CONTENTS
Neural crest development
Formation of tooth
o Bud stage
o Cap stage
o Bell stage
Hard tissue formation
Root formation
Determination of crown pattern
Dentin formation
Enamel formation
Cementum formation
Formation of periodontal ligament
Development of alveolar bone
Development of gingival
Epithelial mesenchymal interactions
Conclusion
1
DEVELOPMENT OF TOOTH AND PERIODONTIUM
Development is the progressive evolution of a tissue and
usually refers to an increase in its complexity and specialization.
Development of the tooth involves many complex biologic
processes including epithelial mesenchymal interactions,
morphogenesis, fibrillogenesis and mineralization.
The primitive cavity is lined by a primitive 2 or 3-layered
epithelium covering an embryonic connective tissue called
ectomesenchyme, because of its origin from the neural crest.
Neural crest development
By about the 8 th day of embryonic development cell
differentiation has already occurred and 2 different cell types are
present – ectoderm and endoderm. These two together form the
BILAMINAR DISC. During the first three weeks there is rapid
cell proliferation and migration and the bilaminar arrangement
separates with the development of the mesoderm between the
ectoderm and endoderm.
2
During the next few weeks the ectoderm thickens and forms
the neural folds and ultimately the neural tube. As the neural
crest develops, a group of cells differentiate from the lateral
border of the neural crest called neural crest cells.
Most of the dental structure like dentin and cementum and
their supporting tissues; periodontal ligament and bone develop
3
from the neural crest cells. Enamel is produced from ectodermal
cells.
After 37 days of development a continuous band of
thickened epithelium forms around the mouth in the presumptive
upper and lower jaws from the fusion of separate plates of
thickened epithelium. These bands correspond in position to the
future dental arches. This is called the PRIMARY EPITHELIAL
BAND (PEB). The PEB gives rise to 2 subdivisions the
vestibular lamina and the dental lamina.
The vestibule forms as a result of the proliferation of the
vestibular lamina into the ectomesencyme. Its cells rapidly
enlarge and degenerate to form a cleft that becomes the vestibule
between the cheek and tooth-bearing area.
During the 6 th week of embryogenesis tooth development
begins with a thickening of the oral epithelium lining the future
4
dental arches to form the dental lamina. Within the dental lamina
continued and localized proliferative activity leads to the
formation of a series of epithelial ingrowths into the
ectomesenchyme, at sites corresponding to the positions of the
future deciduous teeth. At this time the MITOTIC INDEX
LABELING INDEX and GROWTH OF EPITHELIAL CELLS are
significantly lower than corresponding indices in the underlying
ectomesenchyme which suggests that part of the ingrowth is
achieved by ectomesenchymal upgrowth.
The initiation of this development appears to be directly by
subepithelial ectomesenchyme that originates form the neural
crest. The coordination of odontogenesis, morphogenesis and
differentiations occurs through a serious of well-controlled
inductive molecular interactions that have their origins in the
ectoderm (enamel organ) and the ectomesenchyme (dental papilla
and follicle).
The early series of events in tooth development are divided
into three morphologic stages namely the Bud, Cap and Bell
stage.
5
Bud stage
The stage of tooth development is the stage at which
portions of the epithelium of the dental lamina begin to
aggregate and form an invagination into underlying connective
tissue.
Cap stage (Proliferation)
The epithelial ingrowth which superficially resembles a cap
sitting on a ball of condensed ectomesenchyme is called the
dental/enamel organ. Epithelium continues to proliferate forming
a cap like structure. Underneath this epithelial cap the
mesenchymal cells begin to proliferate to form the dental papilla,
which forms the dentin and pulp. The cells from the dental
papilla continue to proliferate around the enamel organ to form
the dental follicle from which cementum, periodontalligamnet
6
and alveolar bone develop. The dental organ, papilla and follicle
together constitute the TOOTH GERM.
Bell stage (Histodifferntiation and Morpodifferentiation)
The enamel organ continues to proliferate to form a bell
shaped structure. By this stage the enamel organ consists of four
types of cells. As the tooth germ transitions from cap to bell
stage important developmental changes occur. Through these
changes called, histodifferentiation a mass of similar epithelial
cells transform themselves into morphologically distinct
components.
