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Osteocytes are one of the four kinds of bone cells. Due to derivation from osteoblasts, these cells are highly specialized in nature and are responsible for the maintenance of the bony matrix. Specially built with innate proteins that help them to survive in hypoxic conditions, osteocytes maintain biomineralization. Not only do osteocytes contribute to bone mass via controlling osteoblast and osteoclast activity, but these cells act as main players in phosphate metabolism. Osteocytic necrosis is caused due to pathologic conditions such as osteoarthritis and osteoporosis, leading to developing skeletal fragility and dysfunctional signal repair and/or microdamage. Immobilization-induced hypoxia and glucocorticoid treatment may also lead to osteocytic necrosis or apoptosis. Osteocytes react to implant biomaterials in dynamic ways and are currently under active stem-cell research for trauma care and bone remodeling purposes.[1]

Degraded or malfunctioning osteocytes may lead to various pathological conditions, such as hypophosphatemic rickets, sclerosteosis, and necrotic bone. Autosomal recessive hypophosphatemic rickets (ARHR) type 1 happens because of a lack of function mutations in dentin matrix protein 1, a type of noncollagenous bone matrix protein found in osteocytes and pre-osteocytic osteoblasts. This protein contributes to osteocyte proliferation and FGF23 downregulation. ARHR 2 happens because of a lack of function mutations in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1); ENPP1 produces inorganic pyrophosphate (PPi), a crucial calcification inhibitor, and is related to ectopic calcification disorders in some cases. SOST codes for a specific protein known as the 190-residue glycoprotein sclerostin, which is mainly released by osteocytes. Sclerostin is an osteogenesis inhibitor that suppresses the canonical Wnt signaling pathway within osteoblast lineage cells. Sclerostin articulates to Wnt-signaling coreceptors LRP5 and LRP6, blockading Wnt particle articulation to those receptors. Sclerosteosis, caused by a decreased sclerostin expression, results in less restrained osteogenesis, leading to progressive hyperostosis. Sclerostin, therefore, relies on its coreceptor, LRP4. Osteonecrosis refers to the classic pattern of cell death and complex osteogenesis and bone resorption processes. Osteocyte necrosis (ON) initiates with hematopoietic and adipocytic cellular necrosis along with interstitial marrow edema. ON happens after about 2 to 3 hours of anoxia; histological signs of osteocytic necrosis do not display until about 24 to 72 hours after hypoxia. ON is first characterized by pyknosis of nuclei, followed by hollow osteocyte lacunae. Capillary revascularization and reactive hyperemia slightly take place at the periphery of the necrosis site, followed by a repair process combining both bone resorption and production that incompletely changes dead with living bone. Nouveau bone overlays onto dead trabeculae along with fragmentary resorption of dead bone. Bone resorption outperforms formation resulting in a net removal of bone, deformed structural integrity of the subchondral trabeculae, joint incongruity, and subchondral fracture.[10][11][12][13]