THE DENTAL PULP

THE DENTAL PULP

INDEX
History of pulp biology
Development of pulpodentin complex
Connective tissue of pulp
Circulation of pulp
Nerve supply of pulp & responses to injury
Pain mechanism of pulpodentin complex
Control of dental pain
Pulpal calcification
INDEX
HISTORY OF PULP BIOLOGY
Early writings from around the world indicate a
recognition of the relationship between caries, pulpal
inflammation & pain.
Fu His is credited with one of the earliest surviving
descriptions of several types of tooth ache including
pain caused by cold & mastication.
Root canal treatments were performed in the
European & ancient Greeks attempted to hermetically
seal root canal systems. At the time caries was thought
to be caused by small worms that existed in the tooth &
consumed enamel.
Jonathan Taft (1858) introduced that the vital pulpodentin
complex was valuable in providing greater resistance to caries.

Adolph Witzel (1879) recommended that after caries removal
& pulpal exposure, cold water should be placed into the cavity:
if that caused acute but transitory pain, then the pulp was
viewed to be reversibly inflamed & could be capped; if pain
lingered, other treatments were recommended.

In the early 20th century many physicians & dentists
believed that teeth with infected pulps were foci of infection for
systemic disease. The focal infection theory was based on
culture results from extracted teeth, with little regard to the
possibility that the bacteria recovered may have been part of
the normal flora of the oral cavity. This theory resulted in
needless extraction of countless teeth.
DEVELOPMENT OF PULPODENTIN
COMPLEX
Dentin & pulp are derived
from dental papilla, whose
cells migrate to the first
branchial arch from within
the ectomesenchyme. The
tissues remain closely
associated during
development & throughout
the life of an adult tooth &
hence are most commonly
referred to as the pulpo-
dentin complex.

CONNECTIVE TISSUE OF PULP
The basic components
arranged in a manner as found
in other loose connective
tissues.
Odontoblasts, the specialized
cells that elaborate dentin,
circumscribes outer most part
of pulp.
The cell bodies lie in the pulp
& long cytoplasmic processes,
the odontoblastic processes,
extend into dentinal tubules.
Tall & columnar cells in the
coronal pulp, short & columnar
in the mid portion & cuboidal to
flat in the root portion.
Network of capillaries called
terminal capillary network
exists within the odontoblast
layer

Nerve fibers between
odontoblasts as free nerve
endings also exist.
Area relatively free of cells
seen, called the cell free
zone or zone of Weil. The
constituents include the rich
network of unmyelinated
nerve fibers, blood capillaries
& processes of fibroblasts.
The zone is often
inconspicuous when the
odontoblasts are actively
forming dentin.
More deeply situated pulp
ward, cell rich zone has high
density of cells. They include
fibroblasts, undifferentiated
mesenchymal cells, defense
cells (macrophages &
lymphocytes), blood
capillaries & nerves.

CELLS BORDERING PULP
EXTRACELLULAR MATRIX OF
PULP
COLLAGEN
ELASTIN
GLYCOSAMINOGLYCANS &
PROTEOGLYCANS
FIBRONECTIN:
CELLS OF THE PULP
ODONTOBLASTS
FIBROBLASTS
UNDIFFERENTIATED
MESENCHYMAL
CELLS
IMMUNOCOMPETENT
CELLS:

LYMPHOCYTES
MACROPHAGES
DENDRITIC CELLS
ODONTOBLASTS:
Most highly differentiated cells of
the pulp, are post mitotic neural
crest-derived cells. They produce
the components of the organic
matrix of predentin and dentin,
including collagens and
proteoglycans. Odontoblasts also
synthesize various non
collagenous proteins, including
bone sialoprotein, dentin
sialoprotein, phosphophoryn,
osteocalcin, osteonectin, and
osteopontin . Odontoblasts are
most active during the early
period of primary dentin formation.
The cell body of actively
synthesizing odontoblasts
columnar.
ODONTOBLASTS:
ODONTOBLAST PROCESSES
Are a direct extension of
the cell body & occupies most
of the space within the
dentinal tubules.
Its diameter is 3-4m at the
pulp predentin border &
gradually narrows as it
passes within the dentinal
tubules.
The process has numerous
side branches that may
contact the branches of other
odontoblasts.
In contrast to main cell
body, the process is virtually
devoid of major organelles for
synthetic activity.
ODONTOBLAST JUNCTIONS
Desmosome like junctions, occur along the lateral
surface of odontoblasts. This type of junctional contact
may promote cell-cell adhesion & play a role in
maintaining the polarity of odontoblasts.


