摘要
目的:研究异位骨化与创伤性颞下颌关节强直发病机制是否具有相似性,为拓展后者的防治提供新思路。方法:选取确诊为肘、髋、膝关节区异位骨化和创伤性颞下颌关节强直的病例各30例,对术中截取的关节区及周边区骨质标本收集保存,分别作为实验组A(A组)和实验组B(B组);另取5个正常完整喙突作为对照组(C组)。H-E染色观察3组标本的组织学结构形态,免疫组织化学法观察标本中BMP-2、BMP-4、CD34阳性表达差异,利用影像资料比较A、B 2组的影像学特征。采用SPSS 17.0软件包对数据进行统计学分析。结果:A组和B组的组织学结构及影像学特点基本一致。免疫组织化学显示,A组和B组的BMP-2、BMP-4、CD34阳性表达均显著强于C组(P<0.05)。结论:创伤性颞下颌关节强直与异位骨化发病机制具有相似性。
PURPOSE:To investigate whether the pathogenesis of heterotopic ossification(HO)was similar to traumatic temporomandibular joint ankylosis(TMJA),and to provide new ideas for the prevention and treatment of TMJA.METHODS:Thirty cases of elbow,hip and knee joint HO and 30 cases of traumatic TMJA were selected.The bone samples of joint area and surrounding area were collected and preserved as experimental group A(group A)and experimental group B(group B)respectively.Five normal and complete coracoids were collected as the control group(group C).Structural forms of bone specimens were detected by H-E staining and expressions of BMP-2,BMP-4,CD34+in the three groups were detected by immunohistochemical assay.Imaging data were used to compare the imaging features of group A and group B.SPSS 17.0 software package was used for data analysis.RESULTS:The histological structure and imaging features of group A and group B were basically the same.Immunohistochemistry showed that the positive expressions of BMP-2,BMP-4 and CD34+in group A and group B were significantly stronger than those in group C(P<0.05).CONCLUSIONS:Traumatic TMJA and HO have similar pathogenesis.
作者
陈云亮
满城
李晓宇
伍靖
魏柳琼
李文龙
CHEN Yun-liang;MAN Cheng;LI Xiao-yu;WU Jing;WEI Liu-qiong;LI Wen-long(Department of Stomatology,Longhua District People's Hospital.Shenzhen 518000,Guangdong Province;Department of Oral and Maxillofacial Surgery,Affiliated Stomatological Hospital of Zunyi Medical University.Zunyi 563000,Guizhou Province,China)
出处
《中国口腔颌面外科杂志》
CAS
2023年第5期461-466,共6页
China Journal of Oral and Maxillofacial Surgery
基金
深圳市龙华区医疗卫生机构区级科研项目(2020137)。
关键词
异位骨化
创伤性颞下颌关节强直
发病机制
Heterotopic ossification
Traumatic temporomandibular joint ankylosis
Pathogenesis