Hypertension meets osteoarthritis — revisiting the vascular aetiology hypothesis

Karen Ching, Xavier Houard, Francis Berenbaum, Chunyi Wen

Research output: Journal article publicationReview articleAcademic researchpeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)533-549
Number of pages17
JournalNature Reviews Rheumatology
Volume17
Issue number9
DOIs
Publication statusPublished - Sep 2021

ASJC Scopus subject areas

  • Rheumatology

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