DENTIN-PULP COMPLEX

BY-
Dr.ANANTHAKRISHNA.S
 INTRODUCTION
• Dentin & pulp are specialized connective tissues of
mesodermal origin, formed from the dental papilla of the
tooth bud.
• These 2 tissues together from the pulp-dentin complex,
with the mineralized dentin comprising the mature end
product of cell differentiation & maturation.
• Dentin is formed by cells called odontoblasts.
Odontoblasts are considered part of bith dentin & pulp
tissues because their cell bodies are in the pulp cavity but
their long, slender cytoplasmic cell processes (TOMES
FIBERS) extend well into the tubules in the mineralized
dentin
 INTRODUCTION
• It is because of these odontoblastic processes that
dentin is considered living tissue with the
capability to react to physiologic stimuli.
• Thus contain peculiarities are imposed on the pulp
by the rigid mineralized dentin in which it is
enclosed.
• This close relationship between dentin,
odontoblasts & pulp is one of the reasons why
dentin & pulp together are considered as a
functional entity.
 DENTIN
• Dentin is the hard tissue portion of
the pulp-dentin complex & forms
the bulk of the tooth.
• 70% inorganic material, 20%
organic & 10% water.
• Its inorganic component consist
mainly of hydroxyapatite & the
organic component is type I
collagen with fractional inclusions
of glycoproteins, proteoglycans &
phosphoproteins.
 DENTIN
• physically, dentin has an elastic quality which is
important for the proper functioning of the tooth
because it provides flexibility & prevents fracture
of the overlying brittle enamel.
• Basically, dentin is characterized by the presence
of multiple closely packed dentinal tubules that
traverse its entire thickness & contain the
cytoplasmic extensions of odontoblasts that once
formed the dentin & now maintain it.
 STRUCTURE OF DENTIN
• Primary dentin/
developmental dentin- is that
which forms during tooth
development.
• Dentin formed
physiologically after the root
is fully developed is referred
to as secondary dentin.
• Mantle dentin- is the first
formed dentin & is situated
immediately subjacent to the
enamel or cementum.
 STRUCTURE OF DENTIN
• This first layer formed by newly differentiated
odontoblasts is approximately 150 micro.m wide
with an organic matrix consisting of ground
substance derived from the dental papilla that
lacks phosphophoryn.
• This matrix is slightly(4%) less mineralized than
the rest of the primary dentin, which is referred to
as circumpulpal dentin.
• Circumpulpal dentin constitutes the major part of
primary dentin.
 STRUCTURE OF DENTIN
• The organic matrix is composed mainly of collgen fibers,
500 A0 in diameter, that are oriented at the right angles to
the long axis of the dentinal tubules.
• Predentin- is the unmineralized organic matrix of dentin
situated between the odontoblast layer & the mineralized
dentin. It is of variable thickness(10-47micro.m) that lines
the innermost (pulpal) portion of dentin. It consist of type I
&type III trimer collagens, glycoproteins & proteoglycans.
Predentin is thickest where active dentinogenesis is
occurring, & its presense is important in maintaining the
integrety of dentin
 HISTOLOGY OF PIMARY
DENTIN
• When dentin is viewed
microscopically, several
structural features can be
identified such as
- dentinal tubules
- intratubular / peritubular
dentin
- intertubular dentin
- icremental growt lines
- granular layer of Tomes-
an area seen solely in the root
portion of the tooth.
 DENTINAL TUBULES
• A characteristic of human dentin is the presence of tubules
that occupy from 20-30% of the volume of intact dentin.
• These tubules house the major processes of odontoblasts.
They form around the odontoblast processes.
• They are slightly tapered, with the wider portion situated
toward the pulp.
• In coronal dentin, the tubules have a gentle ‘S-shape’ as
they extend from DEJ to pulp. The S-shaped curvature is
presumably a result of the crowding of odontoblasts as
they migrate toward the center of the pulp. As they
approach the pulp, the tubules converge.
 DENTINAL TUBULES
• The dentinal tubules are 2.5 micro.m in diameter near pulp
& 1.2 micro.m in the midportion of dentin & 900 nm near
the DEJ.
• The dentinal tubules branches to the extent that dentin is
permeated by a profuse anastamosing canalicular system.
• Lateral tubules containing the branches of the main
odontoblastic processes may form pathways for the
movement of materials between the main processes & the
more distant matrix. Thus the tubular nature of the dentin
bestows an unusual degree of permiability on this hard
tissue that can enhance a carious process & accentuate the
response of the pulp to dental restorative procedure.
DENTINAL TUBULES
 PERITUBULAR / INTRATUBULAR DENTIN

