The document discusses tooth development and the genes involved. It begins by describing the stages of tooth development from the bud stage to the bell stage. It then discusses the cells and components that make up the developing tooth germ during the cap and bell stages. The role of the Hertwig's epithelial root sheath in root formation is explained. The document concludes by discussing some of the key genes involved in each stage of tooth development, such as BMP, FGF, SHH, Wnt, and others, and how they regulate signaling pathways between the dental epithelium and mesenchyme to control the morphogenesis of the tooth.

1. PRESENTED BY :
Dr. ROSHNI MAURYA

2. INTRODUCTION
• Tooth is the hardest living biological structure of
ectomesenchymal origin having various functions.
• It has following structures
a) enamel in the coronal portion;
b) Dentine (in both coronal and radicular portion);
c) Cementum (in radicular portion);
d) Pulp (in coronal and radicular portion)

4. • Stewart & Prescott told “tooth is formed by ectoderm but due
to mesenchymal behaviour and activity it is called of
mesenchymal origin”.
• Migration of neural crest cell takes place at 20-24 I.U period
and during this period development of orofacial region takes
place.
• Stimulation cause differentiation between oral ectoderm with
odontogenic structure a tooth forming potential.

5. During 6.5 week I.U period :
Proliferation of lateral surface dental lamina takes place
Bud shaped deciduous formation takes place (56-86 days)
uniform cell division and
proliferation takes place
Bell shaped structure takes place (14th week)
Initiation of dental matrix takes place.

6. Comparisonof theDental Hard Tissue
Enamel Dentin Cementum Alveolar Bone
Embryological
background
Enamel organ Dental papilla Dental papilla Mesoderm
Type of tissue Epithelial Connective
tissue
Connective
tissue
Connective
tissue
Formative cells Ameloblasts Odontobalsts Cementoblasts Osteoblasts
Incremental
lines
Lines of retzius Imbrication
lines of von
Ebner
Arrest and
reversal lines
Arrest and
reversal lines
Mature cells None(lost with
eruption)
Only dentinal
tubules with
processors
Cementocytes Osteocytes

7. Enamel Dentine Cementum Alveolar
Bone
Resorptive
cells
Odontoclasts Odontoclasts Odontoclasts Osteoclasts
Mineral
Levels
96% 70% 65% 60%
Organic and
Water levels
1% organic &
3% water
20% organic &
10% water
23% organic &
12% water
25% organic
& 15% water
Tissue
formation
after eruption
None Possible Possible Possible
Vascularity None None None Present
Innervation None Present None Present
Table Continued………

8. DENTITION
• The term dentition describes the natural teeth in the jaw
bones . There are two dentitions : (a) Primary Dentition (b)
Permanent Dentition
• Primary Dentition: Primary dentition develops during the
prenatal period and consists of 20 teeth, which erupt
and are later shed or lost
• Permanent Dentition: As the primary teeth are shed and
the jaw grow and mature , the permanent dentition
consists of as many as 32 teeth , gradually erupts and
replaces the primary dentition .
• An overlapping period between the primary and the
permanent dentition during preteen years is referred to as
the mixed dentition period , when an individual has some
teeth from both dentition .

10. FORMULAFORHUMANTEETH
* The dental formula for the primary/deciduous
teeth in humans is as follows :-
I 2/2 C 1/1 M 2/2 = 10
• A dental formula for permanent dentition is as
follows :-
I 2/2 C 1/1 P 2/2 M 3/3 = 16

11. Primary Epithelial Band :-
• Oral Ectoderm is neutral crest or ectomesechyma in origin.
• Lined by Stratified Squamous Epithelium.
• Initial Oral cavity develops after the rupture of buccopharyngeal
membrane at the 4th week of intrauterine life.
• Interaction between oral epithelium and mesenchymal cells result in
tooth development.
• After 37 days of development, a continuous band of thickened epithelium
forms around the mouth in both future upper and lower jaws.
• This occurs from fusion of separate plates of thickened epithelium which
are roughly horseshoe-shaped structure.
• These correspond in position to future dental arches in presumptive
upper and lower jaws.
• Primary epithelial band forms as a result of a change in orientation of the
plane of the dividing cells.

