Department of Trauma Surgery, University of Regensburg Medical Center, Regensburg, Germany.
PM R. 2011 Jun;3(6 Suppl 1):S3-11. doi: 10.1016/j.pmrj.2011.05.009.
Osteoarthritis is the most common degenerative musculoskeletal disease. In healthy cartilage, a low turnover of extracellular matrix molecules occurs. Proper balance of anabolic and catabolic activities is thus crucial for the maintenance of cartilage tissue integrity and for the repair of molecular damages sustained during daily usage. In persons with degenerative diseases such as osteoarthritis, this balance of anabolic and catabolic activities is compromised, and the extent of tissue degradation predominates over the capacity of tissue repair. This mismatch eventually results in cartilage loss in persons with osteoarthritis. Tissue homeostasis is controlled by coordinated actions and crosstalk among a number of proanabolic and antianabolic and procatabolic and anticatabolic factors. In osteoarthritis, an elevation of antianabolic and catabolic factors occurs. Interestingly, anabolic activity is also increased, but this response fails to repair the tissue because of both quantitative and qualitative insufficiency. This review presents an overview of the anabolic and catabolic activities involved in cartilage degeneration and the interplay among different signaling and metabolic factors. Understanding the basic molecular mechanisms responsible for tissue degeneration is critical to identifying and developing means to efficiently block or reverse the pathobiological symptoms of osteoarthritis.
骨关节炎是最常见的退行性肌肉骨骼疾病。在健康的软骨中，细胞外基质分子的周转率较低。因此，合成代谢和分解代谢活动的适当平衡对于维持软骨组织完整性和修复日常使用中持续的分子损伤至关重要。在退行性疾病（如骨关节炎）患者中，这种合成代谢和分解代谢活动的平衡受到损害，组织降解的程度超过组织修复的能力。这种不匹配最终导致骨关节炎患者的软骨丧失。组织动态平衡受多种促合成代谢和抗合成代谢以及促分解代谢和抗分解代谢因素的协调作用和相互作用控制。在骨关节炎中，抗合成代谢和分解代谢因子升高。有趣的是，合成代谢活性也增加，但由于数量和质量不足，这种反应未能修复组织。这篇综述介绍了参与软骨退化的合成代谢和分解代谢活动以及不同信号和代谢因素之间的相互作用。了解导致组织退化的基本分子机制对于识别和开发有效阻止或逆转骨关节炎病理生物学症状的方法至关重要。