• Within the dentinal tubule, there is a

hyper-mineralized ring of dentin (40%
more than intertubular dentin) which is
formed within the tubule, narrowing the
tubular lumen. This is referred to as
INTRATUBULAR DENTIN.
• The matrix of intratubular dentin differs
from that of intertubular dentin in having
relatively fewer collagen fibrils & a
higher proportion of sulfated
proteoglycans.
• Because of its lower content of collagen,
intratubular dentinis more quickly
dissolved in acid than is intertubular
dentin.
 PERITUBULAR /
INTRATUBULAR DENTIN
• By preferentially removing
intratubular dentin, acid-etching
agents used during dental restorative
procedures enlarge the openings of the
dentinal tubules, thus making the
dentin more permiable.
• Since the intratubular dentin is more
highly mineralized than intertubular
dentin dentin, it is harder & may
provide added structural support for
the intertubular dentin, thus
strengthening the tooth.
 INTERTUBULAR DENTIN
• Is located between the dentinal tubules &
constitutes the bulk of dentin.
• These fibrils are oriented approximately at
right angles to the dentinal tubules & the
apatite crystals are generally oriented with
their long axes paralleling the fibril.
 INTERGLOBULAR DENTIN
• Is the term used to describe areas of unminaralized
or hypermineralized dentin where globular zones
of mineralization(calcospherites) have failed to
fuse into a homogeneous mass within mature
dentin.
• It is seen in most frequently in the curcumpulpal
dentin just below the mantle dentin where the
pattern of mineralization is largly globular
• In certain dental anamolies like vit-D resistant
rickets & hypophosphatasia, large areas of
interglobular dentin are a characteristic feature.
 DENTINAL FLUID
• Free fluid occupies about 22% of the total volume
of dentin. This fluid is an ultrafiltrate of blood in
the pulp capillaries.
• The fluid flows outward between the odontoblasts
into the dentinal tubules & eventually escapes
through small pores in the enamel.
• Exposure of the tubules by tooth fracture or during
cavity preparation often results in the outward
movement of fluid to the exposed dentin surface in
the form of tiny droplets.
 DENTINAL FLUID
• Dehydrating the surface of dentin with compressed air, dry
heat, or the application of absorbent paper can accelerate
this outward movement of fluid.
• Rapid flow of fluid through the tubules is thought to be a
cause of dentin sensitivity.
• Bacterial products or other contaminants may be
introduced into the dentinal fluid as a result of dental
caries, restorative procedures, or growth of bacteria
beneath restorations.
• Dentinal fluid may thus serve as a reservoir from which
injurious agents can percolate into the pulp, producing an
inflammatory response.
 DENTIN PERMEABILITY
• The permeability of dentin has been well
characterized. Dentinal tubules are the
major channels for fluid diffusion across
dentin.
• Because fluid permeation is proportional to
tubule diameter & number, dentin
permeability increases as the tubules
converge on the pulp.
 DENTIN PERMEABILITY
• Thus from a clinical standpoint, the dentin beneath
a deep cavity preparation is much more permeable
than dentin underlying a shallow cavity when the
formation of sclerotic or reparative dentin is
negligible.
• Studies have been shown that the permeability of
radicular dentin is much lower than that of coronal
dentin
• This low permeability of outer radicular dentin
should make it relatively impermeable to toxic
substances, such as bacterial products eminating
from plaque
 DENTIN PERMEABILITY
• Dentinal sclerosis beneath a carious lesion reduces
the permeation by obstructing the tubules, thus
the concentration of irritants that are introduced
into the pulp
• The cutting of dentin during cavity preparation
produces microcrystalline grinding debris that
coats the dentin & clogs the dentin & clogs the
orifices of the dentinal tubules. This layer of
debris is termed the smear layer
• Because of the small size of the particles, the
smear layer is capable of preventing bacteria from
penetrating dentin
 DENTIN PERMEABILITY
• Removal of the grinding debris by acid –etching
greatly increases the permeability of the dentin by
decreasing the surface resistance & widening the
orifices of the tubules.
