Osteoarthritis (OA) is the most frequent joint disease and a leading cause of disability in the Western world. Currently, we do not have a cure for this degenerative disorder and despite a high individual and socioeconomic demand, available therapeutic strategies have not changed substantially within the last 40 to 50 years, largely involving basic symptomatic control using analgesics and NSAIDS, physiotherapy and behavioural changes, and eventual prosthetic replacement in end-stage disease. While prosthetic joint replacement constitutes an effective surgical treatment option for patients whose joints are irreversibly damaged by OA, demographic development together with altered physical activities in our aging society increasingly demonstrate the limitations of joint replacement surgery as the only real treatment modality. There is, therefore, an urgent requirement for disease modifying drugs that aim to halt OA disease progression during the early stages and potentially to kick start cartilage regeneration. This need is contrasted, however, by a sustained “translational roadblock” in OA research with very few conceptually novel therapeutic approaches on the horizon. Amongst others, this “translational roadblock” results from a general lack in our understanding of how articular chondrocytes as the only cells in joint cartilage acquire and maintain their specific and highly specialised phenotype and how this phenotype changes during OA onset and progression. Investigation of this developmental aspect of disease pathology in OA patients and using human samples has many limitations, which is why animal models remain to constitute a key element of cartilage and OA research. This lecture summarizes the relevance of different animal models for understanding fundamental principles of cartilage homeostasis and remodelling in health and osteoarthritic cartilage degeneration. By focusing on the analysis of chrondrocyte phenotypic stability, it provides examples for how the use of such models can contribute to understanding OA and to the development of new therapeutic strategies for the disease.
Disclosure of Interest None declared
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