...
首页> 外文期刊>Osteoarthritis and cartilage >Articular collagen degradation in the Hulth-Telhag model of osteoarthritis.
【24h】

Articular collagen degradation in the Hulth-Telhag model of osteoarthritis.

机译:骨关节炎的Hulth-Telhag模型中的关节胶原降解。

获取原文
获取原文并翻译 | 示例
           

摘要

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 as 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 that 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 was 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. Copyright 1999 OsteoArthritis Research Society International.
机译: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)降解的模式。根据先前对原发性骨关节炎(OA)的研究,可以推测CII降解的最坏区域将位于关节软骨的浅表和中上区域,随着OA变得更严重,染色会扩展到深部区域。 。设计:在这种继发性OA模型中,通过横切前后十字韧带并去除半月板,使兔成为骨关节炎。在手术后的不同时间,使用单克隆抗体18:6:D6检查关节软骨的CII降解。当蛋白酶裂解导致CII降解时,此抗体与暴露的表位发生反应。蛋白聚糖(PG)使用Safranin-O / Fast Green进行本地化。使用图像分析软件对染色强度进行定量。结果:在外科手术诱发的OA关节中,CII的降解最早可在3周内见到,大部分降解位于I区和III区。在第14周,CII的破坏更加明显,但是II区却没有令人惊讶的降解。还有其他一些意外发现。例如,假手术的关节旨在作为对照,但在术后3周被杀死的兔子中却观察到CII降解。还预期在内侧from突软骨中会发生更大的CII降解,但是14周后内侧and突与外侧lateral突之间没有显着差异。最后,除了在III区观察到有限的PG损失外,PG染色的损失与CII的降解有关。结论:这种继发性OA模型与原发性OA模型的关节软骨破坏模式存在差异。需要进一步研究两种类型的OA的发展背后的机械和生化过程。版权所有1999国际骨关节炎研究协会。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号