Gap junctions are present between lateral surfaces of
odontoblasts. They provide pathways for intercellular
transfer of ions & small water soluble metabolites & play
role in controlling cyto differentiation of the odontoblasts
& mineralization of dentin
RESPONSES OF
ODONTOBLASTS TO INJURY
Under physiologic conditions, primary odontoblasts
in the adult tooth produce new dentin at a slow rate.

Once the primary odontoblasts are injured, the
dentin production may be accelerated as a defense
reaction.

Depending on the nature, magnitude, and duration
of the injury, the primary odontoblasts may be
reversibly damaged or they may actually die. The
dead cells may be replaced by secondary
odontoblasts that produce new dentin matrix.

FIBROBLASTS OF THE PULP:
Most numerous connective
tissue cells with capacity to
synthesize and maintain
connective tissue matrix also.
Found in high densities in the
cell rich zone of the coronal
pulp. Synthesis of collagens
type 1, type 3
Also, synthesis and secretion
of a wide range of non
collagenous extra cellular
matrix components, such as
proteoglycans and fibronectin.

UNDIFFERENTIATED
MESENCHYMAL CELLS:
Distributed through out the
cell rich zone & the pulp
core, occupying the
perivascular area.
Cells appear as stellate
shaped with a relatively high
nucleus-cytoplasmic ratio.
After receiving stimuli, they
may undergo terminal
differentiation & give rise
either to odontoblasts or
fibroblasts.
In older pulps the number of
mesenchymal cells diminish
& hence the regenerative
potential of pulp.
IMMUNOCOMPETENT CELLS:
The ability of connective tissue to generate &
support local inflammatory & immune reactions
makes it an active participant in host defense.
The cells are recruited from the blood stream
where they reside as transient inhabitants.
Once foreign antigens gain entry into connective
tissue, these cells interact to create mechanisms
that help defend the tissue from antigenic
invasion.
LYMPHOCYTES OF THE PULP:
T lymphocytes are the normal residents of
human dental pulp. They are scattered
predominantly along the blood vessels in
the pulp. The CD8 T lymphocytes
outnumber CD4 T lymphocytes.
The terminally differentiated B
lymphocytes with a specialized capacity
for producing antibody are rarely
encountered in normal dental pulp.
MACROPHAGES:
They are constituents of the mononuclear
phagocyte system.
They primarily act as scavenger cells that
phagocytose & digest foreign particles as well as
self tissues & cells that are injured or dead.
They are activated by variety of stimuli & acquire
several properties that contribute to the defense
& repair of connective tissues
DENDRITIC CELLS:
Discrete populations of
hematopoetically derived
leucocytes sparsely
distributed in almost all
tissues & organs of the body.
They form a continuous
reticular network throughout
the entire pulp.
They are particularly rich in
periphery of the pulp where
they compete for space with
the odontoblasts &
sometimes extend their
processes into dentinal
tubules

