A new hypothesis of sex-differences in temporomandibular disorders: Estrogen enhances hyperalgesia of inflamed TMJ through modulating voltage-gated sodium channel 1.7 in trigeminal ganglion?
A new hypothesis of sex-differences in temporomandibular disorders: Estrogen enhances hyperalgesia of inflamed TMJ through modulating voltage-gated sodium channel 1.7 in trigeminal ganglion?
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DOI：
10.1016/j.mehy.2014.12.010
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发表时间：
2015-02-01
影响因子：
4.7
通讯作者：
Gan, Ye-Hua
中科院分区：
文献类型：
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作者：
Bi, Rui-Yun;Ding, Yun;Gan, Ye-Hua
目的：颞下颌关节紊乱病（TMD）是一组以颞下颌关节疼痛为主要特征的临床疾病。颞下颌关节炎或滑膜炎是TMD患者常见的疾病，也是TMD疼痛的主要原因。TMD在育龄期女性中普遍存在，至少是男性的两倍，这意味着雌激素可能参与了TMD疼痛的处理。雌激素主要通过雌激素受体（ER）影响细胞。雌激素-雌激素受体复合物与特定基因启动子区的雌激素反应元件序列（ERE）结合，发挥其调节作用。电压门控钠通道1.7（Nav1.7），其单次中断导致疼痛的完全丧失，放大神经元中的弱刺激，并作为触发动作电位的阈值通道，在疼痛感知（包括炎症性疼痛）中发挥重要作用。此外，我们以前的研究表明，三叉神经节Nav1.7参与了炎症TMJ的痛觉过敏。我们认为雌激素可能通过调节三叉神经节Nav1.7的表达和通道阈值来降低TMJ或炎症TMJ的伤害性感受阈值，从而增强炎症TMJ的痛觉过敏。(c)2014爱思唯尔有限公司版权所有。
Objective: Temporomandibular disorders (TMD) are an assorted set of clinical conditions characterized mainly by pain in the temporomandibular joint (TMJ). TMJ inflammation or synovitis is frequently observed in TMD patients and is the major reason for TMD pain. TMD is prevalent in women of childbearing age, at least twice than in men, implying that estrogen may be involved in TMD pain processing. Estrogen affects a cell mainly through the estrogen receptors (ER). The estrogen-ER complex binds to estrogen response element sequences (ERE) in the promoter region of specific genes and then exerts its regulatory potential. The voltage-gated sodium channel 1.7 (Nav1.7), whose single disruption leads to a complete loss of pain, amplifies weak stimuli in the neurons and acts as the threshold channel for firing action potentials and plays a prominent role in pain perception, including inflammatory pain. Furthermore, our previous study showed that trigeminal ganglionic Nav1.7 was involved in the hyperalgesia of the inflamed TMJ. We propose that estrogen may enhance hyperalgesia of inflamed TMJ through decrease nociceptive threshold of TMJ or inflamed TMJ by modulating both expression and channel threshold of Nav1.7 in trigeminal ganglion. (c) 2014 Elsevier Ltd. All rights reserved.