• Consequently ,the incidence of pulpal
inflammation may be increased significantly if
cavities are treated with an acid cleanser, unless a
cavity liner, base or dentin bonding agent is used
• Bacterial invasion of dentinal tubules occur more
rapidly in the non vital teeth.
 PULP
• The dental pulp is the soft connective tissue that supports
the dentin.
• When its histology is examined, 4 distinct zones can be
distinguished
1. The odontoblastic zone at the pulp periphery
2. A cell free zone of weil, beneath the odontoblasts, which
is prominent in the coronal pulp
3. A cell rich zone where cell density is high, which is seen
in coronal pulp adjacent to the cell free zone
4. The pulp core which is characterized by the major
vessels & nerves of the pulp
5. Increase of pulp stones & dystrophic mineralization
 PULP
• The principal cells of
the pulp are the
odontoblasts ,
fibroblasts,
undifferentiated
ectomesenchymal cells,
macrophages & other
immunocompetent cells
 ODONTOBLAST LAYER
• The outermost stratum of cells of
the healthy pulp is the
odontoblast layer
• This layer is located
immediatedly subjacent to the
predentin; the odontoblast
processes however pass throu the
predentin into the dentin
• The odontoblast layer in the
coronal pulp contains more cells
per unit area than in the radicular
pulp
 ODONTOBLAST LAYER
• Whereas the odontoblasts of mature
coronal pulp are usually columnar, those
in mid portion of the radicular pulp are
more cuboidal.
• Near the apical foramen the odontoblasts
appear as a flattened cell layer.
• As there are fewer dentinal tubules per
unit area in the root than the crown of the
tooth the
 ODONTOBLAST LAYER
Odontoblast cell bodies are less crowded & are able
to spread out laterally.
• Between adjacent odontoblasts, there are a series
of specialized cell to cell junctions including
desmosomes, gap junctions & tight junctions
• Tight junctions are found mainly in the apical part
of odontoblasts in young teeth
• It appears that tight junctions determine the
permeability of the odontoblast layer by restricting
the passage of molecules , ions & fluid b/n the
extracellular compartments of the pulp & pre
dentin
 CELL FREE ZONE OF WEIL
• Immediately subjacent to the
odontoblast layer in the coronal pulp,
there is often a narrow zone
approximately 40nm in width that is
relatively free of cells
• It is traversed by blood capillaries,
unmyelinated nerve fibers & the
slender cytoplasmic process of
fibroblasts
• The presence or absence of the cell
free zone depends on the functional
status of the pulp.
• It may not be apparent in young pulps,
where dentin forms rapidly, or in older
pulps, where reparative dentin is being
produced.
 CELL RICH ZONE
• Usually conspicuous in the sub-
odontoblastic area is a stratum
containing a relatively high
proportion of fibroblasts,compare
with the more central region of the
pulp.
• It is much more prominent in the
coronal pulp than in the radicular
pulp.
• Besides fibroblasts, the cell-rich zone
may include a variable number of
macrophages, dendritic cells &
lymphocytes.
 PULP PROPER
• It is central mass of the pulp.
• It contains the larger blood vessels and the
nerves.
 ODONTOBLASTS
• The odontoblasts is the most characteristic cell of
the pulp-dentin complex as it is responsible for
dentinogenesis both during tooth development &
in mature tooth.
• During dentinogenesis, the odontoblasts from the
dentinal tubules, & their presence within the
tubules makes dentin a living tissue.
• The number of dentinal tubules range from 59000-
76000/sq.mm in coronal dentin, with a lesser
number in root dentin.
 ODONTOBLASTS
• The odontoblasts in crown are also larger than
odontoblasts in root.
• The odontoblasts synthesizes mainly type I
collagen, although small amounts of type IV
collagen have been found in the extra-cellular
matrix.
• The odontoblasts also secretes alkaline
phosphatase, an enzyme that is closely linked to
mineralization.
 ODONTOBLAST PROCESS
• The odontoblast process occupies most of
the space within the tubule & mediates the
formation of peritubular dentin. Fine
cytofilaments are the other structures found
in the process.
• Microtubules and microfilaments are the
principle ultrastructural components of the
odontoblast process and its lateral branches.
 ODONTOBLAST PROCESS

