ABSTRACT

Glucocorticoid (GC)-induced osteoporosis (GCOP) is the most common cause of iatrogenic osteoporosis (OP). Fractures may occur in 30-50% of patients on chronic GC therapy. Most of the epidemiological data associating fracture risk with GC therapy are from the use of oral GCs. The process of bone remodeling is complex, regulated by an intricate network of local and systemic factors. With prolonged GC administration, cortical bone becomes increasingly affected and long bones show increased fragility. As some patients on a low GC dose show bone loss at a much higher rate than others on a higher GC dose, genetics may play a role in determining this difference. Any patient that is treated with long-term GCs should be suspected as suffering from GCOP. Laboratory evaluation for GCOP should include total blood cell count, markers of renal and liver function, serum electrophoresis, serum and 24-hr urine calcium, serum levels of 25-hydroxyvitamin D, alkaline phosphatase, thyroid-stimulating hormone and parathyroid hormone, estradiol in women and total and free testosterone in men. Changes in BMD early on during GC therapy can be detected by dual-energy X-ray absorptiometry (DXA). In patients under GC treatment fractures tend to occur at BMD values that are lower than the conventional threshold T-score of -2.5. Recently simple adjustments for the calculated fracture risk have been presented that take into account glucocorticoid dosage for the Fracture Risk Assessment tool (FRAX). Guidelines for the prevention and treatment of GCOP have been put forth from various authorities. Prevention of GCOP should start as soon as GCs are administered; bone loss is more rapid in the first months of therapy. Patients on GCs should receive supplementation with calcium and vitamin D. There are several antiresorptive agents available for the prevention and treatment of GCOP - bisphosphonates are the most widely used. Teriparatide and denosumab can also be therapies of choice for patients on GC treatment with or without GCOP. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

INTRODUCTION

Glucocorticoid (GC)-induced osteoporosis (GCOP) is often the result of secondary osteoporosis (OP) (1). It is the most common cause of iatrogenic OP; adults aged 20 to 45 years are mainly affected (1-3). Important bone loss may occur with or without other manifestations and its severity is dependent on both the dose and duration of GC treatment (4). From a retrospective study conducted in the United Kingdom the prevalence of chronic use of oral GCs in the general population was shown to be 0.5%; the prevalence was higher in women over 55 years (1.7%) and as high as 2.5% in subjects older than 70 years (5, 6); more recently experts argued that approximately 2% of the population receives long-term GC treatment (7). It is of practical interest to note that only 4%-14% of patients taking oral steroids were receiving treatment for prevention of osteoporosis (mainly by rheumatologists), indicating that GCOP is often underestimated and left untreated (5, 8).

EPIDEMIOLOGY

The association between glucocorticoid (GC) excess and osteoporosis was first described nearly 80 years ago, but its importance in clinical practice has only recently been recognized (9). Although it shares some similarities with postmenopausal osteoporosis, glucocorticoid-induced osteoporosis (GCOP) has distinct characteristics, including the rapidity of bone loss early after initiation of therapy, the accompanying increase in fracture risk during this time, and the combination of suppressed bone formation and increased bone resorption during the early phase of therapy (10).

Although awareness of GCOP amongst health-care professionals has increased over recent years, several studies indicate that its management remains suboptimal (11, 12). Although increased rates of diagnosis and treatment have been reported, possibly as a result of national guidelines, but overall these rates remain low (12, 13).

There is clear epidemiological association between GC therapy and fracture risk (14-16). Oral GC therapy is prescribed in up to 2.5% of the elderly population (aged 70-79 years) for a wide range of medical disorders (17). Fractures may occur in 30-50% of patients on chronic GC therapy (18). The vertebrae and femoral neck of the hip are specifically involved (19), whereas risk at the forearm (predominantly consisting of cortical bone), is not increased, confirming that GCs affect predominantly cancellous bone (15). Vertebral fractures associated with GC therapy may be asymptomatic (20). When assessed by X-ray-based morphometric measurements of vertebral bodies, more than 1/3 of postmenopausal women on chronic (> 6 months) oral GC treatment have sustained at least one vertebral fracture (20).

Along with the demonstration that fractures can occur early in the course of GC therapy, fracture incidence is also related to the dose and duration of GC exposure (16).

Doses as low as 2.5 mg of prednisone equivalents per day can be a risk factor for fracture, but the risk is clearly greater with higher doses. Chronic use is also associated with greater fracture risk (1, 16). When daily amounts of prednisone - or its equivalent - exceed 10 mg on a continuous basis and duration of therapy is greater than 90 days, the risk of fractures at the hip and vertebral sites is increased by 7- and 17-fold respectively (16). The risk of fractures declines after discontinuation of GCs although the recovery of the lost bone is gradual and often incomplete (1, 16).

