Pathogenesis of temporomandibular disorder induced by matrix degradation

在本研究中，我们研究了炎性细胞因子对滑膜成纤维细胞和软骨细胞在体外的影响。肿瘤坏死因子-α（TNF-α）增强软骨细胞基质金属蛋白酶-13（MMP-13）mRNA的表达。高分子量透明质酸预处理可抑制TNF-α介导的MMP-13的增强作用。另一方面，白细胞介素-17（IL-17）刺激滑液肉瘤细胞中MMP-3 mRNA的表达。免疫荧光染色显示，来自人颞下颌关节（TMJ）的滑膜成纤维细胞的IL-17受体（IL-17 RA）的表达，主要定位于细胞表面，而没有免疫荧光染色被视为软骨细胞。提示IL-17在TMJ中的主要作用靶点是滑膜组织。

In the present study, we examined the effects of inflammatory cytokines on synovial fibroblasts and chondrocytes in vitro. Tumor necrosis factor-alpha (TNF-alpha) enhanced matrix metalloproteinase-13 (MMP-13) mRNA expression in chondrocytes. Pre-treatment with high molecular weight hyaluronic acid suppressed TNF-alpha-mediated enhancement of MMP-13.On the other hand, interleukin-17 (IL-17) stimulates MMP-3 mRNA expression in synovial sarcoma cells. Immunofluorescent staining in synovial fibroblasts derived from human temporomandibular joints (TMJ) revealed that expression of IL-17 receptor (IL-17RA) that was primarily localized on the cell surface, whereas no immunofluorescent staining was seen in chondroyctes. Thesse results suggest that the main target of IL-17 in TMJ is synovial tissue.