Yunus Mohd Heikal Mohd, Nordin Abid, Kamal Haziq
Department of Physiology, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur 56000, Malaysia.
Centre of Tissue Engineering & Regenerative Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur 56000, Malaysia.
Medicina (Kaunas). 2020 Nov 16;56(11):614. doi: 10.3390/medicina56110614.
Osteoarthritis (OA) is the most well-known degenerative disease among the geriatric and is a main cause of significant disability in daily living. It has a multifactorial etiology and is characterized by pathological changes in the knee joint structure including cartilage erosion, synovial inflammation, and subchondral sclerosis with osteophyte formation. To date, no efficient treatment is capable of altering the pathological progression of OA, and current therapy is broadly divided into pharmacological and nonpharmacological measures prior to surgical intervention. In this review, the significant risk factors and mediators, such as cytokines, proteolytic enzymes, and nitric oxide, that trigger the loss of the normal homeostasis and structural changes in the articular cartilage during the progression of OA are described. As the understanding of the mechanisms underlying OA improves, treatments are being developed that target specific mediators thought to promote the cartilage destruction that results from imbalanced catabolic and anabolic activity in the joint.
骨关节炎（OA）是老年人中最常见的退行性疾病，是导致日常生活中严重残疾的主要原因。它具有多因素病因，其特征是膝关节结构发生病理变化，包括软骨侵蚀、滑膜炎症以及伴有骨赘形成的软骨下硬化。迄今为止，尚无有效的治疗方法能够改变OA的病理进程，目前的治疗方法在手术干预之前大致分为药物治疗和非药物治疗措施。在这篇综述中，描述了在OA进展过程中引发关节软骨正常稳态丧失和结构变化的重要危险因素和介质，如细胞因子、蛋白水解酶和一氧化氮。随着对OA潜在机制的理解不断提高，正在开发针对特定介质的治疗方法，这些介质被认为会促进因关节分解代谢和合成代谢活动失衡而导致的软骨破坏。
