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DENTIN
INTRODUCTION:
It provides the bulk and general form of the tooth and is
characterized as a hard tissue with tubules throughout its
thickness.
Since it begins to form slightly before the enamel, it
determines the shape of the crown including the cusps and
ridges and the size of the roots.
As a living tissue it contains within its tubules the
processes of the odontoblasts. Although the cell bodies are
arranged along the pulpal surface of the dentin they are
morphologically cells of dentin because they produce dentin.
Physically and chemically the dentin closely resembles
bone. The main difference is that some of the osteoblasts
exist on the surface of bone and when one of these cells
becomes enclosed within the matrix it is called an osteocyte.
The odontoblast cell bodies remain external to dentin,
but their processes exist within tubules in dentin. Both are
considered as vital tissues because they contain living
protoplasm.
The topic will be discussed under the following sub
titles.
1. Physical and chemical properties.
2. Structure of Dentin.
3. Types of Dentin.
Primary
Secondary
Tertiary
Pre-dentin
4. Histology of Dentin.
Dentinal tubules.
Intratubular / peributular dentin.
Interglobular dentin.
Icremental lines.

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Granular layer of Tomes.
Odontoblast process.
5.Innervation of Dentin:
Intratubular nerves.
Theories of pain transmission.
6. Age and functional changes:
Vitality of Dentin.
Reparative Dentin.
Dead tracts.
Sclerotic Dentin.
7. Development:
Dentinogenesis.
Mineralization.
8. Clinical considerations.
9. Dentin Anomalies (developmental)
Dentin Dysplasia.
Dentinogenis Imperfecta.
PHYSICAL PROPERTIES AND CHEMICAL PROPERTIES:
Dentin is yellowish. Because light can readily pass
through thin highly mineralized enamel and be reflected by
the underlying dentin, the crown of a tooth has a yellowish
appearance. Physically dentin has an elastic quality, which
provides flexibility and prevents fracture of the overlying
brittle enamel. It is somewhat harder in its central part than
near the pulp or on its periphery.
Mature dentin is chemically by weight, approximately
70% inorganic, 20% organic material and 10% water. Its
inorganic component consists mainly of hydroxyapatite which
is composed of several thousand unit cells (Unit = 3 Ca
(PO4)2, Ca(OH)2). Organic phase is type-I collagen with
fractional inclusions of glycoproteins, proteoglycans,
phosphoproteins and some plasma proteins. The inorganic
phase makes dentin slightly harder than bone and softer
than enamel. This difference can be readily distinguished on

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radiographs, where dentin appears more radiolucent than
enamel and more radioopaque than pulp.
STRUCTURE OF DENTIN:
The dentinal matrix of collagen fibres is arranged in a
random network. As dentin calcifies, the hydroxyapatite
crystals mask the individual collagen fibres.
The bodies of the odontoblasts are arranged in a layer
on the pulpal surface of the dentin and only their cytoplasmic
processes are included in the tubules in the mineralized
matrix. Each cell gives rise to one process, which traverses
the predentin and calcified dentin within one tubule and
terminates in a branching network at the junction with
enamel or cementum. Tubules are found throughout normal
dentin and are therefore characteristic of it.
TYPES OF DENTIN:
Primary Dentin:
Most of the tooth is formed by primary dentin, which
outlines the pulp chamber. The outer layer of primary dentin
called mantle dentin which is about 20 m thick differs from
the rest of the primary dentin.
The fibrils formed in this zone are perpendicular to the
DEJ and the organic matrix is composed of larger collagen
(loose) fibrils. Circumpulpal dentin forms the remaining
primary dentin or bulk of the tooth. This is the dentin
formed prior to the root completion. The collagen fibrils in
CPD are much smaller in diameter (0.05 m) and are more
closely packed. It may contain slightly more mineral than
mantle dentin.
Secondary Dentin:

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Secondary dentin is narrow band of dentin bordering the
pulp and representing that dentin formed after root
completion. It contains fewer tubules than primary dentin.
There is usually a bend in the tubules where primary and
secondary dentin interface. It was once thought that
secondary dentin was formed only in response to functional
stimuli, but it has been found in un-erupted teeth as well.
There is a greater deposition of secondary dentin on the
roof and floor of the pulp chamber leads to an asymmetric
reduction in the size and shape of the chamber and of the
pulp horns. These changes which is clinically referred to as
pulp recession can be readily detected on radiographs and
are important in determining the form of cavity preparation
for certain dental restorative procedures. For e.g. Preparation
of the tooth for a full crown in a young patient presents a
substantial risk of involvement of the dental pulp by
mechanically exposing a pulp horn, but in older patient the
horn has recorded, presenting less danger. There is also
evidence suggesting that secondary dentin scleroses more
readily than primary dentin. This leads to reduce the overall
permeability of the dentin, thereby protecting the pulp.
Tertiary Dentin:
 Also referred as reactive, reparative, or irregular secondary
dentin.
It is produced in reaction to noxious stimuli, such as
caries or a restorative dental procedure.
Unlike primary or secondary dentin, which forms along
the entire pulp dentin border, only cells directly affected by
the stimulus produce tertiary dentin.
The quality and quantity of tertiary dentin produced are
related to the cellular response initiated, and this depends on
the intensity and duration of the stimulus.

