João Henriques , Francis Berenbaum , Ali Mobasheri
{"title":"Obesity-induced fibrosis in osteoarthritis: Pathogenesis, consequences and novel therapeutic opportunities","authors":"João Henriques , Francis Berenbaum , Ali Mobasheri","doi":"10.1016/j.ocarto.2024.100511","DOIUrl":null,"url":null,"abstract":"<div><div>Osteoarthritis (OA) is a significant global burden, affecting more than half a billion people across the world. It is characterized by degeneration and loss of articular cartilage, synovial inflammation, and subchondral bone sclerosis, leading to pain and functional impairment. After age, obesity is a major modifiable risk factor for OA, and it has recently been identified as a chronic disease by the World Health Organization (WHO). Obesity is associated with high morbidity and mortality, imposing a significant cost on individuals and society. Obesity increases the risk of knee OA through increased joint loading, altered body composition, and elevated pro-inflammatory adipokines in the systemic circulation. Moreover, obesity triggers fibrotic processes in different organs and tissues, including those involved in OA. Fibrosis in OA refers to the abnormal accumulation of fibrous tissue within and around the joints. It can be driven by increased adiposity, low-grade inflammation, oxidative stress, and metabolic alterations. However, the clinical outcomes of fibrosis in OA are unclear. This review focuses on the link between obesity and OA, explores the mechanism of obesity-driven fibrosis, and examines potential therapeutic opportunities for targeting fibrotic processes in OA.</div></div>","PeriodicalId":74377,"journal":{"name":"Osteoarthritis and cartilage open","volume":"6 4","pages":"Article 100511"},"PeriodicalIF":0.0000,"publicationDate":"2024-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Osteoarthritis and cartilage open","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2665913124000785","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Osteoarthritis (OA) is a significant global burden, affecting more than half a billion people across the world. It is characterized by degeneration and loss of articular cartilage, synovial inflammation, and subchondral bone sclerosis, leading to pain and functional impairment. After age, obesity is a major modifiable risk factor for OA, and it has recently been identified as a chronic disease by the World Health Organization (WHO). Obesity is associated with high morbidity and mortality, imposing a significant cost on individuals and society. Obesity increases the risk of knee OA through increased joint loading, altered body composition, and elevated pro-inflammatory adipokines in the systemic circulation. Moreover, obesity triggers fibrotic processes in different organs and tissues, including those involved in OA. Fibrosis in OA refers to the abnormal accumulation of fibrous tissue within and around the joints. It can be driven by increased adiposity, low-grade inflammation, oxidative stress, and metabolic alterations. However, the clinical outcomes of fibrosis in OA are unclear. This review focuses on the link between obesity and OA, explores the mechanism of obesity-driven fibrosis, and examines potential therapeutic opportunities for targeting fibrotic processes in OA.
骨关节炎(OA)是一个严重的全球性负担,影响着全球 5 亿多人。其特点是关节软骨退化和脱落、滑膜炎症和软骨下骨硬化,从而导致疼痛和功能障碍。继年龄之后,肥胖是导致 OA 的主要可改变风险因素,最近世界卫生组织(WHO)已将其确定为一种慢性疾病。肥胖与高发病率和高死亡率有关,给个人和社会带来巨大损失。肥胖会增加关节负荷、改变身体成分、升高全身循环中的促炎性脂肪因子,从而增加膝关节 OA 的风险。此外,肥胖还会引发不同器官和组织的纤维化过程,包括涉及 OA 的器官和组织。OA 中的纤维化是指关节内和关节周围纤维组织的异常堆积。纤维化可由脂肪增加、低度炎症、氧化应激和代谢改变等因素引起。然而,OA 纤维化的临床结果尚不明确。本综述重点探讨肥胖与 OA 之间的联系,探索肥胖驱动纤维化的机制,并研究针对 OA 纤维化过程的潜在治疗机会。