间接性TMJ损伤后髁突软骨增殖能力的改变  

THE CHANGES OF CONDYLAR CARTILAGE PROLIFERATING CELL AFTER INDIRECT TRAUMA ON THE GOAT TMJ

作　　者：胡开进[1] 王大章[1] 李明哲[1] 赵宗林[1] 

机构地区：[1]华西医科大学口腔医学院

出　　处：《口腔颌面外科杂志》1998年第4期250-252,共3页Journal of Oral and Maxillofacial Surgery

基　　金：国家自然科学基金

摘　　要：目的：探讨间接性颞下颌关节损伤在颞下颌关节骨关节病发生、发展过程中的作用。方法：用撞击装置撞击山羊右侧下颌角部，间接造成ＴＭＪ损伤，以对侧关节为对照，伤后２小时，１、３、６月处死动物，采用免疫组化方法观察髁突软骨细胞ＰＣＮＡ阳性细胞的分布及改变。结果：与对照侧相比，髁突软骨ＰＣＮＡ阳性细胞在伤后２小时无变化，伤后１月时增多而在伤后３月和６月时明显减少。结论：ＴＭＪ损伤导致ＴＭＪＯＡ的机理是由于损伤破坏了髁突面屏障，使胶原纤维裸露于关节腔内，引起关节局部内环境变化，使滑液中的异物在关节内压作用下进入软骨或骨髓，破坏和抑制了软骨的增殖能力，引起软骨组织进行性丧失，导致ＴＭＪＯＡ。Objective: In order to understand the roles of indirect trauma on the temporomandibular joint(TMJ) in the development of TMJ Osteoarthritis(TMJOA). Methods: Trauma to the TMJ was achieved under an impact to the right mandibular angle, the left TMJ was used as a control, The animals were killed after 2h, 1 month, 3 months and 6 months, the expressions of proliferating cell nuclear antigen/cyclin(PCNA/cyclin) were examined with immunohistochemical techniques. Results: compared with the left, the positive cells of PCNA in right condylar cartilage had no difference at 2h posttrauma, were more on 1 month posttrauma, were significant less on 3 months and 6 months posttrauma. Conclusion: The mechanism of the experimental process is probably that trauma to the TMJ damaged its natural barrier, exposed the collagen fibrils and started TMJ autoimmunity, the defect in the condylar surface allows the synovial fluid, under pressure, into the condylar cartilage or marrow space. Proliferating ability of the cartilage cell was destroyed. Cartilage lossed from the joint surface, resulted to TMJOA.

关 键 词：颞下颌关节损伤 增殖细胞核抗原 髁突软骨增殖 

分 类 号：R782.602[医药卫生—口腔医学]