The cells in the centre of the dental organ continue to
synthesize glycosaminoglycans and secrete them into the
extracellular matrix between the epithelial cells.
7
Glycosaminoglycans being hydrophilic pull water into the dental
organ and the increasing amount of water pull the cells apart.
But the cells still maintain connections with each other through
their desmosomal contacts and become star shaped. Thus the
center of the dental organ is termed the stellate reticulum.
At the periphery of the dental organ the cells assume a
cuboid shape and form the external or outer enamel epithelium
(EEE). The cells bordering on the dental papilla differentiate
into histologically distinct components. Those immediately
adjacent to papilla assume a short columnar shape and are
characterized by high glycogen content. Together they form the
internal or inner enamel epithelium.
Between the inner enamel epithelium (IEE) and the stellate
reticulum the epithelial cells differentiate into a layer of
flattened cells called stratum intermedium. The cells of this layer
are characterized by an exceptionally high activity of the enzyme
alkaline phosphatase.
Although cells of stratum intermedium and inner enamel
epithelium are histologically different they should be considered
as a single functional unit responsible for the formation of
enamel. The inner and outer enamel epithelium meet at the rim
of the dental organ and this junctional zone is called the cervical
loop.
8
The important events take place in the dental lamina in the
bell stage. The dental lamina joining the tooth germ to the oral
epithelium breaks up into discrete islands of epithelial cells thus
separating the developing tooth from the oral epithelium. The
fragmentation of the dental lamina results in formation of
discrete clusters of epithelial cells that normally degenerate and
are resorbed. If any persist they may form small cysts called
eruption cysts over the developing tooth and delay eruption.
Second the inner enamel epithelium folds making it possible to
recognize the shape of the further crown pattern of the tooth.
Formation of the permanent dentition
The permanent or secondary dentition also arises from the
dental lamina. The tooth germs that will give rise to the
permanent incisors, canines and premolars form as a result of
9
proliferative activity within the dental lamina at a point where it
joins the dental organs of the deciduous tooth germs. This
increased proliferative activity leads to the formation of another
epithelial cap and associated ectomesenchymal response on the
lingual aspect of the deciduous tooth germ. The molars of the
permanent dentition have no deciduous predecessors and so do
not originate in the same way. Instead when the jaws grow long
enough the dental lamina burrows backward beneath the lining
epithelium of the oral mucosa into the ectomesenchyme. This
backward extension of the dental lamina successively gives off
epithelial ingrowths which together with associated
ecotomesenchal response gives rise to the first, second and third
molars.
Thus the primary and secondary dentin forms in essentially
the same way although at different times. The entire primary
dentition is initiated between the sixth and eighth week of
embryonic development and the successional permanent teeth
between twentieth week in utero and the tenth month after birth.
The permanent molars between the twentieth week in utero for
the first molar and the fifth year of life for the third molar.
Hard tissue formation or crown stage
Late in the bell stage of tooth development the two
principal hard tissues of the tooth, the dentin and enamel are
formed. Formation of dentin always precedes enamel formation
and marks the onset of the crown stage of tooth development.
10
Until the completion of the bell stage, the cells of the inner
enamel epithelium are continually dividing to permit overall
growth of the tooth germ. At the sites of the future cusp tips
where dentin will be first formed, mitotic activity ceases and the
small columnar cells of the inner enamel epithelium elongate and
become tall and columnar in shape with their nuclei aligned
adjacent to the stratum intermedium and away form the dental
papilla. Changes also occur in the adjacent dental papilla. The
undifferentiated ectomesenchymal cells of the dental papilla
increase in size and differentiate into odontoblasts. This
differentiation of the odontoblasts from the undifferentiated cells
of the ectomesenchyme is initiated by an organizing influence
from the elongated cells of the inner enamel epithelium. In the
absence of epithelium no dentin will form.
As development continues there is progressive maturation
of the cells of the inner enamel epithelium down the cusp slopes
and a progressive differentiation of odontoblasts in the papilla.
The odontoblasts as they differentiate begin to elaborate
organic matrix of dentin, collagen and ground substance, which
is ultimately mineralized. As the organic matrix is deposited the
odontoblasts move towards the center of the dental papilla
leaving behind a cytoplasmic extension around which dentin is
formed. This results in the tubular nature of dentin.
