Skip to main content
Log in

Cushing's Syndrome and Bone

  • Published:
Pituitary Aims and scope Submit manuscript


Structural and functional impairment of skeletal system is a relevant cause of morbidity and disability in patients with Cushing's syndrome (CS). Approximately 30–50% of patients with CS experience fractures (particularly at the spinal level) consistent with the 50% incidence of osteoporosis. Growth failure, pubertal arrest are the hallmarks of CS in children and growing adolescents leading to reduced final adult height and peak bone mass. The decrease in osteoblast number and function, through different mechanisms, seems to play a central role in the bone loss in CS. Patients with CS have decreased serum levels of osteocalcin and alkaline phosphatase. Considering the preferential bone loss in the cancellous skeleton it is reasonable to measure BMD, possibly with Dual X-rays absorptiometry (DEXA) at lumbar spine, in all patients with CS.

Patients cured from CS have increased prevalence of spine damage: therefore, a radiological follow-up of the skeleton should be included in the management of patients with CS not only during the active phase but also after cure.

Glucocorticoid-induced osteoporosis is reversible. The recovery of bone loss in CS is slow, taking approximately ten years to become complete. In the meanwhile, patients with severe osteopenia are exposed to a high risk of fracture. Alendronate may induce a more rapid improvement in BMD than cortisol normalization alone and it could be useful in patients with persistent postsurgical hypercortisolism to prevent further bone loss. The decision to discontinue antiresorptive therapy should be based on clinical monitoring and DEXA measurements.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others


  1. Cushing H. The basophil adenomas of the pituitary body and their clinical manifestations (pituitary basophilism). Bulletin of the John Hopkins Hospital 1:137–192.

  2. Manelli F, Giustina A. Glucocorticoid-induced osteoporosis. Trends Endocrinol Metab 2000;11:79–85.

    CAS  PubMed  Google Scholar 

  3. Kaltsas G, Manetti L, Grossman AB. Osteoporosis in Cushing's syndrome. Front Horm Res 2002;30:60–72.

    CAS  PubMed  Google Scholar 

  4. Arnaldi G, Angeli A, Atkinson AB, Bertagna X, Cavagnini F, Chrousos GP, Fava GA, Findling JW, Gaillard RC, Grossman AB, Kola B, Lacroix A, Mancini T, Mantero F, Newell-Price J, Nieman LK, Sonino N, Vance ML, Giustina A, Boscaro M. Diagnosis and complications of Cushing's syndrome: A consensus statement. J Clin Endocrinol Metab 2003;88:5593–5602.

    CAS  PubMed  Google Scholar 

  5. Faggiano A, Pivonello R, Filippella M, Di Somma C, Orio F Jr, Lombard G, Colao A. Spine abnormalities and damage in patients cured from Cushing's disease. Pituitary 2001;4:153–161.

    CAS  PubMed  Google Scholar 

  6. Minetto M, Reimondo G, Osella G, Ventura M, Angeli A, Terzolo M. Bone loss is more severe in primary adrenal than in pituitary-dependent Cushing's syndrome. Osteoporos Int 2004;15:855–861.

    Article  CAS  PubMed  Google Scholar 

  7. Ohmori N, Nomura K, Ohmori K, Kato Y, Itoh T, Takano K. Osteoporosis is more prevalent in adrenal than in pituitary Cushing's syndrome. Endocr J 2003;50:1–7.

    Article  PubMed  Google Scholar 

  8. Abad V, Chrousos GP, Reynolds JC, Nieman LK, Hill SC, Weinstein RS, Leong GM. Glucocorticoid excess during adolescence leads to a major persistent deficit in bone mass and an increase in central body fat. J Bone Miner Res 2001;16:1879–1885.

    CAS  PubMed  Google Scholar 

  9. Canalis E, Bilezikian JP, Angeli A, Giustina A. Perspectives on glucocorticoid-induced osteoporosis. Bone 2004;34:593–598.

    Article  CAS  PubMed  Google Scholar 

  10. Canalis E, Giustina A. Glucocorticoid-induced osteoporosis: Summary of a workshop. J Clin Endocrinol Metab 2001;86:5681–5685.

    Article  CAS  PubMed  Google Scholar 

  11. Francucci CM, Pantanetti P, Garrapa GG, Massi F, Arnaldi G, Mantero F. Bone metabolism and mass in women with Cushing's syndrome and adrenal incidentaloma. Clin Endocrinol (Oxf) 2002;57:587–593.

