate reticulum
Inner enamel epithelium
Dental Papilla
Dental Sac

52. Basal lamina separates
inner/outer epithelial
cells from dental
papilla and dental sac
respectively

53. Stellate reticulum

54. Transient structures
Enamel knot
Clusters of non-dividing
epithelial cells
At deepest portion of
invagination of enamel
organ
Enamel cord
Linear condensation of
cells from inner to
outer enamel
epithelium

55. • When the enamel cord extends to meet the OEE it is
termed as enamel septum, dividing the stellate
reticulum into two parts.
• OEE at the point of meeting shows a small
depression and this is termed as enamel navel.
• These all are temporary structures that disappear
before the enamel formation begins.

56. • Enamel niche
 Enamel organ may be seen to have a double
attachment of dental lamina to the overlying oral
epithelium enclosing ectomesenchyme called
enamel niche between them.
 This appearance is due to funnel shaped
depression of the dental lamina.

57. • FUNCTIONS
• 1) Acts as a reservoir of dividing cells of growing
enamel organ .
• 2) Enamel knot acts as a signaling centre ,many
important growth factors are expressed by the clls of
the enamel knot play an important role in
determining shape of the tooth.

58. BELL STAGE 11 -12TH WEEK IUL
Morpho and histodifferentiation occurs
2 stages
Early advanced

59. Early Bell Stage
• Enamel organ enlarges further and changes shape
to a Bell
• Four layers are seen
- Inner enamel epithelium lining concave or -
invaginated part
- Sratum intermedium
- Stellate reticulum
- Outer enamel epithelium lining the convex
portion
• Dental lamina degenerates

60. Outer enamel epithelium
• Cells become more flattened
• Separated from dental sac by basement
membrane.
• Cells are attached to each other by
desmosomes and to basement membrane by
hemidesmosomes.
• Convex outer boundary is smooth which later
turns to irregular bringing blood vessels closer
to the ameloblasts

61. Stellate reticulum
• Becomes more prominent.
• Net work of strar shaped cells with long
processes anastomosing to each other.
• Cells are attached to each other and to
adjacent layers by desmosomes.
• As tooth dev. progresses this layer collapses
bringing blood vessels further closer to the
ameloblasts.

62. Stratum intermedium
• New layer that appear in the enamel organ between stellate
reticulum and inner enamel epithelium in bell stage.
• Composed of 2- 3 layers of squamous cells, strongly attached
to each other and to adjacent layers by desmosomes.
• Cells are metabolically active and rich in alkaline phosphatase
enzyme, therefore assisting ameloblasts to synthesize
enamel.
• Enamel knot contribute cells for formation of this layer.

63. Inner enamel epithelium
• Differentiate into Ameloblasts, the Enamel forming
cells.
• Cells become tall columnar with width of 4 microns
and height of 40 microns.
• Develop rich synthetic cytoplasmic organelles.
• Before enamel formation starts nucleus of these cells
move away from basal region to the apical portion,
allowing the synthetic organelles to move to basal
region. This is called reversal of polarity.

64. • Separated from dental papilla by basement
membrane.
• Cells are attached to each other by
desmosomes and to basement membrane by
hemidesmosomes.
• Exerts an organizing influence on dental pailla
helping in formation of odontoblsts

65. Membrana preformativa
• The basement membrane lining the invaginated
portion of enamel organ, separating the ameloblast
layer from dental papilla is called Membrana
preformativa.
• This is called blue print of crown of developing tooth
because the shape of the crown depends on the
shape of MP

66. Cervical loop
• The cervical part of enamel organ where outer
enamel epithelium joins to inner enamel epithelium.
• In this region only two layers, outer enamel
epithelium and inner enamel epithelium are present.
• In advanced bell stage cervical loop proliferates to
form Hertwig’s Epithelial Root Sheath that forms root
of tooth.

67. Dental lamina
• Degenerates in bell stage and enamel organ
looses connection with oral ectoderm.
• Remnants are called cell rests of Serres.
• Successional lamina develops lingualy which
forms permanent successors.

