Abstract Summary
The pathogenesis of osteoarthritis (OA) involves both metabolic and biomechanical factors. However, the mechanistic implications of contributing factors – obesity, adiposity, and metabolic syndrome – have been difficult to determine due to the complexities of their interactions. To gain further mechanistic insight, we examined a fat-free mouse model that completely lacks adipose tissue depots. We observed that in the absence of body fat, animals have improved cartilage knee joint integrity compared to controls, suggesting a direct relationship between adipose tissue depots and the onset and progression of OA, independent of biomechanical and metabolic contributors.