Abstract
Glucocorticoid (GC)-induced osteoporosis is the main cause of secondary osteoporosis. Fractures, which are often asymptomatic, can occur in as many as 50% of patients receiving chronic GC therapy. GCs have direct and indirect effects on bone cells (osteoblasts, osteocytes, and osteoclasts) with a suppression of bone formation and an increased bone resorption. The management of patients exposed to GCs should include the use of the minimal effective dose of GC, general health measures, and adequate intakes of calcium and vitamin D. Bisphosphonates are nowadays largely used in GC-induced osteoporosis and teriparatide has proved its efficiency as well.
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References
Cushing H. The basophil adenomas of the pituitary body and their clinical manifestations (pituitary basophilism). 1932. Obes Res. 1994;2:486–508.
Hazard J. Discovery of mineralocorticoid hormones. Hist Sci Med. 2004;38:441–8.
van der Laan S, Meijer OC. Pharmacology of glucocorticoids: beyond receptors. Eur J Pharmacol. 2008;585:483–91.
Stahn C, Lowenberg M, Hommes DW, Buttgereit F. Molecular mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists. Mol Cell Endocrinol. 2007;275:71–8.
McDonough AK, Curtis JR, Saag KG. The epidemiology of glucocorticoid-associated adverse events. Curr Opin Rheumatol. 2008;20:131–7.
Grad I, Picard D. The glucocorticoid responses are shaped by molecular chaperones. Mol Cell Endocrinol. 2007;275:2–12.
Abu EO, Horner A, Kusec V, et al. The localization of the functional glucocorticoid receptor alpha in human bone. J Clin Endocrinol Metab. 2000;85:883–9.
Huang L, Xu J, Kumta SM, Zheng MH. Gene expression of glucocorticoid receptor alpha and beta in giant cell tumour of bone: evidence of glucocorticoid-stimulated osteoclastogenesis by stromal-like tumour cells. Mol Cell Endocrinol. 2001;181:199–206.
Huizenga NA, Koper JW, De Lange P, et al. A polymorphism in the glucocorticoid receptor gene may be associated with and increased sensitivity to glucocorticoids in vivo. J Clin Endocrinol Metab. 1998;83:144–51.
Peng YM, Lei SF, Guo Y, et al. Sex-specific association of the glucocorticoid receptor gene with extreme BMD. J Bone Miner Res. 2008;23:247–52.
van Rossum EF, Koper JW, van den Beld AW, et al. Identification of the BclI polymorphism in the glucocorticoid receptor gene: association with sensitivity to glucocorticoids in vivo and body mass index. Clin Endocrinol. 2003;59:585–92.
Lowenberg M, Stahn C, Hommes DW, Buttgereit F. Novel insights into mechanisms of glucocorticoid action and the development of new glucocorticoid receptor ligands. Steroids. 2008;73:1025–9.
Hofbauer LC, Gori F, Riggs BL, et al. Stimulation of osteoprotegerin ligand and inhibition of osteoprotegerin production by glucocorticoids in human osteoblastic lineage cells: potential paracrine mechanisms of glucocorticoid-induced osteoporosis. Endocrinology. 1999;140:4382–9.
Meyer T, Carlstedt-Duke J, Starr DB. A weak TATA box is a prerequisite for glucocorticoid-dependent repression of the osteocalcin gene. J Biol Chem. 1997;272:30709–14.
Meyer T, Gustafsson JA, Carlstedt-Duke J. Glucocorticoid-dependent transcriptional repression of the osteocalcin gene by competitive binding at the TATA box. DNA Cell Biol. 1997;16:919–27.
Stahn C, Buttgereit F. Genomic and nongenomic effects of glucocorticoids. Nat Clin Pract Rheumatol. 2008;4:525–33.
Cooper MS, Blumsohn A, Goddard PE, et al. 11beta-hydroxysteroid dehydrogenase type 1 activity predicts the effects of glucocorticoids on bone. J Clin Endocrinol Metab. 2003;88:3874–7.
Tomlinson JW, Draper N, Mackie J, et al. Absence of Cushingoid phenotype in a patient with Cushing’s disease due to defective cortisone to cortisol conversion. J Clin Endocrinol Metab. 2002;87:57–62.
Tomlinson JW, Walker EA, Bujalska IJ, et al. 11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response. Endocr Rev. 2004;25:831–66.