68. Ectomesenchymal components
• Dental Papilla
• Dental sac

69. Dental papilla
• Completely enclosed in the invaginated
portion of enamel organ.
• Cells are closely packed with fine collagen and
rich capillary loops.

70. BELL STAGE
Dental sac
Outer enamel epithelium
Stellate reticulum
Strarum intermedium
ameloblasts
Dental papilla
Cervical loop
Odontoblasts

72. Advanced bell stage
Events occuring include--->
1) Crown pattern formation :
inner enamel epithelial cells stop dividing at
“growth center”where future cusp will
develop
Epithelial cells buckle inwards to form cusp
outline

73. Advanced Bell stage
• Also called crown stage of tooth dev.
• All four layers are seen in enamel organ
- Inner enamel epithelium/ Ameloblast layer
- Stratum intermedium
- Stellate reticulum
- Outer enamel epithelium

74. Histological differences
• Dentin deposition starts, followed by enamel.
• Outer enamel epithelium becomes irregular
by developing infoldings.
• Stellate reticulum collapses.
• Source of nutrition to ameloblasts changes
from dental papilla to dental sac.

75. • Dentin is the first hard tissue that is formed.
• Enamel formation can occur only after a layer of
dentin is deposited. The interdependence between
ameloblasts and odontoblasts is called Reciprocal
induction.
• Hard tissue formation starts at future dentino
enamel junction, in the region of incisal edge or
cusp tip and progresses cervically.
• Enamel formation progresses from DEJ outward
with ameloblasts moving to the surface.
• Dentin formation progresses from DEJ inwards with
odontoblasts moving pulpally.

76. Advanced Bell stage
Stellate reticulum
Enamel
Dentin
Odontoblasts
Outer enamel epithelium

77. Bell Stage

78. Primary tooth bud acquires its final shape

79. Tooth bud

80. HERS formed from inner/outer enamel epithelia

82. Root Development
Cervical loop proliferates
Formation of Hertwig’s Epithelial Root
Sheath
Formation of epithelial
diaphragm
Inner cells of HERS causes differntiation
of odontoblasts
Radicular dentin formation

83. • Degeneration of HERS and formation of cell rests of Malassez
Differentiation of cementoblasts from
dental sac
Cementum formation
Orientation of perio.lig

84. Formation of multiple roots

87. NEURAL CREST CELLS
• Group of pleuripotent cells that develop from
ectoderm along lateral margins of neural plate.
• Cells migrate between ectoderm, endoderm and
intramesodermally in developing embryo.
• These cells move around the sides of developing
head beneath ectoderm as sheet of cells. They
migrate and form entire connective tissue of upper
facial region. Hence the connective tissue –
ectomesenchyme.

88. STRUCTURES DEVELOPING FROM NEURAL
CREST CELLS
• Bone, cartilage, dermis, tooth forming tissues,
muscle and arteries of H&N.
• In the trunk region, neural, endocrine and
pigment producing cells. Sensory ganglion,
schwann cells and neurons.

89. DEVELOPMENT
OF
ENAMEL
(AMELOGENESIS)

90. Life cycle of ameloblasts has 6 stages---->
• Morphogenic
• Organizing
• Formative
• Maturative
• Protective
• Desmolytic

91. Morphogenic stage
• Cells short columnar
• Large oval nuclei
• Golgi apparatus and the
centrioles at proximal end
• Mitochondria scattered

92. Organizing stage
• Inner enamel
epithelium cells
become longer
• Golgi body/centrioles
migrate to distal end
(reversal of polarity)
• Mitochondria move
proximally
• Differentiation of
odontoblastsdentin
• Formation begins in
the terminal phase of
this stage.

93. Formative stage
• Begins after the first
dentin deposited
• Cell length increases
further
• Blunt processes develop on
ameloblast surfaces facing
developing enamel
(TOME’S PROCESSES)
• Stage of enamel matrix
formation.

