Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis.
Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis.
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DOI：
10.1038/nrrheum.2016.136
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发表时间：
2016-10
期刊：
影响因子：
--
通讯作者：
Sokolove J
中科院分区：
文献类型：
--
作者：
Robinson WH;Lepus CM;Wang Q;Raghu H;Mao R;Lindstrom TM;Sokolove J
骨关节炎（OA）一直被认为是一种软骨退行性疾病，但越来越多的证据表明炎症在其发病机制中起着关键作用。此外，我们现在认识到OA发病机制不仅涉及软骨的破坏，而且还涉及底层骨的重塑、异位骨的形成、关节囊肥大和滑膜衬里的炎症。也就是说，OA是关节整体的疾病，炎症驱动许多病理变化。OA中的炎症与类风湿性关节炎和其他自身免疫性疾病中的炎症不同：它是慢性的，相对低度的，并且主要由先天免疫系统介导。目前的OA治疗方法只能控制症状，没有一种被FDA批准用于预防或减缓疾病进展。然而，对OA炎症基础的深入了解为开发新的疾病修饰疗法带来了希望。事实上，几种抗炎疗法已经在OA动物模型中显示出前景。需要进一步的工作来确定OA中低度炎症的有效抑制剂，并确定针对这种炎症的治疗是否可以预防或减缓疾病的发展和进展。
Osteoarthritis (OA) has long been viewed as a degenerative disease of cartilage, but accumulating evidence indicates that inflammation has a critical role in its pathogenesis. Furthermore, we now appreciate that OA pathogenesis involves not only breakdown of cartilage, but also remodelling of the underlying bone, formation of ectopic bone, hypertrophy of the joint capsule, and inflammation of the synovial lining. That is, OA is a disorder of the joint as a whole, with inflammation driving many pathologic changes. The inflammation in OA is distinct from that in rheumatoid arthritis and other autoimmune diseases: it is chronic, comparatively low-grade, and mediated primarily by the innate immune system. Current treatments for OA only control the symptoms, and none has been FDA-approved for the prevention or slowing of disease progression. However, increasing insight into the inflammatory underpinnings of OA holds promise for the development of new, disease-modifying therapies. Indeed, several anti-inflammatory therapies have shown promise in animal models of OA. Further work is needed to identify effective inhibitors of the low-grade inflammation in OA, and to determine whether therapies that target this inflammation can prevent or slow the development and progression of the disease.
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影响因子：
7
作者：
Abramson, Steven B.
通讯作者：
Abramson, Steven B.
骨关节炎的炎症。
影响因子：
5.1
作者：
Goldring MB;Otero M
通讯作者：
Otero M
影响因子：
39.2
作者：
Chalasani N;Vuppalanchi R;Navarro V;Fontana R;Bonkovsky H;Barnhart H;Kleiner DE;Hoofnagle JH
通讯作者：
Hoofnagle JH
影响因子：
27.4
作者：
Baker K;Grainger A;Niu J;Clancy M;Guermazi A;Crema M;Hughes L;Buckwalter J;Wooley A;Nevitt M;Felson DT
通讯作者：
Felson DT
DOI：
10.1002/art.24096
发表时间：
2009-03-15
期刊：
ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH
影响因子：
--
作者：
Chevalier, X.;Goupille, P.;Appleton, B. E.
通讯作者：
Appleton, B. E.