11
After this first dentin has formed, the cells of the inner
enamel epithelium differentiate and assume a secretory function
producing an organic matrix against the newly formed dentin
surface. This organic matrix is mineralized almost immediately
to form enamel.
It has been stated the odontoblasts differentiate under an
organizing influence stemming from the cells of the inner enamel
epithelium. Likewise it has been stressed that enamel formation
cannot begin until some dentin has been formed. This
interdependence between the two tissues is an example of
RECIPROCAL INDUCTION.
Before the formation of the first dentin the nutrition of the
dental organ in particular the cells of the IEE comes from the
sources; blood vessels located in the dental papilla and those
situated along the periphery of the EEE. When dentin is formed
it cuts off the papillary source of nutrients. This reduction in
nutrients occurs at a time when the cells of the IEE are about to
secrete enamel and thus there is an increased demand for
nutrients. This demand is satisfied by a collapse of the stellate
reticulum and so the ameloblasts are approximated to the blood
vessels lying outside the EEE. Until this point the ameloblasts
meet their metabolic requirements by using the glycogen stored
in their cytoplasm and also by using some of the extracellular
components of the stellate reticulum.
12
Root formation
Just as in crown formation, epithelial cells are required for
initiation of the odontoblasts that will eventually form the root
dentin. Odontoblasts are formed as epithelial cells of the IEE and
EEE proliferate from the cervical loop of the dental organ to
form a double layer of cells called the Hertwigs epithelial root
sheath. This sheath grows around the dental papilla between the
papilla and the follicle until it encloses all, but the basal portion
of the papilla. The rim of this root sheath encloses the primary
apical foramen. As the cells of the IEE progressively enclose
more and more of the expanding dental papilla they initiate the
differentiation of odontoblasts from the cells at the periphery of
the dental papilla.
Multirooted teeth are formed in essentially the same way.
Only you have to visualize two tongues of epithelium growing
towards each other to enclose two primary apical foramina. If
three tongues are formed three apical foramina are formed.
The root sheath once it forms rapidly initiates root
formation and fragments. The tip of the forming root remains in
a stationary position relative to the inferior border of the
mandible, which means that the free border of the root sheath
must be in a stable position. With the onset of root formation the
crown of the root is growing away from the bony base of the
crypt and the root sheath is not actually growing into the jaw.
Because of these growth changes the root sheath is stretched and
13
eventually fragments to form a fenestrated network around the
tooth. In longitudinal sections this fenestrated network around
the tooth. In longitudinal sections this fenestrated network is
seen as a discrete cluster of epithelial cells known as the
epithelial cells rests of Malassez. In the adult these cell rests
persist next to the root surface in the periodontal ligament. They
are functionless but are the source of the epithelial lining of the
dental cysts that develop in reaction to inflammation of the
periodontal ligament.
Mechanism of crown pattern determination
Crown pattern of the tooth is determined during the bell
stage of tooth development. At this stage the stellate reticulum
cells are separated from each other by ground substance
consisting largely of mucopolysaccharides which attract water so
the dental organ is turgid and exerts pressure on both the IEE
and EEE. The growing dental papilla also exerts pressure on the
IEE since it is contained within the dental follicle. The
epithelium is therefore in a state of equilibrium between two
opposing forces that cancel each other. The folding that occurs
as the crown pattern develops is caused by differential rates of
mitotic activity.
When the tooth germ is growing rapidly in the early bell
stage, cell division occurs throughout the IEE. As development
continues, cell division ceases at a particular point in the IEE as
the cells begin to differentiate and assume their eventual
14
function of producing enamel. The point where maturation of the
cells of the IEE first occurs represents the site of future cusp
development. Since the IEE is constrained at the cervical loop
and because there is continued proliferation of the cells on each
side of the zone of maturation the epithelium buckles and forms
a cuspal outline. Thus the future cusp is pushed upwards towards
the EEE. The zone of maturation eventually sweeps down the
cusp slopes and is followed by dentin and enamel formation. The
occurrence of a second zone of maturation within the IEE leads
to the formation of a second cusp and so on until the final cuspal
pattern of the crown is determined.
Some researchers believe that the factors causing
maturation and cessation of cell division in the IEE reside in the
ectomesenchyme of the dental papilla. Thus it is clear that the
shape of the crown results from interaction between the dental
papilla, ectomesenchyme and the IEE.