94. Tome’s processes

95. Maturative stage
• Mineralization occurs
after matrix
deposition
• Ameloblasts display
microvilli at distal end
• Size of cells reduced
somewhat

96. Protective stage
• Ameloblasts cannot
be differentiated
from other enamel
organ cells
• All layers together
form reduced
enamel epithelium
• Protects mature
enamel
• Separates it from
connective tissue

97. Desmolytic stage
• Reduced enamel epithelium causes atrophy
of connective tissue separating it from oral
epithelia
• Fusion of these epithelia occurs facilitating
eruption
• Epithelial cells secrete enzymes to destroy
connective tissues by desmolysis
• Premature degeneration REE may prevent
eruption of tooth.

98. Reduced enamel epithelium

99. Maturation of enamel
2 stages
Immediate partial maturation starting from
mineralization of crown tip cervically
matrix segments
• Organic matrix thinned down to accommodate
growing crystals

100. DEVELOPMENT
OF
DENTIN
DEVELOPMENT
OF
DENTIN
(DENTINOGENESIS)

101. • Before dentinogenesis,
inner enamel epithelial
cells short columnar
• Dental papillary cells
separated from them
by an acellular zone
• Papillary cells
small,undifferentiated

102. Epithelial cells become
taller,columnar with nuclei
migrated to opposite pole
papillary cells divide with
spindle 90° to basal lamina
acellular zone obliterated as
odontoblast differentiates

103. Daughter cell influenced by
epithelial cell differentiates
into pre-odontoblast
other cell not influenced by
this factor forms sub-
odontoblast
induction factor --->IGF and
others secreted by basal
lamina*
*Sasaki(1996)

104. Finally cells close to basement
membrane develop into
odontoblasts
later start depositing dentin
sub-odontoblast forms
reparative dentin later if at all
need arises

105. Mineralization of dentin
Odontoblasts differentiate
Deposit organic matrix(ground substance)
Type I collagen deposited
Matrix of mantle dentin formed
HAC deposited--->mantle dentin
Primary/circumpulpal dentin
Secondary dentin

107. Deposition of minerals always lags behind the
formation of organic matrix
So there is always a layer of organic matrix
called ----->PRE-DENTIN between
odontoblasts and the mineralization front

108. predentin

109. DEVELOPMENT
OF
PULP

110. • Dental papilla forms pulp
• young papillary cells are highly vascularised
with undifferentiated cells
• Later form stellate shaped fibroblasts
• After ameloblasts/odontoblasts form and
dentin laid down--->pulp organ
• With maturation of dentin, pulp also forms
nerves and develops further

113. DEVELOPMENT
OF
CEMENTUM

115. Deposition of dentin along inner aspect of HERS
Breaks in HERS occur
New dentin comes in direct contact with sac
connective tissue
Collagen/cementoblasts form between epithelial
cells of root sheath
Cementoblasts lay down cementoid

116. Cementoid is lined by cementoblasts
Connective tissue fibres from periodontal
ligament pass between cementoblasts into
cementum
Attach tooth to surrounding bone
Sharpey’s Fibers
Later cementoid gets mineralized rhythmically
Incremental lines of Salter

117. cementum lined by cementoblasts

118. Sharpey’s fibers

119. DEVELOPMENT
OF
PERIODONTAL
TISSUES

120. • After root
cementum is
deposited,some
cells of the dental
sac differentiate
into fibroblasts
• form ground
substance of
periodontal
ligament.
• Fibres embedded in
new cementum and
bone

121. development of periodontal fibers
The group of alveolar crest fibers (arrowheads),
first forming in A,
are initially oblique (B),
then horizontal (C),
and then oblique again (D).

122. DEVELOPMENTAL
ANOMALIES
AND
THEIR
CONSIDERATIONS

123. stages Results of disturbance
initiation
histodifferen
tiation
morphodiffer
entiation
apposition
Lack of initiation results in absence of single tooth
or multiple teeth(anodontia). The upper lateral
incisors followed by third molars and lower second
premolars are commonly involved.
Abnormal initiation mesiodens ,maxillary 4th
molar , geminated teeth.
Examples- dentinogenesis ,atypical dentin seen
Talons cusp, peg shaped tooth,hutchinsons
incisors , dens in dente, macrodontia
Enamel hypoplasia and hypocalcification can
occur
Intrinsic staining or concresence.

