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Amelogenesis & Enamel Surface Structures

This document discusses amelogenesis, the process of enamel formation. It begins by describing the stages of tooth development and the layers of the enamel organ. The life cycle of ameloblasts is then explained, which involves three main stages: pre-secretory, secretory, and post-secretory. The process of enamel matrix formation and mineralization in two steps is summarized. The five main enamel proteins - amelogenin, ameloblastin, enamelin, tuftelin, and amelotin - are also described briefly. Factors that can disrupt amelogenesis like genetic conditions, infections, environmental factors, and fluorosis are then mentioned.
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0% found this document useful (0 votes)
40 views

Amelogenesis & Enamel Surface Structures

This document discusses amelogenesis, the process of enamel formation. It begins by describing the stages of tooth development and the layers of the enamel organ. The life cycle of ameloblasts is then explained, which involves three main stages: pre-secretory, secretory, and post-secretory. The process of enamel matrix formation and mineralization in two steps is summarized. The five main enamel proteins - amelogenin, ameloblastin, enamelin, tuftelin, and amelotin - are also described briefly. Factors that can disrupt amelogenesis like genetic conditions, infections, environmental factors, and fluorosis are then mentioned.
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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AMELOGENESIS

NAMRATA SENGUPTA
MDS 1ST YEAR
ORAL PATHOLOGY &
MICROBIOLOGY
INTRODUCTION
The development of tooth is divided into : bud, cap,
early bell and advanced bell stage.

Enamel organ consists of 4 layers – outer enamel


epithelium, inner enamel epithelium, stratum
intermedium and stellate reticulum.

The cells of the inner enamel epithelium become


more columnar and convert into ameloblasts, which
produce enamel.

Enamel formation begins in the advanced bell stage.


LIFE CYCLE OF AMELOBLASTS

During amelogenesis, the ameloblasts


undergo changes in their morphology ,
starting from pre-secretory phase to
post-secretion phase.

At each stage, the cell rearranges itself


to suit the functional requirements
Broadly classified into 3 stages:

PRE-SECRETORY STAGE

SECRETORY STAGE

POST-SECRETORY STAGE
Each is again sub-classified:

LIFE-CYCLE OF AMELOBLASTS

PRE-SECRETORY SECRETORY POST-SECRETORY

1. MORPHOGENIC 1. MATURATIVE
FORMATIVE 2. PROTECTIVE
2. ORGANIZING
3. DESMOLYTIC
IEE interacts with the adjacent connective tissue cells, which differentiate into
odontoblasts.
Reversal of functional polarity.
During its terminal stage, formation of dentin by odontoblasts begins.
First appearance of dentin - a critical phase in the life cycle of IEE.
FORMATIVE STAGE
Ameloblasts enter formative stage after
the first layer of dentin has been formed.
MUTUAL INTERACTION
Ameloblasts retain same length and
arrangement
Development of cell processes which
penetrate the basal lamina & enter
predentin
MATURATIVE STAGE
Full mineralization occurs after most of the
thickness of enamel matriX has been formed in the
occlusal or incisal area.

Cervical part: matriX formation still progressing.


PROTECTIVE STAGE

Enamel fully calcified

Ameloblasts disarranged

Fuse with stratum intermedium & OEE to


form REE

REE protects mature enamel by separating


it from the connective tissue until the
tooth erupts
DESMOLYTIC STAGE

REE induce atrophy of the connective


tissue

Enzymes destroy connective tissue


fibers by desmolysis
STAGES OF AMELOGENESIS
Amelogenesis ,or enamel formation, is a two step
process.
AMELOGENESIS

Organic matrix
Mineralization
formation

1.Secretion of 1. Deposition of
enamel proteins hydroxyapatite
crystals
2. Produces a 2. Organic matrix and
partial mineralized water are lost and
(30%) enamel mineral is added to
attain greater than
96% mineral content
FORMATION OF THE ENAMEL MATRIX

The ameloblasts begin their


secretory activity when a small
amount of dentin has been laid
down.

As enamel deposition proceeds , a


thin, continuous layer of enamel is
formed along the dentin.
ENAMEL PROTEINS

1) AMELOGENIN
90% of the enamel proteins are a heterogenous group of
low-molecular-weight proteins known as Amelogenins.

Hydrophobic proteins rich in proline, histidine and


glutamine.

Undergoes eXtracellular degradation by proteolytic


enzymes.