Cooper MS, Walker EA, Bland R, et al. Expression and functional consequences of 11beta-hydroxysteroid dehydrogenase activity in human bone. Bone. 2000;27:375–81.
Cooper MS, Bujalska I, Rabbitt E, et al. Modulation of 11beta-hydroxysteroid dehydrogenase isozymes by proinflammatory cytokines in osteoblasts: an autocrine switch from glucocorticoid inactivation to activation. J Bone Miner Res. 2001;16:1037–44.
Ishida Y, Heersche JN. Glucocorticoid-induced osteoporosis: both in vivo and in vitro concentrations of glucocorticoids higher than physiological levels attenuate osteoblast differentiation. J Bone Miner Res. 1998;13:1822–6.
Cheng SL, Yang JW, Rifas L, et al. Differentiation of human bone marrow osteogenic stromal cells in vitro: induction of the osteoblast phenotype by dexamethasone. Endocrinology. 1994;134:277–86.
Bellows CG, Heersche JN, Aubin JE. Determination of the capacity for proliferation and differentiation of osteoprogenitor cells in the presence and absence of dexamethasone. Dev Biol. 1990;140:132–8.
Shalhoub V, Conlon D, Tassinari M, et al. Glucocorticoids promote development of the osteoblast phenotype by selectively modulating expression of cell growth and differentiation associated genes. J Cell Biochem. 1992;50:425–40.
Ito S, Suzuki N, Kato S, et al. Glucocorticoids induce the differentiation of a mesenchymal progenitor cell line, ROB-C26 into adipocytes and osteoblasts, but fail to induce terminal osteoblast differentiation. Bone. 2007;40:84–92.
Atmani H, Audrain C, Mercier L, et al. Phenotypic effects of continuous or discontinuous treatment with dexamethasone and/or calcitriol on osteoblasts differentiated from rat bone marrow stromal cells. J Cell Biochem. 2002;85:640–50.
Atmani H, Chappard D, Baslé MF. Proliferation and differentiation of osteoblasts and adipocytes in rat bone marrow stromal cell cultures: effects of dexamethasone and calcitriol. J Cell Biochem. 2003;89:364–72.
Lane NE, Yao W, Balooch M, et al. Glucocorticoid-treated mice have localized changes in trabecular bone material properties and osteocyte lacunar size that are not observed in placebo-treated or estrogen-deficient mice. J Bone Miner Res. 2006;21:466–76.
Weinstein RS, Jilka RL, Parfitt AM, Manolagas SC. Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone. J Clin Invest. 1998;102:274–82.
Borelli A, Leite MO, Correa PH, et al. Bone histomorphometry in Cushing’s syndrome. J Endocrinol Invest. 1992;15:783–7.
Giustina A, Mazziotti G, Canalis E. Growth hormone, insulin-like growth factors, and the skeleton. Endocr Rev. 2008;29:535–59.
Jia D, Heersche JN. Insulin-like growth factor-1 and -2 stimulate osteoprogenitor proliferation and differentiation and adipocyte formation in cell populations derived from adult rat bone. Bone. 2000;27:785–94.
Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy. Osteoporos Int. 2007;18:1319–28.
Canalis E. Effect of glucocorticoids on type I collagen synthesis, alkaline phosphatase activity, and deoxyribonucleic acid content in cultured rat calvariae. Endocrinology. 1983;112:931–9.
Pereira RC, Durant D, Canalis E. Transcriptional regulation of connective tissue growth factor by cortisol in osteoblasts. Am J Physiol Endocrinol Metab. 2000;279:E570–6.
Pereira RC, Delany AM, Canalis E. Effects of cortisol and bone morphogenetic protein-2 on stromal cell differentiation: correlation with CCAAT-enhancer binding protein expression. Bone. 2002;30:685–91.
Pereira RC, Delany AM, Canalis E. CCAAT/enhancer binding protein homologous protein (DDIT3) induces osteoblastic cell differentiation. Endocrinology. 2004;145:1952–60.
Wu Z, Bucher NL, Farmer SR. Induction of peroxisome proliferator-activated receptor gamma during the conversion of 3T3 fibroblasts into adipocytes is mediated by C/EBPbeta, C/EBPdelta, and glucocorticoids. Mol Cell Biol. 1996;16:4128–36.
Pereira RM, Delany AM, Durant D, Canalis E. Cortisol regulates the expression of Notch in osteoblasts. J Cell Biochem. 2002;85:252–8.
