Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Cheras 56000, Malaysia.
Mediators Inflamm. 2020 Mar 3;2020:8293921. doi: 10.1155/2020/8293921. eCollection 2020.
A joint is the point of connection between two bones in our body. Inflammation of the joint leads to several diseases, including osteoarthritis, which is the concern of this review. Osteoarthritis is a common chronic debilitating joint disease mainly affecting the elderly. Several studies showed that inflammation triggered by factors like biomechanical stress is involved in the development of osteoarthritis. This stimulates the release of early-stage inflammatory cytokines like interleukin-1 beta (IL-1), which in turn induces the activation of signaling pathways, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and mitogen-activated protein kinase (MAPK). These events, in turn, generate more inflammatory molecules. Subsequently, collagenase like matrix metalloproteinases-13 (MMP-13) will degrade the extracellular matrix. As a result, anatomical and physiological functions of the joint are altered. This review is aimed at summarizing the previous studies highlighting the involvement of inflammation in the pathogenesis of osteoarthritis.
关节是我们身体中两块骨头的连接点。关节炎症会导致多种疾病，包括骨关节炎，这是本次综述关注的问题。骨关节炎是一种常见的慢性致残性关节疾病，主要影响老年人。多项研究表明，生物力学应激等因素引发的炎症与骨关节炎的发生发展有关。这会刺激早期炎症细胞因子（如白细胞介素 1β（IL-1））的释放，进而诱导信号通路的激活，如核因子 kappa-轻链增强子的 B 细胞（NF-κB）、磷酸肌醇 3-激酶/蛋白激酶 B（PI3K/AKT）和丝裂原活化蛋白激酶（MAPK）。这些事件反过来又会产生更多的炎症分子。随后，基质金属蛋白酶 13（MMP-13）等胶原酶会降解细胞外基质。结果，关节的解剖和生理功能发生改变。本综述旨在总结之前的研究，强调炎症在骨关节炎发病机制中的作用。