Most of the epidemiological data associating fracture risk with GC therapy, come from the use of oral GCs. There is less data about risk associated with inhaled GCs (21-25); from the data available it can be extrapolated that a small but persistent and clinically significant growth retardation may be expected in children receiving inhaled GCs (26). It is also important to bear in mind that the underlying disorder for which inhaled or systemic GCs is used may also be a cause of bone loss (27). The systemic release of local bone-resorbing cytokines in some of these disorders could stimulate bone loss (28, 29). In addition, there are also local factors to consider. In inflammatory bowel disease, bone loss may be due, in part, to malabsorption of vitamin D, calcium, and other nutrients (28). In chronic lung disease, hypoxia, acidosis, reduced physical activity, and smoking may all contribute to bone loss, independently of the use of inhaled GCs (14, 25, 30, 31).

SECONDARY CAUSES/RISK FACTORS OF BONE LOSS

Factors, such as advancing age, race, sex, menopausal status, family history of OP and fractures, and secondary causes of OP, such as hyperthyroidism, hyperparathyroidism, Cushing’s syndrome, hypogonadism, diabetes (particularly type 1), renal failure, inflammatory bowel disease, and rheumatoid arthritis can add to the effects of GCOP (14, 32-36). Some of the risk factors for GCOP are common to other forms of OP and can be modified; these include: low calcium and high sodium intake (37), high caffeine intake (when calcium intake is low) (38), tobacco and alcohol use, decreased physical activity, immobilization, and a number of medications (32, 39, 40). Medications/treatments that are administered concomitantly with GCs (such as methotrexate, cyclosporine, heparin, medroxyprogesterone acetate, gonadotropin releasing hormone (GnRH) analogs, levothyroxine, anticonvulsants, or radiotherapy) may add to the disease burden of GCOP.

The emerging use of aromatase inhibitors (41), androgen-deprivation therapy in men with prostate cancer (42), and the growing field of bariatric surgery (43) have emerged as novel and important etiologies of secondary osteoporosis.

Patients with classical congenital adrenal hyperplasia (CAH) can be over-treated with GC and show loss of bone mineral density (BMD) (44). The iatrogenic suppression of adrenal androgens production in women with CAH is associated with increased risk for bone loss (45). Young adult men on GCs apparently show more rapid bone loss compared to older men or postmenopausal or premenopausal women. Of note, men are more susceptible to depression-associated bone loss, which may be in part, GC-mediated (46). Postmenopausal women receiving GCs show higher fracture risk compared to premenopausal women that is attributed to lower bone mass when starting GC therapy) (47, 48). Patients with sarcoidosis and those taking steroids to prevent rejection of grafts after heart or kidney transplant, are also more likely to experience rapid bone loss (49-51).

CELLULAR AND MOLECULAR MECHANISMS OF GCOP

The process of bone remodeling is complex, regulated by an intricate network of local and systemic factors. Although normal bone needs endogenous GCs for its development (for osteoblast differentiation in particular, via inhibition of mesenchymal stem-cell differentiation to adipocytes) (52-54), GCs, at least in mice models, exert negative effects on bone maintenance in old age (by lowering survival of osteoblasts and osteocytes and limiting angiogenesis) (52). Quiescent bone is covered by osteoblasts and osteoclasts. In response to bone-resorbing stimuli, osteoclastic migration and bone resorption are activated. Osteoclasts remove both the organic matrix and the mineral component of the bone, producing a pit. This bone remodeling cycle takes place under a canopy of osteoprogenitor cells (55). In the formation phase, osteoblasts deposit osteoid in the pit, which is then mineralized. In normal bone there is – apparently – no appreciable effect of GCs on osteoclasts (52). Quiescence is restored at completion of the cycle (56). GCs can influence bone remodeling in a number of ways and at any stage of the remodeling cycle (Figure 1). We have to note that regarding animal studies of GCOP experts point to the heterogeneity of used models and the need for their standardization (57).

Figure 1.