Determination of tooth shape also depends on such
interactions. Humans being heterodonts the teeth fall into three
groups – incisiform, caniniform and molariform.
There are two theories that try to explain the initiation of
teeth of different families. The question asked is do the neural
crest cells as they migrate and form ectomesenchyme become
programmed to form teeth all of one family that subsequently
become modified in shape by local external factors – FIELD
15
THEORY; or is the tooth-forming ectomesenchyme initially
differentiated to form teeth of different families.
The field theory proposes three separate graded fields in
the jaw for the three families of teeth. Thus a tooth bud forming
at a given location develops according to its location within the
field. The CLONE THEORY states that the ectomesenchyme as it
migrates into the jaws becomes segregated into three clones:
incisor, canine and molar. There is some experimental evidence
to support both claims.
Dentin formation
The differentiation of odontoblasts from the dental papilla
requires the presence of epithelial cells or their products. This
inductive role of epithelium has been recognized for many years
and hence any description of dentin formation should always
begin with histologic changes that occur within the IEE. Apart
from this inductive influence dentin formation is purely a
connective tissue event.
Before dentinogenesis begins the cells of the IEE are short
and columnar in shape and are rapidly dividing to accommodate
the growing tooth germ. The cells are supported by a basement
membrane that supports the epithelium fro the dental papilla.
16
The cells of the dental papilla at this time are separated
from the IEE by an acellular zone and are small undifferentiated
ectomesenchymal cells with a central nucleus and sparse
cytoplasm containing few cytoplasmic organelles.
Cell division stops in the cells of the IEE and their shape
changes to tall columnar and the nucleus migrates to the pole
away from the dental papilla. Immediately after this, the cells of
the dental papilla rapidly enlarge as their cytoplasm increases in
volume to contain increasing amounts of rough endoplasmic
reticulum and golgi complexes. They are highly polarized with
nuclei positioned away from the IEE. The acellular zone between
the dental papilla and the IEE is eliminated as the odontoblasts
differentiate and increase in size to occupy this zone.
Some studies have shown that ectomesenchymal cells must
undergo a number of cell divisions before they develop the
capacity to respond to an epithelial influence and differentiate
into odontoblasts. During the final division of the
ectomesenchymal cells adjacent to the IEE the mitotic spindles
are perpendicular to the basement membrane supporting the IEE
and hence only the daughter cells next to the basement membrane
differentiate into odontoblasts. As a result, two populations of
cells can be differentiated – odontoblasts and subodontoblasts.
17
After the differentiation of the secretory odontoblasts,
mantle dentin is formed containing type I collagen of large
diameter. There large collagen fibrils along with the ground
substance constitute the first formed or mantle dentin.
During the secretion of mantle dentin the cells increase in
size and the extracellular compartment is obliterated. The
odontoblasts move away from the IEE towards the pulp leaving
behind an odontoblastic process. The plasma membranes of the
odontoblasts adjacent to the IEE push out short stubby processes
which on occasion penetrate the basal lamina and interpose
between the cells of the IEE. These are called enamel spindles.
Also small membrane bound vesicles are formed between the
collagen fibrils called matrix vesicles. Hydroxyl apatite is first
formed within the matrix vesicles as single clusters. These
crystals grow rapidly and rupture from the confines of the
vesicle, which fuse with adjacent crystals to form a fully
mineralized matrix. Deposition of mineral always lags behind the
formation of organic matrix and hence there is always a layer of
organic matrix called predentin found between the odontoblasts
and the mineralized front.
After the formation of mantel dentin, primary or
physiologic dentin is formed. The collagen in primary dentin is
in smaller fibrils, which are more closely packed and interwoven.
Matrix vesicles are no longer secreted by the odontoblasts and
mineralization is by heterogenous nucleation, secondary
18
nucleation and crystal growth. Odontoblasts secrete lipids,
phophoproteins. Evidence shows that these lipids are involved in
mineralization of primary dentin.
Mineralization of dentin occurs by globular or calcospheric
calcification which involves the deposition of crystals in several
discrete areas of matrix at any one time. With continues crystal
growth these crystals form globular masses, which eventually
fuse to form a single calcified mass. On occasion these large
globular masses fail to fuse and leave small uncalcified areas
known as interglobular dentin. In the rest of the circumpulpal
dentin the size of the globules progressively decreases until the
mineralization front appears linear. The size of the globules
seems to depend on the rate of dentin deposition, with larger
globules occurring where dentin deposition is fastest.
