Apoptotic Osteocytes and the Control of Targeted Bone Resorption
Open accessAbstract
Studies from the 1950s and 1960s already recognize the fact that osteocytes, although long living cells, die, as evidenced by accumulation of osteocytic lacunae devoid of cells. More recently, it was demonstrated that these cells die by apoptosis. The rate of osteocyte apoptosis is regulated by the age of the bone, as well as by systemic hormones, local growth factors, cytokines, pharmacological agents, and mechanical forces. Apoptotic osteocytes, in turn, recruit osteoclasts to initiate targeted bone resorption. This results in the removal of "dead" bone and may improve the mechanical properties of the skeleton. However, the molecular regulators of osteocyte survival and targeted bone remodeling are not completely known. In this review, the current knowledge on the molecular mechanism that lead to osteocyte death or survival, and the signals that mediate targeted bone resorption is discussed.
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Osteocyte apoptosis has been recognized as a chemotactic signal to osteoclastic bone resorption.
“Moreover, osteocyte apoptosis has been recognized as a chemotactic signal to osteoclastic bone resorption [70–73].”
From Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells (2015) · cites this paper as [72]
HMGB1 and M-CSF have been suggested to be produced by osteocytes that stimulate osteoclast recruitment during bone remodeling.
“High mobility group box protein 1 (HMGB1) [198–200] and M-CSF [201] have also been suggested to be produced by osteocytes that stimulate osteoclast recruitment during bone remodeling [72, 73].”
From Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells (2015) · cites this paper as [72]
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- Authors
- Plotkin, L. I.
- Affiliations
- Indiana University School of Medicine (US)
- Corresponding author
- Plotkin, Lilian I.
- ORCID
- Plotkin, Lilian I.
- Venue
- Current Osteoporosis Reports
- Published
- 2014-01-28
- Volume
- 12
- Issue
- 1
- Pages
- 121-126
- ISSN
- 1544-1873 (ISSN-L)
- 1544-2241
- PMC
- PMC3952244
- OpenAlex
- W2007571035
- Cited by
- 93
- References
- 65
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 10 · 2023: 14 · 2022: 4 · 2021: 6 · 2020: 7 · 2019: 9 · 2018: 9 · 2017: 11 · 2016: 6 · 2015: 4 · 2014: 2
- FWCI
- 0.72
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Osteoporosis Reports (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Purdue University Indianapolis (Indiana University) (submittedVersion)
- PMC
- Funders
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR053643, R01AR067210)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- osteocyte apoptosis, osteocyte survival, osteoclast recruitment, bone remodeling, osteocyte death, bone age, growth factors, cytokines, mechanical loading, osteoporosis
- MeSH terms
- Bone Resorption, Humans, Osteocytes, Signal Transduction, Bone Remodeling, Apoptosis
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