Overview of the mechanisms of glucocorticoid-induced osteoporosis (GCOP). Osteoporosis results from an imbalance between osteoblast and osteoclast activity. BMP-2: bone morphogenic protein-2; Cbfa1: core binding factor a1; Bcl-2: B-cell leukemia/lymphoma-2 apoptosis regulator; Bax: BCL-2-associated X protein; IGF-I: insulin-like growth factor-I; IGFBP: IGF binding protein; IGFBP-rPs: IGFBP-related proteins; HGF: hepatocyte growth factor; RANKL: receptor activator of the nuclear factor-κB ligand; CSF-1: colony-stimulating factor-1; OPG: osteoprotegerin; PGE2: Prostaglandin E 2; PGHS-2 prostaglandin synthase-2

EXTRASKELETAL MECHANISMS OF GCOP

INDIVIDUAL SUSCEPTIBILITY TO GCOP

Some patients on a low GC dose show bone loss at a much higher rate than others on a higher GC dose (202). Genetics may play a role in determining this difference. Little is known about the mechanisms of cellular sensitivity to GCs. Individual factors are also important in determining the risk of fractures when GCs are used. Polymorphisms in the GR gene have been linked to the varied degrees of susceptibility to GCs; these could explain the different rates of GC-associated fractures (97). Individuals that are heterozygous for a polymorphism at nucleotide 1,220 (resulting in an Asparagine-to-Serine change at codon 360), had increased BMI, increased blood pressure and lower spine BMD compared to control subjects (203, 204).

Another explanation for inter-individual variability among those exposed to GCs is related to differential activity of 11β-hydroxysteroid dehydrogenase (11β-HSD) (205). This enzyme system plays a critical role in the regulation of GCs activity (206). Two distinct 11β-HSD enzymes have been described; 11β-HSD1 (converting cortisone [E] to cortisol [F] and 11β-HSD2 (converting F to E) modulate GC and mineralocorticoid hormone action in target organs (205, 207, 208). 11β-HSD1 is widely expressed in GCs target tissues, including bone (206). The reductase activity does not show a large inter-individual variability, whereas the oxidase activity of 11β-HSD2 has a large inter-individual variability. Subjects with higher oxidase activity at bone level may be at greater risk of developing GCOP (209). Men with OP were shown to have increased endogenous GC availability, via apparent 11β-HSD1 activation (210). The activity of 11β-HSD1 and the potential to generate F from E in human osteoblasts is increased by pro-inflammatory cytokines (TNFα, IL-1β and IL-6) and by GCs themselves (211, 212). During inflammation pro-inflammatory cytokines may potentiate GC actions in bone through an “intracrine” mechanism (209, 213). An increase of 11β-SD1 activity occurs with aging, possibly providing an explanation for the enhanced GC effects in the skeleton of elderly subjects (214).

In the future, the characterization of factors accounting for the variability to GC-related bone loss among individuals may identify subjects at higher risk of developing GCOP and, possibly, customize treatment.

DIAGNOSIS OF GCOP

Bone Mineral Density (BMD) Assessment

Changes in BMD early on during GC therapy can be detected by dual-energy X-ray absorptiometry (DXA) and quantitative computed tomography (QCT); classic X-ray studies are useful to detect vertebral compression fractures. Both QCT and DXA can measure cortical and trabecular bone density, however, the former is mostly used to evaluate trabecular bone density, whereas the latter is used to measure cortical and trabecular bone density (231, 232). DXA also helps estimate the risk for fractures, and provides an objective measurement to judge the efficacy of treatment (221, 233, 234). BMD measurement techniques that focus on the vertebral body and exclude the cortical bone of posterior processes, such as lateral DXA scanning, are more sensitive in detecting GCOP (61, 235). However, the selection of a BMD assessment method is influenced by the presence of vertebral deformities, osteophytes, or of calcifications in the aorta that may spuriously elevate spinal BMD values. If this is the case, lateral views of the vertebral bodies are considerably less precise than antero-posterior scans, and therefore less appropriate for following up changes in bone mass. When marked osteophytosis or scoliosis of the spine is seen, proximal femoral densitometry (in the femoral neck) should be chosen (63). The trabecular bone score (TBS), which is a DXA analytical tool that hones on lumber vertebral microarchitecture, may be useful in assessing GCOP (236, 237).

In patients under glucocorticoid treatment fractures tend to occur at BMD values that are lower than the conventional threshold T-score of -2.5 (238, 239). A T-score threshold value of – 1.5 SD is usually the cutoff for GCOP in Europe (5), whereas the American College of Rheumatology (ACR) has defined the T-score cut off to – 1.0 SD to separate “normal” from “not normal” BMD (220). Furthermore, the ACR recommends BMD baseline measurements at the lumbar spine and/or hip before starting any GC treatment longer than 6 months (220). At 6 month intervals from the baseline assessment, or at 12 month intervals, if the patient is receiving therapy to prevent bone loss, follow-up measurements should be done (240, 241). For the United States in particular, Medicare reimburses BMD evaluation for patients on chronic treatment with GC doses higher than 7.5 mg/day of prednisolone equivalent (242).

