Maeda S, Sawai T, Uzuki M, Takahashi Y, Omoto H, Seki M, Sakurai M
Department of Orthopaedic Surgery, Tohoku University, School of Medicine, Sendai, Japan.
Ann Rheum Dis. 1995 Dec;54(12):970-5. doi: 10.1136/ard.54.12.970.
To investigate whether interstitial collagenase (MMP-1) concentration in synovial fluid can be useful as a marker for disease activity in rheumatoid arthritis (RA), to determine the main route by which collagenase degrades the matrix of articular cartilage, and to investigate if an imbalance between metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMP) is responsible for the activity of MMPs in RA.
Collagenase concentrations were measured in synovial fluid and paired serum samples using a specific sandwich enzyme linked immunosorbent assay. Collagenase activities were also assayed in synovial fluid samples. Synovial tissues obtained from the same patient were examined by immunohistochemical staining and the numbers of cells expressing collagenase were counted.
Collagenase concentrations in synovial fluid did not correlate with C reactive protein and collagenase levels in serum, but did correlate positively with the degree of synovial inflammation, and increased with increasing numbers of cells identified as expressing collagenase in synovial tissue. Collagenase activities did not correlate with TIMP-1 concentrations, but did correlate strongly with the ratios of collagenase concentration to TIMP-1 (r = 0.73).
The collagenase concentration in synovial fluid cannot be used as a marker for systemic disease activity, but can be used as a marker for the degree of synovial inflammation in the joint from which the sample is aspirated. In advanced RA, most of the collagenase is probably produced in synovial lining cells and released into synovial fluid, where it degrades the matrix of articular cartilage. An imbalance between MMP and TIMP may be of importance in the degradation of extracellular matrix of articular cartilage in RA.
研究滑膜液中间质胶原酶（MMP - 1）浓度是否可作为类风湿关节炎（RA）疾病活动的标志物，确定胶原酶降解关节软骨基质的主要途径，并研究金属蛋白酶（MMPs）与金属蛋白酶组织抑制剂（TIMP）之间的失衡是否与RA中MMPs的活性有关。
使用特异性夹心酶联免疫吸附测定法测量滑膜液和配对血清样本中的胶原酶浓度。还对滑膜液样本进行胶原酶活性测定。对同一患者获取的滑膜组织进行免疫组织化学染色检查，并对表达胶原酶的细胞数量进行计数。
滑膜液中的胶原酶浓度与血清中的C反应蛋白和胶原酶水平无关，但与滑膜炎症程度呈正相关，并且随着滑膜组织中被鉴定为表达胶原酶的细胞数量增加而升高。胶原酶活性与TIMP - 1浓度无关，但与胶原酶浓度与TIMP - 1的比值密切相关（r = 0.73）。
滑膜液中的胶原酶浓度不能用作全身疾病活动的标志物，但可作为抽取样本的关节滑膜炎症程度的标志物。在晚期RA中，大部分胶原酶可能由滑膜衬里细胞产生并释放到滑膜液中，在那里它降解关节软骨基质。MMP和TIMP之间的失衡可能在RA中关节软骨细胞外基质的降解中起重要作用。