12. Dental Lamina :-
• At the sixth week of gestation period , certain areas of basal cells of oral
ectoderm proliferate more rapidly than adjacent cells.
• Primary epithelial band forms two subdivisions called the dental lamina
and vestibural lamina.
• Dental lamina is a band of epithelium invading the underlying
ectomesenchyme along both the horseshoe-shaped future dental arches.
• Deciduous dentition develops directly from the lamina at the eight week
of fetal life.
• Permanent molars develop from a distal extension of dental lamina.
• Initiation of permanent first , second and third molars occurs at the
fourth month of intrauterine life , one year after birth and five years after
birth respectively.

13. Successional Lamina :-
• It is a lingual extension of dental lamina.
• It is responsible for the development of permanent incisors ,
canine and premolars.
• It is active from fifth month in utero ( from permanent central
incisor) to ten months of age ( second premolars).

14. Dental Anatomists told during 8th week of
I U period thickening of dental lamina
place Known as primary enamel for
deciduous tooth
Behind deciduous tooth germ
5poliferation of tooth germ present known
as
Successional lamina
dura for permanent tooth

15. Fate of Dental Lamina :-
• After initiation of tooth development , the dental lamina
degenerates.
• After functional activity , remnants of dental lamina may
persist in jaw or gingiva forms of island or epithelial pearls.
• It goes an degenerating in anterior teeth and activating in
posterior teeth.
• As the teeth continue to grow the connection of teeth with
dental lamina is lost by mesenchymal invasion.

16. Vestibular Lamina :-
• Facial (labial and buccal) to dental lamina
another their band of epithelium develops in the
maxillary and mandibular dental archer , called
as vestibular lamina or the lip furrow band.
• It hollows out and forms the oral vestibular
between the alveolar portions of jaws and lips
and cheeks.

18. Tooth development / Odontogenesis :-
• The process of development for both dentitions is similar , only the time
frames are different , and each developing tooth develops as an anatomically
distinct unit.
• The initial teeth for both dentition develop in the anterior mandibular region
, followed later by the maxillary region , and then development progresses
posteriorly in both the jaws. This position allows time for the jaw to grow to
accommodate the increased number of the primary teeth , the larger
primary molars and then finally the overall larger permanent teeth.
Tooth formation is a continuous process , characterized by a series of stages .
They are named after the shapes of the epithelial part of tooth germ
( enamel organ) and are called as :-
a. Bud Stage
b. Cap Stage
c. Bell Stage

19. Stages of tooth development
Stage /Time
span*
Main processes
Involved
Description
Initiation
stage/sixth to
seventh weeks
Induction Ectoderm lining stomodeum gives rise to
dental lamina ectomesenchyma which is
influenced by the neural crest cell.
Bud stage/eighth
week.
Proliferation Growth of dental lamina into bud that
penetrates growing ectomesenchyma

20. Table Continued……….
Stage/time
Span*
Main Processes
Involved Description
Cap stage/ninth to tenth
week
Proliferation ,
differentiation ,
morphogenesis
Enamel organ forms into
cap , surrounding mass
dental papilla
surrounded by mass of
dental sac also from the
ectomesenchyme.
Bell - stage/eleventh to
twelfth week
Proliferation ,
differentiation ,
morphogenesis
Differentiation of enamel
organ into bell with four
cell types and dental
papilla into two cell
types.

21. Table Continued………
Stages/time
Span*
Main processes
Involved Description
Apposition stage/ varies
per tooth
Induction , proliferation Dental tissue secreted as
matrix in successive layers
Maturation stage/ varies
per tooth
Maturation Dental tissue fully
mineralized to their
mature levels.

22. Bud Stage Bell Stage
Cap Stage Tooth Apposition Stage

24. Components of tooth germ during
Cap Stage
Components Description of
Components
Future Dental
tissue
Produced
Enamel organ Formation of tooth bud
in a cap shape with deep
central depression
Enamel
Dental papilla Condensed mass of
ectomesenchyme within
the concavity of the
enamel organ
Dental and pulp
Dental sac Condensed mass of
ectomesenchyme
surrounding the enamel
organ
Cementum ,
periodontal ligament ,
alveolar bone

26. Cells of the tooth during the
Bell Stage
Cell Layers Description of
Layers
Role in Tooth
Formation
Dental Sac Increasing amount of
collagen fibers forming
around the enamel organ
Will differentiate into
cementum, periodontal
ligament &alveolar bone
Outer enamel epithelium
(OEE)
Outer cuboidal cells of
enamel organ
Serves as protective barrier
for enamel organ
Stellate reticulum More outer star-shaped
cells in many layers ,
forming a network within
the enamel organ
Support the production of
enamel matrix.
Stratum intermedium More inner compressed
layer of flat to cuboidal
cells
Support the production of
enamel matrix

