Vincent Group | Molecular Pathogenesis of Osteoarthritis

Kennedy

Our research focuses on all aspects of osteoarthritis, from understanding its causes to developing new treatments for the condition to improve people's quality of life.

Osteoarthritis (OA) is the most prevalent joint disease yet it is still very poorly understood.

Although once considered a disease of attrition of the articular surfaces, data that have emerged over the past few years have identified articular cartilage breakdown by two important pathogenic proteases – Adamts5 and Mmp13.

In mice, we have demonstrated that induction of proteases is highly mechanosensitive as disease can be prevented, and proteases suppressed, if the joint is immobilised after disease is induced (by surgical joint destabilisation).

The cells of the joint use a variety of methods by which they sense and respond to mechanical disruption. Some of these methods involve release of growth factors that are stored in the pericellular matrix of cartilage and are released in response to mechanical injury. These growth factors include FGF2, TGFb and connective tissue growth factor (CTGF). Their release does not drive protease induction but more likely drives beneficial responses within the damaged tissue perhaps attempting to drive cartilage regeneration and repair.

The mechanosensitive pathway(s) that drive pathogenic responses in the joint are currently unknown and their identification is paramount.

OA Centre

The OA Centre was created in 2013 with substantial funding from Versus Arthritis, University of Oxford and Kennedy Trust for Rheumatology Research (KTRR). A further five years funding was awarded in 2018. The Centre has strong links with Arthritis Research UK Centre for Sports, Exercise and OA, and other Centres around the UK.

Our team

Tonia Vincent

Professor of Musculoskeletal Biology & Honorary rheumatologist
Jadwiga Zarebska

Senior Postdoctoral Scientist
Linyi Zhu

Senior Postdoctoral Researcher
Thomas Perry

Senior Postdoctoral Researcher in the Molecular Pathogenesis of Knee Osteoarthritis
Vicky Batchelor

Research Assistant
Nicholas Groth Merrild

Postdoctoral Researcher in the Molecular Pathogenesis of Osteoarthritis
Ida Parisi

Lab Manager (Histology Facility)
Jennifer Williams

Senior Clinical Research Manager
Urszula Sleczka

MB DPhil student

PRINCIPAL INVESTIGATOR

Tonia Vincent

Professor of Musculoskeletal Biology & Honorary rheumatologist

RESEARCH QUESTIONS

Can chondroprotective pathways in cartilage be harnessed to improve disease in patients with established OA?
Why does pain develop in OA; what are the key pathways and in which tissues does it originate?
What is the mechanism by which molecules bound into the pericellular matrix are released upon mechanical loading/injury and is this modulated in age and disease?
Can articular cartilage repair and what are the pathways that drive this?
Can the early injury response in the joint help us to predict which patients will develop OA following joint injury?
Can we develop novel biomarkers of superficial cartilage injury in early disease that could be used in individuals with subclinical disease?