Arthritis Research UK Centre for Osteoarthritis Pathogenesis
Professor Tonia Vincent, Director of the Arthritis Research UK Centre for Osteoarthritis Pathogenesis talks to us about the Centre and her work. The Centre was launched in 2013 and coincided with the relocation, from London to Oxford, of the Kennedy Institute of Rheumatology. It’s funded over 5 years by Arthritis Research UK, Oxford University and the Kennedy Trust for Rheumatological Research (KTRR).
Extracted from Issue 7, March 2014 OxfordMedSci News.
What are you hoping to achieve in the new Centre?
Our mission is to discover the pathways that drive joint degeneration in osteoarthritis (OA), the most common form of arthritis in developed societies. These pathways represent potential therapeutic targets and should also lead to the development of biomarkers for early diagnosis, prognosis and treatment response.
And who’s in your team?
The Centre comprises a core of basic and clinician scientists from the Kennedy institute working within the fields of cartilage, matrix and bone biology. It also includes several other groups within Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (largely at the Botnar Research Centre) and further afield within the University such as the Structural Genomics Consortium, Oxford Neurosciences and Oxford Centre for Diabetes, Endocrinology and Metabolism. We have strong links with teams at the MRC Unit at Harwell, complementing the pre-clinical side of our programme.
How has the move to Oxford helped the Centre?
Although it was a challenge applying for this grant when we were still in London our integration into Oxford has been greatly facilitated by the grant and we have already set up several collaborative projects across the Centre. We are also very fortunate to be in a stunning new building on the Old Road Campus within a five minute walk of the Botnar and Nuffield Orthopaedic Centre. The proximity of the institute to the clinical rheumatology and orthopaedic interface will enable us to create a seamless transition from basic science discovery through preclinical models to patient benefit. The conduits that the Centre has created is already allowing this to occur, for instance in the development of new patient cohorts and acquisition of perioperative tissues.
Where do you see your research heading in the next ten years? And what are the challenges you face in getting there?
There has been a phenomenal paradigm shift in OA pathogenesis in recent years; once considered an ‘untreatable’ ‘inevitable disease of ageing’, we now know that this is an active protease-driven disease, where the pathways that drive the proteases are being triggered by abnormal mechanical stress. This means that, at the very least, we should be able to arrest disease in a given individual. But can we go further than this? Another dogma that pervades the OA community is that cartilage, once damaged, is incapable of repair. Old epidemiological data as well as small prospective studies on focal cartilage lesions have suggested that cartilage does repair itself in some individuals. Furthermore, recent clinical trials where the joint has been off-loaded show that established joint damage in OA patients is indeed reversible. We believe that harnessing the pathways that drive this response represents a good future therapeutic strategy in patients.
Perhaps our greatest challenge of all is education. We need to persuade our colleagues and healthcare providers that medical treatments are realisable in this condition. We need to persuade funding bodies that it is worth continuing to invest in basic research in this area. Finally, we need to empower patients with the knowledge that theirs is not a forgotten disease.