Animal models in OA: a means to explore bone

Abstract

Cartilage damage which characterizes osteoarthritis is accompanied with bone lesions. Joint integrity results from the balance in the physiological interactions between bone and cartilage. Several local factors regulate physiological remodeling of cartilage, the disequilibrium of these leading to a higher cartilage catabolism. Several cytokines secreted by bone cells can induce chondrocyte differentiation which suggests their role in the dialogue between both cells. Several animal models of osteoarthritis have been developed in order to assess the mechanism of cartilage loss and chondrocyte functions that encompassed surgical, chemical, or genetic approaches. Indeed, the animal models are helpful to investigate the cartilage changes in relation to changes in bone remodeling. Accumulative in vivo evidence show that increased bone resorption occurs at early stage of the development of osteoarthritis. Inhibition of bone resorbing molecules prevents cartilage damage, confirming the role of bone factors in the cross talk between both tissues. Among these numerous molecules, some participate to the imbalance in cartilage homeostasis and in the pathophysiology of osteoarthritis. These local factors are potential candidates for new drug targets.