Osteoarthritis (OA) is a whole-joint disease characterized by subchondral bone perfusion abnormalities and neovascular invasion into the synovium and articular cartilage. In addition to local vascular disturbance, mounting evidence suggests a pivotal role for systemic vascular pathology in the aetiology of OA. This Review outlines the current understanding of the close relationship between high blood pressure (hypertension) and OA at the crossroads of epidemiology and molecular biology. As one of the most common comorbidities in patients with OA, hypertension can disrupt joint homeostasis both biophysically and biochemically. High blood pressure can increase intraosseous pressure and cause hypoxia, which in turn triggers subchondral bone and osteochondral junction remodelling. Furthermore, systemic activation of the renin–angiotensin and endothelin systems can affect the Wnt–β-catenin signalling pathway locally to govern joint disease. The intimate relationship between hypertension and OA indicates that endothelium-targeted strategies, including re-purposed FDA-approved antihypertensive drugs, could be useful in the treatment of OA.

骨关节炎（OA）是一种全关节疾病，其特征是软骨下骨灌注异常和新生血管侵入滑膜和关节软骨。除了局部血管障碍外，越来越多的证据表明全身血管病理学在 OA 的病因中起着关键作用。这篇综述概述了目前在流行病学和分子生物学的十字路口对高血压（高血压）和 OA 之间密切关系的理解。作为 OA 患者最常见的合并症之一，高血压会在生物物理和生物化学上破坏关节稳态。高血压会增加骨内压力并引起缺氧，进而引发软骨下骨和骨软骨连接处的重塑。此外，肾素-血管紧张素和内皮素系统的全身激活可以局部影响 Wnt-β-catenin 信号通路以控制关节疾病。高血压与 OA 之间的密切关系表明，内皮靶向策略，包括重新利用 FDA 批准的抗高血压药物，可能有助于治疗 OA。