TLR5 and metabolic syndrome: Another observation performed by Guss et al. in a load-induced model of OA with/without a high-fat diet in Toll-like receptor-5 deficient (TLR5KO) mice that spontaneously develop metabolic syndrome due to gut microbiota alterations, suggests that severe obesity and inflammation increased load-induced cartilage damage and the modification of metabolic syndrome-associated phylotypes of gut microbiota may contribute to development of cartilage pathology and subchondral bone morphology [12].