27. Table Continued :-
Cell Layers Description of
layers
Role in tooth
Formation
Inner enamel epithelium
(IEE)
Innermost tall ,columnar
cells of enamel organ
Will differentiate into
ameloblast that form
enamel matrix
Outer cells of dental papilla Outer layer of cells of the
dental papilla nearest the
inner enamel epithelium of
the enamel organ
Will differentiate into
odontoblasts that forms
dentin matrix
Inner cells of dental papilla Inner cell mass of the
dental papilla
Will differentiate into pulp
tissue

29. ADVANCED BELL STAGE
• In this stage two more features of tooth
development are seen.
• FUTURE DEJ-forms from the boundary present
between the inner enamel epithelium and
odontoblasts.
• HERTWIG’S epithelial root sheath-develops
from cervical portion of enamel organ.

30. CROWNPATTERNDETERMINATION
Butler told “Identical tooth germs are influenced by
various area with accurate shape and place for
eruption of tooth.
This theory is known as field theory according to him,
human being has 3 fields
Incisor, Canine and Molar field
Dohlbarg (1945) told human being has 4 fields Incisor,
Canine, Premolar and Molar field

31. Hard Tissue Formation or Crown Stage
It has been stated that odontoblasts differentiate
under an organizing influence stemming from
the cells of the internal dental epithelium.
Likewise, it has been stressed that enamel
formation cannot begin until some dentin has
formed – an example of reciprocal induction.

32. HERTWIG’S EPITHELIAL ROOT SHEATH ANDROOT
FORMATION
• HERS is a double-layered ;formed by enamel
organ;consists of only OEE and IEE,devoid of stratum
intermedium and stellate reticulum.
• It initates formation of root,determines the
number,shape,length,dimensions of roots.

33. ROLE OF GENE IN TOOTH
FORMATION

34. Gene is the biological unit of heredity.
Unit of chromosomes carry the traits
which passes from parents to child.

35. A gene is a combination of DNA
segments which help to form one or
more mRNA molecule.
Several genes react together to form
various structures of body along with
tooth and orodental structures.

36. Anatomist told after few hours of fertilization
zygote formation take place.
After 18 days of IU Period notocord formation
take place, from this “Neural Crest cell” formation
occur.

37. Migration of neural
crest cells take place at
20-24 IU period and
during this period
stimulation
Cause
Differentiation of oral
ectoderm to form
odontogenic sturctures
and tooth.

38. Connective tissue Sensory ganglia
Cranial Neural Crest
Derivatives
ParasympatheticPigment Cell
Accessory Cell

39. Dentin
Bone
Cartilage
Gingival
Dermis
Periodontal
Ligament
Neural Crest Cell

40. Genetic engineers found various genes
during tooth development.
a) Bud Stage Activin A, Amelogenin,
AXIN1 & 2, BRX1,
DLX1,2,3,4,5, FGF 3,4,
MAX1,2, & Other
b) Cap Stage Activin BetaA, Amelogenin,
Antizine1, BMP2,3,4,7,
c) ERbB3, FGFr2, FGF4, Shh
d) Bell Stage BMP, FGF
e) Apposition Enamel matrix, dentinal
Stage protein etc.

41. Genetic engineers told Molecular
development of tooth take place by signaling.
Small peptides (one nucleus) give signals to
other small peptides (another nucleus) who
receive signals lead to gene expression as a
result “change of cell behaviour” take place.

42. Single signal from
mesenchyme to
epithelium help to
form epithelial folding
& give formation of
singlecusped tooth.
Several signals
develop in dental
epithelium for
multicusped tooth.
Gene Causing Signals
1) BMP – 2,3,4,5,6,7
2) FGF -1,2,4,7,8
3) GAS – 1
4) Lfng
5) HIP
6) Shh & Others

43. Clusters of cells help in initiation of
crown formation. Primary enamel
knot take place in the tip of bud and
onset of cap formation take place.
FGF signals stimulate the growth and
multiplication.

44. Pispa (2003) noted dental placodes help to form
ectoderm.
Shh genes & Wnt genes are responsible for
formation of ectoderm.
Wnt genes help to form neural tube and neural
crest.
Before initiation of tooth formation Shh genes is
lost, thus only Wnt genes help to form tooth.

