The DOI matches its Crossref record; 75 of the 75 references it cites were found in a registry or an index.
What old means to bone
Open accessAbstract
The adverse effects of aging of other organs (ovaries at menopause) on the skeleton are well known, but ironically little is known of skeletal aging itself. Evidence indicates that age-related changes, such as oxidative stress, are fundamental mechanisms of the decline of bone mass and strength. Unlike the short-lived osteoclasts and osteoblasts, osteocytes--former osteoblasts entombed in the mineralized matrix--live as long as 50 years, and their death is dependent on skeletal age. Osteocyte death is a major contributor to the decline of bone strength with age, and the likely mechanisms are oxidative stress, autophagy failure and nuclear pore "leakiness". Unraveling these mechanisms should improve understanding of the age-related increase in fractures and suggest novel targets for its prevention.
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“Between 60% and 80% of osteoblasts at resorption lacunae die via apoptosis.282”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [282]
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Cites
Manolagas, S. C. (2000) · Endocrine Reviews · doi:10.1210/edrv.21.2.0395 · Cited by 2,639
Self-citationSacchetti, B., Funari, A., Michienzi, S., Di Cesare, S., Piersanti, S., Saggio, I., Tagliafico, E., Ferrari, S., Robey, P. G., Riminucci, M., et al. (2007) · Cell · doi:10.1016/j.cell.2007.08.025 · Cited by 2,226
Klotzbuecher, C. M., Ross, P. D., Landsman, P. B., Abbott, T. A., & Berger, M. L. (2000) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2000.15.4.721 · Cited by 2,012
Sex Steroids and the Construction and Conservation of the Adult Skeleton
Riggs, B. L., Khosla, S., & Melton, L. J. (2002) · Endocrine Reviews · doi:10.1210/edrv.23.3.0465 · Cited by 1,846
Weinstein, R. S., Jilka, R. L., Parfitt, A. M., & Manolagas, S. C. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2799 · Cited by 1,753
Self-citation(2019) · Elsevier eBooks · doi:10.1016/c2015-1-01622-2 · Cited by 1,690
Manolagas, S. C. (2000) · Endocrine Reviews · doi:10.1210/er.21.2.115 · Cited by 1,318
Self-citationUse of Inhaled Corticosteroids and Risk of Fractures
van Staa, T. P., Leufkens, H. G. M., & Cooper, C. C. (2001) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2001.16.3.581 · Cited by 1,297
Use of oral corticosteroids and risk of fractures
Van Staa, T. P., Leufkens, H. G. M., Abenhaim, L., Zhang, B., & Cooper, C. (2000) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2000.15.6.993 · Cited by 1,263
Manolagas, S. C. (2010) · Endocrine Reviews · doi:10.1210/er.2009-0024 · Cited by 1,234
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- Parfitt, A.M. et al. (1987) Increased bone age: mechanisms and consequences. In Osteoporosis (Christianson, C. et al., eds), pp. 301-308, Osteopress ApS
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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-citationThe role of estrogen and androgen receptors in bone health and disease
Manolagas, S. C., O’Brien, C. A., & Almeida, M. (2013) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2013.179 · Cited by 598
Self-citationBoskey, A. L., & Coleman, R. M. (2010) · Journal of Dental Research · doi:10.1177/0022034510377791 · Cited by 599
“It has been noted that osteocyte apoptosis increases with tissue age, which contributes to bone weakening independent of BMD through at least two mechanisms: (i) the formation of areas of micropetrosis due to mineralization of empty lacunae; and (ii) disruption of the canalicular system, thereby decreasing repair of m…”
BackgroundInfluentialFernández, M., Abbah, S. A., McNamara, L. M., Zeugolis, D. I., Pandit, A. S., & Biggs, M. J. P. (2014) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2014.09.005 · Cited by 524
Crockett, J. C., Rogers, M. J., Coxon, F. P., Hocking, L. J., & Helfrich, M. (2011) · Journal of Cell Science · doi:10.1242/jcs.063032 · Cited by 532
“Osteocyte death (as evidenced by the presence of empty osteocyte lacunae) is increased after oestrogen withdrawal, unloading of bone and during ageing (Manolagas and Parfitt, 2010), conditions that are associated with lower bone mass due to increased remodelling.”
Background
Metadata
- Authors
- Manolagas, S. C., & Parfitt, A. M.
- Affiliations
- Central Arkansas Veterans Healthcare System (US)
- Corresponding author
- Manolagas, Stavros C.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 21
- Issue
- 6
- Pages
- 369-374
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC2880220
- OpenAlex
- W2088789328
- Cited by
- 404
- References
- 74
- Citations by year
- 2026: 11 · 2025: 17 · 2024: 20 · 2023: 30 · 2022: 25 · 2021: 30 · 2020: 30 · 2019: 39 · 2018: 32 · 2017: 30 · 2016: 24 · 2015: 25 · 2014: 25 · 2013: 23 · 2012: 17
- FWCI
- 1.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs
- University of Arkansas for Medical Sciences
- National Institutes of Health (P01 AG13918)
- 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
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Alkaline Phosphatase Research Studies
- Keywords
- skeletal aging, osteocyte death, oxidative stress, bone loss, bone strength, osteoblasts, osteoclasts, menopause
- MeSH terms
- Aging, Animals, Bone and Bones, Bone Diseases, Humans, Menopause, Osteocytes, Cell Death
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