Loss of function causes deposition of thin


hypopastic enamel layer which lacks rods and
interrods.
2) AMELOBLASTIN

Member of non-amelogenin

Constitutes 10% of total matriX

Found mostly in newly formed enamel

Assits ameoblasts in adhering to the forming enamel


surface during the secretory phase

Helps in nucleation and growth of crystals

Mutant Protein: Terminal differentiating ameloblasts


detach from the dentin and enamel formation stops
3) ENAMELIN

Also a member of non-amelogenins

Constitutes 2% of total enamel proteins

Large fragments of enamelin present at growing enamel


surface

Small fragments of enamelin bind stongly to enamel and


inhibit crystal growth

LOSS OF FUNCTION & MUTANT PROTEIN: No


defined enamel layer
4) TUFTLIN

Acidic phosphorylated glycoprotein

Localized to DE junction

Suggested to be involved in cell signalling


5) AMELOTIN

Amelotin is a member of the secretory calcium-binding


phosphoprotein (SCPP) family of proteins

One of the more recently discovered enamel proteins

Rich in proline, leucine, glutamine & threonine

FOUND: Surface basal lamina


Basal lamina located at the surface of junctional epithelium
In humans, there are 5acidic & 18 P/Q rich SCPP
genes,which encode many of the secreted proteins that
play prominent roles in enamel and dentin formation such
as:
AMELX
ENAM
AMBN
AMTN
ODAM
SCPPPQ1
DMP1
DSPP
AMTN, ODAM & SCPPPQ1 expressed during
maturation stage of enamel development when protein is
removed from the fully thick enamel as it becomes the
hardest substance of the body.
AMELOTIN present within the basement
membrane appears to allow a more consistent
hardening of the enamel because without
AMELOTIN the incisor enamel tends to chip
DEVELOPMENT OF TOMES’ PROCESS

Projections of ameloblasts into the enamel


matriX

The proXimal end of the tomes’ process


lays down the interrod enamel

The distal end lays down the enamel which


forms the enamel rods
MINERALIZATION & MATURATION OF
THE ENAMEL MATRIX

No unmineralized matrix like that of predentin and


osteoid

Starts from height of crown to cervically

Ruffle ended ameloblasts : calcium entry into the


forming enamel

OCTOCALCIUM PHOSPHATE

Crystal size increase further after tooth eruption


due to ionic exchange from saliva
THE INITIAL LAYER OF ENAMEL LAID
DOWN ON MANTLE DENTIN &
MINERALIZED IMMEDIATELY.

THUS, INITIAL ENAMEL LAYER DOES NOT


HAVE RODS.
AMELOGENESIS IMPERFECTA
AI represents a group of developmental
conditions, which affect the struccture &
clinical appearance of enamel of all or nearly all
the teeth in a more or less equal manner & may
be associated with morphologic or biochemical
changes elsewhere in the body.

The enamel may be hypoplastic,


hypomineralized or both.

Teeth affected may be discoloured, sensitive or


prone to disintegration.
It may show autosomal dominant, autosomal
recessive, sex-linked or sporadic inheritance
patterns.

In families with x–linked forms: AI result


from mutations in the amelogenin gene
(AMELX).

Enamelin gene ENAM: pathogenesis of


dominant forms of AI.

Mutations in genes coding for enamel


proteases which degrade the enamel
proteins, might also cause AI.
INFECTION ASSOCIATED ENAMEL DEFECTS

Severe infections which occur during enamel


formation can affect enamel formation.

-CONGENITAL SYPHILIS
-CONGENITAL RUBELLA

- PRENATAL CYTOMEGALOVIRUS INFECTION

Enamel hypoplasia is the most common


phenotype associated with these conditions.
ENVIRONMENTAL FACTORS

Amelogenesis is a regulated process at


the molecular level
Can be disrupted by many environmental
factors
FEVER
TRAUMA
CHANGE IN OxYGEN SATURATION
ANTIBIOTICS
FLUOROSIS

Pathologic condition

Hypomineralization of the enamel due to


excessive exposure to fluoride during
enamel mineralization
During the early maturation stage, the relative
quantity of protein is increased in fluorosed
enamel in a dose related manner.

This appears to result from a delay in the


removal of protein during enamel maturation.

A study reported that severe cases of DF were


associated with DLX1 AND DLX2 genes.

Polymorphisms of TIMP1, DLX1 & DLX2 genes –


associated with DF phenotypes.

These genes are expressed in atleast one stage


of enamel development.
MOLAR-INCISOR HYPOMINERALIZATION
Developmental defect of the human dentition
that primarily affects the enamel of the first
permanent molars and can involve the
incisors.

The more severely affected the first


permanent molars, the more likely it is that
there will be incisor environment.

Normal thickness of enamel with abnormal


areas having decreased mineral content and
increased protein and water content.
A study by Bussaneli et al. in the year 2018
reported that there is an association between
the SNP rs10733708 of the TGFBR1 gene and
severe MIH.

Suggesting that alteration in immune response


genes may influence the proper development
of enamel.

Furthermore, the interaction between


polymorphisms in immune response genes &
amelogenesis genes appears to have an
additive effect on susceptibility to the
development of MIH (in the population of
Araraquara, Brazil)
THANK
YOU...

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