Abstract Background Osteocytes form a network through gap junction-coupled cell processes and canaliculi throughout bone; this network extends to the osteoblasts in the bone surface. The osteocyte network is considered to function in mechanosensing and mechanotransduction. However, the lack of suitable animal models makes it difficult to clarify the function of osteocytes. Highlight Any kind of osteocyte death results in necrosis, whereby the intracellular contents, including immunostimulatory molecules, which activate osteoclastogenesis, are released through the canaliculi to the bone surface. This leads to enhanced bone resorption in the damaged region of the bone. Overexpression of Bcl2 in osteoblasts reduces the number of osteoblast processes, resulting in a reduction in the numbers of osteocyte processes and canaliculi. The osteocytes gradually die without enhancement of bone resorption because a severe reduction in the number of canaliculi interrupts the release of intracellular contents to the bone surface. Bcl2 transgenic mice at 4 months of age, in which the osteocyte network is disrupted, are an appropriate mouse model for the evaluation of osteocyte function. These mice show that the osteocyte network enhances bone resorption and inhibits bone formation under physiological conditions, and that these osteocyte functions are augmented under unloaded conditions. Under such conditions, Rankl upregulation in osteoblasts and Sost upregulation in osteocytes are, at least in part, responsible for enhanced bone resorption and suppressed bone formation, respectively. Conclusion Dead osteocytes induce bone resorption, while live osteocytes enhance bone resorption and inhibit bone formation under physiological conditions, while their functions are augmented under unloaded conditions.