摘要
目的探讨病理性滑膜皱襞发病机制中对软骨破坏有基质金属蛋白酶的参与。方法关节镜检查确诊为病理性滑膜皱襞和正常滑膜皱襞,分别进行免疫组化染色,观察金属蛋白酶-1(MMP-1)和组织金属蛋白酶抑制因子-1(TIMP-1)的表达及分布。结果MMP-1、TIMP-1在病理性滑膜皱襞和正常皱襞内的阳性表达,差异具有显著性(2χ=16.014,P=0.000;2χ=4.059,P=0.044)。MMP-1在滑膜衬里层细胞、单核和淋巴细胞、血管内皮细胞和化生的软骨细胞呈阳性表达,而在正常滑膜皱襞组织中不表达。TIMP-1只在滑膜衬里层细胞和少量的成纤维细胞有表达,而MMP-1免疫组化显示阳性细胞数和着色强度强于TIMP-1。结论病理性滑膜皱襞可产生MMP-1、TIMP-1,而且两者分布不平衡,可能是导致软骨破坏的生物学因素。
Objective To explore whether or not the cartilage damage in the pathogenesis of pathologic synovial plicae is due to the matrix metalloproteinase. Methods The immunohistochemical method was used to detect the expression and distribution of matrix metalloproteinase-1 （MMP-1） and tissue inhibitor of metalloproteinase-1 （TIMP-1） in arthroscopically clarified pathologic synovial plicae and normal synovial plicae of the knee joint. Results The positive expression rate of MMP-1 and TIMP-1 had significant differences between the pathologic and normal synovial plicae （χ^2 = 16. 014, P = 0. 000 ;χ^2 = 4. 059, P = 0. 044）. The expression of MMP-1 was positive in the synovial lining cells, monocytes, lymphocytes, endothelial cells, and chondrocytes, but negative in the normal synovial plicae. The TIMP-1 expression was only detected in the synovial lining cells and a small quantity of fibroblast cells. The immunohistochemical analysis revealed a greater number of positive cells and intensity of staining of MMP-1 than TIMP-1. Conclusions The development of pathologic synovial plicae may yield MMP-1 and TIMP-1 with unbalanced distributions, which may be the biological basis of the pathogenesis of cartilage destruction.
出处
《中国微创外科杂志》
CSCD
2006年第8期621-623,共3页
Chinese Journal of Minimally Invasive Surgery
