Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Center, Department of Development and Regeneration, KU Leuven, 3000 Leuven, Belgium.
Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Center, Department of Development and Regeneration, KU Leuven, 3000 Leuven, Belgium; Division of Rheumatology, University Hospitals Leuven, 3000 Leuven, Belgium.
Osteoarthritis Cartilage. 2023 Oct;31(10):1303-1311. doi: 10.1016/j.joca.2023.06.005. Epub 2023 Jun 21.
As more has become known of the pathophysiology of osteoarthritis (OA), evidence that inflammation plays a critical role in its development and progression has accumulated. Here, we aim to review current knowledge of the complex inflammatory network in the OA joint.
This narrative review is presented in three main sections: local inflammation, systemic inflammation, and therapeutic implications. We focused on inflammatory mediators and their link to OA structural changes in the joint.
OA is characterized by chronic and low-grade inflammation mediated mostly by the innate immune system, which results in cartilage degradation, bone remodeling and synovial changes. Synovitis is regarded as an OA characteristic and associated with increased severity of symptoms and joint dysfunction. However, the articular cartilage and the subchondral bone also produce several pro-inflammatory mediators thus establishing a complex interplay between the different tissues of the joint. In addition, systemic low-grade inflammation induced by aging, obesity and metabolic syndrome can contribute to OA development and progression. The main inflammatory mediators associated with OA include cytokines, chemokines, growth factors, adipokines, and neuropeptides.
Future research is needed to deeper understand the molecular pathways mediating the inflammation in OA to provide new therapeutics that target these pathways, or to repurpose existing drugs.
随着对骨关节炎（OA）病理生理学认识的不断深入，越来越多的证据表明炎症在其发生和发展过程中起着关键作用。在这里，我们旨在回顾 OA 关节中复杂的炎症网络的现有知识。
本综述以三个主要部分呈现：局部炎症、全身炎症和治疗意义。我们重点关注炎症介质及其与 OA 关节结构变化的关系。
OA 以主要由先天免疫系统介导的慢性和低水平炎症为特征，导致软骨降解、骨重塑和滑膜变化。滑膜炎被认为是 OA 的特征之一，与症状加重和关节功能障碍有关。然而，关节软骨和软骨下骨也产生几种促炎介质，从而在关节的不同组织之间建立了复杂的相互作用。此外，由衰老、肥胖和代谢综合征引起的全身低度炎症也可能导致 OA 的发生和发展。与 OA 相关的主要炎症介质包括细胞因子、趋化因子、生长因子、脂肪因子和神经肽。
需要进一步研究以深入了解介导 OA 炎症的分子途径，从而提供针对这些途径的新疗法，或重新利用现有药物。