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For e.g.: The stimulus of an active carious lesion causes
extensive destruction of dentin and considerable
rapidly by odontoblast like cells that have
differentiated from pulpal prevascular cells. Such
as dentin displays a sparse and irregular tubular
pattern with frequent cellular inclusions and is
sometimes called Osteodentin.
If the stimulus is less active tertiary dentin is deposited
less rapidly, its tubular pattern is more regular and there are
fewer, cellular inclusions.
The main function of reparative dentin is to protect the
pulp by “sealing off” the dentinal tubules or minimizing the
permeability of potentially harmful contents.
Pre-Dentin (10-47 m):
It lines the innermost portion of the dentin, which is
first formed but unmineralized.
It consists of collagen, glycoproteins and proteoglycans.
As the collagen fibres undergo mineralisation at the
predentin-dentin junction the pre-dentin becomes dentin and
a new layer of pre-dentin forms circumpulpally.
Pre-dentin is the thickest where active dentinogenesis is
occurring and its presence is important in maintaining the
integrity of dentin, since its absence appears to leave the
mineralized dentin vulnerable to restoration of odontoclasts.
HISTOLOGY:
When dentin is viewed microscopically, structural
features identified area:
1. Dentinal tubules.
2. Intertubular (Peritubular) Dentin and Sclerotic Dentin.
3. Intertubular dentin.
4. Interglobular dentin.
5. Incremental growth lines.
6. Granular layer of Tomes.

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7. Odontoblast process.
Dentinal Tubules:
The course of the dentinal tubules follows a gentle curve
in the crown, less so in the root where it resembles an “S” in
shape.
They start at right angles from the pulpal surface and
ends perpendicular to the dentinoenamel and
dentinocementum junctions.
Near the root tip and along the incisal edges and cusps
the tubules are almost straight.
Over their entire lengths the tubules exhibit minute,
relatively regular secondary curvatures that are sinusoidal in
shape.
The ratio between the outer and inner surfaces of dentin
is about 5:1. Accordingly the tubules are further apart in the
peripheral layers and are most closely packed near the pulp.
They are larger in diameter near the pulpal cavity and
smaller at their outer ends (1 m).

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The ratio between the number of tubules/unit area on
the pulpal and outer surfaces of dentin is about 4:1.
The dentinal tubules have lateral branches throughout
dentin called canaliculi originate more or less at right angles
to main tubule entering the intertubular dentin or to distant
tubules.
A few dentinal tubules extend through the DEJ into the
enamel for several mms. There are termed as enamel
spindles.
Dentinal tubules makes the dentin permeable, providing
a pathway for invasion of caries, drugs and chemical present
in restorative materials causing pulpal injury.
Intra-tubular Dentin / Peri-tubular Dentin:
The dentin that immediately surrounds the dentinal
tubules is termed peritubular dentin.
The peritubular dentin is the best calcified of all the
mineralized components of dentin, so it is clearly
demonstrated in cross sections of ground section of un-
decalcified dentin with the light microscope (because it is so
highly mineralized, it is lost in de-calcified sections).
It is twice as thick in outer dentin (0.75 m) than in
inner dentin (0.4 m). By its growth it constricts the dentinal
tubules to a diameter of 1 m near the DEJ.
The deposition of intra-tubular dentin causes a
progressive reduction in the tubule lumen and eventually
obliterates the tubule.
When this occurs in several tubules in the same area
the dentin obtain a glassy appearance. This dentin is termed
Sclerotic dentin.

