Abstract
Both gout and osteoarthritis (OA) are common forms of arthritis that inflict a huge burden to an aging population with the increasing prevalence of obesity. Clinicians have long observed the link between these two conditions. In this review, we summarize the evidence from epidemiologic and immunological studies that described the possible relationship between the two conditions. The recent new understanding on monosodium uric acid crystal-induced inflammation has given insight into probable shared pathogenesis pathways for both conditions. We describe the potential therapeutic implications, particularly regarding the possibility of repurposing traditional gout medications for use in OA.
Highlights
The risk of mobility and disability attributable to osteoarthritis (OA) alone is greater than any other medical condition among elderly [1]
Another cross-sectional study involving over 4,000 participants in China has shown that women with the highest tertile of uric acid showed the highest degree of radiographic features suggestive of knee OA after adjusted for various confounding risk factors including body mass index (BMI) [17]
A study of knee OA subjects without gout showed that serum uric acid levels significantly distinguished non-progressors from progressors defined by joint space narrowing on radiography over 24 months [18]
Summary
The risk of mobility and disability attributable to osteoarthritis (OA) alone is greater than any other medical condition among elderly [1]. Gout is a crystal-induced arthritis caused by deposition of the monosodium uric acid crystal (MSU) related to long standing hyperuricemia. It is a common inflammatory arthritis affecting around 5% of the middle-aged and elderly population worldwide [5]. Should gout and OA prove to have a causative relationship, and share common pathological pathway, effective treatment for gout might potentially be useful for OA. In this narrative review, the possible associations and pathological mechanisms between hyperuricemia, gout, and OA are discussed
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