Wei Yingliang, Bai Lunhao
a Department of Orthopedic Surgery, Sheng-Jing Hospital , China Medical University , ShenYang , China.
Connect Tissue Res. 2016 Jul;57(4):245-61. doi: 10.1080/03008207.2016.1177036. Epub 2016 Jun 10.
Osteoarthritis (OA), the most common form of degenerative joint disease, is linked to high morbidity. It is predicted to be the single greatest cause of disability in the general population by 2030. The development of disease-modifying therapy for OA currently face great obstacle mainly because the onset and development of the disease involve complex molecular mechanisms. In this review, we will comprehensively summarize biological and pathological mechanisms of three key aspects: degeneration of articular cartilage, synovial immunopathogenesis, and changes in subchondral bone. For each tissue, we will focus on the molecular receptors, cytokines, peptidases, related cell, and signal pathways. Agents that specifically block mechanisms involved in synovial inflammation, degeneration of articular cartilage, and subchondral bone remodeling can potentially be exploited to produce targeted therapy for OA. Such new comprehensive agents will benefit affected patients and bring exciting new hope for the treatment of OA.
骨关节炎(OA)是退行性关节疾病最常见的形式,与高发病率相关。预计到2030年,它将成为普通人群中导致残疾的单一最大原因。目前,针对OA的疾病修饰疗法的开发面临巨大障碍,主要是因为该疾病的发生和发展涉及复杂的分子机制。在本综述中,我们将全面总结三个关键方面的生物学和病理机制:关节软骨退变、滑膜免疫发病机制以及软骨下骨变化。对于每个组织,我们将关注分子受体、细胞因子、肽酶、相关细胞和信号通路。特异性阻断滑膜炎症、关节软骨退变和软骨下骨重塑相关机制的药物有可能被用于开发针对OA的靶向治疗。这类新型综合药物将使受影响的患者受益,并为OA的治疗带来令人振奋的新希望。