Role and Mechanism of Mechanical Load in the Homeostasis of the Subchondral Bone in Knee Osteoarthritis: A Comprehensive Review.

IF 4.2 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2024-11-21 eCollection Date: 2024-01-01 DOI:10.2147/JIR.S492415
Lin Chen, Zhan Zhang, Xueyong Liu
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引用次数: 0

Abstract

Osteoarthritis (OA) is one of the most prevalent degenerative joint diseases, and the knee joint is particularly susceptible to it. It typically affects the entire joint and is marked by the erosion of cartilage integrity, chondrocytopenia, subchondral bone sclerosis and the mild synovial inflammation. Pathological changes in the subchondral bone often serve as initiating factors for joint degeneration. Various predisposing factors, including metabolic disorders, oxidative stress, and abnormal mechanical loading, regulate OA pathogenesis. Of them, mechanical loading is closely associated with the maintenance of the subchondral bone. Disrupted mechanical loading, leading to subchondral bone remodeling, can potentially trigger OA, whereas appropriate loading might ameliorate its progression. Therefore, this narrative review aimed to discuss existing knowledge and explore how mechanical loading mediates changes in the subchondral bone, influencing the development of knee osteoarthritis. Special emphasis is placed on its role and underlying mechanisms in maintaining joint homeostasis.

机械负荷在膝关节骨性关节炎软骨下骨平衡中的作用和机制:全面综述》。
骨关节炎(OA)是最常见的关节退行性疾病之一,膝关节尤其易受其影响。它通常影响整个关节,以软骨完整性受到侵蚀、软骨细胞减少、软骨下骨硬化和轻度滑膜炎症为特征。软骨下骨的病理变化通常是关节退化的起始因素。各种致病因素,包括代谢紊乱、氧化应激和异常机械负荷,都会影响 OA 的发病机制。其中,机械负荷与软骨下骨的维护密切相关。紊乱的机械负荷导致软骨下骨重塑,有可能诱发 OA,而适当的负荷可能会改善其进展。因此,本综述旨在讨论现有知识,探讨机械负荷如何介导软骨下骨的变化,从而影响膝关节骨性关节炎的发展。其中特别强调了机械负荷在维持关节平衡中的作用和内在机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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