Fassbender H G
Zentrum fuer Rheuma-Pathologie (World Health Organization Center), Mainz, Federal Republic of Germany.
Am J Med. 1987 Nov 20;83(5A):17-24. doi: 10.1016/0002-9343(87)90846-1.
The chondrocyte holds a key position in the development of osteoarthritis. As the only living element of the articular cartilage, it produces the components of the matrix, i.e., collagens and proteoglycans. In the course of its life, the chondrocyte is susceptible to nutrient and toxic dangers. This leads to a qualitative and quantitative jeopardy of the matrix production. Collagens and proteoglycans are also subject to metabolic influences. Whatever the cause(s), osteoarthritis results in deficient masking of the collagen fibers and in roughening of the cartilaginous surface. Thus, the phase of "wear and tear" is initiated, which is characteristic of osteoarthritis. This process may provoke a total loss of cartilage and opening of the subchondral medullary spaces. However, osteoarthritis probably only becomes clinically manifest when a secondary synovitis supervenes, which is caused by mediators developing from degradation products of the cartilaginous matrix. Thus, osteoarthritis can be considered to develop from a disproportion between the quality of the matrix and load to the cartilage. Aside from avoiding non-physiologic overload to the articular cartilage, therapy must influence the secondary synovitis. Furthermore, an attempt should be made to interfere effectively with the chondrocytic metabolism by means of "chondroprotective substances."
软骨细胞在骨关节炎的发展过程中占据关键地位。作为关节软骨唯一的活性成分,它能产生基质成分,即胶原蛋白和蛋白聚糖。在其生命过程中,软骨细胞易受营养和毒性危害影响。这会导致基质产生在质量和数量上出现问题。胶原蛋白和蛋白聚糖也会受到代谢影响。无论病因如何,骨关节炎都会导致胶原纤维的遮盖不足以及软骨表面粗糙化。于是,就引发了以骨关节炎为特征的“磨损”阶段。这一过程可能导致软骨完全丧失以及软骨下骨髓腔开放。然而,骨关节炎可能只有在继发滑膜炎时才会出现临床症状,继发滑膜炎是由软骨基质降解产物产生的介质所引发的。因此,骨关节炎可被认为是由基质质量与软骨负荷之间的失衡所导致的。除了避免对关节软骨施加非生理性过载外,治疗还必须针对继发滑膜炎。此外,应尝试通过“软骨保护物质”有效干预软骨细胞代谢。