Osteoarthritis (OA) is a prevalent disease of most mammalian species and is a significant cause of welfare and economic morbidity in affected individuals and populations. In vitro models of osteoarthritis are vital to advance research into the causes of the disease, and the subsequent design and testing of potential therapeutics. However, a plethora of in vitro models have been used by researchers but with no consensus on the most appropriate model. Models attempt to mimic factors and conditions which initiate OA, or dissect the pathways active in the disease. Underlying uncertainty as to the cause of OA and the different attributes of isolated cells and tissues used mean that similar models may produce differing results and can differ from the naturally occurring disease. This review article assesses a selection of the in vitro models currently used in OA research, and considers the merits of each. Particular focus is placed on the more prevalent cytokine stimulation and load-based models. A brief review of the mechanism of these models is given, with their relevance to the naturally occurring disease. Most in vitro models have used supraphysiological loads or cytokine concentrations (compared with the natural disease) in order to impart a timely response from the cells or tissue assessed. Whilst models inducing OA-like pathology with a single stimulus can answer important biological questions about the behaviour of cells and tissues, the development of combinatorial models encompassing different physiological and molecular aspects of the disease should more accurately reflect the pathogenesis of the naturally occurring disease.
The prevalence of radiographic signs of degenerative joint disease (including appendicular osteoarthritis) among a hospital population of 218 cats was 33.9 per cent (74 cats), and the prevalence of signs of appendicular joint osteoarthritis was 16.5 per cent (36 cats). Half of the cases of appendicular joint osteoarthritis had no apparent radiographic or historical cause, and clinical signs of lameness were recorded in only six of them, all of which had an apparent radiographic cause. The 74 cats with radiographic signs of degenerative joint disease were on average significantly older than the 144 cats in which there were no radiographic signs of the disease.
Medical and/or surgical management were usually successful in resolving infection (94 per cent). However, they were frequently unsuccessful in restoring full joint function; this may in part have been due to the nature of the underlying joint
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