Type II collagen degradation in articular cartilage fibrillation after anterior cruciate ligament transection in rats
Type II collagen degradation in articular cartilage fibrillation after anterior cruciate ligament transection in rats
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DOI：
10.1053/joca.2000.0390
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发表时间：
2001-05-01
影响因子：
7
通讯作者：
van den Berg, WB
中科院分区：
文献类型：
--
作者：
Stoop, R;Buma, P;van den Berg, WB
目的：探讨机械诱导骨关节炎（OA）的早期软骨变化的动力学，以及这些机会与II型胶原network.Methods：实验性OA诱导大鼠膝关节前交叉韧带横断（ACLT-OA）的损害的关联。在2、7、14、28和70天后处死动物。使用常规组织学和变性（未缠绕）II型胶原免疫组织化学评价膝关节，以检测胶原损伤。结果：前交叉韧带切断后，关节软骨的变化首先发生在关节软骨的表浅区。这些变化包括表面软骨细胞的损失、剩余软骨细胞的肿胀和表面纤维化。软骨细胞的肿胀不是由于向肥大表型的变化，因为这些细胞没有染色的X型胶原。在原纤维化区域中，变性II型胶原蛋白染色显著增加。胶原酶切割位点的染色显示与变性胶原蛋白相同的分布，但强度明显较低。胶原蛋白的损伤可能永远不会被检测到之前发生的纤维性颤动，并不存在于non-fibrillated areas.Conclusions：这些结果表明，在这个模型中，软骨退化开始在关节面，这种退化与局部表达的II型胶原蛋白降解产物。(C)2001年国际骨关节炎研究学会。
Objective: To investigate the kinetics of early cartilage changes in mechanically induced osteoarthritis (OA) and the association of these chances with damage to the type II collagen network.Methods: Experimental OA was induced by anterior cruciate ligament transsection in the rat knee joint (ACLT-OA). Animals were sacrificed after 2, 7, 14, 28 and 70 days. Knee joints were evaluated using routine histology and immunohistochemistry for denatured (unwound) type II collagen to detect collagen damage. An antibody recognizing the collagenase cleavage site in type II collagen was used to study the role of collagenase in this process,Results: The first changes of the articular cartilage after anterior cruciate ligament transection occurred in the superficial zone. These changes included loss of superficial chondrocytes, swelling of the remaining chondrocytes and superficial fibrillation. The swelling of the chondrocytes did not result from a change towards the hypertrophic phenotype, since these cells did not stain for type X collagen. A marked increase in denatured type II collagen staining was present in the fibrillated areas, Staining of the collagenase cleavage site showed the same distribution as denatured collagen but was clearly less intense. Collagen damage could never be detected before fibrillation occurred and was not present in non-fibrillated areas.Conclusions: These results indicate that in this model cartilage degeneration starts at the articular surface and that this degeneration is associated with a localized expression of type II collagen degradation products. (C) 2001 OsteoArthritis Research Society International.