DENTAL PULP

Guided by:
Dr. Bobbin Gill
Dr. Nirmala Bishnoi Presented by:
Dr. Vaishak Augustin Dr. Ritu Khichar
Contents
 Introduction
 Cellular Structures of Pulp
 Extracellular Matrix
 Pulpal Microvasculatures
 Regulation of Pulpal blood flow
 Lymph Vessels
 Nerves in the pulp
Introduction
 Dental pulp is a connective tissue situated within the rigid
encasement of mineralized dentin.
 Unique location of dental pulp imposes several special
constraints on its development, maintenance, and response to
injury.
 Pulp and dentin exist in intimate embryologic and functional
relation, which is why dentin and pulp are considered
together as inseparable functional unit termed pulpodentin
complex.
 Histological Zones of Pulp
Odontoblast layer
Cell-free zone
Cell-rich zone
Pulp proper
 Pulp Core
 Itis central region of pulp
 Contains major blood vessels and nerves of pulp
 Pulpal cells and fibroblasts are also seen
Functions Of Dental Pulp
 Formative

 Nutritive

 Defense

 Nervous
Formative function
Steps in reparative dentin formation
 Injury to odontoblasts
 Inflammatory response of the subjacent pulpal tissue
 Differentiation of new odontoblasts
 Secretion of ground substance matrix and collagen
precursors
 Formation of collagen fibrils
 Attraction of mineral salts
Nutritive
 Dental pulp maintains the vitality of dentin by
providing oxygen and nutrients to the odntoblast.

 Also provides continuing source of dentinal fluid.

 Nutrition made possible by rich peripheral

capillary network
Defensive
 Pulp as remarkable reparative abilities responds
to irritation by producing reparative dentin and
mineralizing dentinal tubules .

 Mild to moderate irritation results in continued

peritubular dentin formation , sclerosis and
intratubular calcification(tubular sclerosis).
 Stimuli like operative procedures abrasion ,
carries can result rapid dentin formation(Tertiary
dentin).
 Inflamed pulp due to bacterial infection the cells
in the pulp add in the process of repair(macro
phages , Lymphocytes , neutrophils, monocytes,
plasma, mast cells)
Nervous
 Pulphelps in recognition of stimuli like heat,
cold, pressure, chemicals by way of sensory nerve
fibres.

 Vasomotor innervation controls the muscular wall

of blood vessels. This regulates the blood volume
and rate of blood flow and hence the intrapulpal
pressure .
Cells of Pulp
o Odontoblasts
o Fibroblasts
o Immune cells
o Stem cells
Odontoblast
 The principal cell of the dentin-forming layer, is the
first cell type encountered as the pulp is approached
from the dentin.
 Synthesis and secretory activities render the
odontoblast highly polarized, with synthesis occurring
in the cell body and secretion from the odontoblastic
process.
 The cell body contains organelles that represent
different stages of secretion of collagen,
glycoproteins, and calcium salts.
 The initial mineral seeding of predentin at the
dentinoenamel junction is by the formation of “matrix
vesicles, similar to bone mineralization.
 odontoblasts appear to vary from tall, pseudostratified
columnar cells in the coronal pulp, to a single row of
cuboidal cells in the radicular pulp to a flattened, almost
squamous shape near the apex.
 The cell body manufactures the matrix material; the
material is transported to and secreted from the
odontoblastic process.
 the odontoblastic process was determined to be
limited to the inner third of dentin, with the outer two
thirds of the tubule devoid of processes or of nerves,
but filled with extracellular fluid.
 After initial dentin formation, the odontoblast, via its
process, can still modify the dentin structure by
producing peritubular dentin.
 Fibroblast
 Cells that occur in greatest number in the pulp.
 Function is to form , maintain the matrix that consists of
collagen fibers and ground substance throughout the pulp.
 Fibroblastsrelease proteolytic enzymes such as the matrix
metalloproteinase (MMP) family.
 Inhibitorsto MMPs, called tissue inhibitors of
metalloproteinases, are also secreted by fibroblasts to
regulate extracellular degradation.
 Intracellular
degradation is for the normal physiological
turnover and remodelling of collagenous connective tissue.
Immune Cells
Dendritic cells
Macrophages
T lymphocytes
Plasma Cells

