Table 1.

Evidence in favour of targeting inflammation in osteoarthritis

Human and preclinical animal model data consistently shows upregulation and activation of inflammatory and immune pathways in the joint and systemically. Data from selective preclinical in vitro and in vivo models confirm that genetically or pharmacologically inhibiting specific inflammatory cytokines and immune cells can reduce structural and/or symptomatic OA. High priority, and potentially joint-tissue and OA-phenotype specific inflammatory pathways identified from unbiased genome-wide human OA expression studies. Many efficacious therapeutics already developed, approved and in clinical use in other diseases, could be repurposed for specific OA phenotypes. Treating systemically with an inhibitor of IL1β (canakinumab) shows disease modification in patients with a systemic inflammatory phenotype.