Ultrastructural, biochemical, and behavioral assessments reveal that the Crtap^-/- mouse model of severe, recessive Osteogenesis Imperfecta presents with defects in tendon structure and strength that correlate with severe motor deficits.

Under metabolic syndrome, joint subchondral preosteoclasts acquire a senescence-associated secretome, which causes a rapid structural alteration of subchondral bone and contributes to the development of osteoarthritis.

The method presented here allows researchers to retrieve accurate and reproducible biomechanical properties of mouse cartilage.

Low expression of Cbfb may be the cause of osteoarthritis, and local admission of Cbfb may rescue and protect against osteoarthritis through decreasing Wnt/β-catenin signaling, and increasing Hippo/Yap signaling and Tgfβ/Smad2/3 signaling in osteoarthritis articular cartilage.