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Osteoarthritis (OA) is a common, painful disease. Currently OA is incurable, and its etiology largely unknown, partly due to limited understanding of OA as a whole-joint disease. Here we report that two homologous microRNAs,  miR-204  and  miR-211 , maintain joint homeostasis to suppress OA pathogenesis. Specific knockout of  miR-204/-211  in mesenchymal progenitor cells (MPCs) results in Runx2 accumulation in multi-type joint cells, causing whole-joint degeneration. Specifically,  miR-204/-211  loss-of-function induces matrix-degrading proteases in articular chondrocytes and synoviocytes, stimulating articular cartilage destruction. Moreover,  miR-204 / -211  ablation enhances NGF expression in a Runx2-dependent manner, and thus hyper-activates Akt signaling and MPC proliferation, underlying multiplex non-cartilaginous OA conditions including synovial hyperplasia, osteophyte outgrowth and subchondral sclerosis. Importantly,  miR-204 /- 211 -deficiency-induced OA is largely rescued by Runx2 insufficiency, confirming the  miR-204 /- 211- Runx2 axis. Further, intraarticular administration of  miR-204 -expressing adeno-associated virus significantly decelerates OA progression. Collectively,  miR-204 / -211  are essential in maintaining healthy homeostasis of mesenchymal joint cells to counteract OA pathogenesis.

The microRNAs miR-204 and miR-211 maintain joint homeostasis and protect against osteoarthritis progression