The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
Osteocyte control of osteoclastogenesis
Open accessAbstract
Multiple lines of evidence support the idea that osteocytes act as mechanosenors in bone and that they control bone formation, in part, by expressing the Wnt antagonist sclerostin. However, the role of osteocytes in the control of bone resorption has been less clear. Recent studies have demonstrated that osteocytes are the major source of the cytokine RANKL involved in osteoclast formation in cancellous bone. The goal of this review is to discuss these and other studies that reveal mechanisms whereby osteocytes control osteoclast formation and thus bone resorption.
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Cites
Osteoclast differentiation and activation
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“Although both cytokines are essential for osteoclastogenesis, M-CSF is primarily involved in stimulating the replication of osteoclast progenitors while RANKL is responsible for stimulating their differentiation [12].”
BackgroundOPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph node organogenesis.
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Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems
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Mechanical Stimulation of Bone in Vivo Reduces Osteocyte Expression of Sost/Sclerostin
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Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST)
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Autoamplification of NFATc1 expression determines its essential role in bone homeostasis
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Self-citationRole of RANK ligand in mediating increased bone resorption in early postmenopausal women
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“Studies in estrogen-deficient women demonstrated that RANKL abundance is increased on the surface of bone marrow lymphocytes and stromal cells, compared to estrogen-replete women [75].”
BackgroundIdentification of a 52 kb deletion downstream of the SOST gene in patients with van Buchem disease
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Osteocyte Apoptosis Controls Activation of Intracortical Resorption in Response to Bone Fatigue
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MLO-Y4 Osteocyte-Like Cells Support Osteoclast Formation and Activation
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“They demonstrated that osteocyte apoptosis localizes to areas containing fatigue damage whereas expression of factors that support focal bone resorption, such as RANKL and VEGF, is elevated in osteocytes surrounding the apoptotic osteocytes [83].”
BackgroundOsteocyte apoptosis and control of bone resorption following ovariectomy in mice
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Cited by
Estrogens and androgens in skeletal physiology and pathophysiology
Almeida, M., Laurent, M. R., Dubois, V., Claessens, F., O'Brien, C. A., Bouillon, R., Vanderschueren, D., & Manolagas, S. C. (2017) · Physiological Reviews · doi:10.1152/physrev.00033.2015 · Cited by 860
Self-citationAgidigbi, T. S., & Kim, C. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20143576 · Cited by 511
The Regulation of Bone Metabolism and Disorders by Wnt Signaling
Maeda, K., Kobayashi, Y., Koide, M., Uehara, S., Okamoto, M., Ishihara, A., Kayama, T., Saito, M., & Marumo, K. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20225525 · Cited by 353
p38 MAPK Signaling in Osteoblast Differentiation
Rodríguez-Carballo, E., Gámez, B., & Ventura, F. (2016) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2016.00040 · Cited by 316
Macrophages and bone inflammation
Gu, Q., Yang, H., & Shi, Q. (2017) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2017.05.002 · Cited by 221
Metadata
- Authors
- O'Brien, C. A., Nakashima, T., & Takayanagi, H.
- Venue
- Bone
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 54
- Issue
- 2
- Pages
- 258-263
- ISSN
- 1873-2763 (ISSN-L)
- 8756-3282
- OpenAlex
- W2159180461
- Cited by
- 235
- References
- 22
- FWCI
- 6.74
- Type
- journal article
- Language
- en
- Open access
- green
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