• Microtubules extend from the cell body out into

the process. These straight structures follow a
course that is parallel with the long axis of cell and
impart the impression of rigidity.
• Although their precise role is unknown, theories as
to their functional significance suggest that they
may be involved in cytoplasmic extension,
transport of materials or the provision of a
structural framework.
 ODONTOBLAST PROCESS
• Occasionally mitochondria can be found in the
process where it passes through the predentin.
In restoring a tooth , preparation of a cavity or
crown often disrupts odontoblasts. Consequently
,it would be of considerable clinical importance
to establish conclusively the extent of the
odontoblastic processes.
• With this knowledge the clinician would be in a
better position to estimate the impact of restorative
procedure on the underlying odontoblasts
 OTHER CONTENTS OF THE
TUBULE
• Recently it has become evident that collagen is a
significant component of the dentinal tubule.
Intratubular collagen has been shown to be a
significant feature of dentin, with increasing
amounts occuring in tubules of inner dentin
• In addition to collagen ( type I & V) & nerve
fibrils, proteolycan, tenascin, fibronectin, serum
proteins albumin & transferrin may all be present
 FIBROBLASTS
• Fibroblasts are the most numerous cells of the
pulp
• They appear to be tissue specific cells that are
capable of giving rise to cells that are committed
to differentiation. Eg- odontoblast like cells ,if the
condition demands so
• These cells synthesize type I & III collagen as
well as proteoglycans
• Fibroblasts are responsible for collagen turn over
in the pulp. Although distributed through out
pulp, they are particularly abundant in the coronal
portion of the pulp, where they form the cell rich
zone
 UNDIFFERENTIATED
ECTOMESENCHYMAL CELLS
• They represent the pool from which connective
tissue cells of the pulp are derived
• Depending on the stimulus, these cells may give
rise to odontoblasts & fibroblasts
• They are often found throughout the cell rich area
& the pulp core & are often related to blood
vessels
• In older pulps their no. diminishes along with the
no. of other cells of pulp core. This reduction , in
association with other aging factors reduces the
regenerative potential of pulp
 MACROPHAGES
• They tend to be centrally located in the pulp
• Due to their mobility & phagocytic activity, they
are able to act as scavengers, removing
extravascular RBCs, dead cells & foreign bodies
from the tissue. Ingested material is destroyed by
the action of lysosomal enzymes
• Another suset of macrophages participates in
immune reactions by processing antigen &
presenting it to memory T cells
• When activated by appropriate inflammatory
stimuli, macrophages are capable of producing a
large variety of soluble factors, including
interleukin 1, tumor necrosis factor, growth factors
& other cytokines
 DENDRITIC CELLS
• Antigen presenting dendritic cells are found in & around
the odontoblast layer in non erupted teeth & in erupted
teeth beneath the odontoblastic layer, with the dendritic
processes extending b/n the odontoblats.
• They have close relationship with the vascular & neural
elements & they capture & present foreign antigen to the
T-cells.
• These cells are non phagocytic & participate in pulp
immuno-surveillance, & increase in no. in carious teeth,
where they come to occupy the odontobalstic layer &
protect their processes into the tubules
 LYMPHOCYTES