In summary dentinogenesis result in the production of an
organic matrix calcified with apatite crystals through which run
cytoplasmic extensions of the odontoblasts occupying dentinal
tubules. Coronal dentin deposition occurs at a rate of about 4
micron meter per day in an incremental manner.
Root dentin formation differs only very slightly from
coronal dentin formation in that the rate of deposition is slower
and the orientation of the collagen fibers is different. The
differentiation of odontoblasts that form root dentin is initiated
by the epithelial cells of the Hertwigs root sheath.
19
Secondary dentin formation is achieved essentially the
same way as primary dentin although the rate of formation is
slower. Secondary dentin stains less well for glysoaminoglycans
and also is less mineralized.
Tertiary or reparative dentin is deposited at specific sites in
response to injury. The rate of its deposition depends on the
degree of injury; the more severe the injury, the more rapid the
rate of dentin deposition with as much as 3.5 microns being
deposited in a single day. As a result of this rapid rate of
deposition, odontoblasts often become trapped in the newly
formed matrix.
Enamel formation
Enamel is ectodermally derived tissue covering the
anatomic crown of the tooth. It is formed by the enamel organ,
which is derived from a localized proliferation of the oral
epithelium. The ameloblasts are derived from the IEE of the
enamel organ. This process of differentiation requires presence
of dentin it begins at the future cusp tip and follows the
developing dentin down the slopes of the cusp.
In dentinogenesis, the odontoblasts retreat centrally leaving
behind formed dentin. The ameloblasts also retreat but in a
peripheral direction leaving newly formed enamel over dentin.
The IEE terminates at the cervical loop and this determines the
extent of enamel deposition. Enamel differs form other hard
20
tissues, which are all derived from connective tissue, in that it is
an ectodermal product, and it has a unique matrix and a
distinctive pattern of mineralization.
Enamel formation comprises of 2 stages: secretion and
mineralization. The first stage is formative and involves the
secretion of at an average rate of 0.023mm per day of an organic
matrix, that is almost immediately partially mineralized.
Secretion and partial mineralization continue until almost all of
the entire thickness of enamel has been formed. The organic
matrixes when first secreted have two types of proteins –
amelogenins and enamelins. Amelogenins exceed enamelins by a
ratio of 19:1. During this phase the enamel gets mineralized up
to 30% and retains a soft consistency.
Enamel then undergoes a maturation process where the
apatite crystals continue to grow and the protein and water
content goes down. Maturation begins at the DENTINOENAMEL
JUNCTION (DEJ) at about the same time the enamel secretion
has reached its complete thickness. It starts at the DEJ and takes
place at a rate twice as fast as matrix secretion.
The IEE and stratum intermedium which is rich in alkaline
phosphatase should be considered together during enamel
formation. In the cervical loop region the IEE cells are short and
columnar and as we move coronally they become tall and
columnar and their nuclei are aligned to the proximal end of the
21
cells adjacent to the stratum intermedium. The acellular zone of
the dental papilla seems to disappear as dentin formation has
begun. After dentin secretion has begun the cells of the IEE now
called ameloblasts begin to secrete the enamel matrix, which is
immediately partially mineralized. As this first increment of
enamel is formed the ameloblasts begin to move away from the
dentin surface and soon each cell forms a short conical
projection called Tomes processes that jut into the newly
forming enamel, giving the junction between the enamel and the
ameloblasts a picket fence like appearance.
During this time the enamel organ collapses. The volume of
the stellate reticulum is reduced by loss of intercellular
substance. This brings the blood vessels in the follicle close to
the ameloblasts as they lose their nutrient supply from the
papilla due to formation of dentin.
As enamel formation continues, the cells of the EEE,
stratum intermedium and stellate reticulum lose their discrete
identities and form a stratified layer of epithelium adjacent to the
ameloblasts, which have now become short and have lost their
tomes processes join together with the adjacent stratified
epithelium to form the REE.
