The dental pulp contains both sensory and autonomic
nerves to fulfill its vasomotor and defensive
functions.
Sensory nerves
The sensory nerves, which are involved in pulp pain
perception and transduction, are branches of the
maxillary and mandibular divisions of the trigeminal
nerve. The small branches enter the apical foramina
and progress coronally and peripherally following the
route of the blood vessels, and they branch extensively
subjacent to the cell-rich zone, forming the plexus of
Raschkow. The plexus contains both large myelinated
A- and A- fibres (2–5µm in diameter) and the smaller
unmyelinated C fibres (0.3–1.2µm). At about the level
of the cell-rich zone, myelinated fibres lose their myelin
sheath. In the cell-free zone, they form a rich network
of free nerve fibres that are specific receptors for pain.
From there, the free nerve terminals may enter the
odontoblastic layer, and penetrate into the predentine
zone or to the inner dentine next to the odontoblastic
cell process, but not every dentinal tubule will contain
nerve endings. Myelinated nerves do not reach their
maximal development and penetration into the pulp
until the tooth is fully formed, which may explain why
young teeth are less sensitive than adult teeth. The
branching of nerve axons has been observed not only
within the pulp but also occurs in the periapical region
where these axons may branch to supply the pulps of
adjacent teeth just prior to entering the pulp.
It has been postulated that the A- and A- fibres
produce the initial rapid sharp pain in response to
external stimuli without the presence of tissue injury
because of their peripheral location, low threshold of
excitability and fast conduction. On the other hand, the
smaller C fibres cause a slow, dull and crawling pain
related to pulp tissue damage and the inflammatory
process due to their much higher threshold of excitability
and slow conduction. Almost all of the A- fibres are
located in the coronal portion of the pulp, with the
greatest nerve density in the pulp horns. In contrast,
C-fibres are located in the pulp proper, extending most
likely into the cell-rich zone.
Pulp usually responds to various stimuli as one
sensation, i.e., pain. However, the exact mechanism
that transmits the stimuli through the dentine to initiate
pain is largely unknown.
Several hypotheses about dental pain transmission
have been proposed including hydrodynamic
mechanism, odontoblastic transduction and dentine
innervation.
Among these hypotheses, the hydrodynamic theory
enjoys the most popularity.
The free nerve endings at
the periphery of the pulp are exquisitely sensitive to
sudden pressure changes and fluid movement. The
dentine contains thousands of capillary-like tubules
that are filled with water-like dentinal fluid. A stimulus
such as cold or compressed air will extract tubular fluid
from its outer surface and cause an outward flow
whereas other stimuli, such as heat or chewing pressure
on a loose filling, will drive the tubular fluid inward
towards the pulp. This rapid fluid movement, either
inward or outward, exerts a direct mechanical
deformation on the low-threshold A- fibres within the
tubules or in the subjacent pulp tissue. The fluid
movement may also cause a concomitant movement of
odontoblasts, which may in turn deform nerve fibres in
contact with their process or cell body. The deformed
nerve membrane increases its permeability to Na+ions.
The rapid inward movement of the sodium depolarizes
the A- fibre membrane, and an action potential (pain
impulse) is initiated.
The dentine innervation theory postulates that nerve
endings penetrate dentine and extend to the dentino-enamel junction.
Direct mechanical stimulation of these
nerves will initiate an action potential. Free nerves have
been demonstrated to penetrate into the dentine, but
these nerves are confined to the inner one-third of
dentine. Moreover, pain producing substances such as
bradykinin fail to induce pain when applied to dentine,
and bathing dentine with local anesthetic solutions
does not prevent pain.
The transduction theory states that odontoblasts can
transduce a mechanical stimulus and transfer that
signal to a closely opposed nerve terminal.
Odontoblasts are derived from the neural crest and
their cellular processes extend into the dentinal tubules
which extend to the dentino-enamel junction.
Odontoblasts communicate with each other via gap
junctions, and are closely associated with nerve
terminals. Nonetheless, odontoblasts are matrix-
forming cells and hence they are not considered to be
excitable cells, and no synapses have been demonstrated
between odontoblasts and nerve terminals. That is,
they have no means of chemical transmission.
Dental pain is also modulated and influenced by the
higher centres in the body. It is a subjective experience
and to a great extent depends on psychological
phenomena. The precise mechanism for the transmission
of pain and the specific pathway to the higher centre is
not completely understood. The gate control theory has
been proposed but it is still speculative.
This theory
suggests that there is a gating mechanism in the
substantia gelatinosa of the spinal cord and brainstem
on which both peripheral nerve fibres and descending
central influences exert their effect in the pain
experience.
Depending on the degree of activity in
large diameter and small diameter afferent nerve fibres,
the gating mechanism either inhibits or facilitates
transmission of impulses: the large diameter fibres are
activated by non-noxious stimuli and close the gate,
whereas the small diameter fibres are activated by
noxious stimuli and open the gate. Descending control
mechanisms from higher central nervous centres, such
as cognitive, motivational and affective processes, also
modulate the gate. Ascending pain pathways, the
sensory-discriminative pathway, allows localization of
pain and reticular information pathway deals with the
unpleasant, aversive and emotional aspects of pain.