Articular collagen degradation in the Hulth-Telhag model of osteoarthritis
Articular collagen degradation in the Hulth-Telhag model of osteoarthritis
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DOI：
10.1053/joca.1999.0258
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发表时间：
1999-11-01
影响因子：
7
通讯作者：
Chichester, CO
中科院分区：
文献类型：
--
作者：
Rogart, JN;Barrach, HJ;Chichester, CO
目的：本研究采用免疫组织化学方法研究骨关节炎急性损伤模型中 II 型胶原 (CII) 的降解模式。根据先前对原发性骨关节炎 (OA) 的研究，推测 CII 降解最严重的区域将位于关节软骨的浅层和中上层区域，随着 OA 变得更加严重，染色会延伸到深部区域。 设计：在继发性 OA 模型中，通过横断前十字韧带和后十字韧带并去除半月板来使兔子患上骨关节炎。在术后不同时间，使用单克隆抗体 18:6:D6 检查关节软骨的 CII 降解情况。当 CII 因蛋白酶切割而降解时，该抗体会对暴露的表位发生反应。使用 Safranin-O/Fast Green 定位蛋白多糖 (PG)。使用图像分析软件对染色强度进行定量。结果：在手术诱发 OA 的关节中，CII 的降解最早出现在 3 周内，大部分降解集中在 I 区和 Iii 区。第 14 周时，CII 的破坏更加明显，但 II 区的降解却出人意料地缺乏。还有其他一些意想不到的发现。例如，假手术关节旨在作为对照，但在手术后 3 周处死的兔子中观察到 CII 降解。还预计内侧髁的软骨会发生更大的 CII 降解，但 14 周后，内侧髁和外侧髁之间没有显着差异。最后，PG 染色的损失与 CII 的降解相关，但 III 区除外，其中 PG 损失有限：结论：继发性骨关节炎模型与原发性骨关节炎模型的关节软骨破坏模式存在差异。需要对两种 OA 发展背后的机械和生化过程进行进一步研究。 (C) 1999 年国际骨关节炎研究协会。
Objective: This study employed immunohistochemistry to investigate the pattern of type II collagen (CII) degradation in an acute injury model of osteoarthritis. It was hypothesized, based on previous studies of primary osteoarthritis (OA), that the worst areas of CII degradation would be located in the superficial and upper middle zones of the articular cartilage, with staining extending into the deep zone as the OA became more severe.Design: In this model of secondary OA, rabbits were made osteoarthritic by transecting the anterior and posterior cruciate ligaments and removing the meniscus. At various times post surgery, articular cartilage was examined for CII degradation using monoclonal antibody 18:6:D6. This antibody reacts to an epitope that is exposed when CII is degraded as the result of protease cleavage. Proteoglycans (PG) were localized using Safranin-O/Fast Green. Staining intensities were quantitated using image analysis software.Results: In the joints with surgically induced OA, degradation of CII was seen as early;Is 3 weeks with the majority of the degradation localized in zones I and Iii. At 14 weeks the destruction of CII was more pronounced, but there was a surprising lack of degradation in zone II. There were also several other unexpected findings. The sham-operated joints, for example, were intended to serve as controls yet CII degradation was observed in rabbits killed 3 weeks after surgery. It was also expected thai greater CII degradation would occur in cartilage from medial condyles, but after 14 weeks there was no significant difference between medial and lateral condyles. Finally, the loss of staining for PG correlated with the degradation of CII except in zone III where limited PG loss wa:; observed.Conclusion: Differences were observed between the pattern of articular cartilage destruction in this model of secondary OA and that of primary OA. Further investigation of the mechanical and biochemical processes underlying the development of both types of OA needs to be conducted. (C) 1999 OsteoArthritis Research Society International.