咬合创伤在颅颌紊乱症中的作用机制研究  

Pathogenic mechanism of traumatic occlusion in craniomandibular disorders

作　　者：王海鹰[1,2,3,4] 周继林[1,2,3,4] 洪民[1,2,3,4] 李维华[1,2,3,4] 杨梅芳[1,2,3,4] 王沛英[1,2,3,4] 邓斌[1,2,3,4] 郝秀华[1,2,3,4] 张曙光[1,2,3,4] 侯宁[1,2,3,4] 王东胜[1,2,3,4] 

机构地区：[1]解放军总医院口腔科 [2]解放军总医院病理科 [3]解放军总医院基础所生化室 [4]解放军总医院耳研所

出　　处：《军医进修学院学报》1998年第1期37-39,共3页Academic Journal of Pla Postgraduate Medical School

摘　　要：目的：深入研究咬合创伤在颅颌紊乱症中的作用机制。方法：在小型猪一侧下颌磨牙上粘固联冠，建立咬合创伤动物模型，并对其同时进行颞颌关节（ＴＭＪ）和咀嚼肌的组织病理学观察，ＴＭＪ软组织Ｐ物质和前列腺素Ｅ２的免疫组化实验以及咀嚼肌前列腺素Ｅ２和Ｆ２α的放免分析。结果：咬合创伤确实引起了ＴＭＪ和咀嚼肌的伤害性反应和病理性变化。结论：咬合创伤的靶器官主要是ＴＭＪ盘周附着组织，关节滑膜，翼外肌上头和嚼肌。咬合创伤的致病机制包括神经源性和非神经源性两个方面，并应考虑外周与中枢的相互作用。Objective:The purpose of this research was to further study the pathogenic mechanism of traumatic occlusion in craniomandibular disorders (CMD).Methods:Animal model of traumatic occlusion was established by way of the wrought crown of unilateral mandibular molars of miniature pigs. The temporomandibular joint (TMJ) and the masticatory muscles of the pigs were observed and studied with histopathologic methods, immunohistochemical staining of substance P(SP) and prostaglandin E2(PEG2), and radioimmunologic analyses of PGE2 and PGE2α. Results:The results indicated that such traumatic occlusion caused nociceptive reactions and pathologic changes in TMJ and masticatory muscles.Conclusion:The disc attachment and the synovial membrane of TMJ, the upper head of the lateral pterygoid muscle and the masseter are the target ougans of traumatic occlusion. It is shown that the pathogenic mechanism of the traumatic occlusion is borh neurogenous and nonneurogenous, and the interactons between peripheral and central nerves should alsobe taken into account.

关 键 词：颅颌紊乱症 咬合创伤 病理学 

分 类 号：R782.402[医药卫生—口腔医学]