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Type II collagen degradation in articular cartilage fibrillation after anterior cruciate ligament transection in rats.

机译:大鼠前十字韧带横断后关节软骨纤颤中的II型胶原降解。

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OBJECTIVE: To investigate the kinetics of early cartilage changes in mechanically induced osteoarthritis (OA) and the association of these changes 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. Copyright 2001 OsteoArthritis Research Society International.
机译:目的:探讨机械性骨关节炎(OA)早期软骨变化的动力学,以及这些变化与II型胶原网络受损的关系。方法:实验性OA是由大鼠膝关节前交叉韧带横断(ACLT-OA)诱发的。在第2、7、14、28和70天后处死动物。使用常规组织学和免疫组织化学方法评估变性(未缠绕)II型胶原蛋白的膝关节,以检测胶原蛋白的损伤。使用识别II型胶原中胶原酶切割位点的抗体来研究胶原酶在此过程中的作用。结果:前十字韧带横断后关节软骨的首次变化发生在浅表区。这些变化包括浅表软骨细胞的丢失,剩余软骨细胞的肿胀和浅表纤维颤动。软骨细胞的肿胀不是由于向肥大表型的变化而引起的,因为这些细胞不会染色X型胶原蛋白。在原纤维化区域中变性的II型胶原蛋白染色明显增加。胶原酶切割位点的染色显示与变性胶原相同的分布,但强度明显较低。在发生原纤维形成之前,永远无法检测到胶原蛋白损伤,并且在非原纤维形成区域中不存在。结论:这些结果表明在该模型中,软骨变性始于关节表面,并且该变性与II型胶原降解产物的局部表达有关。版权所有2001国际骨关节炎研究协会。

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