Ohnaka K, Taniguchi H, Kawate H, et al. Glucocorticoid enhances the expression of dickkopf-1 in human osteoblasts: novel mechanism of glucocorticoid-induced osteoporosis. Biochem Biophys Res Commun. 2004;318:259–64.
Ohnaka K, Tanabe M, Kawate H, et al. Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts. Biochem Biophys Res Commun. 2005;329:177–81.
Wang FS, Ko JY, Yeh DW, et al. Modulation of Dickkopf-1 attenuates glucocorticoid induction of osteoblast apoptosis, adipocytic differentiation, and bone mass loss. Endocrinology. 2008;149:1793–801.
Wang FS, Lin CL, Chen YJ, et al. Secreted frizzled-related protein 1 modulates glucocorticoid attenuation of osteogenic activities and bone mass. Endocrinology. 2005;146:2415–23.
Hayashi K, Yamaguchi T, Yano S, et al. BMP/Wnt antagonists are upregulated by dexamethasone in osteoblasts and reversed by alendronate and PTH: potential therapeutic targets for glucocorticoid-induced osteoporosis. Biochem Biophys Res Commun. 2008.
Leclerc N, Noh T, Cogan J, et al. Opposing effects of glucocorticoids and Wnt signaling on Krox20 and mineral deposition in osteoblast cultures. J Cell Biochem. 2008;103:1938–51.
Camps M, Nichols A, Arkinstall S. Dual specificity phosphatases: a gene family for control of MAP kinase function. FASEB J. 2000;14:6–16.
Canalis E. Notch signaling in osteoblasts. Sci Signal. 2008;1:pe17.
Iu MF, Kaji H, Sowa H, et al. Dexamethasone suppresses Smad3 pathway in osteoblastic cells. J Endocrinol. 2005;185:131–8.
Liu Y, Porta A, Peng X, et al. Prevention of glucocorticoid-induced apoptosis in osteocytes and osteoblasts by calbindin-D28k. J Bone Miner Res. 2004;19:479–90.
Espina B, Liang M, Russell RG, Hulley PA. Regulation of bim in glucocorticoid-mediated osteoblast apoptosis. J Cell Physiol. 2008;215:488–96.
Planey SL, Derfoul A, Steplewski A, et al. Inhibition of glucocorticoid-induced apoptosis in 697 pre-B lymphocytes by the mineralocorticoid receptor N-terminal domain. J Biol Chem. 2002;277:42188–96.
Gohel A, McCarthy MB, Gronowicz G. Estrogen prevents glucocorticoid-induced apoptosis in osteoblasts in vivo and in vitro. Endocrinology. 1999;140:5339–47.
Rubin J, Biskobing DM, Jadhav L, et al. Dexamethasone promotes expression of membrane-bound macrophage colony-stimulating factor in murine osteoblast-like cells. Endocrinology. 1998;139:1006–12.
Hofbauer LC. Osteoprotegerin ligand and osteoprotegerin: novel implications for osteoclast biology and bone metabolism. Eur J Endocrinol. 1999;141:195–210.
Sasaki N, Kusano E, Ando Y, et al. Changes in osteoprotegerin and markers of bone metabolism during glucocorticoid treatment in patients with chronic glomerulonephritis. Bone. 2002;30:853–8.
Sasaki N, Kusano E, Ando Y, et al. Glucocorticoid decreases circulating osteoprotegerin (OPG): possible mechanism for glucocorticoid induced osteoporosis. Nephrol Dial Transplant. 2001;16:479–82.
Kim HJ, Zhao H, Kitaura H, et al. Glucocorticoids suppress bone formation via the osteoclast. J Clin Invest. 2006;116:2152–60.
Weinstein RS, Chen JR, Powers CC, et al. Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids. J Clin Invest. 2002;109:1041–8.
Meunier PJ, Dempster DW, Edouard C, et al. Bone histomorphometry in corticosteroid-induced osteoporosis and Cushing’s syndrome. Adv Exp Med Biol. 1984;171:191–200.
Dempster DW, Arlot MA, Meunier PJ. Mean wall thickness and formation periods of trabecular bone packets in corticosteroid-induced osteoporosis. Calcif Tissue Int. 1983;35:410–7.
Chappard D, Legrand E, Baslé MF, et al. Altered trabecular architecture induced by corticosteroids: a bone histomorphometric study. J Bone Miner Res. 1996;11:676–85.