A. They play a major role in local inflammation

and immunity.
B. They are recruited from blood stream and remain as
transient inhabitants in pulp.
Stem Cells
 Dental pulp stem cells (DPSC) are highly
proliferative, have the capacity for self-renewal,
and have the ability to differentiate in response
to injury.
Extra cellular matrix
 Extracellular matrix (ECM), or ground substance, is a structure less
mass making up the bulk of the pulp tissue. It consists complexes of
glycosaminoglycans, namely hyaluronic acid, chondroitin sulfate, and
other glycoproteins.
 Proteoglycans are a large group of extracellular and cell surface-
associated molecules that consist of a protein core, to which
glycosaminoglycan chains are attached, which binds them to water.
 Hyaluronic acid, a large glycosaminoglycan, forms a
viscous hydrated gel.
 Proteins, glycoproteins, and proteoglycans of the ECM
function in cell–matrix adhesion and signaling; regulate
diffusion of nutrients, waste products, and soluble
signaling molecules.
Fibers
Collagen

Elastin

fibronectin
 Collagen is the major organic component in the
dental pulp
 Tropocollagen is an immature collagen fiber that
remains thin and stains black with silver nitrate.
 If tropocollagen molecules aggregate into larger
fibers, they no longer stain with silver and are
then termed “collagen fibers.” If several collagen
fibers aggregate (cross-link) and grow denser, they
are termed “collagen bundles.”
 Collagen generally becomes more coarse (i.e.,
develops more bundles) as the patient ages.
 Collagen fibers are inelastic but have great
tensile strength, giving its consistency and
strength to the tissue.
 Collagen type I and III make up the bulk of the
tissue collagen. Collagen type IV is found in
basement membranes.
 In the pulp, type III collagen appears as fine-
branched filaments, whose distribution is similar
to reticular fibers.
 Fibronectin is insoluble and the fibrils form part
of the ECM. It acts as a mediator for cell–cell and
cell–matrix adhesion.
 Integrins are transmembrane receptors that link
intracellular actin network with ECM.
Lymph Vessels
 The only known mechanism for the removal of proteins and
macromolecules that may leak out from the blood vessels in any
tissue is the lymphatics.
 Recovery of inflammation depends on the removal of
macromolecules and plasma proteins from the tissue, thus a
reversible pulpitis is dependent on functional lymph vessels.
 The lymphatics in the peripheral pulp zone join to form larger
collecting vessels. These vessels unite with progressively larger
lymphatic vessels that pass through the apex together with the
blood vessels.
 Theopen endothelial margins and incomplete basal
lamina permit the entry of large molecules and even
microorganisms into the lymphatics.
 Thefact that materials placed in the dental pulp can
migrate to lymph nodes indicates the possibility of the
spread of microorganisms or their products from the
pulp.
 Theanastomoses of pulpal, periodontal, and alveolar
lymphatics may be important routes for the spread of
pulpal inflammation into adjacent tissues.
 In the low-compliant pulp, this would imply that the
increased local tissue pressure, as measured during
pulpitis, induces increased lymph flow that will
normalize the pressure and also drain off
microorganisms and their byproducts, promoting
healing of the pulp.
 The relationship of teeth to the cardiovascular and
lymphatic systems is intimate and absolute.
 Clinicians should remember this when performing
dental procedures, because placement of materials on
dentin or the pulp may result in widespread distribution
of that material or medicament
Pulp reaction to permeating substances
 Pulpal microvasculatures
• The arterial supply of the dental pulp has its origin from the
posterior superior alveolar arteries and the infraorbital and the
inferior alveolar branch of the internal maxillary arteries.
• Near the dentin, around the odontoblastic area, they form a
dense terminal capillary network in the subodontoblastic region.
• The tooth lacks a collateral or alternative blood supply that
makes the apical region a critical point. Thus, increased tooth
movement in the apical area due to trauma, periodontitis, or
excessive and uncontrolled orthodontic tooth movement may
damage the pulpal blood supply.
Arteriovenous Anastomosis and U- Turn
Loops
 Before the arterioles break up into capillary beds,
arteriovenous anastomosis (AVA) often arise to connect the
arteriole directly to a venule.
 AVAs play a role in the regulation of blood flow.
 They could provide a mechanism for shunting blood away
