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The Mechanism of Articular Cartilage Degeneration in Osteoarthritis and Rheumatoid Arthritis

骨关节炎和类风湿关节炎的关节软骨退变机制

基本信息

批准号：
05671236
负责人：
FUJII Katsuyuki
金额：
$ 1.41万
依托单位：
JIKEI UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1994
项目状态：
已结题

项目摘要

Immunohistochemical and biochemical studies were undertaken in order to investigate the mechanism of articular cartilage degeneration if patients with osteoarthritis and rheumatoid arthritis. Polyclonal antibodies against cyanogen bromide (CB) peptide of Type II colagen that specifically react with unwound alpha-chains and CB-derived peptides of human Type II collagen were utilized to identify degradation of Type II collagen fibers in articular cartilage. In the case of human osteoarthritic cartilage with mild degeneration, the most prominent staining by the anti-CB peptide antibodies was found in the superficial fibrillation and in the interterritorial matrix of the superficial and mid-zones. Incontrast, these regions showed weak staining by both anti-Type II collagen antibodies and anti-proteoglycan antibodies. Moreover, Staining by anti-fibronectin antibodies and anti-dermatan sulfate proteoglycan antibodies was observed around cell clusters in the superficial zone. On the other hand, in the case of rheumatoid arthritis, deep zone of the articular cartilage was well stained by the anti-CB peptide antibodies.Synthesis of the Type II collagen and proteoglycans was also investigated using cultured human chondrocytes obtained from osteoarthritic and rheumatoid arthritis cartilage. Chondrocytes from mildly degenerated osteoarthritic cartilage showed increased synthetic activity, while cells from moderately degenerated cartilage showed decreased activity. Chondrocytes from rheumatoid arthritis were found to synthesize decreased level of Type II collagen and proteoglycan molecules.These findings indicate that degeneration in osteoarthritic cartilage was initiated in the superficial zone and then gradually progressed to the mid and deep zones, While degeneration in the rheumatoid arthritic cartilage was initiated in the deep zone.

为探讨骨关节炎和类风湿关节炎患者关节软骨退变的机制，进行了免疫组织化学和生物化学研究。利用针对与人II型胶原的解绕α链和CB衍生肽特异性反应的II型胶原的溴化氰（CB）肽的多克隆抗体来鉴定关节软骨中II型胶原纤维的降解。在人骨关节炎软骨轻度变性的情况下，最突出的染色由抗CB肽抗体被发现在浅表纤维化和在interterritorial基质的浅表和中间区。相反，这些地区表现出弱染色的抗II型胶原抗体和抗蛋白多糖抗体。此外，抗纤维连接蛋白抗体和抗硫酸皮肤素蛋白聚糖抗体染色观察周围的细胞簇在浅区。另一方面，在类风湿性关节炎的情况下，关节软骨的深层被抗CB肽抗体很好地染色。II型胶原和蛋白多糖的合成也使用从骨关节炎和类风湿性关节炎软骨中获得的培养的人软骨细胞进行了研究。轻度退行性骨关节炎软骨的软骨细胞显示合成活性增加，而中度退行性软骨的细胞显示活性降低。发现类风湿关节炎软骨细胞合成Ⅱ型胶原和蛋白多糖分子的水平下降，表明骨关节炎软骨的退变始于浅层，然后逐渐向中深层发展，而类风湿关节炎软骨的退变始于深层。