Abstract
Although odontogenic infections are often accompanied by pain, little is known about
the potential mechanisms mediating this effect. In this study we tested the hypothesis
that trigeminal nociceptive neurons are directly sensitized by lipopolysaccharide
(LPS) isolated from an endodontic pathogen, Porphyromonas gingivalis. In vitro studies conducted with cultures of rat trigeminal neurons demonstrated
that pretreatment with LPS produced a significant increase in the capsaicin-evoked
release of calcitonin gene-related peptide (CGRP) when compared with vehicle pretreatment,
thus showing sensitization of the capsaicin receptor, TRPV1, by LPS. Furthermore,
confocal microscopic examination of human tooth pulp samples showed the colocalization
of the LPS receptor (toll-like receptor 4, TLR4) with CGRP-containing nerve fibers.
Collectively, these results suggest the direct sensitization of nociceptors by LPS
at concentrations found in infected canal systems as one mechanism responsible for
the pain associated with bacterial infections.
Key Words
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© 2011 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.
