Abstract
Transient receptor potential (TRP) channels function in diverse processes such as
acting as second messenger systems, regulating of ionic concentrations, and aiding
in thermoception. TRPM2 channels, members of the melastatin subfamily, mediate calcium
influx in response to oxidative stress but during pathological states facilitate hyperexcitability
and cellular necrosis via calcium excitotoxicity. We hypothesized that TRPM2 channel
expression is upregulated in pulpal tissue of symptomatic teeth with signs of irreversible
pulpitis. TRPM2 channel expression was significantly increased in pulp from clinically
diagnosed symptomatic teeth compared with pulp from asymptomatic teeth. Additionally,
increased TRPM2 expression in symptomatic pulp was the result of increased immunoreactivity
in fibroblasts, whereas neural expression of TRPM2 was absent. We provide a possible
mechanism explaining the association between TRPM2 channel expression with pain and
necrosis. We suggest that TRPM2 channel antagonists could be administered in attempts
to inhibit the progression of or even reverse pulpal degradation.
Key Words
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© 2007 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.
