患类风湿关节炎时,滑膜层增厚伴单核细胞浸润,肉芽组织翳形成,邻近的关节内面的软骨被破坏,随后发生跛行。人们久已认为软骨退化主要是由于滑膜细胞,尤其是血管翳中的细胞释放的酶。新的观察支持这种解释。软骨的主要蛋白质是糖蛋白和Ⅱ型胶原。多数溶酶体的蛋白酶在酸性环境中活性最大,但这些酶在接近正常的情况下,对细胞外软骨降解可能仅起较小的作用。巨噬细胞和其它细胞分泌的许多蛋白酶在接近中性时活性最大。这些蛋白酶包括胶原酶,纤溶酶原活化剂和裂解补体第三成分的酶。用类风湿滑膜作体外培养的研究表明,释放的酶能降解糖蛋白和胶原。由蛋白酶消化类风湿滑膜所释出和粘附于培养皿的细胞能产生大量的胶原酶和前列 In rheumatoid arthritis, thickening of the synovial membrane with infiltration of mononuclear cells, formation of granulation tissue,, adjacent to the cartilage inside the joints were destroyed, followed by limp. It has long been thought that cartilage degeneration is mainly due to the release of enzymes from synovial cells, especially cells in the blood vessels. New observations support this interpretation. The main cartilage proteins are glycoproteins and type II collagen. Most lysosomal proteases are most active in acidic environments, but these enzymes may play only minor roles in extracellular cartilage degradation near normal conditions. Many proteases secreted by macrophages and other cells are most active near neutral. These proteases include collagenases, plasminogen activators, and enzymes that cleave the third component of complement. Studies using in vitro rheumatoid synovial cultures have shown that the released enzyme degrades glycoproteins and collagen. Cells released by the protease-digested rheumatoid synovial membrane and adherent to the culture dish produce a large amount of collagenase and forefront