In mature bones, osteocytes and their processes reside inside spaces called lacunae (Latin for a pit) and canaliculi, respectively.

They are networked to each other via long cytoplasmic extensions that occupy tiny canals called canaliculi, which are used for exchange of nutrients and waste through gap junctions.

[5] Osteocytes form an extensive lacunocanalicular network within the mineralized collagen type I matrix, with cell bodies residing within lacunae, and cell/dendritic processes within channels called canaliculi.

[9] Although recently it was shown that vascular smooth muscle cells drive osteocyte differentiation [10], most aspects of osteocytogenesis remain largely unknown.

[11] The embedded "osteoid-osteocyte" must do two functions simultaneously: regulate mineralization and form connective dendritic processes, which requires cleavage of collagen and other matrix molecules.

[14] Although osteocytes are relatively inert cells, they are capable of molecular synthesis and modification, as well as transmission of signals over long distances, in a way similar to the nervous system.

[15][16] Osteocytes contain glutamate transporters that produce nerve growth factors after bone fracture, evidence of a sensing and information transfer system.

[6] Osteocytes are mechanosensor cells that control the activity of osteoblasts and osteoclasts[16] within a basic multicellular unit (BMU), a temporary anatomic structure where bone remodeling occurs.

[17] Osteocytes generate an inhibitory signal that is passed through their cell processes to osteoblasts for recruitment to enable bone formation.

[15] Osteocyte-specific proteins such as sclerostin have been shown to function in mineral metabolism, as well as other molecules such as PHEX, DMP-1, MEPE, and FGF-23, which are highly expressed by osteocytes and regulate phosphate and biomineralization.

[15][19][16][14] Osteocytes synthesize sclerostin, a secreted protein that inhibits bone formation by binding to LRP5/LRP6 coreceptors and blunting Wnt signaling.

The results confirm that the human CD34+ stem cells possess unique osteogenic differentiation potential and can be used in the early regeneration of injured bone.

[24] Mechanical stimulation of osteocytes results in opening of hemichannels to release PGE2 and ATP, among other biochemical signaling molecules, which play a crucial role in maintaining the balance between bone formation and resorption.

[25] Osteocyte cell death can occur in association with pathologic conditions such as osteoporosis and osteoarthritis, which leads to increased skeletal fragility, linked to the loss of ability to sense microdamage and/or signal repair.