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Inter-tubular Dentin:
The main body of the dentin is composed of intertubular
dentin. It is located between the dent tubules.
Although it is highly mineralized, this matrix like bone
and cementum is retained after decalcification where as
peritubular dentin is not.
About one half of its volume is organic matrix, especially
collagen fibres, which are randomly oriented around the
dentinal tubules.
Hydroxyapatite crystals, which average 0.1 m in length
are formed along their fibres with their long axis oriented
parallel to the collagen fibres.
Inter globular Dentin:
Sometimes mineralisation of dentin begins in small
globules areas that fail to coalesce into a homogeneous mass.
This results in zones of hypomineralisation between the
globules, which are known as globular dentin or inter-
globular spaces. Seen commonly in Vitamin D deficiency and
exposure to high levels of fluoride during dentin formation.
It is seen most frequently in the circumpulpal dentin
where the pattern of mineralisation is largely globular.
Because this irregularity of dentin is a defect of
mineralisation and not of matrix formation, the architectural
pattern of the tubules remains unchanged and they run
uninterruptedly through the interglobular areas.
Incremental Lines: (Von Ebner)
These are imbrication lines, appear as fine lines or
striations in dentin.

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They run at right angles to dentinal tubules and
correspond to the incremental lines in enamel or bone.
These lines reflect the daily rhythmic recurrent
deposition of dentin matrix as well as hesitation in the daily
formative process.
The distance between lines varies from 4 – 8 m in the
crown to much less in the root.
The daily increment decreases after a tooth reaches
functional occlusion. The course of lines indicates the growth
pattern of dentin.
Some of the incremental lines are accentuated because
of disturbances in the matrix and mineralizaation process.
Such lines demonstrated in ground sections are called
contour lines (Owen) (hypocalcified bands).
In the deciduous teeth and in the first permanent
molars where dentin is formed partly before and partly after
birth, there is an accentuated contour line due to the abrupt
change in the environment during dentin matrix formation,
which may be a zone of hypocalcification termed as Neonatal
line (as in enamel).
Granular layer of Tome’s:
When dry ground sections of the root dentin are
visualized in transmitted light, there is a zone adjacent to the
cementum that appears granular known as Tomes granular
layer.
This zone increases slightly in amount from the CEJ to
the root apex and is believed that it is caused by coalescing
and looping of the terminal portions of the dentinal tubules.

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The cause of development of this zone is probably
similar to the branching and beveling of the tubules at the
DEJ.
Odontoblast process:
Odontoblast processes are the cytoplasmic extension of
the odontoblasts.
Odontoblast cells reside in the peripheral pulp at the
pulp - predentin border and their processes extend into the
dentinal tubules.
The processes are largest in diameter near the pulp (3 -
4 mm) and taper approximately 1 m further into the dentin.
Odontoblast process transverse the thickness of dentin.
In other areas a shortened process may be characteristic in
tubules that are narrow or obliterated by mineral deposit.
Odontoblast process is composed of microtubules of 20
m in diameter and small filaments 5 to 7.5 m in diameter.
Occasionally mitochondria, dense bodies, resembling
lysosomes, micro vesicles and coated vesicle that may open to
extracellular space are also seen.
The ododontoblast processes divide near the DEJ and
may indeed extend into enamel in the enamel spindles.
Innervation of dentin:
Intratubular nerves:
Dentinal tubules contain numerous nerve endings in the
predentin and inner dentin no farther than 200 to 150 m
from the pulp.
Most of these small vesciculated endings are located in
tubules in the coronal zone, specifically in the pulp horn
(because the tubule diameter is largest here and the
peritubular dentin is very little or absent).
The nerves and their terminals are found in close
association with the odontoblast process within the tubule.

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The nerve endings interdigitate with the odontoblast
process indicating an intimate relationship to this cell. It is
believed that most of these are terminal processes of the
mylenated nerve fibres of the dental pulp.
Theories of pain transmission through dentin:
There are three basic theories of pain conduction
through dentin.
i. Direct neural stimulation:
Stimuli in some manner, reach the nerve endings in the
dentin and the dentin is stimulated. There is little scientific
support of this theory.
ii. Fluid or Hydrodynamic theory:
Various stimuli such as heat, cold, air blast,
desiccation, or mechanical or osmotic pressure affect fluid
movement in the dentinal tubules.
The fluid movement either inward/outward stimulates
the pain mechanism in the tubules by mechanical
disturbance of the nerves closely associated with the
odontoblast and its process.
Thus these endings may act as mechanoreceptors as
they are affected by mechanical displacement of the tubular
fluid.
iii. Transduction theory:
This theory presumes that the odontoblast process is
the primary structure excited by the stimulus and that the
impulse is transmitted to the nerve endings in the inner
dentin, through its membrane.
This is not a popular theory since there are no
neurotransmitter vesicles in the odontoblast process to
facilitate the synapse.
In short, no single proposed mechanism fully explains
all the facts related to dentin sensitivity may be more than
one mechanism operates at any one time.

