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TRPM8 axonal expression is decreased in painful human teeth with irreversible pulpitis and cold hyperalgesia

机译:TRPM8轴突表达在患有不可逆牙髓炎和冷痛觉过敏的痛苦人牙中减少

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摘要

Pulpitis pain may 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 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 two groups. These results suggest that TRPM8 is most likely not involved in cold-mediated noxious pulpal pain mechanisms.
机译:感冒刺激可能会引发牙髓炎疼痛,但造成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响应热感受器的直接激活。这项研究的目的是评估TRPM8热感受器在冷介导的有害牙髓疼痛机制中的可能作用,方法是比较健康对照磨牙与感冒性牙痛伴不可逆性牙髓炎的牙髓神经中的表达模式。用间接免疫荧光法对样品进行相同处理,并通过共聚焦显微镜获得图像。定量鉴定的N52 / PGP9.5神经纤维内TRPM8的免疫荧光强度和面积。结果显示,相对于正常样品,TRPM8神经区表达在冷敏感疼痛样品中明显减少(34.9%对8%,p <0.03),但两组之间的免疫荧光强度没有显着差异。这些结果表明,TRPM8最有可能不参与冷介导的有害牙髓疼痛机制。

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