45. Wnt gene is combination of many
genes such as – MAX1, MAX2,
BMP2, BMP7, FGF4, BMP, FGF and
other.
These genes react together and
ultimately enamel formation take
place.

46. According to Pax9 gene theory
MAX1 and MAX2 gene help to form incisor and
canine
DLX1 & DLX2 gene - Multicuspid tooth
BARX1, DLX1, DLX2 - Help to form Molar
tooth
MAX 2MAX 1
DLX 2DLX 1
DLX 2DLX 1BARX 1
MAX 2MAX 1
MAX 2MAX 1

47. Various Genes During Tooth
Development
• Dental Epithelium :- Activin Bet A ; Ameloblastin ;
Amelogenin ;
Aquaporine(2,3,4,5,9) ; BMP (4,5,6,7) ;
Collagen type ; Alpha (I,II,III,IV,V, VII) ;
Cytokeratin (1,10,13,18).
• Ameloblast :- Ahr ; Ameloblastin ; Amelogenin ;
Enamelin
Artht ; Bax ; Laminin 5B.
• Developing Tooth :- Aquaporin (1,2,3,4,5,9 ) ; Fibronectin ;
Cytokeratin (4,5,7,8,13,18,19) ; DLX 5 ;
Amelogenin ; Enamelin

48. • Enamel :- Amelogenin ; Ameloprotese 1 ; Laminin 5 ;
L(alpha)
(beta) 3 ; Laminin (gamma) 2 ; Tuffelin ; BMP 7
;
Enamelin.
• Dentin :- Activin (beta) A ; Amelogenin ; Ameloblastin ;
BMP (2,3,4) ; Aquapain (2,3,4,5,9) ; Collagen
(I,III,IV, VIII) ; Dentin phosphoprotein ; DLX
(2,3,4,5,6)
• Dental papilla :- Activin Bet A ; Alkaline phosphatase ;
Ameloblastin ; Amelogenin ; Aquapanin
(2,3,4,5,9)
• Cementum :- BMP (2,3,4,7) ; MAX 1 ; Osteocalcin ;
Osteopotin ; Rhax 2 ; Shh
• Root :- Amelogenin ; BMP (2,3,4,7) ; MAX 1,2 ;
Osteocalcin ;
Shh ; Run X2

49. Disturbances Stage Description Etiological
Factors
Clinical
Ramifications
Anodontia Initiation
Stage
Absence of
single or
multiple teeth
Hereditary
,
Endocrine
dysfunctio
n,systemic
disease,
Excess
radiation
exposure
May cause
disruption
of oclussion
and
aesthetic
problems .
May need
partial or
full
dentures,
bridges,
and/or
implants to
replace
teeth.
Common Dental Development Disturbances

50. Table continued………….
Disturbance Stage Description Etiological
Factors
Clinical
Ramification
Supernumerary Initiation Development
of one or
more extra
teeth
Hereditary Occurs
commonly
between the
maxillary CI,
distal to third
molars and
PM region.
May cause
crowding
abnormal
eruption,
disruption of
occlusion

51. Table continued………..
Disturbance Stage Description Etiological
Factors
Clinical
Ramification
Macrodontia
Microdontia
Bud
stage
Abnormally
large or
small teeth
Hereditary in
localized
form
Endocrine
Dysfunction
is complete
Commonly
involves
permanent
maxillary
lateral incisor
and third
molars

53. Table continued……..
Disturbance Stage Description Etiological
Factor
Clinical
Ramification
Dens in dente Cap stage Enamel organ
inavigates into
the dental
papilla
Hereditary Commonly
affects the
permanent
maxillary
lateral incisor.
Tooth may have
deep lingual pit
and need
endodontic
therapy

54. Table Continued :-
Description Stage Description Etiological
Factor
Clinical
Ramification
Gemination Cap
Stage
Tooth germ
tries to divide
Hereditary Large single
– rooted
tooth with
one pulp
cavity and
exhibits
“twinning” in
crown area.
Normal no. of
teeth in
dentition.
May cause
problems in
appearance
and spacing.

55. Table continued……..
Disturbance Stage Description Etiological
Factors
Clinical
Ramification
Fusion Cap Stage Union of two
adjacent tooth
germs
Pressure on
area
Large tooth
with two pulp
cavities. One
fewer tooth in
dentition. May
cause problem
in appearance
and spacing.