Chappard D, Josselin N, Rougé-Maillart C, et al. Bone microarchitecture in males with corticosteroid-induced osteoporosis. Osteoporos Int. 2007;18:487–94.
Vedi S, Elkin SL, Compston JE. A histomorphometric study of cortical bone of the iliac crest in patients treated with glucocorticoids. Calcif Tissue Int. 2005;77:79–83.
Stellon AJ, Davies A, Compston J, Williams R. Bone loss in autoimmune chronic active hepatitis on maintenance corticosteroid therapy. Gastroenterology. 1985;89:1078–83.
van Staa TP, Leufkens HG, Abenhaim L, et al. Use of oral corticosteroids in the United Kingdom. Q J Med. 2000;93:105–11.
Reid IR, Evans MC, Wattie DJ, et al. Bone mineral density of the proximal femur and lumbar spine in glucocorticoid-treated asthmatic patients. Osteoporos Int. 1992;2:103–5.
Laan RF, van Riel PL, van Erning LJ, et al. Vertebral osteoporosis in rheumatoid arthritis patients: effect of low dose prednisone therapy. Br J Rheumatol. 1992;31:91–6.
Buckley LM, Leib ES, Cartularo KS, et al. Effects of low dose corticosteroids on the bone mineral density of patients with rheumatoid arthritis. J Rheumatol. 1995;22:1055–9.
Laan RF, van Riel PL, van de Putte LB, et al. Low-dose prednisone induces rapid reversible axial bone loss in patients with rheumatoid arthritis. A randomized, controlled study. Ann Intern Med. 1993;119:963–8.
Sambrook P, Birmingham J, Kempler S, et al. Corticosteroid effects on proximal femur bone loss. J Bone Miner Res. 1990;5:1211–6.
McKenzie R, Reynolds JC, O’Fallon A, et al. Decreased bone mineral density during low dose glucocorticoid administration in a randomized, placebo controlled trial. J Rheumatol. 2000;27:2222–6.
van Staa TP, Leufkens HG, Cooper C. The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporos Int. 2002;13:777–87.
Natsui K, Tanaka K, Suda M, et al. High-dose glucocorticoid treatment induces rapid loss of trabecular bone mineral density and lean body mass. Osteoporos Int. 2006;17:105–8.
Decramer M, Rennard S, Troosters T, et al. COPD as a lung disease with systemic consequences—clinical impact, mechanisms, and potential for early intervention. COPD. 2008;5:235–56.
Ardizzone S, Puttini PS, Cassinotti A, Porro GB. Extraintestinal manifestations of inflammatory bowel disease. Dig Liver Dis. 2008;40(S2):S253–9.
Katz S. Osteoporosis in patients with inflammatory bowel disease: risk factors, prevention, and treatment. Rev Gastroenterol Disord. 2006;6:63–71.
Wang HH, Chang PC, Chu SH, et al. Osteoporosis after kidney transplantation: preliminary report from a single center. Transplant Proc. 2008;40:2412–3.
Kanis JA, Johansson H, Oden A, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19:893–9.
Cooper C, Coupland C, Mitchell M. Rheumatoid arthritis, corticosteroid therapy and hip fracture. Ann Rheum Dis. 1995;54:49–52.
Hooyman JR, Melton LJIII, Nelson AM, et al. Fractures after rheumatoid arthritis. A population-based study. Arthritis Rheum. 1984;27:1353–61.
Van Staa TP, Leufkens HG, Abenhaim L, et al. Use of oral corticosteroids and risk of fractures. J Bone Miner Res. 2000;15:993–1000.
Angeli A, Guglielmi G, Dovio A, et al. High prevalence of asymptomatic vertebral fractures in post-menopausal women receiving chronic glucocorticoid therapy: a cross-sectional outpatient study. Bone. 2006;39:253–9.
Vestergaard P, Rejnmark L, Mosekilde L. Fracture risk associated with systemic and topical corticosteroids. J Intern Med. 2005;257:374–84.
Vestergaard P. Skeletal effects of systemic and topical corticosteroids. Curr Drug Saf. 2008;3:190–3.
Vestergaard P, Rejnmark L, Mosekilde L. Fracture risk associated with different types of oral corticosteroids and effect of termination of corticosteroids on the risk of fractures. Calcif Tissue Int. 2008;82:249–57.
