Inflammation in joint injury and post-traumatic osteoarthritis.
Inflammation in joint injury and post-traumatic osteoarthritis.
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DOI：
10.1016/j.joca.2015.08.015
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发表时间：
2015-11
影响因子：
7
通讯作者：
Scanzello CR
中科院分区：
文献类型：
--
作者：
Lieberthal J;Sambamurthy N;Scanzello CR
炎症是骨关节炎（OA）的一个可变特征，与关节症状和疾病进展相关。在有发生创伤后骨关节炎（PTOA）风险的关节损伤患者的关节液和组织中可以观察到炎症体征。此外，炎症机制被假设为有助于损伤后OA发展和进展的风险。PTOA的动物模型有助于理解诱发性损伤后观察到的慢性进行性软骨退化的因素和机制。在PTOA模型中也观察到在人中观察到的炎症的特定方面，包括细胞因子和趋化因子产生、滑膜反应、细胞浸润和炎症途径活化。这些模型中的许多现在被用于了解损伤后炎症反应对PTOA发展和进展的影响，包括进行性软骨退化的风险和损伤后慢性症状的发展。从这些模型中可以看出，关节损伤后早期会出现剧烈的炎症反应，但在后期阶段会维持在较低水平。这种早期炎症反应有助于PTOA特征的发展，包括软骨侵蚀，并且可能是可改变的，但特定的介质也可能在组织修复中发挥作用。虽然关节损伤后抗炎干预的最佳方法和时机尚未确定，但这项工作应该为PTOA疾病修饰的未来提供希望。
Inflammation is a variable feature of osteoarthritis (OA), associated with joint symptoms and progression of disease. Signs of inflammation can be observed in joint fluids and tissues from patients with joint injuries at risk for development of post-traumatic osteoarthritis (PTOA). Furthermore, inflammatory mechanisms are hypothesized to contribute to the risk of OA development and progression after injury. Animal models of PTOA have been instrumental in understanding factors and mechanisms involved in chronic progressive cartilage degradation observed after a predisposing injury. Specific aspects of inflammation observed in humans, including cytokine and chemokine production, synovial reaction, cellular infiltration and inflammatory pathway activation, are also observed in models of PTOA. Many of these models are now being utilized to understand the impact of post-injury inflammatory response on PTOA development and progression, including risk of progressive cartilage degeneration and development of chronic symptoms post-injury. As evidenced from these models, a vigorous inflammatory response occurs very early after joint injury but is then sustained at a lower level at the later phases. This early inflammatory response contributes to the development of PTOA features including cartilage erosion and is potentially modifiable, but specific mediators may also play a role in tissue repair. Although the optimal approach and timing of anti-inflammatory interventions after joint injury are yet to be determined, this body of work should provide hope for the future of disease modification tin PTOA.