• In normal pulp , T- lymphocytes are found

but B- lymphocytes are scarcely found
 CONNECTIVE TISSUE FIBERS
OF THE PULP
• The fibres are principally type I & III collagen in an
approximate ratio of 55:45
• Whereas the overall collagen content of the pulp increases
with age , the ratio b/w type I & III fibres remain stable
• Greatest con of collagen is generally seen in the apical
portion of pulp.
• This fact is imp when pulpectomy is done during the
course of treatment. Engaging the pulp with a barbed
broach in the region of the apex affords a better
opportunity to remove the tissue intact than does engaging
the broach more coronally where pulp is more gelatinous
& liable to tear
 GROUND SUBSTANCE
• It is composed of principally of glycosamino
glycans, glycoproteins & water
• It supports the cells & acts as the medium of
transport of nutrients from the medium for
transport of nutrients from the vasculature to the
cells & of metabolites from cells to the vasculature
• Alterations in the composition of ground
substance caused by age or disease interfere with
this function , producing metabolic changes ,
reducing cellular function & irregularities in
mineral deposition
 INNERVATION OF DENTIN –
PULP COMPLEX
• The dentin pulp is richly innervated. Nerves enter the pulp
through the apical foramen, along with afferent blood
vessels & together form the neurovascular bundle
• Each nerve fiber has been estimated to provide atleast 8
terminal branches , which ultimately contribute to an
extensive plexus of nerves in the cell free zone just below
the cell bodies of the odontoblasts in the crown portion of
the tooth. This plexus of nerves called the sub
odontoblastic plexus of raschkow occupies the cell free
zone of weil & discharges various proteins associated with
nerves (eg- nerve growth factor receptor)
 INNERVATIONS OF DENTIN
PULP COMPLEX
• In the root no corresponding plexus exists
• The nerve bundles that enter the tooth- pulp consists
principally of sensory afferents of the trigeminal ( V
nerve) & sympathetic branches from the superior cervical
ganglion
• Each bundle contains both myelinated & unmylinated
axons . The myelinated axons are classified according to
their diameter & conduction velocities. The majority are
A fibers which are fast conducting & have a diameter in
range of 1 – 6 micronmtr.
• About 1% have diameters of 6-12 micronmtr & identified
as A fibers
 INNERVATIONS OF DENTIN PULP
COMPLEX
• Non myelinated fibers are designated as C- fibres & have
smaller diameter in the range smaller diameter in the range
of 0.4 – 1.2 micro.m
• It is believed that A fibers are associated with sharp ,
localized pain experienced when dentin is first exposed,
whereas C- fibers are associated with a dull & more diffuse
pain
• The A- fibers are associated with sharp, localized pain
experienced when dentin is first exposed, whereas C-
fibers are associated with a dull & more diffuse pain
• The A fibers are located principally in the central region
of pulp( pulp- dentin junction) where as C-fibers are
probably distributed throughout pulp
 INNERVATIONS OF DENTIN PULP COMPLEX

• Although most of the nerve bundles terminate in the sub-

odontoblastic plexus as free, unmyelinated nerve endings ,
a small no. of axons pass b/n the odontoblast cell bodies to
enter the dentinal tubules in close approximation to
odontoblast process.
• The intratubular nerves characteristically contain
neurofilaments, neurobundles, numerous mitochondria &
many small vesicular structures
• Intratubular nerve endings are most numerous in the area
of the pulp horns, where as many as upto 40 % of the
tubules contain fibers
• Their no. decreases in other parts of dentin, & in root
dentin, only about one tubule in a 100 contains fibers
 INNERVATIONS OF DENTIN PULP COMPLEX
• Of considerable clinical interest id the evidence
that nerve fibers of the pulp are relatively resistant
to necrosis.
• This is apparently as nerve bundles are more
resistant to autolysis than other tissue elements.
Even in degenerating pulps, C- fibers might still
be able to respond to stimulation
• Furthermore, it may be that C- fibers remain
excitable even after blood flow has been
compromised in the diseased pulp, for C- fibers
are often able to function in the presence of
hypoxia
• This may offer an explanation as to why
instrumentation of root canal of apparently non
vital teeth sometimes elicits pain
 VASCULAR SUPPLY
• Blood from the dental artery enters the tooth via arterioles
having diameter of 100nm or less
• These vessels pass through the apical foramen or foramina
with nerve bundles
• Smaller vessels may not enter the pulp via lateral /
accessory canals
• The arterioles course up through the central portion of the
radicular pulp & give off branches that spread laterally
towards the odontoblast layer beneath which they ramify to
form a capillary plexus
• The arterioles pass into the coronal pulp, they fan out
toward the dentin, diminish in size & give rise to a
capillary network in the sub-odontoblastic layer.
 VASCULAR SUPPLY
• this network provides the odontoblasts with a rich
source metabolites
• Capillary blood flow in the coronal portion of the
pulp is nearly twice that in the root portion
• Moreover blood flow in the region of the pulp
horns is greater than in other ares of the pulp
• In young teeth, capillaries commonly extend into
the odontoblast layer, thus assuring an adequate
supply of nutrients for the metabolically active
odontoblasts
 VASCULAR SUPPLY
• Blood passes from the capillary plexus, first into
post capillary venules & then into larger venules