Pedersen S. Clinical safety of inhaled corticosteroids for asthma in children: an update of long-term trials. Drug Saf. 2006;29:599–612.
Schlienger RG, Jick SS, Meier CR. Inhaled corticosteroids and the risk of fractures in children and adolescents. Pediatrics. 2004;114:469–73.
Gulliver T, Morton R, Eid N. Inhaled corticosteroids in children with asthma: pharmacologic determinants of safety and efficacy and other clinical considerations. Paediatr Drugs. 2007;9:185–94.
Cosman F, Nieves J, Herbert J, et al. High-dose glucocorticoids in multiple sclerosis patients exert direct effects on the kidney and skeleton. J Bone Miner Res. 1994;9:1097–105.
Ebeling PR, Erbas B, Hopper JL, et al. Bone mineral density and bone turnover in asthmatics treated with long-term inhaled or oral glucocorticoids. J Bone Miner Res. 1998;13:1283–9.
Kotowicz MA, Hall S, Hunder GG, et al. Relationship of glucocorticoid dosage to serum bone Gla-protein concentration in patients with rheumatologic disorders. Arthritis Rheum. 1990;33:1487–92.
Vihinen MK, Kolho KL, Ashorn M, et al. Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids. Eur J Endocrinol. 2008;159:693–8.
Prummel MF, Wiersinga WM, Lips P, et al. The course of biochemical parameters of bone turnover during treatment with corticosteroids. J Clin Endocrinol Metab. 1991;72:382–6.
Vegiopoulos A, Herzig S. Glucocorticoids, metabolism and metabolic diseases. Mol Cell Endocrinol. 2007;275:43–61.
Lane NE, Lukert B. The science and therapy of glucocorticoid-induced bone loss. Endocrinol Metab Clin North Am. 1998;27:465–83.
Yao W, Cheng Z, Busse C, et al. Glucocorticoid excess in mice results in early activation of osteoclastogenesis and adipogenesis and prolonged suppression of osteogenesis: a longitudinal study of gene expression in bone tissue from glucocorticoid-treated mice. Arthritis Rheum. 2008;58:1674–86.
Quarles LD. Prednisone-induced osteopenia in beagles: variable effects mediated by differential suppression of bone formation. Am J Physiol. 1992;263:E136–41.
Chavassieux P, Buffet A, Vergnaud P, et al. Short-term effects of corticosteroids on trabecular bone remodeling in old ewes. Bone. 1997;20:451–5.
Eberhardt AW, Yeager-Jones A, Blair HC. Regional trabecular bone matrix degeneration and osteocyte death in femora of glucocorticoid- treated rabbits. Endocrinology. 2001;142:1333–40.
Gluer CC, Scholz-Ahrens KE, Helfenstein A, et al. Ibandronate treatment reverses glucocorticoid-induced loss of bone mineral density and strength in minipigs. Bone. 2007;40:645–55.
Pufe T, Claassen H, Scholz-Ahrens KE, et al. Influence of estradiol on vascular endothelial growth factor expression in bone: a study in Gottingen miniature pigs and human osteoblasts. Calcif Tissue Int. 2007;80:184–91.
Scholz-Ahrens KE, Delling G, Stampa B, et al. Glucocorticosteroid-induced osteoporosis in adult primiparous Gottingen miniature pigs: effects on bone mineral and mineral metabolism. Am J Physiol Endocrinol Metab. 2007;293:E385–95.
Barrett R, Chappell C, Quick M, Fleming A. A rapid, high content, in vivo model of glucocorticoid-induced osteoporosis. Biotechnol J. 2006;1:651–5.
Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis: 2001 update. American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis. Arthritis Rheum. 2001;44:1496–503.
Buckley LM, Leib ES, Cartularo KS, et al. Calcium and vitamin D3 supplementation prevents bone loss in the spine secondary to low-dose corticosteroids in patients with rheumatoid arthritis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med. 1996;125:961–8.
Sambrook P, Birmingham J, Kelly P, et al. Prevention of corticosteroid osteoporosis. A comparison of calcium, calcitriol, and calcitonin. N Engl J Med. 1993;328:1747–52.
Adachi JD, Bensen WG, Bianchi F, et al. Vitamin D and calcium in the prevention of corticosteroid induced osteoporosis: a 3 year followup. J Rheumatol. 1996;23:995–1000.
