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TRPM2 Immunoreactivity Is Increased in Fibroblasts, but not Nerves, of Symptomatic Human Dental Pulp

  • Kevin C. Rowland
    Correspondence
    Address requests for reprints to Dr. Kevin C. Rowland, Section Head of Physiology, Department of Applied Dental Medicine, Southern Illinois University, School of Dental Medicine, Alton, IL 62002.
    Affiliations
    Southern Illinois University, School of Dental Medicine, Alton, Illinois

    Saint Louis University, Center for Advanced Dental Education, St. Louis, Missouri.
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  • Courtney B. Kanive
    Affiliations
    Southern Illinois University, School of Dental Medicine, Alton, Illinois

    Saint Louis University, Center for Advanced Dental Education, St. Louis, Missouri.
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  • Jason E. Wells
    Affiliations
    Southern Illinois University, School of Dental Medicine, Alton, Illinois

    Saint Louis University, Center for Advanced Dental Education, St. Louis, Missouri.
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  • John F. Hatton
    Affiliations
    Southern Illinois University, School of Dental Medicine, Alton, Illinois

    Saint Louis University, Center for Advanced Dental Education, St. Louis, Missouri.
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      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.

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