The two key components in pulp inflammation are
the microcirculation and the sensory nerve activity.
Injury to the pulp may activate the intradental sensory
nerves to release neuropeptides, which in turn cause
alteration of microcirculatory haemodynamics.
The response of sensory nerves to stimuli depends
upon the severity of the pulp injury and the stages of
inflammation. Within the first few minutes of injury,
destruction and disruption of nerve fibres in the injured
dentine and pulp occurs, followed by hypersensitivity
of the surviving nerve fibres and the release of
neuropeptides into the pulp. Inflammatory mediators,
such as bradykinin and the prostaglandin E, may also
evoke the neurosecretion of CGRP.
These neuropeptides cause vasodilatation and
increased vascular permeability, hence the neurogenic
inflammation. The tissue becomes oedematous as a
result of filtration of serum proteins and fluid from the
vessels. In the low-compliant environment of the pulp,
the increase in both interstitial fluid volume and blood
volume leads to an increase in the tissue pressure,
which in turn causes compression of the thin-walled
venules, resulting in a decrease in blood flow and an
increase in flow resistance in the venules. The flow
stasis causes an aggregation of red blood cells and an
elevation of blood viscosity. It also produces tissue
hypoxia or ischaemia, which suppress cellular
metabolism in the affected area of the pulp. This results
in tissue necrosis. An increase in carbon dioxide and a
decrease in pH levels alter the local micro-environment,
and may lead to vasodilatation in the adjacent area and
the gradual spread of inflammation.
However, it should be remembered that pulp is
capable of localizing the inflammation and the tissue
adjacent to the inflammatory lesion may be completely
normal.
If healing is favourable, the increase in tissue
pressure may open the shunt vessels and subsequently
redirect the blood before it reaches the inflamed region
of the pulp.
This prevents a further increase in blood
flow and tissue pressure. Also the increase in tissue
pressure may initiate increased lymph flow and
absorption of fluid into capillaries in nearby non
inflamed tissue.
All these factors will transport
fluid away from the affected area and out of the tooth
which will consequently lower the tissue pressure.
Furthermore, increased tissue pressure will promote
outward flow of fluid through exposed dentine tubules
and thereby help to protect the pulp against the entry
of harmful substances.
Sprouting of sensory nerve terminals and up-regulation
of the neuropeptides may also occur.
It would be expected that sensory nerves participate in
the inflammatory process by an increased release of the
neuropeptides. The nerve growth factor produced by
pulp fibroblasts may mediate the nerve sprouting
reactions.
Should the irritant be eliminated or become inactive,
tissue granulation becomes predominant as it replaces
inflammation and nerve sprouting subsides when
reparative dentine covers the injury site. There is a
proliferation of small blood vessels and fibroblasts
together with the deposition of collagen fibres.
Alternatively, if the irritant overwhelms the pulp’s
defense ability, blood flow to the area ceases and the
injured tissue undergoes necrosis. Neutrophils in the
area degenerate and release intracellular lysosomal
enzymes to digest the surrounding tissue, forming
necrotic tissue. Pulp microcirculation may also be
adversely affected by accidental injury or any event that
causes long-term interruption of the blood supply to
the pulp.
As time progresses, necrotic pulp tissue will become
infected by oral micro-organisms penetrating into the
root canal system via caries, cracks or marginal break-down of restorations.
The microbes will migrate
apically through the tooth root and digest the pulp
tissue which renders the tooth pulpless.
Thrombi in pulp blood vessels and collagen sheaths
around vessel walls may become nidi for mineralization,
resulting in pulp calcification. Pulp canal calcification is
a protective mechanism to trauma, or other continual
stimuli (such as caries). It may be also a normal
physiologic response to ageing and genetic predisposition
may play a role.
During the transition from pulpitis to necrosis of the
pulp, the inflammation in the pulp may transform it
into a vascularized inflammatory tissue and this could
initiate resorption of adjacent hard tissue by the
formation and activation of dentinoclasts. These cells
are believed to be derived from undifferentiated reserve
connective tissue cells in the pulp stroma or they may
be recruited from blood in the general circulation.
These cells fuse to form the multinucleated clastic cells
that resorb the dentinal wall, advancing through the
dentine from the root canal wall towards the periphery
until perforation of the root occurs.
Pain
Pain will be present when tissue damage or
inflammation is occurring, not after the damage is
done.
Inflammatory mediators lower the sensory
nerve threshold. The increased tissue pressure acts
directly on sensory nerve receptors. An increase in pulp
blood flow causes excitation of both A- and C fibres
via an increase in tissue pressure, whereas reduction in
blood flow has an inhibitory effect on A- fibres due to
hypoxia, but no discernible effect on C fibre activity. As
a consequence, the gate remains open and stimuli that
were not noxious to a normal pulp (such as heat and
cold) trigger a more painful response because of the
small-fibre activity (unmyelinated C fibres).
During neurogenic inflammation, sodium channel
expression shifts from tetrodotoxin-sensitive (TTXs) to
tetrodotoxin-resistant (TTXr), leading to hyperalgesia
of C fibres.
These TTXr sodium channels are
relatively resistant to local anaesthetics compared with
TTXs channels. In this situation, bupivicaine may be
the anaesthetic of choice because it is found to be more
potent than lidocaine in blocking TTXr channels.