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Molecular mechanisms of glucocorticoid-induced osteoporosis.
Abstract
Bone loss resulting from long-term glucocorticoid therapy is common and clinically relevant. A number of different glucocorticoid-mediated effects are responsible for the reduction in bone density: (i) glucocorticoid-induced direct impairment of osteoblast, osteocyte, and osteoclast function leads to reduced bone remodeling and diminished repair of microdamage in bone; (ii) the effects of parathyroid hormone (PTH) might be more pronounced in the presence of glucocorticoids, whereas vitamin D plays a lesser role in the pathogenesis of steroid-induced osteoporosis; (iii) glucocorticoids antagonize gonadal function and inhibit the osteoanabolic action of sex steroids; and (iv) increased renal elimination and reduced intestinal absorption of calcium lead to a negative calcium balance that has been suggested to promote secondary hyperparathyroidism. From a mechanistic point of view, all of the aforementioned effects have long been considered to be mediated at the molecular level exclusively by genomic actions. However, there is now increasing evidence for the existence of rapid glucocorticoid effects that are incompatible with this classical mode of action. These rapid effects, termed nongenomic effects, are mediated by glucocorticoid interactions with biological membranes, either through binding to membrane receptors or by physicochemical interactions. It is possible, but has yet to be shown, that these effects play a role in the pathogenesis of glucocorticoid-induced osteoporosis.
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“Glucocorticoids also have remarkably complex effects on bone, virtually all of which are detrimental, and these influences have been summarized in recent reviews (241,242).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [242]
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Metadata
- Authors
- Patschan, D., Loddenkemper, K., & Buttgereit, F.
- Affiliations
- Humboldt-Universität zu Berlin (DE)
- Corresponding author
- Buttgereit, F.
- Venue
- Bone
- Publisher
- Elsevier BV
- Published
- 2001-12
- Volume
- 29
- Issue
- 6
- Pages
- 498-505
- ISSN
- 1873-2763 (ISSN-L)
- 8756-3282
- OpenAlex
- W2005326563
- Cited by
- 201
- References
- 80
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 11 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 6 · 2016: 8 · 2015: 9 · 2014: 8 · 2013: 6 · 2012: 6
- FWCI
- 8.19
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Bone (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Keywords
- glucocorticoid-induced osteoporosis, bone loss, bone remodeling, osteoblast activity, osteoclast function, osteocyte function, parathyroid hormone, vitamin D, sex steroids, gonadal function, calcium balance, secondary hyperparathyroidism, glucocorticoid receptor signaling
- MeSH terms
- Calcium, Glucocorticoids, Humans, Intestinal Absorption, Kidney, Osteoblasts, Osteoclasts, Osteoporosis, Parathyroid Hormone, Gonadal Steroid Hormones, Vitamin D
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