Anatomical Analysis of TRPV1 and TRPV2 Expression in Dental Pulp

Transient receptor potential ion channels (TRPs) respond to thermal and chemical stimuli and are important in mediating inflammatory pain states. TRPV2 is a homolog of the capsaicin receptor, TRPV1. Although TRPV2 is not activated by capsaicin and is expressed in a distinct population of sensory neurons from TRPV1, both channels are activated by noxious heat. Objectives: In this study we evaluated the expression of these channels in rat dental pulp and studied the extent to which these TRP channels are coexpressed with other markers of primary afferent “pain” fibers. Methods: Animals were deeply anesthetized and perfused with 10% formalin. Jaws were removed and decalcified, sectioned using a cryostat, and processed for immunhistochemistry. Antibodies were visualized using an avidin–biotin HRP protocol with DAB as chromogen, or with fluorescent secondary antibodies when we performed double labeling experiments. Controls included evaluation of immunoreactivity in the tissues of TRPV1 knockout mice and withholding of the TRPV2 antibody. Results: TRPV2 immunoreactivity was abundantly expressed in dental pulp. The channel colocalized with N52, a marker of myelinated afferents. TRPV1 immunoreactivity was also detected in dental pulp, but to a lesser extent than TRPV2. Both channels were found to almost exclusively colocalize with calcitonin gene-related (CGRP) peptide, a marker of the peptidergic population of nociceptors. We found very little overlap with isolectin B4 (IB4), a marker of the non-peptide populations of nociceptors. Conclusion: We conclude that TRPV1 and TRPV2 are predominantly expressed in peptidergic pulpal neurons and likely transmit painful thermal information via both unmyelinated and myelinated nociceptors. This research was funded by a grant from the AAE Foundation.