124. DENTAL AGENESIS
The dental agenesis is a common developmental
anomaly that affects approximately 20% of the population.
 Dental agenesis is classified according to the number of teeth
involved and may be classified into hypodontia,oligodontia,
and full anodontia.
 Hypodontia is defined as the congenital absence of less than
six permanent teeth ,oligodontia as the congenital absence of
more than 6 teeth and full anodontia as the absence of all
permanent teeth.
• The early diagnosis and treatment are important to improve
masticatory function, speech, and self-appearance to reduce
the psychosocial impact.
Correia MF etal. aesthetic rehabilitaion of Oligodontia in
Primary dention with adhesive partial denture; case reports
in dentistry2013.

125.  The absence of teeth is a clinical and public health problem since
the patients in these conditions may present several signs and
symptoms as reduction of the chewing ability, malocclusion,
problems in articulating words, and also the aesthetic may be
compromised.
 These complications may affect self-esteem, behavior pattern,
and social life of these patients .
 Regarding the diagnosis of oligodontia, it is normally based on
radiographic evidence and routine clinical examination, detecting
absence of teeth or delayed eruption of them.

126. Intraoral view of
dental agenesis
Intraoral view of oral
rehabilitation
Partial dental
prosthesis

127. GILLDSETAL,COUNSELLING PATIENTS WITH HYPODONTIA;DENTAL
UPDATE JUNE 2008
• Importance of dental disease prevention
• In patients with a reduced number of teeth, the importance of
maintaining the teeth which are present in a healthy condition
should be emphasized. Preventive techniques which should be
considered include:
• Diet analysis and advice;
• Oral hygiene instruction including techniques for keeping
microdont spaced teeth clean;
• Fissure sealing;
• Fluoride supplementation;
• Sports guards to protect protrusive maxillary incisors;
• Artificial saliva in patients with xerostomia (eg Ectodermal
Dysplasia).

128. • Screening siblings
• It is important to take a family history when a child is
diagnosed with hypodontia because of the genetic
association of this condition.
• Often, the affected patient will have a younger sibling and it
is beneficial to suggest to the parent that the brother or sister
be screened for hypodontia at an early stage.
• This will allow the patient to receive preventive advice and
possible interceptive treatment at an appropriate time, which
may simplify later treatment.

129. • Psycho-social implications
• Bullying
• Bullying within school children is a very common problem,
with up to 21% of children having reported being bullied at
some stage.
• Chronic bullying can lead to depression, loneliness, anxiety,
low self-esteem and underachievement at school.
• Children who bully tend to focus on one characteristic of the
victim that is considered a weakness
• . However, if this focus is removed, they are likely to find a
second focus, as it is often more general factors about the
individual which initiate the bullying, such as general
attractiveness, odd mannerisms or physical disabilities.
• Hence counseling should be provided.

130. • Financial implications
• At present in the United Kingdom the National Health Service
funds dental care for children and, typically, implant related
treatment for young adults with six or more missing teeth
• Another financial implication to be considered is the time
parents have to take off work to accompany their children for
treatment (particularly self-employed parents) and travel
costs.

131. MICRODONTIA
• Most common
example is peg
shaped lateral
incisor
• Usually no
treatment is
necessary unless
desired for
aesthetic
restoration to full
size by porcelain
crowns

132. GEMINATION AND FUSION• Usually requires
selected shaping of
teeth with or
without placement
of full crowns
• In severe cases,
teeth are surgically
removed and
prosthetic
replacement is
performed.