• Arteriovenus ansastomoses maybe present in both

the coronal & radicular protions of pulp,
particularly in the latter

• Theoretically , they could provide a mechanism

for shunting blood away from areas of injury or
inflammation where damage to the
microcirculation may result in thrombosis and
hemorrhage
RETROGRESSIVE & AGE CHANGES
OF THE DENTIN & PULP
• Among the age changes that have been reported to occur
in the pulp & dentin are-
1. Decrease in cellular component
2. Dentinal sclerosis
3. Decrease in number & quality of blood vessels & nerves
4. Dead tracts in primary dentin
5. Reduction in size & volume of the pulp, owing to
secondary dentin deposition & to reparative dentin
formation
6. Increase in number & thickness of collagen fibers
 DECREASE IN CELLULAR
COMPONENTS
• Aging effects a reduction in number of
cells of the pulp, possibly as a
consequence of reduced circulation.
• There is also a significant decrease in
the number of regenerable cells.
 DENTINAL SCLEROSIS
• The (primary) dentinal tubules are
also affected by aging. Increase in
peritubular dentin or increased
deposit of apatite crystals occur.
The dentinal tubules are ultimately
occluded, a condition called
sclerosis of dentin.
• Sclerosis of dentinal tubules in the
apical 3rd of the root occurs
consequently with aging
 DENTINAL SCLEROSIS
• Sclerosis of dentin is also initiated by dental
caries. Dental caries elicits reactions within the
primary dentinal tubules which tend to slow down
the progress of the disease. The pulp defends itself
against the lesion of caries quite efficiently.
• Sclerosis of dentin also occurs in response to slow,
external irritations such as abrasion, attrition &
erosion.
 DENTINAL SCLEROSIS
• There appears to be 2 patterns of
dentinal tubule mineralization
1. Continuous of peritubular dentin &
2. Intratubular crystal deposition
• Certain drugs like Ca(OH)2 &
corticosteroids, when placed on the
dentin after cavity preparation, also have
been demonstrated to cause sclerosis.
• Thus sclerosis which results in
decreased permeability of dentin, limits
the diffusion of noxious substances
through it & helps to shield the pulp
from irritation.
 DEAD TRACTS IN PRIMARY DENTIN
• When caries progresses rapidly, the
odontoblasts degenerate. The tubules
are no longer filled with living
protoplasm & ‘dead tracts’ results.
• A similar occurrence follows fractures
of the crowns of the teeth(with sudden
exposure of dentinal tubules), severe
operative injuries, such as deep cavity
cutting with out coolant, & drug
injuries by application of phenol, silver
nitrate, or ionization to the base of the
cavity preparation.
• Caries progress more rapidly in the
presence of dead tracts.
 DECREASE IN NUMBER & QUALITY OF
BLOOD VESSELS & NERVES

