“…ACL rupture initiates a sequence of events involving persistent inflammation and altered walking biomechanics [ 6 , 7 ], which significantly contributes to the onset and progression of post-traumatic OA [ 8 , 9 ] Extensive evidence indicates ACL injury triggers an initial inflammatory response associated with poor patient-reported outcomes at 2-year follow-up [ 10 , 11 ] Subsequent ACLR then reinitiates this inflammatory response leading to elevated inflammatory biomarkers (i.e., IL-1β, IL-6, IFNγ) persisting ≥5 year post-operatively [ 12 , 13 ] Moreover, the presence of effusion-synovitis, an imaging marker of inflammation, is frequently detected on magnetic resonance imaging (MRI) at 3 and 6 months post-ACLR, and this finding relates to degenerative joint changes by 2 years after surgery [ 14 , 15 ] Concurrently, altered walking biomechanics, including vertical ground reaction force peak magnitude (vGRF)and loading rate (vGRF-LR), are pervasive post-ACLR and by modifying knee joint loads are considered instrumental in development of OA [ 6 , 16 ] Beyond their individual significance, there seems to be an intricate interplay between walking biomechanics and inflammation that could be pivotal in determining an individual’s susceptibility to developing OA [ 8 , 9 ] Specifically, using real-time gait biofeedback in participants post-ACLR to change their vGRF during walking will alter the levels of pro-inflammatory biomarkers and enzymes that break down cartilage [ 17 ], thus escalating the risk of chronic inflammation and joint damage [ 18 , 19 ] However, the exact nature of the interaction between biomechanics and chronic inflammation following ACLR remains unclear.…”