Raymond Purves Bone & Joint Research Laboratory

It has long been known that individuals with OA have a nearly 2-fold greater risk of CVD. This connection has been associated with shared risk factors (ageing, obesity) and OA, reducing physical activity. Our novel research, funded by an NHMRC Ideas Grant (2024-26) and the Hillcrest Foundation through Perpetual Philanthropies (2021-22 & 26-28), is defining a new pathway where molecules released from injured and diseased OA joint tissues enter the blood and directly damage heart cells. Identifying these factors and defining how they injure and affect heart cells, will open new avenues to diagnose and manage CVD risk.  

Despite active injury prevention programs Australia leads the world in rising rates of ACL ruptures. Our research has revealed that this increasing burden reflects two key limiting factors: unresolved biological risk whereby prior mild/non-rupture knee injuries cause a progressive remodelling of the ACL, silently eroding tissue strength until failure occurs during normal activity;absence of widely accessible prognostic toolsto identify individuals with silent, load-induced ACL weakening and elevated rupture risk who would benefit from targeted injury-prevention efforts. In studies funded by the Hillcrest Foundation (2023-25), Arthritis Australia (2024) and Sydney Musculoskeletal Health (2026), we are defining the sex-specific biological tissue changes driving load-induced ACL weakening. We aim to translate mechanistic insights into real-world solutions by defining blood-based biomarkers to identify individuals whose ACLs are on a trajectory toward rupture; and with colleagues in Melbourne develop enhanced quantitative measures of ACL loads in people to enable detection of injury-inducing events. This work will critically advance ACL injury prevention by enabling the right individuals to be targeted at the right time.

Progressive joint breakdown and chronic pain following joint injury is known as post-traumatic osteoarthritis (ptOA). Current treatments including surgery and bracing can restore joint biomechanics and return individuals to activity, but they fail to prevent long-term consequences with ~50% of individuals developing ptOA within 15 years irrespective of intervention. Our research funded by NHMRC (2013-17), Arthritis Australia (2015) and the Hillcrest Foundation (2019-20 & 22-23), has identified specific inflammatory and immune cell responses that occur in the joint acutely after ptOA-inducing but not non-OA-inducing knee injuries. Critically, inhibiting these immune cell changes just in the immediate 3-5 day peri-injury period modifies long-term joint inflammation and most importantly ptOA joint pathology. We are now defining the optimal therapeutic agent(s) and treatment window for joint immune reprogramming by repurposing already available immune-therapeutics to enable rapid clinical implementation. Targeting the rising prevalence of knee ptOA in a younger active population is a critical research priority to prevent lifelong disability. Our research program will shift clinical practice from ptOA management towards ptOA prevention.