Purpose of Review

Metabolic syndrome (MetS), also called the ‘deadly quartet’ comprising obesity, diabetes, dyslipidemia, and hypertension, has been ascertained to have a causal role in the pathogenesis of osteoarthritis (OA). This review is aimed at discussing the current knowledge on the contribution of metabolic syndrome and its various components to OA pathogenesis and progression.

Recent Findings

Lately, an increased association identified between the various components of metabolic syndrome (obesity, diabetes, dyslipidemia, and hypertension) with OA has led to the identification of the ‘metabolic phenotype’ of OA. These metabolic perturbations alongside low-grade systemic inflammation have been identified to inflict detrimental effects upon multiple tissues of the joint including cartilage, bone, and synovium leading to complete joint failure in OA. Recent epidemiological and clinical findings affirm that adipokines significantly contribute to inflammation, tissue degradation, and OA pathogenesis mediated through multiple signaling pathways. OA is no longer perceived as just a ‘wear and tear’ disease and the involvement of the metabolic components in OA pathogenesis adds up to the complexity of the disease.

Summary

Given the global surge in obesity and its allied metabolic perturbations, this review aims to throw light on the current knowledge on the pathophysiology of MetS-associated OA and the need to address MetS in the context of metabolic OA management. Better regulation of the constituent factors of MetS could be profitable in preventing MetS-associated OA. The identification of key roles for several metabolic regulators in OA pathogenesis has also opened up newer avenues in the recognition and development of novel therapeutic agents.

中文翻译：

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肥胖、代谢综合征和骨关节炎——最新综述

审查目的

代谢综合征（MetS）也被称为由肥胖、糖尿病、血脂异常和高血压组成的“致命四重奏”，已被证实在骨关节炎（OA）的发病机制中具有因果作用。本综述旨在讨论目前关于代谢综合征及其各个组成部分对 OA 发病机制和进展的影响的知识。

最近的发现

最近，代谢综合征的各个组成部分（肥胖、糖尿病、血脂异常和高血压）与 OA 之间的关联性不断增强，从而确定了 OA 的“代谢表型”。这些代谢紊乱以及低度全身炎症已被确定会对关节的多个组织（包括软骨、骨和滑膜）造成有害影响，导致 OA 中的关节完全衰竭。最近的流行病学和临床研究结果证实，脂肪因子通过多种信号通路显着促进炎症、组织降解和 OA 发病机制。OA 不再被认为只是一种“磨损”疾病，OA 发病机制中代谢成分的参与增加了该疾病的复杂性。

概括

鉴于全球肥胖率激增及其相关的代谢紊乱，本综述旨在阐明目前有关 MetS 相关 OA 病理生理学的知识，以及在代谢 OA 管理背景下解决 MetS 的必要性。更好地调节 MetS 的构成因素可能有助于预防 MetS 相关的 OA。多种代谢调节因子在 OA 发病机制中关键作用的确定也为新型治疗药物的识别和开发开辟了新途径。