Abstract
Purpose: As a multifactorial disease, Osteoarthritis (OA) has many associated risk factors. One of which, joint trauma, is the primary cause for approximately 12% of all OA cases. This accelerated form of OA, termed Post-traumatic, or secondary Osteoarthritis (PTOA), is caused by one or more injurious, high impact loading events which result in chondrocyte cell death and a ‘phenotypic shift’ in residual cartilage cells toward a more catabolic state. Conversely, cyclic loading within the physiological range has been shown to have beneficial effects on joint health with longitudinal patient studies demonstrating that a lack of rhythmic mechanical stimulation of the joint can result in cartilage atrophy/thinning (Vanwanseele et al., 2008). Recent in vivo data has also indicated the potential benefit of post-injury cyclic loading. Mice subjected to a daily sinusoidal loading regime following destabilisation of the medial meniscus developed OA slower than their sham counterparts (Holyoak et al., 2019). The diverse and contrasting effects of mechanical stimulation on cartilage tissue health has directed us to investigate the cellular mechanisms responsible for driving the chondrocyte response to both physiological and pathological loading with the aim of identifying potential therapeutic targets in the future.