Chen Di, Shen Jie, Zhao Weiwei, Wang Tingyu, Han Lin, Hamilton John L, Im Hee-Jeong
Department of Biochemistry, Rush University Medical Center , Chicago, IL, USA.
Department of Orthopaedic Surgery, Washington University , St Louis, MO, USA.
Bone Res. 2017 Jan 17;5:16044. doi: 10.1038/boneres.2016.44. eCollection 2017.
Osteoarthritis (OA) is the most common degenerative joint disease and a major cause of pain and disability in adult individuals. The etiology of OA includes joint injury, obesity, aging, and heredity. However, the detailed molecular mechanisms of OA initiation and progression remain poorly understood and, currently, there are no interventions available to restore degraded cartilage or decelerate disease progression. The diathrodial joint is a complicated organ and its function is to bear weight, perform physical activity and exhibit a joint-specific range of motion during movement. During OA development, the entire joint organ is affected, including articular cartilage, subchondral bone, synovial tissue and meniscus. A full understanding of the pathological mechanism of OA development relies on the discovery of the interplaying mechanisms among different OA symptoms, including articular cartilage degradation, osteophyte formation, subchondral sclerosis and synovial hyperplasia, and the signaling pathway(s) controlling these pathological processes.
骨关节炎(OA)是最常见的退行性关节疾病,也是成年人疼痛和残疾的主要原因。OA的病因包括关节损伤、肥胖、衰老和遗传。然而,OA发生和进展的详细分子机制仍知之甚少,目前尚无干预措施可恢复退化的软骨或减缓疾病进展。滑膜关节是一个复杂的器官,其功能是承受体重、进行体育活动并在运动时展现特定关节的活动范围。在OA发展过程中,整个关节器官都会受到影响,包括关节软骨、软骨下骨、滑膜组织和半月板。全面了解OA发展的病理机制依赖于发现不同OA症状之间的相互作用机制,包括关节软骨降解、骨赘形成、软骨下硬化和滑膜增生,以及控制这些病理过程的信号通路。