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Post-traumatic osteoarthritis: The role of stress induced chondrocyte damage

机译:创伤后骨关节炎:应激诱导的软骨细胞损伤的作用

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Post-traumatic osteoarthritis is the form of osteoarthritis (OA) that develops following joint injury. Although its end-stage is indistinguishable from idiopathic OA, many patients with post-traumatic OA are younger than those with idiopathic OA, and they have a well-defined precipitating insult. Clinical and experimental studies suggest that excessive acute impact energy or chronic mechanical overload cause the degeneration of the articular surface responsible for post-traumatic OA. Yet, the mechanisms by which excessive mechanical force causes OA remain unknown. For these reasons it has not been possible to develop effective methods of preventing or decreasing the risk of post-traumatic OA. We hypothesized that mechanical loading that exceeds the tolerance of the articular surface causes chondrocyte damage due to oxidative stress. Our in vitro tests of human articular cartilage samples showed that shear stress causes chondrocyte death and that anti-oxidants decrease the shear stress induced cell death. These observations suggest that specific patterns of loading are particularly damaging to articular surfaces and that improved treatments of joint injuries may include mechanical methods of minimizing shear stresses and biologic methods of minimizing oxidative damage.
机译:创伤后骨关节炎是在关节损伤后发展为骨关节炎(OA)的形式。尽管其终末期与特发性OA并无区别,但许多创伤后OA的患者比特发性OA的患者年轻,并且有明确的沉淀性损伤。临床和实验研究表明,过多的急性冲击能量或慢性机械过载会导致造成创伤后OA的关节表面变性。然而,过大的机械力导致OA的机制仍然未知。由于这些原因,尚不可能开发出预防或降低创伤后OA风险的有效方法。我们假设超过关节表面承受力的机械负荷会由于氧化应激而导致软骨细胞损伤。我们对人体关节软骨样品的体外测试表明,剪切应力可导致软骨细胞死亡,而抗氧化剂可降低剪切应力引起的细胞死亡。这些观察结果表明,特定的负荷模式对关节表面尤其有害,并且对关节损伤的改进治疗可能包括使剪切应力最小的机械方法和使氧化损伤最小的生物方法。

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