• Blood vessels of aged pulps undergo

arteriosclerotic changes, resulting in a diminished
blood supply to the cells of the coronal portion of
the pulps.
• The blood vessels decrease in number in older
teeth, regardless of whether or not the pulp
exhibited mineralization.
• There is s reduction in the number of nerve
branches in the coronal portion of the aged pulp.
 FORMATION OF SECONDARY
DENTIN
• Continuous deposition of the dentin, which tends
to reduce the volume of dental pulp takes place
throughout life.
• Such secondary dentin formation occurs in the
absence of inflammation. It increases when a tooth
is worn down through chewing, thereby exposing
the dentin. The irritation is mild, yet is sufficient
to elaborate dentin.
 FORMATION OF SECONDARY
DENTIN
• The secondary dentin formed is highly irregular,
with fewer dentinal tubules. Thus the pulp
chamber ‘shrinks’ in an occluso-radicular direction
much more than it does mesio-distally. As a result,
the horns of the pulp in molars are left behind.
• Care must be exercised during cavity preparation
to avoid cutting the so-called recessional lines of
the pulp.
 FORMATION OF REPARATIVE
DENTIN
• The formation of reparative/ irregular/ tertiary/
irritation dentin is an important mechanism in the
defense against disease processes in the pulp.
• It is formed when the pulp is more severely
injured & the injury is accompanied by an
inflammatory response.
• Reparative dentin is found in all instances under
the involved dentinal tubules in dental caries,
restorations, abrasion & attrition.
 FORMATION OF REPARATIVE
DENTIN
• If odontoblasts are injured as a result of either
dental caries or operative procedures, some may
die, & dentin that is formed subsequently is less
regular. This dentin is known as reparative dentin.
• This new dentinal tissue is elaborated by other
pulp cells which have been transformed into
odontoblasts or cells like odontoblasts.These new
odontoblasts may be derived from peri-vascular
cells.
• The reparative dentin is much more amorphous or
irregular.
 FORMATION OF REPARATIVE
DENTIN
1) Reparative dentin under dental caries is less
abundant & much more regular than that found
under restorations. If caries is rampant, the
reparative dentin is decayed as readily as
primary dentin.
2) Reparative dentin restorations is much more
amorphous & irregular than the reparative dentin
found in other conditions. The reparative dentin
is also softer than primary dentin in the same
tooth.
 FORMATION OF REPARATIVE
DENTIN
• The daily rate of reparative dentin formation after
the operative procedures varies with time. It is
about 2.8micro.m for deciduous & 1.5m for
permanent teeth
• The quantity of reparative dentin formed after
operative procedures depends on the depth of the
cavity. In deep cavities there may be a lag period
in the onset of predentin followed by the
elaboration of huge amounts under the cut dentinal
tubules
 FORMATION OF REPARATIVE
DENTIN
3. Reparative dentin in root canals is present in
significant amts that are clinically inflamed &
especially in those that are periodontally involved.
In both these circumstances the root canals are
excessively narrowed & are almost obliterated
Clinical correlations:
The formation of reparative dentin is an attempt of
the pulp to wall off the injured odontoblasts. Thus
when this is formed in large quantities it means
greater damage has occurred.
Once the reparative dentin has been elaborated there
is no assurance that the pulp wall will remain
uninflammed
 INCREASE IN NUMBER & THICKNESS
OF COLLAGEN FIBERS(FIBROSIS)
• In intact uninflammed pulp collagen fibers are
infrequent or absent in the coronal portions of
posterior teeth that are free of caries & have not been
operated on.
• In anterior teeth the quantity of coronal collagen is
significantly more. In the apical third there is a
gradual transition from the cellular pulp to more
collagenous less cellular tissue in which blood vessels
& nerves are present.
• Histologic examination reveals that , in older pulps
there is a relative increase in the number of
arygophilic reticular fibers & in the no. of collagen
fibers as compared to young pulps.
 Increase in no. & thickness of
collagen fibres ( fibrosis)
• The relative increase is due to reduction in the
volume of the pulp by continuous deposition of
secodary dentin. Moreover , actual increase in the
no. of collagen fibrils also occurs
• Fibrosis in the coronal portion of the pulp
increases under the influence of caries, abrasion,
attrition & markedly, after operative procedures
with a concurrent filling in of the pulp horns with
reparative dentin.
 DYSTROPHIC
MINERALIZATION
• It is found in varying amounts & degrees in most
pulps
• The presence of mineralization appears to be
unrelated to any known condition or cause
• Dystrophic mineralization also apparently increases
markedly as a result of disease process such as caries
& periodontal disease.
• In teeth with caries & / or restoration there is a
significant increase in coronal mineralization
 DENTICLES
• The larger mineralizations are called
denticles. These are large mineralized
bodies which sometimes result from fusion
of several smaller ones. They can become
extremely large at times almost
obliterating the pulp chamber or the root
canal.
• Denticles maybe classified
1. Structurally – as true & false denticles .
True denticle is supposed to be made up of
dentin & is lined by odontoblasts.
Generally found in apical portion of tooth.
False denticles are formed from
degenerating cells of the pulp that tend to
mineralize.
2. According to size- fine , diffuse
mineralizations also known as fibrillar
mineralizations & denticles
 DENTICLES
The former are found more
frequently in the root
canals , but they may also
be present in the coronal
portion of the pulp.
3. According to location:
embedded/interstitial,
adherent/ free denticles
 DENTIN SENSITIVITY
• One of the most unusual features of the pulp-dentin
complex is its sensitivity.
• Why this complex should be so sensitive is difficult to
explain, but the overwhelming sensation appreciated by
this complex is pain.
• Among the numerous stimuli that can evoke a painful
response when applied to dentin are many that are related
to clinical dentinal practice, such as cold air or water,
mechanical contact by a probe or bur, & dehydration with
a stream of air or cotton.
 DENTIN SENSITIVITY
• 3 mechanisms, all involving an understanding of the
structure of dentin & pulp, might explain dentin
sensitivity.
1. The dentin contains nerve endings that respond when it
is stimulated.
2. The odontoblasts serve as receptors & are coupled to
nerves in the pulp. And
3. The tubular nature of dentin permits fluid movement to
occur within the tubules when a stimulus is applied- a
movement registered by pulpal free nerve endings
enclose to the dentin.
 1st MECHANISM

