骨关节炎滑液中肿瘤坏死因子α活性检测及滑膜组织超微结构观察

Bioassay of TNF α in synovial fluid and ultrastructural observation of synovium from patients with osteoarthritis

目的进一步探讨滑膜参与骨关节炎病理进程的机理。方法采用Ｌ９２９细胞毒活性法检测了２４例急、慢性关节内损伤及晚期骨关节炎（ＯＡ）患者关节滑液中肿瘤坏死因子（ＴＮＦ－α）生物活性，并用光镜和电镜观察比较三者滑膜组织间的形态学差异。结果ＯＡ滑液中所含ＴＮＦ－α水平较高；ＯＡ滑膜细胞性内膜，细胞增殖与脱落同时发生，内膜下层呈现明显的纤维增生性变、滑膜增厚；Ｂ型和Ａ型滑膜细胞的超微结构变化分别呈现旺盛的蛋白分泌相和活跃的吞噬功能。结论ＯＡ滑膜细胞的功能改变是其滑液中ＴＮＦ－α升高的原因之一；滑膜的变性既可受变性软骨产物的介导，又可导致ＯＡ的进展。

Objective To better define the role of synovium in the pathogenesis of osteoarthritis (OA).Methods We measured the bioactivity of tumor necrosis factor α(TNF α) in synovial fluid (SF) and exammined the histologic and ultrastructural features of the synovium from patients with OA and from patients with acute and chronic traumatologic joint. Results The results showed that the levels of TNF α in SF from OA were significantly elevated.Marked fibrosis and thickened intima were found in OA synovium, with much dense collagen,which,in some cases, was banded,but no specific inflammtory changes were detected.Type B cells in OA synovium had the characteristics of organelles of cells active in synthesizing and secreting protein.Type A cells in OA synovium had the features of the macrophage. Conclusion Evident fibrosis in synovium may be either mediated by the cartilage degradation product or by the enchanced joint damage process in OA.