Skeletal Diseases in Cushing’s Syndrome: Osteoporosis versus Arthropathy
Open accessAbstract
Structural and functional impairment of the skeletal system remains an important cause of morbidity and disability in patients with Cushing’s syndrome (CS). Glucocorticoid (GC) excess inhibits bone formation and calcium absorption from the gut, increases bone resorption, and alters the secretion of gonadotropin and growth hormones, cytokines and growth factors influencing bone. Both overt and subtle endogenous hypercortisolism affect bone, leading to vertebral fractures in up to 70% of patients. Fracture risk is related to age at onset, duration and severity of the disease and individual susceptibility to GCs that is genetically determined. Bone mineral density (BMD) measurement at the lumbar spine should be performed as a screening test in all patients with CS due to the preferential loss of trabecular bone induced by GCs. The higher risk of fractures at comparable BMD values with controls suggests that bone quality features, not assessed by routine BMD approaches, are also important and should be addressed when indicated applying specific radiological means. Successful treatment of GC excess is associated with improvement in bone mass which, although delayed and often incomplete, reduces the risk of osteoporotic fractures. Bisphosphonates can induce a more rapid improvement in BMD than cortisol normalization alone and can be used in patients with increased risks for further fractures and/or persistent hypercortisolemia to prevent further bone loss. Anabolic agents have not as yet been systemically used. Avascular necrosis, mainly of the femoral neck, and growth arrest in children are the most common skeletal disorders unrelated to osteoporosis encountered in patients with endogenous hypercortisolism.
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Hypercorticism affects bone metabolism through a variety of mechanisms.
“Hypercorticism affects bone metabolism in a variety of mechanisms [3].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
Glucocorticoid-induced osteoporosis occurs in two phases: a rapid early phase in which BMD is reduced by bone resorption, followed by a slower progressive phase in which BMD declines because of impaired bone formation.
“GIO occurs in two phases, a rapid early phase in which BMD is reduced as a result of bone resorption, followed by a slower, progressive phase in which BMD declines because of impaired bone formation [3].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
Endogenous hypercortisolism changes bone structure and causes vertebral fractures in up to 70% of patients.
“Endogenous hypercortisolism changes bone structure and causes vertebral fractures in up to 70% of patients.”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
Treatment of growth hormone deficiency protects the skeleton from the adverse effects of glucocorticoid overtreatment in hypopituitary patients.
“It seems that treatment of GHD protects the skeleton from the adverse effects of glucocorticoid overtreatment in hypopituitary patients [3, 17].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
Administration of alendronate or clodronate provides faster BMD recovery in comparison with untreated patients.
“Administration of alendronate or clodronate provides faster BMD recovery in comparison with untreated patients [3].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
Subclinical hypercortisolism might cause osteoporosis and increased risk of vertebral fractures.
“It is thought that even subclinical hypercortisolism (SH) might be the cause of osteoporosis and increased risk of vertebral fractures [3, 13].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
Factors associated with fracture risk in Cushing's syndrome include age at onset, span and severity of disease, and individual susceptibility to glucocorticoids.
“Factors associated with fracture risk include age at the onset, span and severity of the disease, and individual susceptibility to GCs [3].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
Glucocorticoids prolong the life span of mature osteoclasts directly or through increased expression of macrophage colony-stimulating factor.
“GCs prolong the life span of mature osteoclasts by acting directly or through the increased expression of macrophage colony-stimulating factor (M-CSF) [3].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
In both endogenous and exogenous hypercortisolism, fractures may be asymptomatic and occur in patients with normal or only slightly decreased BMD values.
“In both endogenous and exogenous hypercortisolism fractures might be asymptomatic and occur in patients with normal or only slightly decreased BMD values [3, 10, 12].”
From Pituitary Disorders and Osteoporosis (2015) · cites this paper as [3]
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References 22 · Cited by 71
- Authors
- Kaltsas, G., & Makras, P.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- Venue
- Neuroendocrinology
- Publisher
- S. Karger AG
- Published
- 2010
- Volume
- 92
- Issue
- Suppl. 1
- Pages
- 60-64
- ISSN
- 0028-3835 (ISSN-L)
- 1423-0194
- OpenAlex
- W2008913383
- Cited by
- 71
- References
- 22
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 6 · 2020: 4 · 2019: 2 · 2018: 2 · 2017: 6 · 2016: 2 · 2015: 5 · 2014: 11 · 2013: 6 · 2012: 6
- FWCI
- 4.49
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- DSpace - NTUA (National Technical University of Athens) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Keywords
- Cushing's syndrome, glucocorticoid excess, osteoporosis, hypercortisolism, bone mineral density, vertebral fractures, fracture risk, bone quality, bisphosphonates, avascular necrosis, femoral neck, growth arrest, bone disease, bone resorption, bone formation
- MeSH terms
- Cushing Syndrome, Diphosphonates, Humans, Osteoporosis, Bone Density, Bone Density Conservation Agents, Osteoporotic Fractures
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