The Fracture Risk Assessment tool (FRAX) estimates the 10-year risk for osteoporotic fractures at the hip and other sites. FRAX is criticized since it uses hip BMD, whereas vertebral fractures may be more common than hip fractures in subjects receiving GCs (243). Recently simple adjustments for the calculated fracture risk have been presented that take into account glucocorticoid dosage (244) (Figure 2). Use of FRAX is currently advised to stratify GC-treated patients in low, moderate and high fracture risk categories (245, 246).

Figure 2.

Fracture risk stratification and FRAX fracture risk corrections according to glucocorticoid usage (modified from (245); # fracture; T: T-score; postmenop: postmenopausal; corr: corrected; * x 1.15 if glucocorticoid dose > equivalent to 7.5 mg prednisone/day; **x 1.20 if glucocorticoid dose > equivalent to 7.5 mg prednisone/day; ***for > 6months; Z: Z-score; GC Rx: glucocorticoid therapy

PREVENTION AND TREATMENT OF GCOP

Guidelines for the prevention and treatment of GCOP have been put forth from the ACR in 2001, in 2010 (220, 247) and more recently in 2017 (245), the UK Consensus group in Management of GCOP (240) and the Belgian Bone Club (248), among others.

FUTURE THERAPEUTIC OPTIONS

Currently, denosumab is being evaluated for pediatric GCOP (293). Other newer agents that are tentatively evaluated for the treatment of osteoporosis either inhibit osteoclast resorption or stimulate osteoblast bone forming activity. These include antibodies against RANKL (RANKL inhibitors), recombinant osteoprotegrin, inhibitors of osteoclast enzymes, integrin antagonists and agonists to LRP5 (308).

At the time of writing, abaloparatide (PTHrp) and romosozumab (humanized monoclonal antibody that targets sclerostin) have been cleared by the FDA for the treatment of OP in women only (8, 329, 330). One would expect the former to be a good candidate for GCOP in analogy to teriparatide. However, this therapy is not yet approved for GCOP and to the best of our knowledge there are no relevant clinical studies to support its use in GCOP (331). Furthermore, we have to bear in mind that administration of GC > 15 mg/day may attenuate the osseous effects of teriparatide, and this has also been shown with abaloparatide in rodent GCOP models (331, 332). There is an ongoing trial of romosozumab in GCOP but at present this medication has no firm indication for GCOP (313); experimental studies in rodents were encouraging (333).

Other promising future therapeutic options target GC therapy per se. These include the use of disease-modifying antirheumatic drugs or tumor-necrosis factor agents, which could lead to the need for lower GC dosage for autoimmune disease. Furthermore, deflazocort (a prednisone derivative) and liposomal prednisone may be less onerous to bone (334). The search continues to find selective GR agonists (SGRMs) that possess the anti-inflammatory benefits of traditional GCs without the associated adverse effects (335). The SGRMs are selective ligands of the GR, which maintain the transrepressive properties of GCs (usually associated with their beneficial anti-inflammatory effect) while they do not have their transactivating properties (usually associated with metabolic negative effects, including perhaps those on the bone). Some of these molecules may represent an alternative to traditional GCs in the chronic treatment of inflammatory disorders (334, 336). Inhibitors to cathepsin K (which is involved in systemic bone resorption) (337) hold promise for treating GCOP (295, 338). There is interest in therapeutic inhibitors of 11β-HSD1 for patients with endogenous hypercortisolemia such as Cushing’s disease; these inhibitors – in theory – could also mitigate GCOP but no relevant research has been put forth (53).

GLUCOCORTICOID DISCONTINUATION AND REVERSIBILITY OF GCOP

There is no consensus on the reversibility of GCOP. Bone mineral density increases after curative surgery for Cushing’s disease or interruption of exogenous GC treatment (339-341). A prospective study in patients with rheumatoid arthritis showed partial bone regain after discontinuation of low-dose GC therapy that was given for five months (67). If GCs are discontinued and treatment for GCOP is continued, a return to baseline BMD is to be expected within 9 to 15 months (303). In patients with sarcoidosis younger than 45 years, full recovery of bone mass was reported two years after cessation of therapy (342). However, it is unlikely that the large (10% or more) bone mass that is lost during high-dose GC therapy can be completely regained, with full recovery of the mechanical properties of the bone. The likelihood of bone regain may be negatively correlated with the duration of treatment as well as unknown host-related factors. Most complications of osteoporotic fractures, such as vertebral deformities and chronic back pain, are permanent. A sensible approach is to stop anti-osteoporotic treatment 6 to 12 months after discontinuation of GCs administration (303).

