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Aims: To investigate the presence of proteinase-activated receptor 2 (PAR2) in the human tooth pulp and to determine whether there are any changes in receptor expression with caries and pain. Methods: Forty-four mandibular first permanent molars were collected from children (n = 36, mean age 9.96 years ± 2.11) requiring dental extractions under general anesthesia. Teeth were categorized as either intact (n = 22) or carious (n = 22). Carious teeth were further subdivided into asymptomatic (n = 10) and painful (n = 12). The coronal pulp was removed and processed for indirect immunofluorescence by using antibodies raised against PAR2 and double labeled with either a neuronal marker (protein gene product 9.5) or both a smooth muscle cell (SMA) and endothelial (UEIL) marker, in order to examine PAR2 presence in both neuronal and vascular tissue. In addition, hemotoxylin and eosin staining was performed to identify pulpal fibroblasts. Results: PAR2 expression was found to be present in pulpal nerve fibers, vascular tissue, and pulpal fibroblasts. PAR2 neuronal expression was not affected by the presence of caries (P > .05) but was significantly less in carious painful teeth than in carious asymptomatic teeth (P < .05). No changes in vascular PAR2 expression were found (P > .05); however, the number of PAR2-labeled fibroblast-like cells per mm2 was significantly greater in carious teeth (P < .05). Conclusion: These findings indicate that PAR2 receptors and changes in their level of expression may have relevance and clinical importance in nociception. Keywords: caries, human tooth pulp, immunohistochemistry, pain, proteinase-activated receptor 2

Aims: To investigate the presence of vanilloid receptor 1 (TRPV1) in human dental pulp and to correlate any expression with caries and pain. Methods: Permanent mandibular first molars were collected and categorized as intact or grossly carious. Grossly carious teeth were further categorized as carious asymptomatic or carious painful samples. Coronal pulps were removed and processed for indirect immunofluorescence using antibodies raised against TRPV1 and a neuronal marker, either protein gene product 9.5 or alpha-smooth muscle actin, in conjunction with Ulex europaeus agglutinin 1 lectin to fully label the pulp vasculature. Results: Analysis revealed that TRPV1 labeling was not confined to pulpal nerve fibers. TRPV1 was also consistently expressed within pulp microvasculature. Expression of neuronal TRPV1 was significantly increased throughout the pulp in grossly carious samples (P < .05). No significant differences were found between carious asymptomatic and carious painful samples. A significant increase in vascular TRPV1 expression was observed in arterioles present in the midcoronal pulp in carious painful compared with carious asymptomatic samples (mean area ± SEM [%] of TRPV1 to vascular labeling; 6.48% ± 4.5% for carious asymptomatic teeth, n = 9; 31.21% ± 9.6% for carious painful teeth, n = 9; P = .02). Conclusion: Expression of TRPV1 in pulpal nerve fibers undergoes marked changes with caries. This may be of relevance in the development of pulpal inflammation, but its relationship to dental pain is still unclear. However, vascular TRPV1 expression does appear to be positively correlated with dental pain, thus providing new insights into symptomatic pulpitis. Keywords: blood vessels, inflammation, pain, tooth pulp, vanilloid receptor 1