22
A= ERS; B=dental papilla; C=dental follicle; D=odontoblasts; E=epithelial
rests; F=cementoblasts; G=developing alveolar bone; H=developing
cementum; J=developing periodontal ligament; K=root dentine
Cementum development
Cementum is deposited on the surface of root dentin. Once
root dentin formation has begun the continuous root sheath
fragments and forms network that enables follicular cells to pass
between the cells of the root sheath and to come into apposition
with the newly formed root surface. Here the follicular cells now
known as cementoblasts differentiate and begin to deposit the
23
organic matrix of cementum, consisting of intrinsic collagen
fibres and ground substance against the root surface and around
the forming ligament fiber bundles or extrinsic fibers.
Mineralization of this cementoid occurs in a similar manner
to dentin by the formation of apatite crystals within the matrix
vesicles. The cementum is laid down slowly as the tooth is
erupting and the cells retreat in to the periodontal ligament and
so this cementum is acellular. Once the tooth is in occlusion
more cementum forms usually around the apical two thirds of the
root, which has a greater proportion of collagen and the
cementoblasts become trapped in lacunae within this matrix so
that the cementum is cellular.
24
Enamel matrix proteins such as amelogenins, enamellins
and tuftelins seem to play an important role in cementogenesis.
They seem to help in the differentiation of cementoblasts from
the dental follicle. The commercially available form of these
enamel matrix proteins, which has a porcine source, is called
EMDOGAIN, which is being used, increasingly in periodontal
regenerative procedures.
Periodontal ligament development
The periodontal ligament spans the space between the root
surface and the alveolar bone. It is a fibrous connective tissue
that arises from the fibroblasts that differentiate from the
undifferentiated cells of the dental follicle. The first formed
fibres are parallel to the root surface. These fibres later become
the dentogingival and transseptal fibres. The periodontal
ligament forms shortly after root formation begins. The ligament
develops from the dental follicle. Before the tooth erupts the
crest of the alveolar bone is above the CEJ and the developing
fiber bundles of the ligament are all directed obliquely. As the
tooth moves during eruption the alveolar crest comes to coincide
with the CEJ and the oblique fibres below the free gingival fibres
become horizontal.
When the tooth finally comes into occlusion the alveolar
crest is positioned near the apex and the fibers become oblique
25
again with the cemental attachment being coronal to the apical
attachment. The principal fibres of the periodontal ligament
come into their final position only after tooth eruption is
complete.
Alveolar bone development
Teeth are located within the bony sockets in the alveolar
processes of the maxilla and mandible. The thin lamella of bone
that lines the socket wall and contains inserting Sharpeys fibers
is known as the alveolar bone. The alveolar bone is formed
during root development and is derived from cells originating in
the dental follicle. Its development is independent of other
portions of the alveolar process and in intimately associated with
the presence and development of teeth and the subsequent
development of the periodontal attachment apparatus.
26
Primary teeth and permanent teeth that do not have any
precursor tooth develop alveolar bone around their roots during
development and subsequent eruption. Initially the succedaneous
teeth are located within the same osseous cavity as their
deciduous precursors. However as the deciduous teeth erupt,
alveolar bone is deposited around the developing roots and
serves to separate the erupting deciduous tooth from the
underlying developing succedaneous tooth crown. Only when the
permanent tooth erupts into the oral cavity, is new alveolar bone
deposited around the tooth and the alveolar process assumes its
final form.
Development of gingiva
Before the tooth begins to erupt the crown of the tooth is
covered by a double layer of epithelial cells. Those in contact
with enamel are the post secretory ameloblasts that develop
hemidesmosomes and attach themselves to a basal lamina and
become firmly attached to the enamel surface.
The outer layer consists of more flattened cells which are
the remnants of all the remaining layers of the dental organ.
These two layers of cells are called the reduced enamel
epithelium. Between the REE and the overlying oral epithelium
is the connective tissue. When tooth eruption begins this
connective tissue breaks down. In response to hits break down of
27
connective tissue, the epithelium responds in the characteristic
manner in which epithelium supported by damaged connective
tissue responds. A widening of the intercellular spaces between
the epithelial cells occurs as they proliferate and migrate. As a
result the cells of the outer layer of the REE and the basal cells
of the oral epithelium proliferate and migrate into the
degenerating connective tissue and eventually fuse to form a
mass of epithelial cells over the erupting tooth. This leads to the
formation of an epithelium-lined canal through which the tooth
erupts without hemorrhage.
