Aigner T, Vornehm S I, Belke J, von der Mark K, Kirchner T
Pathologisches Institut, Universität, Erlangen.
Verh Dtsch Ges Pathol. 1996;80:282-7.
Increased levels of inflammatory cytokines such as II-1 and TNF-alpha are described in rheumatoid and osteoarthritic synovial fluid. These mediators are also very well established anti-anabolic modulators of chondrocyte synthetic activity in vitro. Our study aimed to investigate, whether chondrocytes in rheumatoid and osteoarthritic cartilage in situ show reaction pattern compatible with the putative effects of these modulatory agents. Immunohistochemical analysis using type II collagen specific antibodies showed considerable loss of staining in many sites of osteoarthritic and rheumatoid articular cartilage. mRNA analysis showed besides an overall activation of synthetic activity in rheumatoid and osteoarthritic cartilage, a decreased expression of cartilage matrix proteins in the upper zone. The cease of the anabolic activity of rheumatoid and osteoarthritic chondrocytes and the increased catabolism of matrix components contributes to the anabolic-catabolic imbalance in rheumatoid and osteoarthritic cartilage and is suggestive to be a crucial event in the progress of the disease. It correlates well to the putative anti-anabolic effect of inflammatory cytokines such as II-1 and TNF-alpha and could indicate a potential role of these mediators in rheumatoid and osteoarthritic cartilage destruction.
类风湿性关节炎和骨关节炎的滑液中炎症细胞因子如白细胞介素 -1（IL-1）和肿瘤坏死因子 -α（TNF-α）水平升高。在体外，这些介质也是软骨细胞合成活性的公认的抗合成代谢调节剂。我们的研究旨在调查类风湿性关节炎和骨关节炎软骨中的软骨细胞在原位是否表现出与这些调节因子的假定作用相符的反应模式。使用II型胶原特异性抗体的免疫组织化学分析显示，在骨关节炎和类风湿性关节炎关节软骨的许多部位染色明显减少。mRNA分析表明，除了类风湿性关节炎和骨关节炎软骨中合成活性的整体激活外，上层区域软骨基质蛋白的表达降低。类风湿性关节炎和骨关节炎软骨细胞合成代谢活性的停止以及基质成分分解代谢的增加导致类风湿性关节炎和骨关节炎软骨中合成代谢 - 分解代谢失衡，提示这是疾病进展中的关键事件。它与IL-1和TNF-α等炎症细胞因子的假定抗合成代谢作用密切相关，并可能表明这些介质在类风湿性关节炎和骨关节炎软骨破坏中具有潜在作用。