133. ANODONTIA
• Complete dentures for
both functional and
cosmetic purposes
• Dentures in relatively
young patients also but
must be reconstructed
periodically as the jaws
continue to grow

134. Amelogenesis imperfecta
Treatment depends on specific
type of defect
Hypo plastic type---
• Composite resins/porcelain
veneers bonded to anterior
teeth
• Often retain intracoronal
restorations (amalgam,
composite resins)
• If enamel too thin, full
coverage crowns needed

135. Hypocalcified type
• Treatment begins early
• Primary teeth need
stainless steel crowns
• Early permanent
dentition open faced
stainless crowns with
composite inserts
needed
• In permanent dentition
PFM crowns for
anteriors; full coverage
for posteriors

136. Hypocalcified teeth
Composite crowns
PFM crowns

137. Dentinogenesis imperfecta
• ----->
Prevent attrition
Rehabilitate worn dentition
Restore aesthetics
Prevent caries
• Primary teeth-stainless
Steel crowns,open faced
anteriorly
• Permanent---PFM
bleaching
full crowns
Aim of treatment

138. after
before

139. SUMMARY

141. •Gupta SK etal. Prevalence and distribution of selected
developmental anomalies in an indian population. J oral
sci;2011,vol 53,no 2,231-238
• The study included 1123 patients visiting the outpatient clinic
in GDC indore.
• Among the 1123 subjects, a total of 385 individuals(34.82%)
presented with selected developmental dental anomalies.
• Patient were examined for the following dental anomalies :
• Shape anomalies-microdontia, talons cusp, dens evaginatus,
fusion ,taurodontism
• Number anomalies-hypodontia,olligodontia,anadontia
• Structure anomalies-amelogenesis imperfecta, dentinogenesis
impeerfecta
• Position anomalies-rotation ectopic eruption, impaction

142. • Most common developmental anomaly was rotation (10.42%)
• Followed by ectopic eruption (7.93%),next common was
hypodontia (4.19%), microdontia (2.58%), taurodontism
(2.49%), dens evaginatus (2.40%),talons (0.97%) , DI (0.09%),
• AI (0.27%)

143. • Risk assessment
• Screening
• It has sometimes been suggested that children should be
screened for the presence of occlusal anomalies, at about the
age of ten years
(Chung and Kerr 1987).

144. • Conclusions
 It is difficult to prevent malocclusion—most of the effort
that is expended on interceptive orthodontics is directed
towards early treatment rather than prevention.
 Careful timing of the extraction of poor quality first
permanent molars can prevent the development of local
malocclusions, as can prompt extraction of retained primary
teeth that are deflecting the eruption of their permanent
successors.
 Early treatment of tuberculate supernumerary teeth will
certainly encourage spontaneous eruption of the permanent
incisors, and greatly simplify their subsequent alignment.

145. • Preventive measures may be effective in dealing with
environmental factors, but are unlikely to influence
the outcome in cases where the genetic background
is one of the more important determining factors.
(Mills1978)

146. CONCLUSION
The ultimate test of dental education is to
see how well it prepares the practitioner
to serve the patient.
Knowledge of development of teeth is
indispensable for a dentist,helping him not
only to diagnose a developmental disorder but
also to exactly pinpoint the event where
development was anomalous.
Bioengineering teeth seem to be a reality due
to the knowledge of teeth development.

147. “An understanding of basic sciences can be
the difference between an excellent
clinician and one who can treat his patients
only as a technician, between a leader and a
follower, between an innovator and one
whose clinical resources are limited and
dated!!”

148. REFERENCES
• Tencate’s Oral histology 6th Edn Antonio Nanci
• Orban’s Oral histology and embryology 11th Edn
Bhaskar S.N.
• Essentials of oral histology and embryology-A
Clinical approach 2nd Edn James K Avery
• The developing Human Moore & Persaud
• Arch Oral Biology 1970:1315:15 Ruch/Linde

149. Colour atlas of oral pathology
4th Edn Hamiltan; Robbinson ; Miller
•Text book of oral pathology 4th Edn Shafer
•Gupta SK etal. Prevalence and distribution of
selected developmental anomalies in an indian
population. J oral sci;2011,vol 53,no 2,231-238
•Text book of Prevention of oral diseases 4th
edition .Jhon J Murray
•Gilldsetal,counselling Patients With
Hypodontia;dental Update June 2008
Various sites on the Internet