The DOI matches its Crossref record; 37 of the 39 references it cites were found in a registry or an index.
The effects of androgen deficiency on murine bone remodeling and bone mineral density are mediated via cells of the osteoblastic lineage.
Abstract
Both estrogens and androgens act on bone marrow stromal/osteoblastic cells to inhibit the production of local factors that promote osteoclast development. Based on this and the evidence that loss of sex steroids up-regulates not only osteoclastogenesis but also osteoblastogenesis, we have hypothesized that cells of the osteoblastic lineage are the mediators of the adverse effects of sex steroid deficiency on bone. To test this hypothesis, we used the senescence-accelerated mouse (SAMP6), a model of defective osteoblast development, and examined the effects of orchidectomy on static and dynamic histological features of bone remodeling and on bone mineral density. After orchidectomy in SAMP6 mice, the expected increases in osteoblast precursors, cancellous osteoclasts and osteoblasts, frequency of remodeling events, trabecular spacing, and rate of bone formation were absent or greatly attenuated. Moreover, whereas bone mineral density decreased in orchidectomized controls, it did not change in SAMP6. Our data indicate that when osteoblast development is defective, orchidectomy fails to result in bone loss. This evidence suggests that cells of the osteoblastic lineage are essential mediators of the changes in the rate of bone remodeling and loss of bone mass that ensue following loss of androgens.
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“Preclinical orchiectomy (ORX) models have utility in examining the consequences of androgen ablation and androgen deprivation therapy on bone (210 -212).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [212]
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Self-citationManolagas, S. C., & Jilka, R. L. (1995) · New England Journal of Medicine · doi:10.1056/nejm199502023320506 · Cited by 1,670
Self-citationIncreased Osteoclast Development After Estrogen Loss: Mediation by Interleukin-6
Jilka, R. L., Hangoc, G., Girasole, G., Passeri, G., Williams, D. C., Abrams, J. S., Boyce, B. F., Broxmeyer, H. E., & Manolagas, S. C. (1992) · Science · doi:10.1126/science.1621100 · Cited by 1,440
Self-citationEstrogen promotes apoptosis of murine osteoclasts mediated by TGF–β
Hughes, D. E., Dai, A., Tiffee, J. C., Li, H. H., Mundy, G. R., & Boyce, B. F. (1996) · Nature Medicine · doi:10.1038/nm1096-1132 · Cited by 813 · cited 1×
“Alternatively, sex steroid deficiency, which is known to delay apoptosis of osteoclasts (44), may not have such an antiapoptotic effect on osteoblasts, thereby creating an imbalance in bone turnover.”
Girasole, G., Jilka, R. L., Passeri, G., Boswell, S. H., Boder, G. B., Williams, D. C., & Manolagas, S. C. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115668 · Cited by 677
Self-citationTemporal relationship between bone loss and increased bone turnover in ovariectomized rats
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Self-citationIsolation and characterization of osteoblast precursor cells from human bone marrow
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Manolagas, S. C. (2000) · Endocrine Reviews · doi:10.1210/edrv.21.2.0395 · Cited by 2,639
Self-citationWeinstein, 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-citationIncreased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
Jilka, R. L., Weinstein, R. S., Bellido, T., Roberson, P. K., PARFITT, A. M., & Manolagas, S. C. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6610 · Cited by 1,042
Self-citationPrevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
Plotkin, L. I., Weinstein, R. S., Parfitt, A. M., Roberson, P. K., Manolagas, S. C., & Bellido, T. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6800 · Cited by 890
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Metadata
- Authors
- Weinstein, R. S., Jilka, R. L., Parfitt, A. M., & Manolagas, S. C.
- Affiliations
- University of Arkansas for Medical Sciences (US)
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1997-09-01
- Volume
- 138
- Issue
- 9
- Pages
- 4013-4021
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W1972472172
- Cited by
- 126
- References
- 39
- Citations by year
- 2026: 1 · 2024: 3 · 2023: 2 · 2022: 1 · 2021: 5 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 5 · 2012: 2
- FWCI
- 4.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institutes of Health
- National Institute on Aging (P01-AG-13918-01, P01AG013918)
- 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 › Endocrinology › Estrogen and related hormone effects
- Keywords
- androgen deficiency, bone remodeling, bone mineral density, osteoblast lineage, osteoblastogenesis, osteoclastogenesis, orchiectomy, sex hormone deficiency, bone loss, trabecular bone, bone formation
- MeSH terms
- Androgens, Animals, Body Weight, Bone Marrow Cells, Cell Count, Male, Mice, Mutant Strains, Orchiectomy, Osteoblasts, Stem Cells, Bone Density, Bone Remodeling, Mice
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