THE CIRCULATION OF THE
PULP:
Microcirculatory system as it
lacks true arteries & veins; the
largest vessels are arterioles &
venules.
Its primary function to regulate
local interstitial environment via
the transport of nutrients,
hormones, gases & removal of
metabolic waste products.
It is a dynamic system that
regulates blood flow in
response to nearby metabolic
events. It also responds to
inflammatory stimuli with a
change in circulatory properties
& also leading to the
recruitment of immune cells to
the site of tissue injury.
ARTERIOLS:
The pulp has an extensive vascular
supply. The arterioles are resistance
vessels, measuring app. 50m in
diameter, & have several layers of
smooth muscle which regulate
vascular tone. The transitional
structure between arterioles &
capillaries is called the terminal
arteriole.
This segment of arteriole has same
dimensions as a capillary but is
surrounded by a few smooth muscle
cells.
The arterioles then divide into
terminal arterioles & then
precapillaries.
Serve as the workhouse of
circulatory system, as they
function as the exchange
vessels regulating the
transport or diffusion of
substances (gases, fluids,
proteins, etc.) between blood
& local interstitial tissue
elements.
At any moment, only about
5% of the blood supply
circulates in capillaries, but
this is major site of nutrient &
gas exchange with local
tissues. The wall of capillary
is about 0.5m thick &
serves as a semi permeable
membrane.
CAPILLARIES
There are several major classes of
capillaries that differ dramatically in their
properties as semi permeable membranes.
These include:
Fenestrated
Continuous (Non fenestrated)
Discontinuous
The venular organization in
dental pulp has important
characteristics. First, the
collecting tubules receive
pulpal blood flow from the
capillary bed & transfer it to
the venules.
These structures are
characterized by a spiral
organization of smooth
muscle. The arterio venous
anastomosis shunts permit
regional control of pulpal
blood flow via direct
shunting of blood from
arterioles to venules.
VENULES
LYMPHATIC VESSELS
The lymphatic system plays a
critical role in tissue homeostasis
& response to injury. Because of
the semi permeable nature of
capillaries, they do not absorb
solutes of high molecular weight.
Instead the lymphatic system is
the dominant mechanism for
removal of high molecular weight
solutes from the interstitial fluid
Lymph from the dental pulp
drains into the sub maxillary &
sub mental lymph glands & then
to superficial & deep cervical
glands.
REGULATION OF PULPAL
BLOOD FLOW:

THREE MECHANISMS TO REGULATE BLOOD FLOW:

METABOLIC

NEURONAL

PARACRINE/ENDOCRINE
Metabolic regulation

The arteriolar vascular tone is regulated by locally
released metabolic by-products.
Studies have suggested that adenosine, low
interstitial pO2 levels, low Ph or elevated pCO2 levels
may increase pulpal blood flow via vasodilatory
effects.
The localized increases in the pulpal activity e.g.
dentinogenesis may lead to localized increases in
pulpal blood flow.
Neuronal regulation
Three major neuronal systems are
implicated in the regulation of pulpal
blood flow:

1.Sympathetic fibres

2. Parasympathetic fibres

3. Afferent fibres
SYMPATHETIC FIBERS
Dental pulp is innervated by sympathetic nervous system.

Sympathetic fibers terminate as free nerve endings in pulp
& innervate predominantly the arterioles.

Depolarization Local release of several
neurotransmitters
Constriction of blood vessels
Activation of sympathetic nervous
system
Reduces the pulpal
blood flow
PARASYMPATHETIC FIBERS
It does not have as dominant role as sympathetic
nervous system in regulating pulpal blood flow.

Neurotransmitters include:
Acetylcholine & vasoactive intestinal
polypeptide

Local administration of Ach to dentinal tubules
produce increase in pulpal blood flow.
AFFERENT FIBERS
Dental pulp is innervated by sensory neurons
originating from trigeminal ganglion.

Neuropeptides released by these fibers include:
Substance P &
Calcitonin gene related peptide (CGRP)

Both are released from terminals of pulpal
nociceptors consisting of unmyelinated C & thinly
myelinated A- delta fibers.

