Osteoarthritis: toward a comprehensive understanding of pathological mechanism.

Osteoarthritis: toward a comprehensive understanding of pathological mechanism.
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骨关节炎:迈向对病理机制的全面理解

DOI:
10.1038/boneres.2016.44
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发表时间:
2017
期刊:
影响因子:
12.7
通讯作者:
Im HJ
Im HJ
中科院分区:
医学1区
文献类型:
--
作者:
Chen D;Shen J;Zhao W;Wang T;Han L;Hamilton JL;Im HJ

文献摘要

被引文献

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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然知之甚少,目前还没有可用的干预措施来恢复退化的软骨或减缓疾病进展。关节是一个复杂的器官,其功能是承受重量,进行体力活动,并在运动过程中表现出关节特异性的活动范围。在OA发展过程中,整个关节器官都受到影响,包括关节软骨、软骨下骨、滑膜组织和半月板。要全面了解OA的病理机制,需要发现OA不同症状(包括关节软骨退化、骨赘形成、软骨下硬化和滑膜增生)之间的相互作用机制,以及控制这些病理过程的信号通路。
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.