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Age and functional changes:
i. Vitality of dentin.
ii. Reparative dentin.
iii. Dead tracts.
iv. Scelerotic or transparent dentin.
Vitality of dentin:
Since the odontoblast and its process are an integral
part of the dentin, there is no doubt that dentin is a vital
tissue.
If vitality is understood to be the capacity of the tissue to
react to physiologic and pathologic stimuli, dentin must be
considered a vital tissue.
Dentin is laid down throughout life, although after the
teeth have erupted and have been functioning for a short
time, dentinogeneis slows and further dentin formation is at a
much slower rate.
Reparative dentin:
If by extensive abrasion, erosion, caries or operative
procedures, the odontoblast process are exposed or cut, the
odontoblasts die or if they live, deposit reparative dentin.
The odontoblasts that are killed are replaced by the
migration of undifferentiated cells arising in deeper regions of
the pulp is believed to be originated from the cell rich zone or
perivascular cells deeper in the pulp.
Reparative dentin is characterized as having fewer and
more twisted tubules than dentin.
Dead tracts:
In dried ground sections of normal dentin the
odontoblast processes disintegrate and the empty tubules are
filled with air.
They appear black in transmitted light and white in
reflected light.

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They extend from the DEJ to the corresponding area of
dentin pulp interface.
In most instances, the dead tracts are sealed at their
pulpal aspect by the formation of reparative dentin.
These areas demonstrate decreased sensitivity and
appear to a greater extent in older teeth.
Sclerotic / transparent dentin:
In case of caries, abrasion, erosion, cavity preparation,
sufficient stimuli are generated to cause collagen fibres and
appetite crystals to fill the tubules with a fine meshwork,
thus obliterating it.
Such calcified tubular space assumes a difference in
refractive index becoming transparent which is observed in
the teeth of elderly people especially in the roots.
It is also found under slowly progressing caries reducing
the permeability of dentin and may prolong pulp vitality.
It is also found beneath warm enamel, which occurs in
the incisal area of anterior teeth in elderly and in cervical
area of older teeth where cervical cementum has been
exposed to the oral cavity due to gingival recession.
DEVELOPMENT:
Dentinogenesis:
Dentinogenesis begins at the cusp tips after the
odontoblasts have differentiated and begin collagen
production. As the odontoblasts differentiate they change
from an ovoid to a columnar shape, and their nuclei become
basally oriented.

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One or several processes excise from the apical end of
the cell in contact with the basal lamina. The length of
odontoblasts then increases to approximately 40 m although
its width remains constant.
Proline appears in the rough surface endoplasmic
reticulum and golgi apparatus. The proline then migrates
into the cell process in dense granules and is emptied into
the extracellular collagenous matrix of the predentin. As the
cell recede it leaves behind a single extension, and the several
initial processes join into one, which becomes enclosed in a
tubule.
As the matrix formation continues, the odontoblast
process lengthens, as does the dentinal tubule. Daily 4 m of
dentin are formed initially, which continues until the crown is
formed and the teeth erupt and move into occlusion.
After this dentin production slows to about 1 m/day.
After root development is complete, dentin formation may
decrease further, although reparative dentin may form at a
rate of 4 m/day for several months after a tooth is restored.
Dentinogenesis is a two-phase sequence in that collagen
matrix is first formed and then calcified. As each layer of
predentin is formed along the pulp border, it remains a day
before it is calcified and the next increment of predentin
forms.
Korff’s fibres have been described as the initial dentin
deposition along the cusp tips. Because of the argyrophilic
reaction (stain black with silver) it was long believed that
bundles of collagen formed among the odontoblasts.
Recently, ultrastructural studies revealed that the
staining is of the ground substance among the cells and not
collagen consequently; all predentin is formed in the apical
end of the cell and along the forming tubule wall.

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The finding of formation of collagen fibres in the
immediate vicinity of the apical ends of the cells is in
agreement with the general concept of collagen synthesis in
C.T. and bone. The odontoblasts secrete both collagen and
other components of the extracellular matrix.
Mineralisation:
The earliest crystal deposition is in the form of very fine
plates of hydroxyapatite on the surfaces of the collagen fibrils
and in the ground substance.
Subsequently, crystals are laid down within the fibril
themselves. The crystals associated with the collagen fibrils
are arranged in an orderly fashion, with their long axis
paralleling the fibril long axes and in rows conforming to the
64 nm. Striation pattern.
Within the globular islands of mineralisation, crystal
deposition appears to take place radically from common
centers, in a so-called spherulite form. These are seen as the
first sites of calcification of dentin.
The general calcification process is gradual, but the
peritubular region becomes highly mineralized at a very early
stage.
Although there is obviously some crystal growth as
dentin matures, the ultimate crystal size remains very small,
about 3 nm in thickness and 100 nm in length. The appetite
crystals of dentin resemble those found in bone and
cementum.
They are 300 times smaller than those formed in the
enamel. It is interesting that two cells so closely allied at the
dentinoenamel junction procedure crystals of such a
difference but at the same time produce chemically the same
hydroxyapatite crystals.