from the area of injury or inflammation, where damage to the
microcirculation may result in thrombosis and hemorrhage.
 ‘‘U”-turn loops are frequently found in the pulp
vascular network, and it is believed that their functions
are similar to that of AVA’s .
 In most arterioles and in some venules, smooth muscle
cells maintain a state of partial vasoconstriction at all
times, and a variety of substances such as
neurotransmitters, hormones, and local factors
influence this muscle tone and, ultimately, the blood
flow.
Regulation of Pulpal Blood Flow
 Pulpal blood flow is regulated by sympathetic α-adrenergic
and neuropeptide Y (NPY) vasoconstriction, β-adrenergic
vasodilation, sympathetic cholinergic vasoactive system,
and an antidromic vasodilation, that is, a sensory axon
reflex.
 When the sympathetic nerve fibers are stimulated, the
muscle fibers contract, decreasing the diameter of the blood
vessel and reducing blood flow.
 A unique feature of the dental pulp is that it is rigidly
encased within dentin. This places it in a low-compliant
environment.
 The sympathetic nerve-induced vasoconstriction
of pulpal vessels is accomplished by the release
of the α-adrenergic agonist noradrenalin, and
NPY from sympathetic nerve endings.
 Activationof sensory nerves in the pulp cause
increased blood flow, so-called vasodilation.
 Thus, the dental pulp tissue has limited ability to
expand, so vasodilation and increased vascular
permeability, evoked during an inflammatory reaction,
result in an increase in pulpal hydrostatic pressure.
 iftissue pressure increases to the point that it equals the
blood pressure, the thin-walled venules would be
compressed, thereby increasing the vascular resistance
and reducing the pulpal blood flow.
The Stealing theory
 The pressure difference from the arterioles entering the pulp to
the venules leaving is only about one-fourth of the total
arteriovenous pressure difference.
 a considerable part of the vascular resistance that regulates the
pulpal blood circulation is located in the venules and also outside
the pulp.
 This implies that changes in circulation in the neighboring
adjacent tissues, such as the gingiva, alveolar bone, and PDL,
will change the blood flow to the pulp because it will affect the
feeding pulpal arterial blood pressure.
 By normal vessel permeability, the increased
pressure causes fluid absorption according to “the
Starling forces” that lowers the tissue pressure.
 Using the laser Doppler technique to study pulpal
blood flow in dogs, Sasano et al.suggested that an
increase or a decrease in pulpal blood flow is
more dependent on systemic blood pressure than
on local vasoconstriction or vasodilation.
• Any vasodilation in tissues that receive their blood
supply through side branches of the end arterioles
feeding the pulp will, according to the Poisseuille
law, “steal” blood pressure from the pulp.
• clinical treatment causing vasodilatation in
adjacent tissues, may decrease the circulation to
the dental pulp.
Low-Compliance system Theory
 Dental pulp is encased in rigid structures, namely dentin,
enamel, and cementum, creating a low-compliance
system.
 In this system, any increase in blood flow or vasodilation
has a limit, depending on the degree of increase in tissue
pressure.
 When the tissue pressure exceeds that of the venular
pressure, a passive compression can cause a decrease in
pulpal blood flow.
 vasodilators caused a biphasic flow response, an increase
followed by a decrease in pulpal blood flow.
Nerves in the Pulp
 The dental pulp has an abundant supply of both sensory
and sympathetic nerves.
 The trigeminal ganglion supplies sensory innervation to
the pulp via the maxillary and mandibular nerves.
Sympathetic nerves are less numerous with its source from
the superior cervical ganglion
 Postganglionic sympathetic nerves travel with the internal
carotid nerve, reach the trigeminal ganglion, and supply
teeth and supporting structures via the maxillary and the
inferior alveolar nerve.
 Sympathetic fibers in fully developed teeth have been
reported to make up no more than ~10% of the nerve
fibers.
 Parasympathetic fibers have been suggested to exist in
the pulp.
 according to their diameter and conduction velocity pulp
contains two types of sensory nerve fibers: A fibers that
are myelinated and C fibers that are unmyelinated.
 A fibers include both A-β and A-δ with A-δ amounting to
~90% of the total A fibers.
Neuropeptides
 Nerve fibers release biologically active peptides,
known as neuropeptides that influence neural
activity and functioning.
 released from the peripheral terminals of mainly
A-δ and C fibers.
 Sensory
CGRP, SP, NKA