Adachi JD, Bensen WG, Brown J, et al. Intermittent etidronate therapy to prevent corticosteroid-induced osteoporosis. N Engl J Med. 1997;337:382–7.
Roux C, Oriente P, Laan R, et al. Randomized trial of effect of cyclical etidronate in the prevention of corticosteroid-induced bone loss. Ciblos Study Group. J Clin Endocrinol Metab. 1998;83:1128–33.
Adachi JD, Roux C, Pitt PI, et al. A pooled data analysis on the use of intermittent cyclical etidronate therapy for the prevention and treatment of corticosteroid induced bone loss. J Rheumatol. 2000;27:2424–31.
Saag KG, Emkey R, Schnitzer TJ, et al. Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis. Glucocorticoid-Induced Osteoporosis Intervention Study Group. N Engl J Med. 1998;339:292–9.
Wallach S, Cohen S, Reid DM, et al. Effects of risedronate treatment on bone density and vertebral fracture in patients on corticosteroid therapy. Calcif Tissue Int. 2000;67:277–85.
Ringe JD, Dorst A, Faber H, et al. Three-monthly ibandronate bolus injection offers favourable tolerability and sustained efficacy advantage over two years in established corticosteroid-induced osteoporosis. Rheumatology. 2003;42:743–9.
Boutsen Y, Jamart J, Esselinckx W, Devogelaer JP. Primary prevention of glucocorticoid-induced osteoporosis with intravenous pamidronate and calcium: a prospective controlled 1-year study comparing a single infusion, an infusion given once every 3 months, and calcium alone. J Bone Miner Res. 2001;16:104–12.
Reid DM, Devogelaer JP, Saag K, et al. Zoledronic acid and risedronate in the prevention and treatment of glucocorticoid-induced osteoporosis (HORIZON): a multicentre, double-blind, double-dummy, randomised controlled trial. Lancet. 2009;373:1253–63.
Sambrook P, Devogelaer J, Reginster J, et al. Effect of a single 5-mg infusion of zoledronic acid on bone turnover markers versus oral risedronate (5 mg/day) over 1 year in patients with glucocorticoid-induced osteoporosis. J Bone Miner Res. 2008;23:S464.
Saag KG, Shane E, Boonen S, et al. Teriparatide or alendronate in glucocorticoid-induced osteoporosis. N Engl J Med. 2007;357:2028–39.
Lukert BP, Johnson BE, Robinson RG. Estrogen and progesterone replacement therapy reduces glucocorticoid-induced bone loss. J Bone Miner Res. 1992;7:1063–9.
Reid IR, Wattie DJ, Evans MC, Stapleton JP. Testosterone therapy in glucocorticoid-treated men. Arch Intern Med. 1996;156:1173–7.
Cranney A, Welch V, Adachi JD, et al. Calcitonin for the treatment and prevention of corticosteroid-induced osteoporosis. Cochrane Database Syst Rev. 2000. doi:10.1002/14651858.
Shiraki M, Shiraki Y, Aoki C, Miura M. Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. J Bone Miner Res. 2000;15:515–21.
Cohen SB, Dore RK, Lane NE, et al. Denosumab treatment effects on structural damage, bone mineral density, and bone turnover in rheumatoid arthritis: a twelve-month, multicenter, randomized, double-blind, placebo-controlled, phase II clinical trial. Arthritis Rheum. 2008;58:1299–309.
Kleiman A, Tuckermann JP. Glucocorticoid receptor action in beneficial and side effects of steroid therapy: lessons from conditional knockout mice. Mol Cell Endocrinol. 2007;275:98–108.
Schacke H, Berger M, Rehwinkel H, Asadullah K. Selective glucocorticoid receptor agonists (SEGRAs): novel ligands with an improved therapeutic index. Mol Cell Endocrinol. 2007;275:109–17.
Compston J. US and UK guidelines for glucocorticoid-induced osteoporosis: similarities and differences. Curr Rheumatol Rep. 2004;6:66–9.
Acknowledgment
This study was made possible by grants from the Bioregos “Pays de la Loire” program and INSERM and was also supported by a grant from the French Society for Rheumatology (SFR).
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Bouvard, B., Legrand, E., Audran, M. et al. Glucocorticoid-Induced Osteoporosis: A Review. Clinic Rev Bone Miner Metab 8, 15–26 (2010). https://doi.org/10.1007/s12018-009-9051-9
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DOI: https://doi.org/10.1007/s12018-009-9051-9