Martin J A, Buckwalter J A
University of Iowa Department of Orthopaedics and Rehabilitation, Iowa City, IA, USA.
Biorheology. 2006;43(3,4):517-21.
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.
创伤后骨关节炎是关节损伤后发生的骨关节炎（OA）形式。尽管其终末期与特发性OA难以区分，但许多创伤后OA患者比特发性OA患者更年轻，并且他们有明确的诱发损伤。临床和实验研究表明，过度的急性冲击能量或慢性机械过载会导致创伤后OA所涉及的关节表面退变。然而，过度机械力导致OA的机制仍不清楚。由于这些原因，尚未开发出预防或降低创伤后OA风险的有效方法。我们假设，超过关节表面耐受能力的机械负荷会因氧化应激导致软骨细胞损伤。我们对人体关节软骨样本的体外测试表明，剪切应力会导致软骨细胞死亡，而抗氧化剂可减少剪切应力诱导的细胞死亡。这些观察结果表明，特定的负荷模式对关节表面具有特别的损害作用，而改进的关节损伤治疗方法可能包括将剪切应力降至最低的机械方法以及将氧化损伤降至最低的生物学方法。