Once the tip of the cusp has erupted into the oral cavity,
oral epithelial cells begin to migrate partially over the REE in an
apical direction. The attachment of the gingival epithelium to
tooth is maintained through the reduced ameloblasts and their
hemidesmosomes and basal lamina adjacent to the enamel
surface. This is the primary epithelial attachment. This
eventually forms the junctional epithelium.
Gradually the reduced ameloblasts change their morphology
and are transformed into squamous epithelial cells that retain
their attachment to the enamel surface. The cells of the outer
layer of the REE also change into squamous epithelial cells but
retain their ability to divide. Due to this continuous cell division,
the ameoloblasts are eventually replaced by the daughter cells of
the REE. As the epithelial cells of the cuff stratify they further
28
separate the cells of the transformed dental epithelium from the
nutritive supply with the consequence that these latter cells
degenerate and create a gingival sulcus.
After the development of the gingiva and dentogingival unit
is complete the dentogingival junction extends to the CEJ and its
epithelial component consists of junctional epithelium formed by
transformation of REE and sulcular epithelium derived from the
epithelial cuff.
The epithelium thus has many important roles in tooth
formation. The main ones being
1. Morphogenetic function that helps to determine crown
pattern of the tooth.
2. Inductive role in initiating coronal and root dentin
formation and hence determines the size, shape and number
of roots of a tooth.
3. It has a formative function in that its cells secrete enamel.
4. It permits tooth eruption without the exposure of
connective tissue.
5. It assists in establishing the dentogingival junction.
Epithelial-Mesenchymal interactions
During embryonic development of all orans an intricate and
functional relationship exists between the epithelial and
mesenchymal tissues. The studies of Spemann as early as 1938
showed that the presence of this type of communication was
essential for organogenesis. Odontogenesis has proved to be an
29
excellent model for studying these interactions since epithelial
mesenchymal interactions occur at all stages of tooth
development. Once the enamel organ has formed during tooth
development the cells of the IEE appear to induce the adjacent
cells in the dental papilla to differentiate into odontoblasts.
However enamel formation by ameloblasts cannot proceed until
odontoblasts have begun to secrete dentin. Such an interaction
between the two tissues in known as RECIPROCAL INDUCTION.
Signaling molecules are required for these interactions to
proceed. The important signaling molecules are transcription
factors and growth factors.
Transcription factors are involved in gene expression. The
important transcription factors are the Homeobox genes and the
Dlx-1 and Dlx-2 genes. These transcription factors are involved
in specifying the spatial location of future tooth germs.
Following gene expression cell differentiation and organ
development continue to be controlled by locally produced
molecules such as growth factors.
Growth factors are soluble polypeptides secreted by cells
that act within the local environment either in a paracrine or
autocrine function. They exert their influence on cells via cell
surface receptors. During odontogenesis, the BMP’s, TGF- and
FGF have been found to be expressed differentially according to
the stage of development, morphogenesis and cell differentiation.
30
Other growth factors including PDGF and EGF have also been
associated with different stages of tooth development.
Reciprocal relationships between epithelium and its
sustaining connective tissue are involved in many aspects of
dental development and include
Initiation of tooth formation
Determination of tooth’s crown pattern
Initiation of dentinogenesis
Initiation of amelogenesis
Determination of size, shape and number of tooth roots
The determination of the anatomy of the dentogingival unit
Conclusion
Tooth development is a very complex yet well defined
series of events driven by molecular processes that are still in
the early stages of research and study.
Knowledge about the development of these tissues is
important since it will help us understand better the mechanisms
required for inducing repair and regeneration of damaged tissues.
31
REFERENCES
1. Janlindhe: Clinical periodontology and Implant dentistry
2. Orbans: Oral histology and Embrology cementum mosby
3. Tencates, Antonio Nanai: Oral histology Development,
Structure and Junction.
4. Carranza: Clinical periodontology tooth supporting
structures, Savunders , 2003 (Pg: 42-45)
5. Berkowitz BKB, Holland GR and Moxham BJ. Oral
anatomy, embryology and histology
6. Neville, Damn, Allen and Bouquot. Oral and maxillofacial
pathology – 2nd ed, 2002
7. Shafer, Hine and Levy. Shafer’s textbook of oral pathology.
32