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Calcospherite mineralisation is seen occasionally along
the pulp pre-dentin forming front.
Clinical considerations / importance:
Bacterial toxins, strong drugs, undue operative trauma,
unnecessary thermal changes or irritating restorative
materials should not insert the cells of the exposed dentin.
It should be remembered that when 1 mm2 of dentin is
exposed, about 30,000 living cells are damaged. It is
advisable to seal the exposed dentin surface with a non-
irritating insulating substance.
The rapid penetration and spread of caries in the dentin
is the result of the tubule system in the dentin. The enamel
may be undermined at the DEJ, even when caries in the
enamel is confined to a small surface area. This is due to the
spaces created at the DEJ by enamel tuffs, spindles and open
and branched dentinal tubules.
The dentinal tubules provide a passage for invading
bacteria and their products through either a thin or thick
dentinal layer.
Electron micrographs of carious dentin show regions of
massive bacterial invasion of dentinal tubules. The tubules
are enlarged by the destructive action of the microorganisms.
Dentin sensitivity of pain, unfortunately, may not be a
symptom of caries until the pulp is infected and responds by
the process of inflammation leading to tooth ache. Thus
patients are surprised at the extend of damage to their teeth
with little or no warning from pain.
Under trauma from operative instruments also may
damage the pulp. Air driven cutting instruments cause
dislodgement of odontoblasts from the periphery of the pulp
and their “aspiration” within the dentinal tubule. This could
be an important factor in survival of the pulp if it is already
inflamed.

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Repair requires the mobilization of the macrophage
system as healing takes place, as this progresses there is the
contribution of deeper pulpal cells, through
cytodifferentiation into odontoblasts, which produces
reparative dentin.
The sensitivity of the dentin has been explained by the
concept that alteration of fluid and cellular contents of the
dentinal tubules causes stimulation of nerve endings in
contact with these cells. This theory explains pain
throughout dentin since fluid movement will occur at the
DEJ as well as near the pulp.
Teeth with deep carious lesions can be saved by indirect
pulp capping. By partial removal of the carious dentin and
insertion of a Ca(OH)2 dressing for a few weeks. During this
period the odontoblasts form new dentin along the pulpal
surface underlying the carious lesion, and then dentist can
reopen the cavity and remove the remaining bacteria laden
decay without endangering the pulp.
The smear layer formed on the cavity floor during cavity
preparation although reduces permeability temporarily, it is a
bacteria laden mass and its important to remove it. Or else
toxic product may migrate to the pulp. A cavity liner is then
recommended to line the cavity.
DENTIN ANOMALIES:
i. Dentin Dysplasia (Rootless teeth)
It is a rare disturbance of dentin formation characterized
by normal enamel by atypical dentin formation with
abnormal pulpal morphology.
Clinically the tooth appears normal both dentitions.
ii. Dentinogenesis imperfecta:
Type-I: Occurs in families with osteogenesis imperfecta.
Type-II: Not associated with osteogenesis Imperfecta. Both
dentitions are equally affected (hereditary opalscent dentin).
Type-III: (Brandywine type): Is a racial isolate and is
characterized by some clinical appearance as I and II but
with multiple pulp exposures of dec teeth both dentition are
affected.

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Clinically they exhibit a characteristic unusual
translucent hue.
Because of abnormal DEJ, the scalloping is lost, leading
to early loss of enamel by fracturing away after which the
dentin undergoes rapid attrition and teeth are severely
flattened.
Radiographically obliteration of the pulp chambers and
root canals by continuing formation of dentin is seen.
In type-III, there is a great variability in deciduous teeth,
they appear as “shell teeth”. The enamel of the tooth appears
but dentin is extremely thin and pulp chambers are
enormous. This large size of pulp chambers is not due to
resorption, but rather due to insufficient and defective dentin
formation.
Histologocally- irregular tubules often with areas of
uncalcified matrix can be seen. In some areas there may be
absence of tubules.
Treatment: Cast metal crowns for posteriors and JC with
anteriors.
REFERENCES:
1. Textbook of Oral Histology and Embryology by
Orbans.
2. Textbook of Oral Histology by Tencate.
3. Pathways of the Pulp, 7th Edition by Cohen.