Both of these cause vasodilatation & hence increase
in pulpal blood flow
Paracrine /endocrine regulation
Paracrine: Locally produced at the site of action & do
not circulate in blood stream.
Endocrine: produced from a distant gland & circulate
in blood stream to modify activity of target cell.
Important hormones: epinephrine & nor epinephrine.
Example of paracrine factors that regulate pulpal
blood flow is bradykinin. locally produced at site of
inflammation. Bradykinin levels are elevated in
irreversible pulpitis. About one half of bradykinins
effect is lost in denervated pulp, suggesting that this
paracrine factor acts partly by activating sensory
neuron release of neuropeptides & partly by a direct
action on pulpal vasculature.
Effect of local anesthetics on
pulpal circulation:
Vasoconstrictors are added to local anesthetic agents
for the purpose of prolonging the anesthetic state & for
obtaining deeper anesthesia. This effect is the result of
arteriolar constriction which reduces pulpal blood flow
by increasing vascular resistance. Dental pulp
recovers from the periods of reduced blood flow.
Both infiltration & intraligamentary routes of injection of
local anesthetic with vasoconstrictor produce a
profound reduction in pulpal blood flow. The infiltration
route of injection produced about a 50% greater
reduction in pulpal blood flow than the
intraligamentary.
Effect of dental procedures on
pulpal circulation:
Dental procedures alter pulpal microcirculation via 2 major
routes:
Thermal stimulation when hand pieces or certain techniques
are used
The effect of dental treatment including restorative materials

Heat generated by tooth preparation can cause major
changes in the pulpal microcirculation including extensive
extravasations. Water spray minimizes the development of
pulpal inflammatory changes after restorative procedures. E.g.
crown preparation without water spray cause about 95%
reduction in pulpal blood flow by 1 hour after preparation. In
contrast, the use of water spray eradicates any alteration in
pulpal blood flow
Endodontic therapy:
If the pulp is partially extirpated during
endodontic therapy, a profuse hemorrhage
may result because of the rupture of wide
diameter vessels in the central part of the
pulp. There would be less hemorrhage if the
pulp were extirpated closer to the apex of the
tooth. Therefore excessive bleeding during
instrumentation of the canal indicates that
some tissue remains in the apical portion of
the root canal
Inflammation:
The two major actions of mediators of acute inflammation are:
Alterations in pulpal blood flow &
increases in capillary permeability,
leading to plasma extravasation. The increased permeability
of the vessels permits the escape of plasma proteins &
leucocytes from the capillaries into the inflamed area to carry
out neutralization, dilution, & phagocytosis of the irritant.

In the acute pulpitis stage following cavity preparation without
water coolant, increased permeability of the blood vessels is
seen not in the superficial, terminal capillaries just beneath
the cavity but in the venular & capillary networks. In the
inflamed pulp, vascular loops, AVA shunts, increased blood
flow & increased lymphatic outflow may represent protective
changes against inflammation.
NERVE SUPPLY OF THE PULPODENTIN COMPLEX
Most densely innervated tissues
in the body.
Preservation of enamel over
many decades requires healthy
dentin & pulp. The profuse
innervations of pulp & dentin
contains many neuropeptide-
rich fibers that can release
those peptides when stimulated.
Neural agents are an important
signal for neurogenic
inflammation, for stimulation of
repair, & for assisting with
everyday functions in the dentin
pulp border area
Types of innervation &
terminal locations:
The sensory innervation of teeth
terminates primarily in the
coronal odontoblast layer,
predentin, & inner dentin &
morphologically it is made up of
at least 6 different kinds of nerve
fiber. A small portion is medium
sized (A-beta) myelinated fibers.
They innervate mainly dentin &
the dentin-pulp border near the
pulp horn tip. They are the most
sensitive fibers to mechanical
stimulation of dentin.
About 25% to 50% of dental nerve
fibers are small myelinated (A-delta)
fibers. Most of it innervates dentin,
predentin & the odontoblast layer in the
coronal regions underlying enamel.

It is progressively less frequent towards
the cervical region & least prevalent in
the root dentin.

The majority of nerve fibers in the teeth
are unmyelinated, slowly conducting C-
fibers. They terminate in peripheral pulp
or along blood vessels & they are mostly
activated by pulpal damage.

