Maintenance of mitochondrial function and energy homeostasis is essential for mammalian cells to adapt to various stressors throughout their life. It is not clear, however, how osteocytes imprisoned in the mineralised bone matrix maintain their mitochondrial function in response to various pharmacological and mechanical stresses in bone. Here using florescence confocal imaging on both live and fixed cells, we revealed the distribution of dendritic mitochondria in primary osteocytes, and the   dynamic dendritic mitochondria transfer between cultured MLO-Y4 cells. Remarkably, administration of glucocorticoid (GC) significantly impeded the distribution and motility of dendritic mitochondria in osteocytes. Specifically, by using two-dimensional co-culture and established three-dimensional tetraculture system, we showed that functional dendritic mitochondria preferentially transferred into stressed adjacent osteocytes to attenuate the level of accumulated ROS, and recover the level of ATP. In detail, GC stressed ER was accumulated onto mitochondria, and the stress factor MKP1 which induced by GC translocated onto ER-mitochondria contact site to negatively regulate mitochondria function by inducing mitochondrial fission and inhibiting mitochondria membrane potential. Collectively our data demonstrated for the first time that dendritic mitochondrial transfer occurs between osteocytes within their dendritic network to potentially maintain the osteocytes homeostasis, and GC induced MKP1 excessively impeded this processes by regulating ER-mitochondria function.