• The pulp is well innervated, especially below the

odontoblasts(plexus of Raschkow). Some nerves
penetrate a short distance in to some tubules in
human teeth.
• How these intratubular nerves are exactly involved
in dentin sensitivity is not exactly understood.
• No evidence has been found for nerves in the
outer dentin, which is reputedly the most sensitive.
 1st MECHANISM

• Development studies have shown that the plexus of

Raschkow & the intratubular nerves do not establish
themselves until sometime after the tooth has erupted, yet
newly erupted teeth are sensitive. In addition, the
application of local anesthetics to exposed dentin does not
eliminate dentin sensitivity(& pharamacological agents
that cause pain when applied to skin do not do so when
applied to dentin.
• Hence it can be stated that there are some nerves within
some tubules in the inner dentin, but that dentin sensitivity
does not depend solely, if at all, on the stimulation of such
nerve endings.
 2nd MECHANISM
• This is proposed to explain dentin sensitivity
involves movement of fluid through the dentinal
tubules. This HYDRODYNAMIC THEORY,
proposes that fluid movement through the tubule
distorts the local pulpal environment & is sensed
by the free nerve endings in the plexus of
Raschkow.
• Thus when dentin is first exposed, small blebs of
fluid can be seen on the cavity floor. When the
cavity is dried with air or cotton wool, a greater
loss of fluid is induced, leading to more movement
& a further painful experience.
 2nd MECHANISM

• The increased sensitivity at the DEJ is

explained by the profuse branching of the
tubules in this region(the hydrodynamic
hypothesis also explains why local
anesthetics fail to block dentin sensitivity &
why pain is produced by thermal change,
mechanical probing, hypertonic solutions &
dehydration).
 3rd MECHANISM

• This mechanism considers the odontoblasts to be a

receptor cell.
• This concept has been considered, abandoned &
reconsidered for many reasons.
• Since the odontoblast is of neural crest origin. It was
thought that it retains an ability to tranduce & propagate an
impulse, but the demonstration of a synaptic relationship
between the odontoblast & pulpal nerves was not very
evident.
• When it was thought that the odontoblast process probably
does not extend much further than 1/3rd the way through
dentin, this explanation of dentin sensitivity was largely
abandoned .
 3rd MECHANISM

• The possibility that the odontoblast process

extends to the DEJ & the demonstration of
the gap junctions b/w the odontoblasts(&
possibly b/w odontoblasts & pulpal nerves),
combined with the knowledge that the such
junctions permit electronic coupling, have
revived the interest in the odontoblasts role
in dentin hypersensitivity.