Osteoblast/osteocyte-specific inactivation of Stat3 decreases load-driven bone formation and accumulates reactive oxygen species

► Specific knockout of Stat3 in osteoblast/ostecyte leads to a lower bone mass and mechanical properties. ► Stat3 deficiency suppresses loading induced bone formation. ► Stat3 deficiency inhibits mitochondrial function and causes Reactive Oxidative Species (ROS) accumulation in calvarial osteoblasts. ► Fluid shear stress may enhance mitochondrial function, but fails to do so in Stat3 deficient calvarial osteoblasts.