Purpose: There is strong evidence that local inflammation plays an important role in causing pain in osteoarthritis (OA) and in contributing to worsening structural deterioration of the affected joint. The metabolic syndrome, which increases the risk of heart disease, may influence OA by magnifying articular inflammation or may increase OA risk through other means. The metabolic syndrome consists of a combination of centralized obesity, elevated triglycerides, reduced HDL cholesterol, hypertension and elevated fasting blood sugar, all of which occur more often in obese persons. The purpose of this talk is to review and critically evaluate evidence on the association of metabolic syndrome and OA. Methods: Narrative review Results: A large number of epidemiologic studies have examined the relationship between metabolic syndrome and the occurrence of OA, especially in the knees. Findings from these studies are challenging to interpret. In general, when the studies have adjusted for obesity, a major risk factor for knee OA that confers increased mechanical load on knees, findings have not shown a consistent association of metabolic syndrome with knee OA. The association of obesity with an increased risk of hand OA has suggested that there is something about systemic adipose tissue accumulation that increases OA risk which might be related to metabolic syndrome. Studies examining the relationship of hand OA with metabolic syndrome have been more positive although not uniformly so. These will be reviewed. A high prevalence of hand OA has been reported in HIV-positive men with metabolic syndrome and this is strong evidence in favor of a relationship between metabolic syndrome and hand OA. A related question is whether any elements of the metabolic syndrome are particularly associated with the risk of OA rather than the metabolic syndrome itself. Initial studies suggested that central obesity may be uniquely related, with visceral fat being a major source of inflammatory adipokines. However the analytic approach to examining central obesity is challenging because central obesity and BMI are collinear and straightforward adjustment for BMI is probably not adequate to evaluate the effect of central obesity in causing OA. Several studies have suggested that hypertension is uniquely related to OA risk, and there is conflicting evidence regarding the relation of OA to diabetes. Conclusions: The evidence so far does not identify a clearcut association of metabolic syndrome with OA but is suggestive, especially for hand OA. Longitudinal studies are needed including those that focus on specific elements of metabolic syndrome and that explore biologically why elements of this syndrome might be related to OA risk.
Felson, D. (2017). Metabolic OA; Does it Exist? Osteoarthritis and Cartilage, 25, S6. https://doi.org/10.1016/j.joca.2017.02.020