Cited by 340Bone Metabolism and DiseasesBone health and osteoporosis researchCell death mechanisms and regulation

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Osteocyte Apoptosis Controls Activation of Intracortical Resorption in Response to Bone Fatigue

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Cardoso, Luis, Herman, Brad C, Verborgt, Olivier, Laudier, Damien, Majeska, Robert J, Schaffler, Mitchell B·2009·Journal of Bone and Mineral Research

DOI 10.1359/jbmr.081210PMC PMC2659511

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Abstract

Osteocyte apoptosis is spatially and temporally linked to bone fatigue-induced microdamage and to subsequent intracortical remodeling. Specifically, osteocytes surrounding fatigue microcracks in bone undergo apoptosis, and those regions containing apoptotic osteocytes co-localize exactly with areas subsequently resorbed by osteoclasts. Here we tested the hypothesis that osteocyte apoptosis is a key controlling step in the activation and/or targeting of osteoclastic resorption after bone fatigue. We carried out in vivo fatigue loading of ulna from 4- to 5-mo-old Sprague-Dawley rats treated with an apoptosis inhibitor (the pan-caspase inhibitor Q-VD-OPh) or with vehicle. Intracortical bone remodeling and osteocyte apoptosis were quantitatively assessed by standard histomorphometric techniques on day 14 after fatigue. Continuous exposure to Q-VD-OPh completely blocked both fatigue-induced apoptosis and the activation of osteoclastic resorption, whereas short-term caspase inhibition during only the first 2 days after fatigue resulted in >50% reductions in both osteocyte apoptosis and bone resorption. These results (1) show that osteocyte apoptosis is necessary to initiate intracortical bone remodeling in response to fatigue microdamage, (2) indicate a possible dose-response relationship between the two processes, and (3) suggest that early apoptotic events after fatigue-induced microdamage may play a substantial role in determining the subsequent course of tissue remodeling.

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Authors: Cardoso, L., Herman, B. C., Verborgt, O., Laudier, D., Majeska, R. J., & Schaffler, M. B.
Affiliations: These authors contributed equally to this study
Icahn School of Medicine at Mount Sinai (US)
AZ Sint-Lucas (BE)
City College of New York (US)
Corresponding author: Schaffler, Mitchell B
ORCID: Verborgt, Olivier
Laudier, Damien
Majeska, Robert J
Schaffler, Mitchell B
Venue: Journal of Bone and Mineral Research
Publisher: Oxford University Press (OUP)
Published: 2009-04-01
Volume: 24
Issue: 4
Pages: 597-605
ISSN: 0884-0431 (ISSN-L)
1523-4681
DOI: 10.1359/jbmr.081210
PMC: PMC2659511
OpenAlex: W2021115829
Cited by: 340
References: 88
Citations by year: 2026: 11 · 2025: 6 · 2024: 11 · 2023: 8 · 2022: 13 · 2021: 23 · 2020: 22 · 2019: 15 · 2018: 18 · 2017: 18 · 2016: 24 · 2015: 26 · 2014: 27 · 2013: 26 · 2012: 28
FWCI: 8.65
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
Locations: Journal of Bone and Mineral Research (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Aeronautics and Space Administration (NASA NCC 9‐58, NCC958)
National Space Biomedical Research Institute (NASA NCC 9‐58, NCC 9‐58)
National Institutes of Health (NCC9-58)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR41210, R01AR041210)
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, bone fatigue, osteoclast resorption, bone microdamage, caspase inhibition, Q-VD-OPh, ulna
MeSH terms: Amino Acid Chloromethyl Ketones, Animals, Bone and Bones, Bone Resorption, Cell Differentiation, Cells, Cultured, Enzyme Inhibitors, Female, Osteoclasts, Osteocytes, Quinolines, Time Factors, Weight-Bearing, Bone Remodeling, Rats, Sprague-Dawley, Apoptosis, Rats, Caspase Inhibitors

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Osteocyte Apoptosis Controls Activation of Intracortical Resorption in Response to Bone Fatigue

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