Sympathetic
Neuropeptides NPY

Parasympathetic
VIP
 CGRP is a potent vasodilator and can function in the
transmission of pain.In the dental pulp, CGRP seems to be
mainly responsible for the increase in blood flow and
interstitial fluid pressure during tooth stimulation.
 SP is found in small-diameter, predominantly
unmyelinated sensory axons. It is a vasodilator, increases
vessel permeability and other aspects of inflammatory
process, and is important in pain perception.
 The CGRP with SP has a synergistic effect on edema
formation during inflammatory reactions.
 NPY, a neuropeptide released from sympathetic
nerve terminals.
 Release of NPY causes vasoconstriction.NPY has
also been reported to be a modulator of the
immune function in the dental pulp and
surrounding structures.
 Vasoactiveintestinal peptide (VIP), neuropeptide
has been shown to be released from
parasympathetic nerves.
Distribution
 Sensory nerves fibers containing CGRP or CGRP
immunoreactive (-IR) nerve fibers enter the pulp via the
apical foramen in bundles either surrounding the blood
vessels or individually, and ramify into a network of fine
fibers in the coronal pulp.
 Coronally, individual fibers penetrate the odontoblast
layer and predentin to terminate in the inner 100 µm of
the dentinal tubules.
 CGRP, SP, and NKA neuropeptides have been shown to
coexist in the same nerve fibers in the dental pulp.
Neuropeptide containing nerve fibers are found in close
contact with immune cells suggesting important
neuroimmune interactions.
 Sympathetic nerve fibers containing NPY or NPY-
IR fibers are thin with varicosities.
 VIP-IR nerve fibers in the dental pulp are
associated with blood vessels,or occur as free and
interlacing nerves in the central pulp and the
subodontoblastic plexus.
Neurogenic Inflammation
 Sensory neuropeptides have been shown to cause
neurogenic inflammation.
 During inflammation, neuropeptide containing nerve fibers
exhibit changes in number, density, and architecture.
 sensory nerves fibers containing neuropeptides CGRP and
SP showed sprouting during pulpal injury.

 In experimental pulp exposure studies, sprouting occurs as

early as one day after pulp exposure and stays high until
healing or pulp necrosis occurs.
 Sympathetic fibers containing NPY, unlike sensory
nerve fibers, do not sprout immediately after
injury in experimental studies but a few weeks
later.
 In clinical situations, neuropeptide levels are
increased in dental pulp diagnosed as irreversible
pulpitis.
 Electrical stimulation of teeth causes release of
neuropeptides, creating a local neurogenic
inflammation such as increased blood flow,
transendothelial migration of inflammatory cells.
 When sympathectomy was performed, granulocytes were
not recruited after electrical stimulation.
 It has been reported that while sensory neuropeptides
have a pro-inflammatory role in the dental pulp,
sympathetic neuropeptide, NPY, may have an anti-
inflammatory role on the immune system.
 Sensory neuropeptides increase vascular permeability
during inflammation, and stimulate the production of
other inflammatory cytokines such as interleukin-1 (IL-1),
interleukin-6 (IL-6), and tumor necrosis factor-alpha
(TNFα) .
 Sympathetic nerves inhibit the production of
proinflammatory cytokines, while stimulating the
production of anti-inflammatory cytokines.
 Teethlacking sympathetic nerves also tend to
undergo necrosis more frequently indicating anti
inflammatory role of sympathetic nervous system.
 Sympathetic nerves have also been shown to have
an inhibitory effect on osteoclast resorption
activity and on the cytokine IL-1α.
Receptors
 Neuropeptides cannot cross the cell membrane and,
therefore, their action is dependent on the existence of
specific receptors.
 NK1 receptors, specific for SP, are present in the blood
vessels in the root pulp and smaller vessels along the
odontoblast layer.
THANK
YOU