56. Table Continued :-
Disturbance Stage Description Etiological
Factors
Clinical
Ramification
Tubercle Cap Stage Extra cusp
due to effects
on enamel
organ
Trauma,
pressure or
metabolic
disease
Common on
permanent
molars or
cingulum of
anterior teeth.
Enamel pearl Apposition
and
maturation
stages
Sphere of
enamel on
root
Displacement
of ameloblast
to root
surface
May be
confused as
calculus
deposit on
root.

57. Table Continued :-
Disturbance Stage Description Etiological
Factors
Clinical
Ramification
Enamel
dysplasia
Apposition
and
maturation
stages
Faulty
development
of enamel from
interference
involving
ameloblast
Local or
systematic or
hereditary
Pitting and
intrinsic color
changes in
enamel
possible.
Problem in
function and
aesthetics.
Concrescence Apposition
and
maturation
stages
Union of root
structure of
two or more
teeth by
cementum
Traumatic
injury or
crowding of
teeth
Common with
permanent
maxillary
molars

58. Hereditary defect of enamel
usually unassociated with other
general defects is known as
Amelogenesis imperfecta which is
a developmental defect.

59. Incidence maybe of AD/AR/X lined. Dental scientists
first primary tooth development occur at 4th week
of I.U period.
Amelogenis imperfecta is classified into 3 basic
type.
A) Hypoplastic (Occur during formation stage)
B) Hypocalcification (Occur during calcification
stage)
C) Hypomaturation (Occur during maturation &
crystallization stage)

60. According to Cowsen
Amelogenesis may be :-
a) Pitted type
b) X linked
c) Hypomaturation type
d) Hypocalcification type
e) Hypoplastic

61. Classification of Amelogenisis Imperfecta
(According to Naville and other – 2002)
Type Pattern Specific Features Inheritence
1A Hypoplastic Generalised pitted AD
1B Hypoplastic Localised pitted AD
1C Hypoplastic Localised pitted AR
1D Hypoplastic Diffuse smooth AD
1E Hypoplastic Diffuse smooth X linked dominant
1F Hypoplastic Diffuse Rough AD
1G Hypoplastic Enamel agenesis AR

62. Classification of Amelogenisis Imperfecta
(According to Naville and other – 2002)
Type Pattern Specific Features Inheritence
IIA Hypomaturation Diffuse Pigmented AR
IIB Hypomaturation Diffuse X
Linked R
IIC Hypomaturation Snow Capped X
Linked
IID Hypomaturation Snow Capped AD

63. Classification of Amelogenisis Imperfecta
(According to Naville and other – 2002)
Type Pattern Specific Features Inheritence
IIIA Hypocalcification Diffuse
AD
IIIB Hypocalcification Diffuse
AR
IVA Hypomaturation hypoplastic Taurodontism AD
IVB Hypoplastic hypomaturation Taurodontism AD

64. Genes with mutation associated with
Amelogenesis imperfecta
According to Aldred and Crawford (1995)
Causetive gene Gene coding
Structural
Protein
Secreted by
ameloblasts

65. Etiology of Amelogenesis Imperfecta
a) Epidermolysis Bullosa
b) Pseudo hypoparathyroidism
c) Tri-coloro-dento-osseous Syndrome
d) Oculdodento osseous dysplasia
e) Oculdodento osseous syndrome
f) Amelo cerebro hypohydrotic syndrome
g) Muccopolysaccirodosis
h) Cystic Fibrosis

66. Common Clinical type of
Amelogenesis imperfecta
a) Hypoplastic
b) Hypocalcification
c) Hypomaturation
d) Mixed type

67. Amelogenesis due to hypocalcification take
place due to defect in formation of
structure of matrix formation along with
calcification.
In amelogenesis due to hypomaturation
where formation of enamel rod, rod sheath
are defective.

68. Hypoplastic Amelogenesis imperfecta.
Some portion of enamel does not rich
normal thickness due to improper
development of enamel. Thin enamel, loss
of mesiodistal width of tooth, loss crown
length, having vertical or horizontal
fissures and presence of pits in enamel.
(Type I)

69. Autosomal dominant thin & smooth
hypoplastic type (Type IA)
Enamel is thin, hard glossy and smooth
surface. Colour of tooth is yellow / opaque
– white, chalky white interproximally. Loss
of enamel structure in incisor, occlusal
and mesiodistally.

