Mohr W
Abteilung Pathologie, Universität Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany.
Z Rheumatol. 2003 Dec;62(6):539-46; discussion 547. doi: 10.1007/s00393-003-0513-z.
Inflammatory cartilage destruction in chronic arthritides is usually regarded as the process owing to chondrocytic chondrolysis or ingrowth of pannus tissue. Besides these two mechanisms a third one-cartilage degradation directly mediated by polymorphonuclear granulocytes (PMN's) of the synovial fluid-seems to be underestimated. There is growing evidence that PMN's are involved in several non-bacterial organ destructions (e.g., alcoholic hepatitis); thus, two case reports are presented demonstrating cartilage destruction by PMN's via the synovial fluid. It is shown by light and electron microscopy that in florid rheumatoid arthritis, PMN's from the inflamed synovial fluid can gain access to the cartilaginous surface. The adherence of PMN's to the superficial matrix, eventually mediated by immunocomplexes, may activate these cells with the subsequent secretion of destructive enzymes as well as reactive oxygen species. Cartilage degradation may be the consequence. From the morphological findings it is deduced that this mechanism may have important implications for inflammatory cartilage loss.
慢性关节炎中的炎性软骨破坏通常被认为是由于软骨细胞溶解或血管翳组织长入所致。除了这两种机制外,第三种机制——由滑液中的多形核粒细胞(PMN)直接介导的软骨降解——似乎被低估了。越来越多的证据表明,PMN参与了几种非细菌性器官破坏(如酒精性肝炎);因此,本文报告了两例病例,证明了PMN通过滑液导致软骨破坏。光镜和电镜显示,在活动性类风湿关节炎中,来自炎症滑液的PMN可接触到软骨表面。PMN对表面基质的黏附最终可能由免疫复合物介导,这可能会激活这些细胞,随后分泌破坏性酶和活性氧。软骨降解可能就是结果。从形态学发现推断,这种机制可能对炎性软骨丢失具有重要意义。