Epidemiological and imaging findings indicate that gout frequently affects damaged joints. Recent studies suggest that the relationship between gout and joint damage may be more complex than a simple unidirectional link and that joint damage may promote the development of gout at affected sites. In this article, we review the clinical associations and recent laboratory research identifying events in the setting of osteoarthritis or joint injury that can alter the intraarticular microenvironment and locally regulate monosodium urate crystallisation and deposition or amplify the inflammatory response to deposited crystals. This includes cartilage matrix proteins or fibres released into the articular space that accelerates the crystallisation process, as well as the lack of lubricin and fibroblast priming that enhances the immune response towards the deposited crystals. These findings provide new insights into gout pathogenesis and offer a possible explanation for the site preference of gout in the damaged joint.
- Crystal arthropathies
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Handling editor Josef S Smolen
HX and HQ contributed equally.
Contributors YH and ND designed and supervised the research project; HX and HQ completed literature search, paper writing and figure design; YH, HX and ND revised the draft.
Funding The study was supported by CSC grant (ID 202106100140) to HX.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.