The elucidation of the pathogenic mechanism and the transition of pathological condition at the bone and cartilage destruction of IL-17 in temporomandibular arthrosis.

白细胞介素(IL)-17存在于类风湿关节炎患者的关节滑膜中，是骨吸收因子之一。然而，关于IL-17对软骨细胞软骨基质蛋白代谢影响的研究报道较少。然后，本研究通过持续刺激研究了IL-17F对人正常软骨细胞软骨基质的影响。然后，我们重点研究了纤溶酶原/纤溶蛋白途径对软骨基质蛋白的降解及其调控。探讨IL-17F对软骨细胞纤溶酶原激活物（PA）和纤溶酶原激活物抑制剂(PAI)-1表达的直接影响以及IL-17F通过前列腺素（PG）E2的间接影响。

Interleukin(IL)-17 exists in a rheumatoid arthritis patient's joint synovia, and is one of the bone resorptive factors. However, there are few reports investigated about the influence which IL-17 has on the cartilage matrix protein metabolism of a cartilage cell. Then, this research investigated that the effect of IL-17F on the cartilage matrix in a human normal chondrocytes by continuous stimulation. Then, we focused on the cartilage matrix protein degradation and its regulation by plasminogen/plasmin pathway. It was investigated that the direct effect of IL-17F on expression of plasminogen activator (PA) and plasminogen activator inhibitor(PAI)-1 of chondrocytes and the indirect effect of IL-17F through prostaglandin(PG)E2.