Osteoarthritis (OA) has long been considered as the consequence of tear and wear due to mechanical triggers. In that paradigm, the increased risk of OA in obese patients can be explained by overload on weight-bearing joints. The discovery of an increased risk of hand OA in obese patients has changed the paradigm by opening up an additional hypothesis (not ruling out the mechanical hypothesis) based on systemic factors secreted by the adipose tissue (even the central one or/and the intraarticular one), which could have a deleterious effect on joints. More recently, cohorts data have suggested that obese patients with a metabolic syndrome (MetS) (an association of cardiometabolic factors that increase the risk of cardiovascular events i.e. diabetes, hypertension, dyslipidemia) have an increased risk of OA compared to obese patients without MetS. The most recent researches in that field highlight the role of metabolic-triggered inflammation (called meta-inflammation) on the initiation/progression of OA and the role of each of the components of the MetS independently (hyperglycemia, insulinoresistance, oxLDL, endothelial dysfunction, etc.). A better understanding of this newly defined OA phenotype, namely the MetS-associated OA, should lead to the discovery of new drugs specifically targeting this phenotype or/and to assess the efficacy of drugs in OA already on the market for diabetes, hypertension or dyslipidemia.
Disclosure of Interest F. Berenbaum Grant/research support from: Servier, TRB Chemedica, Consultant for: Pfizer, AbbVie, GSK, Flexion Therapeutics, Nordic Bioscience, MerckSerono, Jansen, Expanscience