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Glucocorticoids and Bone: Consequences of Endogenous and Exogenous Excess and Replacement Therapy
Open accessAbstract
Osteoporosis associated with long-term glucocorticoid therapy remains a common and serious bone disease. Additionally, in recent years it has become clear that more subtle states of endogenous glucocorticoid excess may have a major impact on bone health. Adverse effects can be seen with mild systemic glucocorticoid excess, but there is also evidence of tissue-specific regulation of glucocorticoid action within bone as a mechanism of disease. This review article examines (1) the role of endogenous glucocorticoids in normal bone physiology, (2) the skeletal effects of endogenous glucocorticoid excess in the context of endocrine conditions such as Cushing disease/syndrome and autonomous cortisol secretion (subclinical Cushing syndrome), and (3) the actions of therapeutic (exogenous) glucocorticoids on bone. We review the extent to which the effect of glucocorticoids on bone is influenced by variations in tissue metabolizing enzymes and glucocorticoid receptor expression and sensitivity. We consider how the effects of therapeutic glucocorticoids on bone are complicated by the effects of the underlying inflammatory disease being treated. We also examine the impact that glucocorticoid replacement regimens have on bone in the context of primary and secondary adrenal insufficiency. We conclude that even subtle excess of endogenous or moderate doses of therapeutic glucocorticoids are detrimental to bone. However, in patients with inflammatory disorders there is a complex interplay between glucocorticoid treatment and underlying inflammation, with the underlying condition frequently representing the major component underpinning bone damage.
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“the deleterious effects of chronic glucocorticoid excess on bone mineral density leading to osteoporosis are well established (258).”
From Adrenal incidentaloma (2020) · cites this paper as [258]
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Sherlock, M., Scarsbrook, A., Abbas, A., Fraser, S., Limumpornpetch, P., Dineen, R., & Stewart, P. M. (2020) · Endocrine Reviews · doi:10.1210/endrev/bnaa008 · Cited by 347
“Similarly, the deleterious effects of chronic glucocorticoid excess on bone mineral density leading to osteoporosis are well established (258).”
BackgroundMolecular Mechanisms of Glucocorticoid-Induced Insulin Resistance
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Pathophysiology and treatment of osteoporosis: Challenges for clinical practice in older people
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Pathogenic mechanisms of glucocorticoid-induced osteoporosis
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Metadata
- Authors
- Hardy, R. S., Zhou, H., Seibel, M. J., & Cooper, M. S.
- Affiliations
- University of Birmingham (GB)
- Anzac Research Institute (AU)
- The University of Sydney (AU)
- Corresponding author
- Cooper, Mark S
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2018-06-13
- Volume
- 39
- Issue
- 5
- Pages
- 519-548
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W2808631980
- Cited by
- 258
- References
- 271
- Citations by year
- 2026: 28 · 2025: 32 · 2024: 34 · 2023: 46 · 2022: 35 · 2021: 33 · 2020: 31 · 2019: 14 · 2018: 5
- FWCI
- 4.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Reviews (publishedVersion)
- PubMed (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion, other-oa)
- Funders
- Versus Arthritis (20843)
- Medical Research Council (MR/P021220/1)
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Keywords
- glucocorticoids, bone health, glucocorticoid-induced osteoporosis, Cushing's disease, subclinical Cushing's syndrome, autonomous cortisol secretion, glucocorticoid replacement therapy, adrenal insufficiency, glucocorticoid receptor, bone metabolism, inflammatory diseases, glucocorticoid metabolism
- MeSH terms
- Cushing Syndrome, Glucocorticoids, Humans, Osteoporosis, Bone Density, Hormone Replacement Therapy, Pituitary ACTH Hypersecretion
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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