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Review
. 2011 Feb;26(2):229-38.
doi: 10.1002/jbmr.320.

The amazing osteocyte

Lynda F Bonewald  1
Affiliations
Review

The amazing osteocyte

Lynda F Bonewald. J Bone Miner Res. 2011 Feb.

Abstract

The last decade has provided a virtual explosion of data on the molecular biology and function of osteocytes. Far from being the "passive placeholder in bone," this cell has been found to have numerous functions, such as acting as an orchestrator of bone remodeling through regulation of both osteoclast and osteoblast activity and also functioning as an endocrine cell. The osteocyte is a source of soluble factors not only to target cells on the bone surface but also to target distant organs, such as kidney, muscle, and other tissues. This cell plays a role in both phosphate metabolism and calcium availability and can remodel its perilacunar matrix. Osteocytes compose 90% to 95% of all bone cells in adult bone and are the longest lived bone cell, up to decades within their mineralized environment. As we age, these cells die, leaving behind empty lacunae that frequently micropetrose. In aged bone such as osteonecrotic bone, empty lacunae are associated with reduced remodeling. Inflammatory factors such as tumor necrosis factor and glucocorticoids used to treat inflammatory disease induce osteocyte cell death, but by different mechanisms with potentially different outcomes. Therefore, healthy, viable osteocytes are necessary for proper functionality of bone and other organs.

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Figures

Fig. 1
Fig. 1
Expression of markers during osteoblast-to-osteocyte ontogeny. The osteocyte appears to be the descendant of the matrix-producing osteoblast, which is a descendant of the mesenchymal stem cell known to express markers such as Stro1, CD29, CD105, CD166. Matrix-producing osteoblasts express Cbfa1 and Osterix, necessary for osteoblast differentiation, followed by alkaline phosphase and collagen, necessary for the production of osteoid. Osteocalcin is produced by the late osteoblast and continues to be expressed by the osteocyte. By some unknown mechanism, some designated cells begin to embed in osteoid and begin to extend dendritic projections, keeping connections with already embedded cells and cells on the bone surface. Molecules such as E11/gp38 and MT1-MMP appear to play a role in dendrite/canaliculi formation, whereas molecules such as destrin and CapG regulate the cytoskeleton. PHEX, MEPE, and DMP-1 regulate biomineralization and mineral metabolism, and FGF-23 regulates renal phosphate excretion. FGF-23 is elevated not only in osteocytes from hypophosphatemic animals but also in those of normal rats.(112) Sclerostin is a marker of the mature osteocyte and is a negative regulator of bone formation.(45) ORP150 may preserve viability of this cell in a hypoxic environment.(23)
Fig. 2
Fig. 2
Visualization of early, embedding osteocytes. Using anti-E11 immunostaining and visualization of the actin cytoskeleton by alexa488 staining for phalloidin, one can visualize the embedding osteocyte and the early osteocyte in 12-day murine calvaria. The merged image shows that the majority of the E11 is on the cell surface and along the dendritic processes. Also, if one looks closely, the dendrites that end on the cell surface have a bulbous tip of unknown function. This structure must interface with the cells on the bone surface. The image is provided by Dr Sarah Dallas, University of Missouri at Kansas City. The second image is of an acid-etched resin-embedded murine sample showing an osteocyte lacuna sending canaliculi to the bone surface. Note the rough surfaces of canaliculi toward the bone surface and the smooth surface of canaliculi that project away from the bone surface, suggesting a difference between forming and formed canaliculi. Both sets of images demonstrate the complexity of this network and the interface of osteocytes with the bone surface.
Fig. 3
Fig. 3
The Wnt/β-catenin pathway plays an important role in osteocyte function and viability and the maintenance of normal bone. Deletion of β-catenin in osteocytes results in bone with a “moth-eaten appearance.” The calvaria shown are from 14-week-old female control and conditional knockout (cKO) mice in which β-catenin is deleted using a Dmp1-Cre. The long bones from these animals show even greater porosity and fragility, thought to be responsible for death of these transgenic animals at an early age.(34) This bone porosity was due to increased osteoclast number and activity most likely owing to reduced expression of osteoprotegerin and an increase in RANKL, both found to be expressed in osteocytes. These observations support the role of β-catenin in osteocyte viability. The diagram integrates a number of observations regarding how mechanical loading in the form of fluid-flow shear stress regulates osteocyte viability,(40) function.(34) and communication(59) through the Wnt/β-catenin pathway. The unique triggering or crosstalk between prostaglandin and this pathway has been detailed previously.(58)
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References

    1. Recklinghausen FV. Untersuchungen uber Rachitis und Osteomalacia. Jena: Gustav Fischer; 1920.
    1. Belanger LF, Robichon J. Parathormone-induced osteolysis in dogs: a microradiographic and alpharadiographic survey. J Bone Joint Surg Am. 1964;46:1008–1012. - PubMed
    1. Belanger LF. Osteocytic osteolysis. Calcif Tissue Res. 1969;4:1–12. - PubMed
    1. Baylink DJ, Wergedal JE. Bone formation by osteocytes. Am J Physiol. 1971;221:669–678. - PubMed
    1. Pead MJ, Suswillo R, Skerry TM, Vedi S. Lanyon LE. Increased 3H-uridine levels in osteocytes following a. single short period of dynamic bone loading in vivo. Calcif Tissue Int. 1988;43:92–96. - PubMed

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