The Burden of Metabolic Syndrome on Osteoarthritic Joints

Bruce M. Dickson; Anke J. Roelofs; Justin J. Rochford; Heather M. Wilson; Cosimo De Bari

Disclosures

Arthritis Res Ther. 2019;21(289) 

In This Article

Conclusions

Our understanding of the pathogenesis of OA has come a long way from the long-standing paradigm of a disease caused by 'wear and tear'. A plethora of new evidence has emerged highlighting the importance of chronic, low-grade inflammation in the pathogenesis of this debilitating condition. Macrophages, as crucial mediators of the innate and adaptive immune response, have been extensively studied, and it is now clear that an imbalance in macrophage phenotype is contributing to this condition. Given the association of OA with obesity in an increasingly overweight population, the impact of metabolic factors on the development of joint disease has become an area of intense investigation. As such, dyslipidaemia, hyperglycaemia, and aberrant adipokine secretion have emerged as important metabolic regulators capable of influencing the chronic inflammation seen in OA. These discoveries reaffirm the role weight loss plays in the management of OA, how weight loss could per se result in resolving inflammation, metformin can alter metabolic regulators, and how dietary fatty acids might be promising targets for DMOADs. Whilst new therapies will require substantial further work to reach fruition, the studies reviewed here offer significant encouragement that novel treatments will emerge for this prevalent and debilitating condition.

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