Osteocyte
Osteocyte | |
---|---|
Details | |
Location | Bone |
Identifiers | |
Latin | osteocytus |
MeSH | D010011 |
TH | H2.00.03.7.00003 |
FMA | 66779 |
Anatomical terms of microanatomy |
An osteocyte, an oblate shaped type of
In mature bones, osteocytes and their processes reside inside spaces called
Although osteocytes have reduced synthetic activity and (like osteoblasts) are not capable of mitotic division, they are actively involved in the routine turnover of bony matrix, through various mechanosensory mechanisms. They destroy bone through a rapid, transient (relative to
Structure
Osteocytes have a stellate shape, approximately 7 micrometers deep and wide by 15 micrometers in length.[3] The cell body varies in size from 5–20 micrometers in diameter and contain 40–60 cell processes per cell,[4] with a cell to cell distance between 20–30 micrometers.[3] A mature osteocyte contains a single nucleus that is located toward the vascular side and has one or two nucleoli and a membrane.[5] The cell also exhibits a reduced size endoplasmic reticulum, Golgi apparatus and mitochondria, and cell processes that radiate largely towards the bone surfaces in circumferential lamellae, or towards a haversian canal and outer cement line typical of osteons in concentric lamellar bone.[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.[6]
Development
The fossil record shows that osteocytes were present in bones of jawless fish 400 to 250 million years ago.[7] Osteocyte size has been shown to covary with genome size; and this relationship has been used in paleogenomic research.[8]
During bone formation, an
Palumbo et al. (1990) distinguish three cell types from osteoblast to mature osteocyte: type I preosteocyte (osteoblastic osteocyte), type II preosteocyte (osteoid osteocyte), and type III preosteocyte (partially surrounded by mineral matrix).[10] 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.[11] The transformation from motile osteoblast to entrapped osteocyte takes about three days, and during this time, the cell produces a volume of extracellular matrix three times its own cellular volume, which results in 70% volume reduction in the mature osteocyte cell body compared to the original osteoblast volume.[12] The cell undergoes a dramatic transformation from a polygonal shape to a cell that extends dendrites toward the mineralizing front, followed by dendrites that extend to either the vascular space or bone surface.[11] As the osteoblast transitions to an osteocyte, alkaline phosphatase is reduced, and casein kinase II is elevated, as is osteocalcin.[11]
Osteocytes appear to be enriched in proteins that are resistant to hypoxia, which appears to be due to their embedded location and restricted oxygen supply.[13] Oxygen tension may regulate the differentiation of osteoblasts into osteocytes, and osteocyte hypoxia may play a role in disuse-mediated bone resorption.[13]
Function
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.[6] They are the most common cell type in bone (31,900 per cubic millimeter in bovine bone to 93,200 per cubic millimeter in rat bone).[6] Most of the receptor activities that play an important role in bone function are present in the mature osteocyte.[6]
Osteocytes are an important regulator of bone mass.[14][15] Osteocytes contain glutamate transporters that produce nerve growth factors after bone fracture, evidence of a sensing and information transfer system.[6] When osteocytes were experimentally destroyed, the bones showed a significant increase in bone resorption, decreased bone formation, trabecular bone loss, and loss of response to unloading.[6]
Osteocytes are mechanosensor cells that control the activity of
Osteocytes are also a key endocrine regulator in the metabolism of minerals such as phosphates.
Sclerostin
Osteocytes synthesize sclerostin, a secreted protein that inhibits bone formation by binding to LRP5/LRP6 coreceptors and blunting Wnt signaling.[15][7] Sclerostin, the product of the SOST gene, is the first mediator of communication between osteocytes, bone forming osteoblasts and bone resorbing osteoclasts, critical for bone remodeling.[19] Only osteocytes express sclerostin, which acts in a paracrine fashion to inhibit bone formation.[19] Sclerostin is inhibited by parathyroid hormone (PTH) and mechanical loading.[19] Sclerostin antagonizes the activity of BMP (bone morphogenetic protein), a cytokine that induces bone and cartilage formation.[16]
Pathophysiology
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.[20]
Clinical significance
Clinically important research of gel based in vitro 3D model for the osteocytic potentiality of human CD34+ stem cells has been described. 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.[21] Osteocytes die as a consequence of senescence, degeneration/necrosis, apoptosis (programmed cell death), and/or osteoclastic engulfment.[1] The percentage of dead osteocytes in bone increases with age from less than 1% at birth to 75% after age 80.[22] Osteocyte apoptosis is thought to be related to decreased mechanotransduction, which possibly leads to the development of osteoporosis.[23] Apoptotic osteocytes release apoptotic bodies expressing RANKL to recruit osteoclasts.[11]
Mechanical loading increases osteocyte viability in vitro, and contributes to solute transport through the lacuno-canalicular system in bone, which enhances oxygen and nutrient exchange and diffusion to osteocytes.
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.[24] 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.[11][25] Oxygen deprivation that occurs as the result of immobilization (bed rest), glucocorticoid treatment, and withdrawal of oxygen have all been shown to promote osteocyte apoptosis.[11] It is now recognized that osteocytes respond in a variety of ways to the presence of implant biomaterials.[26]
See also
- List of human cell types derived from the germ layers
- List of distinct cell types in the adult human body
References
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- ^ PMID 32040934. Retrieved 8 March 2022.
- ^ a b ran Bezooijen Rl, Ran; Papapoulos, SE; Hamdy, NA; ten Dijke, P; Lowik, C (2005). "Control of Bone Formation by Osteocytes". BoneKEy-Osteovision. 2 (12): 33–38.
- PMID 1419377.
- ^ "Soft and weak bones? Have you heard of X-linked hypophosphatemia (XLH)? Learn more about this disease and its symptoms". XLHLink. Retrieved 9 March 2022.
- ^ doi:10.1138/20070272.
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External links
- Histology image: 02003loa – Histology Learning System at Boston University – "Cartilage and Bone and Bone Histogenesis: cells of* Histology image: 02705loa – Histology Learning System at Boston University – "Cartilage and Bone and Bone Histogenesis: compact bone"* =D Histology at ou.edu