Lieberthal J, Sambamurthy N, Scanzello C R
University of Pennsylvania Perelman School of Medicine, Division of Rheumatology, Philadelphia, PA, USA.
University of Pennsylvania Perelman School of Medicine, Division of Rheumatology, Philadelphia, PA, USA; Translational Musculoskeletal Research Center, Corporal Michael J. Crescenz Department of Veterans Affairs Medical Center, Philadelphia, PA, USA.
Osteoarthritis Cartilage. 2015 Nov;23(11):1825-34. doi: 10.1016/j.joca.2015.08.015.
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.
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。在有创伤后骨关节炎(PTOA)发生风险的关节损伤患者的关节液和组织中可观察到炎症迹象。此外,据推测炎症机制会导致损伤后OA发生和进展的风险。PTOA动物模型有助于理解在易患性损伤后观察到的慢性进行性软骨降解所涉及的因素和机制。在PTOA模型中也观察到了在人类中所观察到的炎症的特定方面,包括细胞因子和趋化因子的产生、滑膜反应、细胞浸润和炎症途径激活。现在许多这类模型被用于理解损伤后炎症反应对PTOA发生和进展的影响,包括进行性软骨退变的风险以及损伤后慢性症状的发展。从这些模型可以看出,关节损伤后很早就会出现强烈的炎症反应,但在后期会维持在较低水平。这种早期炎症反应会导致包括软骨侵蚀在内的PTOA特征的发展,并且可能是可调节的,但特定介质也可能在组织修复中起作用。尽管关节损伤后抗炎干预的最佳方法和时机尚未确定,但这一系列研究工作应该为PTOA疾病修饰的未来带来希望。