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Abstract: Osteoarthritis (OA) is the commonest form of arthritis, and presents us with an enormous healthcare burden. Identifying new ways of intervening non-surgically in this disease would seem essential. An overview of our work in clinical translation of laboratory findings in the Arthritis Research UK Centre for OA Pathogenesis will be given, which aims to identify new tests and treatments for OA.

Joint injury is the greatest risk factor for development of OA. Our translational studies investigate how tissues respond to injury with the aim of increasing our understanding of the initiating processes in this disease. In laboratory studies, we have shown that articular cartilage, but also other connective tissues, respond within seconds to injury. A range of inflammatory signalling pathways are activated, inducing a discrete set of inflammatory response genes implicated in inflammation but also cartilage repair. The release of FGF-2 from articular cartilage appears important in activation of many pathways on damage of connective tissues. Elements of this response, regulated by mechanical load, appear necessary for development of later disease.

To investigate whether this response translates to humans, the Knee Injury Cohort at the Kennedy (KICK) study is following 150 individuals with acute knee injury, with clinical, biological sampling and imaging over 5 years. The majority of candidate biomarkers from our pre-clinical studies were also found to be highly up-regulated in the synovial fluid of those with acute joint injury. This biomarker response, best characterised by synovial fluid IL-6, was significantly associated with symptoms and function at the time of the injury, but also over the following 3 months. Studying the development of symptomatic OA in this setting may lead to better understanding of underlying mechanisms of disease initiation, but also resolution, and we hope will help to develop much-needed prognostic tests and novel therapies for OA.