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作 者:王海鹰[1] 周继林[1] 洪民[1] 王东胜[1] 邓斌[1] 李维华[2]
机构地区:[1]解放军总医院口腔科,北京100853 [2]解放军总医院病理科,北京100853
出 处:《口腔颌面修复学杂志》2000年第1期10-13,共4页Chinese Journal of Prosthodontics
摘 要:目的:深入研究过度张口引起口面痛的作用机制。方法:观察过度张口动物模型TMJ和咀嚼肌的组织病理改变及SP和PGE_2、PGF_(2a)。的免疫反应;检测24名健康志愿者过度张口前后口面部的痛阈变化。结果:过度张口引起了TMJ和咀嚼肌的损伤,损伤局部有SP和PGE_2、PGF_(2a)的明显聚积;过度张口后口面部的痛阈明显下降,24-48小时后痛阈基本恢复同前;对过度张口的反应存在个体差异和部位差异。结论:过度张口可损伤TMJ和咀嚼肌,引起口面部疼痛,此过程有内源性致痛物质的参与。To make a further study on the Pathogenic mechanism of orofacial pain caused by overextended opening. Methods: Observation of the histopathological changes and the immunologic reactions of SP and PGE2, PGF2α in TMJ and masticatory muscles of the animal model of overextended opening; measure of the pressure pain thresholds in orofacial area of twenty-four healthy volunteers before and after overextended opening. Results: Both TMJ and masticatory muscles were suffered injury from overextended opening , there were obvious cumulation of SP and PGE2, PGF2α in the injury areas; the pressure pain thresholds in orofacial area were decreased significantly after overextended opening, and that had almost recovered during 24-48 hours after overextended opening; there were individual difference and anatomical position feature in the reactions to overextended opening. Conclusion: Overextended opening can do an injury to TMJ and masticatory muscles and an initiation into orofacial pain, endogenous algogenic substances had a hand in the course.
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