Arokoski J P, Jurvelin J S, Väätäinen U, Helminen H J
Department of Physical and Rehabilitation Medicine, Kuopio University Hospital, Finland.
Scand J Med Sci Sports. 2000 Aug;10(4):186-98. doi: 10.1034/j.1600-0838.2000.010004186.x.
Joints are functional units that transmit mechanical loads between contacting bones during normal daily or specialized activities, e.g., sports. All components of the joint, i.e. articular cartilage, bone, muscles, ligaments/tendons and nerves, participate in load transmission. Failure in any of these components can cause joint malfunction, which, in turn, may lead to accumulation of damage in other joint components. Mechanical forces have great influence on the synthesis and rate of turnover of articular cartilage molecules, such as proteoglycans (PGs). Regular cyclic loading of the joint enhances PG synthesis and makes cartilage stiff. On the other hand, loading appears to have less evident effects on the articular cartilage collagen fibril network. Continuous compression of the cartilage diminishes PG synthesis and causes damage of the tissue through necrosis. The prevailing view is that osteoarthrosis (OA) starts from the cartilage surface through PG depletion and fibrillation of the superficial collagen network. It has also been suggested that the initial structural changes take place in the subchondral bone, especially when the joint is exposed to an impact type of loading. This in turn would create an altered stress pattern on joint surfaces, which leads to structural damage and mechanical failure of articular cartilage. The importance of the neuromuscular system to the initiation and progression of OA is still poorly understood. Many surgical extra- and intra-articular procedures have been used for the treatment of OA. Although some of the new methods, such as autologous chondrocyte transplantation and mosaicplasty, have given good clinical results, it is reasonable to emphasize that the methods still are experimental and more controlled studies are needed.
关节是在日常正常活动或特殊活动（如运动）期间在相互接触的骨骼之间传递机械负荷的功能单元。关节的所有组成部分，即关节软骨、骨骼、肌肉、韧带/肌腱和神经，都参与负荷传递。这些组成部分中的任何一个出现故障都可能导致关节功能失常，进而可能导致其他关节组成部分的损伤积累。机械力对关节软骨分子（如蛋白聚糖 (PGs)）的合成和更新速率有很大影响。关节的定期循环负荷可增强 PG 合成并使软骨变硬。另一方面，负荷对关节软骨胶原纤维网络的影响似乎不太明显。软骨的持续压缩会减少 PG 合成并通过坏死导致组织损伤。普遍的观点是骨关节炎 (OA) 始于软骨表面，通过 PG 耗竭和浅表胶原网络的纤维化。也有人认为初始结构变化发生在软骨下骨，尤其是当关节受到冲击型负荷时。这反过来会在关节表面产生改变的应力模式，导致关节软骨的结构损伤和机械故障。神经肌肉系统对 OA 起始和进展的重要性仍知之甚少。许多外科关节外和关节内手术已用于治疗 OA。尽管一些新方法，如自体软骨细胞移植和镶嵌成形术，已取得良好的临床效果，但有理由强调这些方法仍处于实验阶段，需要更多对照研究。
