Likely due to ignored heterogeneity in disease pathophysiology, osteoarthritis has become the most common disabling joint disease, without effective disease-modifying treatment causing high social and economic burden

Advancements in clinical development are hampered by a lack of tailored biomimetic human preclinical models mimicking different aspects of osteoarthritis pathophysiology

Is it possible to set up personalized human preclinical models of osteoarthritis that mimic different aspects of the osteoarthritic pathophysiology such as inflammation, hypertrophy or mechanical stress?

An inflammatory OA trigger (IL-1β) mainly induced catabolic chondrocyte signalling and cartilage breakdown, mechanical stress at a strain of 65% induced moderate catabolic chondrocyte signalling and changed the cartilage matrix integrity, while T3 initiated expression of hypertrophic and mineralization markers

This demonstrates that it is possible to set up personalized human OA disease models reflecting different relevant aspects (inflammation, hypertrophy and mechanical stress) of osteoarthritic pathophysiology readily applicable in future drug testing