Rowland Kevin C, Kanive Courtney B, Wells Jason E, Hatton John F
Southern Illinois University, School of Dental Medicine, Alton, Illinois 62002, USA.
J Endod. 2007 Mar;33(3):245-8. doi: 10.1016/j.joen.2006.11.020.
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.
瞬时受体电位（TRP）通道在多种过程中发挥作用，如充当第二信使系统、调节离子浓度以及协助热感受。TRPM2通道是褪黑素亚家族的成员，可介导氧化应激反应时的钙内流，但在病理状态下，会通过钙兴奋毒性促进兴奋性过高和细胞坏死。我们假设，在出现不可逆性牙髓炎体征的有症状牙齿的牙髓组织中，TRPM2通道表达上调。与无症状牙齿的牙髓相比，临床诊断为有症状牙齿的牙髓中TRPM2通道表达显著增加。此外，有症状牙髓中TRPM2表达增加是成纤维细胞免疫反应性增强的结果，而TRPM2在神经中无表达。我们提供了一种可能的机制来解释TRPM2通道表达与疼痛和坏死之间的关联。我们建议，可以尝试使用TRPM2通道拮抗剂来抑制牙髓退变的进展甚至使其逆转。
