BONE QUALITY SEMINARS: SUBCHONDRAL BONE Animal models in OA: a means to explore bone M. Cohen-Solal & E. Hay & T. Funck-Brentano Received: 1 May 2012 / Accepted: 25 June 2012 / Published online: 22 November 2012 # International Osteoporosis Foundation and National Osteoporosis Foundation 2012 Abstract Cartilage damage which characterizes osteoar- thritis 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 cyto- kines secreted by bone cells can induce chondrocyte differ- entiation 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 resorb- ing 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. Keywords Bone . Cartilage . Osteoarthritis Introduction Although the cartilage use is the main hallmark of osteoar- thritis (OA), the disease damages the whole joint including the bone, synovial tissues, and ligaments. In humans, the characterization of each tissue lesion that lead to cartilage degradation in a longitudinal manner is restricted. Recent data based on imaging provided useful information in the lesions developed in the joints at the early stages of OA [1]. Such evaluations have the advantage of providing the local- ization and the time course of the tissues alterations such as the cartilage, synovium, meniscus, and bone. For example, synovial inflammation and meniscus and bone marrow lesions are good predictors of OA rapid progression at the knee [2–6]. However, this approach gives only descriptive information and is not fully contributive to the cause of the disease. Therefore, animal models are valuable tools to fully characterize the kinetics of the changes in the tissues. Other advantages are that they can be performed in a short amount of time and that they give access to the mechanism of action and efficacy of new molecules. Animal models in OA The final goal of animal models is to reproduce human OA. Given the heterogeneity of profiles in human OA, many models are needed. Most of them focused in one factor that favors the development of OA such as aging, mechanical stress (surgery), chemical defect (enzyme), or in genetic factors. All of them differ in terms of severity, localization of lesions, and pathogenesis. Hence, the choice of the model should be appropriate to the addressed question. For exam- ple, the choice should be focused on either the role of tissues or molecules that could trigger OA, the development under a M. Cohen-Solal (*) : E. Hay : T. Funck-Brentano INSERM U606, University Paris-Diderot Paris 7, Lariboisière Hospital, 2 rue Ambroise Paré, 75010 Paris, France e-mail: martine.cohen-solal@inserm.fr E. Hay e-mail: eric.hay@inserm.fr T. Funck-Brentano e-mail: thomas.funck-brentano@inserm.fr Osteoporos Int (2012) 23 (Suppl 8):S853–S856 DOI 10.1007/s00198-012-2163-y