Alvarado Lisa T, Perry Griffin M, Hargreaves Kenneth M, Henry Michael A
Department of Endodontics, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229-3900, USA.
J Endod. 2007 Oct;33(10):1167-71. doi: 10.1016/j.joen.2007.06.018. Epub 2007 Aug 16.
Pulpitis pain might be triggered by a cold stimulus, yet the cellular mechanisms responsible for this phenomenon are largely unknown. One possible mechanism involves the direct activation of cold-responsive thermoreceptors. The purpose of this study was to evaluate the possible role of the TRPM8 thermoreceptor in cold-mediated noxious pulpal pain mechanisms by comparing expression patterns in pulpal nerves from healthy control molars to cold-sensitive painful molars with irreversible pulpitis. Samples were identically processed with the indirect immunofluorescence method, and images were obtained with confocal microscopy. The immunofluorescence intensity and area occupied by TRPM8 within N52/PGP9.5-identified nerve fibers were quantified. Results showed that relative to normal samples, TRPM8 nerve area expression was significantly less in the cold-sensitive painful samples (34.9% vs 8%, P <0.03), but with no significant difference in immunofluorescence intensity between the 2 groups. These results suggest that TRPM8 is most likely not involved in cold-mediated noxious pulpal pain mechanisms.
牙髓炎疼痛可能由冷刺激引发，然而导致这种现象的细胞机制在很大程度上尚不清楚。一种可能的机制涉及冷敏性温度感受器的直接激活。本研究的目的是通过比较健康对照磨牙与患有不可逆性牙髓炎的冷敏感疼痛磨牙的牙髓神经中的表达模式，评估瞬时受体电位香草酸亚型8（TRPM8）温度感受器在冷介导的有害牙髓疼痛机制中的可能作用。样本采用间接免疫荧光法进行相同处理，并用共聚焦显微镜获取图像。对TRPM8在神经纤维瘤病52/嗜铬粒蛋白A（N52/PGP9.5）识别的神经纤维内的免疫荧光强度和所占面积进行定量分析。结果显示，相对于正常样本，冷敏感疼痛样本中TRPM8神经面积表达显著减少（34.9%对8%，P<0.03），但两组间免疫荧光强度无显著差异。这些结果表明，TRPM8很可能不参与冷介导的有害牙髓疼痛机制。