The key feature of all the nerve fibers is
that they have specific membrane
receptors for chemical signaling with
their neighboring cells
SYMPATHETIC&PARASYMPATHETIC INNERVATION
OF TEETH:
The vasodilatory functions of
sensory innervation in teeth are
opposed by vasoconstriction by
the sympathetic fibers. The
sympathetic fibers are much
less numerous than the sensory
fibers. Sympathetic fibers also
differ from sensory fibers in that
they are located mainly in the
deeper pulp & along blood
vessels. Parasympathetic
activity can affect blood flow in
teeth but the importance is
much less than that of the
sympathetic activity.
DEVELOPING & PRIMARY TEETH:
During tooth development, the innervation enters
the pulp during the crown stage & makes branches
near the pulp horn odontoblasts. There is rapid
increase in nerve fiber entry into dentin when
eruption starts & then innervation density continues
to increase during maturation of the tooth. The
sensory innervation adjusts its location to maintain
its greatest association with the surviving
odontoblasts close to the pulp horn tip. With
increasing loss of primary dentin, tooth innervation
decreases.
NEUROANATOMIC RESPONSES TO TOOTH INJURY
& INFECTION:
Injury to the pulpodentin
complex produces
numerous neuronal
responses. The nerve
fibers not only send rapid
signals to the ganglion &
central pain pathways,
but they also release
neuropeptides from their
peripheral terminals that
regulate vasodilatation &
leukocyte invasion of the
injury site
NEUROPHYSIOLOGY OF PULPAL NOCICEPTORS
& DENTINAL SENSITIVITY
The type of pain vary according to
type of stimulus applied, the type of
neuronal fiber activated or the
condition of the pulp. Tissue injury
& inflammation can sensitize &
activate certain pulpal neurons.
Pulpal inflammation has been
associated with reduced threshold
to external stimulation &
spontaneous discharges of pulpal
nerve fibers. It is due to synthesis
or release of a number of
inflammatory mediators which
activate pulpal nerves & sensitize
them to external stimuli.
SENSORY FUNCTIONS OF PULPAL NERVES
UNDER NORMAL CONDITIONS:
The quality of pain vary depending on stimuli & range from
sharp, stabbing pain to dull, aching, and throbbing pain
sensations. The variation is caused by activation of different
nerve fiber types & differences in the nerve fiber patterns.
The pulpal C-fibers are polymodal as they respond several
different modes of stimulation & have high threshold for
activation.
Activated only if stimuli reach their terminal endings inside
the pulp.
They also respond to histamine & bradykinin indicating that
this fiber group also may be activated in connection with
pulpal inflammatory reactions. Thus the dull pain induced by
pulpitis may be evoked by C-fiber activation.
MECHANISMS OF DENTAL PAIN CAUSED
BY INFLAMMATION:
Pulpal C nociceptors are thought to have a
predominant role in encoding inflammatory pain
arising from dental pulp & periradicular tissue. This
hypothesis is supported by distribution of C fibers in
dental pulp, their responsiveness to inflammatory
mediators & strikingly similar qualities of pain
associated with C fiber activation & pulpitis.
Application of histamine & bradykinin primarily
produced reports of dull, aching pain.
The A delta fibers respond to stimulation of dentinal
tubules whereas pulpal C fibers respond to
bradykinin.
PHARMACOLOGIC CONTROL OF DENTAL PAIN:
The integrated method to control dental pain called
the 3D method for pain control:

Diagnosis

Definitive dental treatment

Drugs
PULPAL CALCIFICATIONS:
Calcification of pulp tissue is very
common occurrence. One or
more pulp calcifications are
present in at least 50% of the
teeth. In the coronal pulp,
calcification usually takes the
form of discrete, concentric pulp
stones whereas in radicular pulp,
calcification tends to be diffuse.
Pulp stones range in size from
small microscopic particles to
accretions that occupy almost the
entire pulp chamber. The mineral
phase of pulp calcifications
consist of typical hydroxyapatite.
Histologically two types of pulp
stones are known:
Those that are round or
ovoid, with smooth surfaces &
concentric laminations
Those that assume no
particular shape, lack
laminations & have rough
surface.
The cause of pulpal
calcification is largely
unknown. Calcification may
occur around a nidus of
degenerating cells, blood
thrombi, or collagen fibers.
This may be a type of
dystrophic calcification.
Classified according to its structure into:
True & False
True denticles: have dentinal tubules like
dentin, odontoblastic processes & few
odontoblasts
False denticles: are concentric layers of
calcified tissue with a central cellular area
(which might be necrotic & acts as nidus of
denticle formation)
Classified according to its structure into:
free, attached & embedded
Pulp stones