Metabolism and arthritis

A few years ago, we started to look at the role of tissue interactions in osteoarthritis (OA), a disease initially considered as cartilage-driven. OA is a much more complex disease, with inflammatory mediators released by cartilage, bone and synovium interacting into the joint. Because obesity is a risk factor for OA in non-weight-bearing joints such as the hand, adipokines were suggested to play a role in OA. Starting from our work on the involvement of adipokines in OA, we address the hypothesis of a role of metabolic syndrome in OA progression. Metabolic syndrome-associated OA (MetS-OA) has recently been highlighted among the overall group of OA phenotypes, but the molecular mechanisms underlying the role of MetS in cartilage degradation has been poorly studied. Indeed, studies suggest that OA structural progression may result from altered communication between subchondral bone cells (e.g., osteoblasts, osteocytes) and cartilage cells (chondrocytes) and atheromatous vascular disease of subchondral bone.

In parallel, we have launched a cohort of patients suffering from hand OA going to be followed at least 6 years in order to collect biological, imaging and clincal data to better understand the pathophysiology and the prognosis of this disease.