Yeon K Y, Chung G, Shin M S, Jung S J, Kim J S, Oh S B
National Research Laboratory for Pain, Dental Research Institute and Department of Physiology, School of Dentistry, Seoul National University, 28-2 Yeongeon-Dong Chongno-Ku, Seoul 110-749, Korea.
J Dent Res. 2009 Apr;88(4):328-32. doi: 10.1177/0022034509334100.
Dentin hypersensitivity is a common symptom treated in the dental clinic, yet the underlying cellular and molecular mechanisms are not clear. We hypothesized that odontoblasts detect noxious thermal stimuli by expressing temperature-sensing molecules, and investigated whether temperature-activated TRP channels (thermo-TRP channels), which are known to initiate temperature signaling, mediate temperature sensing in odontoblasts. mRNA expression of dentin sialophosphoprotein and collagenase type 1, odontoblast-specific proteins, was shown in acutely isolated adult rat odontoblasts by single-cell RT-PCR, while TRPV1, TRPV2, TRPM8, and TRPA1 were not detected. Application of noxious temperatures of 42 degrees C and 12 degrees C, as well as capsaicin, menthol, and icilin, agonists of thermo-TRP channels, failed to increase intracellular calcium concentration. Immunohistochemical study also revealed no expression of TRPV1. Thus, it is unlikely that odontoblasts serve as thermal sensors in teeth via thermo-TRP channels.
牙本质过敏是牙科诊所中常见的一种症状,但其潜在的细胞和分子机制尚不清楚。我们推测成牙本质细胞通过表达温度感应分子来检测有害热刺激,并研究了已知可启动温度信号传导的温度激活型瞬时受体电位通道(热TRP通道)是否介导成牙本质细胞的温度感应。通过单细胞逆转录聚合酶链反应在急性分离的成年大鼠成牙本质细胞中显示了牙本质涎磷蛋白和1型胶原酶(成牙本质细胞特异性蛋白)的mRNA表达,而未检测到TRPV1、TRPV2、TRPM8和TRPA1。应用42℃和12℃的有害温度以及热TRP通道激动剂辣椒素、薄荷醇和艾考糊精,未能增加细胞内钙浓度。免疫组织化学研究也显示未表达TRPV1。因此,成牙本质细胞不太可能通过热TRP通道作为牙齿中的热传感器。