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 anti-hypertensive drugs, could be useful for treating OA.[H1] Introduction Osteoarthritis (OA) is a prevalent disease that affects 500 million people worldwide 1 , and is not only a leading cause of chronic pain and disability in older adults, but is also a risk factor for cardiovascular events and all-cause mortality 2-4 . OA is no longer thought of as a simple wear-andtear problem affecting articular cartilage, but rather as a whole-joint disorder subject to interactions between a variety of local and systemic risk factors. The prevalence of knee OA has doubled since the mid-20th century 5 , alongside expanding populations of older individuals and those with obesity.However, neither ageing nor obesity can entirely explain this phenomenon. Therefore, interest is This is the Pre-Published Version.
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