    Article  CAS  Google Scholar 

  12. Cooper MS, Rabbitt EH, Goddard PE, Bartlett WA, Hewison M, Stewart PM. Osteoblastic 11beta-hydroxysteroid dehydrogenase type 1 activity increases with age and glucocorticoid exposure. J Bone Miner Res 2002;17:979–986.

    CAS  PubMed  Google Scholar 

  13. Hermus AR, Smals AG, Swinkels LM, Huysmans DA, Pieters GF, Sweep CF, Corstens FH, Kloppenborg PW. Bone mineral density and bone turnover before and after surgical cure of Cushing's syndrome. J Clin Endocrinol Metab 1995;80:2859–2865.

    Article  CAS  PubMed  Google Scholar 

  14. Bonadonna S, Burattin A, Nuzzo M, Bugari G, Agabiti Rosei E, Valle D, Iori N, Bilezikian JP, Veldhuis JD, Giustina A. Chronic glucocorticoid treatment alters spontaneous pulsatile parathyroid hormone secretory dynamics in human subjects. Eur J Endocrinol 2005;152:199–205.

    Article  CAS  PubMed  Google Scholar 

  15. Malerba M, Bossoni S, Radaeli A, Mori E, Bonadonna S, Giustina A, Tantucci C. Growth hormone response to growth hormone-releasing hormone is reduced in adult asthmatic patients receiving long-term inhaled corticosteroid treatment. Chest 2005;127:515–521.

    Article  CAS  PubMed  Google Scholar 

  16. Karavitaki N, Ioannidis G, Giannakopoulos F, Mavrokefalos P, Thalassinos N. Evaluation of bone mineral density of the peripheral skeleton in pre- and postmenopausal women with newly diagnosed endogenous Cushing's syndrome. Clin Endocrinol (Oxf) 2004;60:264–270.

    Article  CAS  Google Scholar 

  17. Tauchmanova L, Rossi R, Nuzzo V, del Puente A, Esposito-del Puente A, Pizzi C, Fonderico F, Lupoli G, Lombardi G. Bone loss determined by quantitative ultrasonometry correlates inversely with disease activity in patients with endogenous glucocorticoid excess due to adrenal mass. Eur J Endocrinol 2001;145:241–247.

    Article  CAS  PubMed  Google Scholar 

  18. Manning PJ, Evans MC, Reid IR. Normal bone mineral density following cure of Cushing's syndrome. Clin Endocrinol (Oxf) 1992;36:229–234.

    CAS  Google Scholar 

  19. Di Somma C, Pivonello R, Loche S, Faggiano A, Klain M, Salvatore M, Lombardi G, Colao A. Effect of 2 years of cortisol normalization on the impaired bone mass and turnover in adolescent and adult patients with Cushing's disease: A prospective study. Clin Endocrinol (Oxf) 2003;58:302–308.

    Google Scholar 

  20. Luisetto G, Zangari M, Camozzi V, Boscaro M, Sonino N, Fallo F. Recovery of bone mineral density after surgical cure, but not by ketoconazole treatment, in Cushing's syndrome. Osteoporos Int 2001;12:956–960.

    Article  CAS  PubMed  Google Scholar 

  21. Di Somma C, Colao A, Pivonello R, Klain M, Faggiano A, Tripodi FS, Merola B, Salvatore M, Lombardi G. Effectiveness of chronic treatment with alendronate in the osteoporosis of Cushing's disease. Clin Endocrinol (Oxf) 1998;48:655–662.

    Google Scholar 

  22. Lane NE, Sanchez S, Modin GW, Genant HK, Pierini E, Arnaud CD. Bone mass continues to increase at the hip after parathyroid hormone treatment is discontinued in glucocorticoid-induced osteoporosis: Results of a randomized controlled clinical trial. J Bone Miner Res 2000;15:944–951.

    CAS  PubMed  Google Scholar 

  23. Manelli F, Carpinteri R, Bossoni S, Burattin A, Bonadonna S, Agabiti Rosei E, Giustina A. Growth hormone in glucocorticoid-induced osteoporosis. Front Horm Res 2002;30:174–183.

    CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations


Corresponding author

Correspondence to Andrea Giustina.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Mancini, T., Doga, M., Mazziotti, G. et al. Cushing's Syndrome and Bone. Pituitary 7, 249–252 (2004).

Download citation

  • Published:

  • Issue Date:

  • DOI:

Key Words