70. Autosomal dominant rough hypoplastic
(Type – I B)
Enamel is hard with rough surface. Colour
may be light yellow to dark brown. Loss of
mesiodistal width of crown. Effect of
enamel rod take place.

71. Autosomal dominant pitted hypoplastic
(Type – IC)
Pin point or Pin headed sized pits are
found on labial surface of enamel
hypocalcification found on pin point along
with line of Retzius.

72. Autosomal dominant local hypoplastic
amelogenesis imperfecta (Type – ID)
Found in both deciduous and permanent
teeth where incisor or occlusal surface is
not effected. Hypoplastic defect in
horizontal row. Hypoplastic and
hypocalcification found in buccal surface
of middle third of enamel.

73. X Linked hypoplasia – (Type -1F)
Where one X chromosome is defective
other and normal. Teeth exhibit
alternating zone of normal and abnormal
enamel. Colour may vary from brown to
yellowish brown. Rough pattern – Thin,
hard and rough. Colour varies from white
to yellow. Rough surface found in incisor
& occlusal region.

74. DENTINOGENESIS IMPERFECTA
(DGI)
• The term DGI is defined as a genetic, which leads in
the formation of defective dentine.
• Dentine is poorly formed with an abnormal low
mineral content.
• Enamel is normal but the pulp chamber and pulp canal
are obliterated.
• The condition is associated with discoloration of
teeth (dusky blue to brown).
• The problem affects both the primary and permanent
teeth.

75. TYPES OF DGI :-
• Shields Types I DGI :- Associated with osteogenesis
imperfecta (OI) , a condition where bones are congenitally
brittle and easily broken. Teeth may show an amber
translucent color. Crowns are bulbous and pulp chambers
show obliteration in radiographs.
• Shields Types II DGI :- In this type only the dentine is
affected . The teeth are blue – gray or brown and opalescent.
On dental radiographs , teeth have bulbous crowns, roots are
narrower , pulp chambers and root canals are smaller or
completely obliterated.
• Shields Types III DGI :- It is called the brandywine form after
the city of Brandywine in Maryland where a large population
of patients were affected with this disorder. It is associated with
shell – like teeth having multiple pulp exposures.

76. GENETICS OF DGI
• The deficiency of dentine sialophosphoprotein (DSPP) causes
DGI . DSPP is responsible for coding dentine
sialophosphoprotein
• Mutation in DSPP gene gives rise to DGI types II and III and
dentin dysplasia .

77. Life – cycle of a Tooth
Life-cycle is the complete cycle of a tooth from the beginning of development to
eruption , arrangement , attrition and finally exfoliation of the tooth.
ERUPTION
Eruption is described as the emergence of teeth into the oral cavity Every tooth in
the dentition has a different eruption schedule .
Factors responsible for eruption are:
a. Vascular pressure exerted around and beneath the root.
b. Continuous growth of the root.
c. Bone remodeling.
d. Traction of the periodontal membrane.
e. Deposition of dentine.
f. Narrowing of pulp.
g. Functional movement of the muscels.

78. ATTRITION
It is a physiological process characterized by wearing away of a tooth during
tooth - to - tooth contact as in mastication . The surface involve are incisal ,
occlusal and proximal. Basically attrition is an aging process and it continues
throughout the life.
REGRESSIVE CHANGES OF PULP
Regressive changes of the pulp are characterized by a reduction in the cellular
components of the pulp associated with a decrease in the number of
odontoblasts. But the teeth are clinically symptomless and give normal
response to the vitality test. As the age of an individual advances , the
cellular component of the pulp decreases gradually and the number of
odontoblasts is reduced.
.

79. RESORPTION OF TEETH
Resorption of teeth occurs under normal conditions.It can occur on
external or internal surfaces called as external or internal resorption
respectively.Root is the most involved part,intensity being mixed in
nature. Resorption starts from CEJ or at site of root apex.
EXFOLIATION OF TEETH
It is the last stage in life cycle of a tooth. In deciduous dentition ,
shedding occurs due to resorption of their root . It is brought about by
pressure exerted by erupting permanent teeth .Factors for shedding of
deciduous teeth are pressure of the erputing permanent teeth ,
activation of osteoclastic and odontoclastic cells , increasing masticatory
forces due development of the muscles lead to weakened dentition and
help in shedding.

80. THANK YOU !