Goldring Mary B, Berenbaum Francis
Tissue Engineering, Regeneration and Repair Program, Hospital for Special Surgery, New York, NY, USA; Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, NY, USA.
Department of Rheumatology, AP-HP Saint-Antoine Hospital, 75012 Paris, France.
Curr Opin Pharmacol. 2015 Jun;22:51-63. doi: 10.1016/j.coph.2015.03.004. Epub 2015 Apr 10.
Osteoarthritis (OA) is a destructive joint disease in which the initiation may be attributed to direct injury and mechanical disruption of joint tissues, but the progressive changes are dependent on active cell-mediated processes that can be observed or inferred during the generally long time-course of the disease. Based on clinical observations and experimental studies, it is now recognized a that it is possible for individual patients to exhibit common sets of symptoms and structural abnormalities due to distinct pathophysiological pathways that act independently or in combination. Recent research that has focused on the underlying mechanisms involving biochemical cross talk among the cartilage, synovium, bone, and other joint tissues within a background of poorly characterized genetic factors will be addressed in this review.
骨关节炎(OA)是一种破坏性关节疾病,其发病可能归因于关节组织的直接损伤和机械破坏,但疾病进展过程中的变化则依赖于活跃的细胞介导过程,这些过程在疾病通常较长的病程中可以观察到或推断出来。基于临床观察和实验研究,现在已经认识到,由于不同的病理生理途径独立或联合起作用,个别患者可能会出现常见的症状和结构异常。本文将综述近期的研究,这些研究聚焦于在遗传因素特征不明的背景下,软骨、滑膜、骨和其他关节组织之间生化相互作用的潜在机制。