Scanzello Carla R
Corporal Michael J. Cresenz VA Medical Center, Division of Rheumatology and Translational Musculoskeletal Research Center, and University of Pennsylvania Perelman School of Medicine, Division of Rheumatology, 3900 Woodland Ave. Bldg. 21, Rm A213, Philadelphia, Pennsylvania, 19104.
J Orthop Res. 2017 Apr;35(4):735-739. doi: 10.1002/jor.23471. Epub 2017 Mar 8.
Evidence has been building that the pathologic drive for development of osteoarthritis (OA) involves more than simple mechanical "wear and tear." Inflammatory mechanisms play an important role in the tissue response to joint injury, and are involved in development of post-traumatic OA. Inflammation also appears integral to the progression of OA, whether post-traumatic or spontaneous, contributing to the evolution of joint tissue degradation and remodeling as well as joint pain. Both patient-based studies and in vivo models of disease have shed light on a number of inflammatory pathways and mediators that impact various aspects of this disease, both structurally and symptomatically. Recent work in this field has implicated inflammatory chemokines in osteoarthritis pathogenesis. Expression of multiple chemokines and their receptors is modulated during disease in both patients and animal models. Although best known for their effects on leukocyte migration and trafficking within the immune system, chemokines can have a wide variety of effects on both motile and non-motile cell types, impacting proliferation, differentiation, and activation of cellular responses. Their role in OA models has also demonstrated diverse effects on disease that exemplify their wide-ranging effects. Understanding how these important mediators of inflammation impact joint disease, and whether they can be targeted therapeutically, is actively being investigated by many groups in this field. This narrative review focuses on evidence published within the last 5 years highlighting chemokine-mediated pathways with mechanistic involvement in osteoarthritis and joint tissue repair. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:735-739, 2017.
越来越多的证据表明，骨关节炎（OA）发展的病理驱动因素不仅仅是简单的机械性“磨损”。炎症机制在组织对关节损伤的反应中起重要作用，并参与创伤后骨关节炎的发展。炎症似乎也是骨关节炎进展的一个组成部分，无论是创伤后还是自发性的，都会导致关节组织降解、重塑以及关节疼痛的演变。基于患者的研究和疾病的体内模型都揭示了一些影响该疾病各个方面（包括结构和症状）的炎症途径和介质。该领域的最新研究表明炎症趋化因子与骨关节炎发病机制有关。在患者和动物模型的疾病过程中，多种趋化因子及其受体的表达均受到调节。尽管趋化因子最出名的是它们对免疫系统内白细胞迁移和运输的影响，但它们对活动和非活动细胞类型都可能有广泛的影响，影响细胞反应的增殖、分化和激活。它们在骨关节炎模型中的作用也证明了对疾病有多种影响，体现了它们的广泛作用。该领域的许多研究小组正在积极研究这些重要的炎症介质如何影响关节疾病，以及它们是否可以作为治疗靶点。这篇叙述性综述重点关注过去5年发表的证据，突出趋化因子介导的途径在骨关节炎和关节组织修复中的机制作用。©2016骨科研究协会。由Wiley Periodicals, Inc.出版。《矫形外科学研究》35:735 - 739, 2017。
