Activation of sensory nerves in the pulp (either by
electrical stimulation of the inferior alveolar nerve or
directly on the tooth crown) induces a long-lasting
blood flow increase in the pulp and increased vascular
permeability. Furthermore, excitation of A- fibres
seems to have an insignificant effect on pulp blood flow
(PBF), whereas C fibre activation causes an increase in
PBF. Neurogenic inflammation is thought to be mediated
by neuropeptides released from sensory nerves, such as
substance P (SP) and calcitonin-gene-related-peptides
(CGRP), and possibly the reactive oxygen species at the
site of inflammation.
However, little is known about the correlation between the
symptoms and levels
of neuropeptides in the pulp except that the amount of
SP increases with the progression of caries.
Furthermore, its expression is significantly higher in
painful pulp with large carious lesions than in
asymptomatic pulps with similar size carious lesions.
Excitatory amino acids have been suggested to activate
sensory nerves to release CGRP.
Neuropeptides may also have some modulatory role
in the pulp immune defense system.
Pulp dendritic
cells may interact with T lymphocytes by the generation
of cytokines, which up regulate the expression of
adhesion molecules on vascular endothelial cells to
facilitate immune-cellular infiltration. They may induce
transendothelial migration of immunocompetent cells,
such as CD43+cells during acute neurogenic
inflammation.