REFERENCES

1.

Mazziotti G, Angeli A, Bilezikian JP, Canalis E, Giustina A. Glucocorticoid-induced osteoporosis: an update. Trends Endocrinol Metab. 2006 May-Jun;17(4):144–9. [PubMed: 16678739]

2.

Khosla S, Lufkin EG, Hodgson SF, Fitzpatrick LA, Melton LJ 3rd. Epidemiology and clinical features of osteoporosis in young individuals. Bone. 1994 Sep-Oct;15(5):551–5. [PubMed: 7980966]

3.

Alesci S, De Martino MU, Ilias I, Gold PW, Chrousos GP. Glucocorticoid-induced osteoporosis: from basic mechanisms to clinical aspects. Neuroimmunomodulation. 2005;12(1):1–19. [PubMed: 15756049]

4.

Canalis E. Clinical review 83: Mechanisms of glucocorticoid action in bone: implications to glucocorticoid-induced osteoporosis. J Clin Endocrinol Metab. 1996 Oct;81(10):3441–7. [PubMed: 8855781]

5.

Orcel P. Prise en charge de l'osteoporose cortisonique. Presse Med. 2006 Oct;35(10 Pt 2):1571–7. [PubMed: 17028523]

6.

Walsh LJ, Wong CA, Pringle M, Tattersfield AE. Use of oral corticosteroids in the community and the prevention of secondary osteoporosis: a cross sectional study. Brit Med J. 1996 Aug 10;313(7053):344–6. [PMC free article: PMC2351752] [PubMed: 8760745]

7.

Lupsa BC, Insogna KL, Micheletti RG, Caplan A. Corticosteroid use in chronic dermatologic disorders and osteoporosis. Int J Womens Dermatol. 2021 Dec;7 5Part A:545–51. [PMC free article: PMC8721058] [PubMed: 35024411]

8.

Ayub N, Faraj M, Ghatan S, Reijers JAA, Napoli N, Oei L. The Treatment Gap in Osteoporosis. J Clin Med. 2021 Jul 5;10(13):3002. [PMC free article: PMC8268346] [PubMed: 34279485]

9.

Compston J. Management of glucocorticoid-induced osteoporosis. Nat Rev Rheumatol. 2010;6:82–8. [PubMed: 20125175]

10.

Compston JE. Emerging consensus on prevention and treatment of glucocorticoid-induced osteoporosis. Curr Rheumatol Rep. 2007;9:78–84. [PubMed: 17437672]

11.

Feldstein AC, Elmer PJ, Nichols GA, Herson M. Practice patterns in patient at risk for glucocorticoid-induced osteoporosis. Osteoporos Int. 2005;16:2168–74. [PubMed: 16142501]

12.

Curtis JR, Westfall AO, Allison JJ, Becker A, Casebeer L, Freeman A, et al. Longitudinal patterns in the prevention of osteoporosis in glucocorticoid-treated patients. Arthritis Rheum. 2005;52:2485–94. [PubMed: 16052570]

13.

Duyvendak M, Naunton M, Atthobari J, van den Berg PB, Brouwers JR. Corticosteroid-induced osteoporosis prevention: longitudinal practice patterns in The Nederlands 2001-2005. Osteoporos Int. 2007;18:1429–33. [PubMed: 17323108]

14.

van Staa TP. The pathogenesis, epidemiology and management of glucocorticoid-induced osteoporosis. Calcif Tissue Int. 2006 Sep;79(3):129–37. [PubMed: 16969593]

15.

van Staa TP, Leufkens HGM, Cooper C. The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporos Int. 2002;13:777–87. [PubMed: 12378366]

16.

Steinbuch M, Youket TE, Cohen S. Oral glucocorticoid use is associated with an increased risk of fractures. Osteoporos Int. 2004;15:323–8. [PubMed: 14762652]

17.

van Staa TP, Leufkens HG, Abenhaim L, Begaud B, Zhang B, Cooper C. Use of oral corticosteroids in the United Kingdom. QJM. 2000;93:105–11. [PubMed: 10700481]

18.

Shaker JL, Lukert BP. Osteoporosis associated with excess glucocorticoids. Endocrinol Metab Clin North Am. 2005 Jun;34(2):341–56. viii-ix. [PubMed: 15850846]

19.

Chotiyarnwong P, McCloskey EV. Pathogenesis of glucocorticoid-induced osteoporosis and options for treatment. Nat Rev Endocrinol. 2020 Aug;16(8):437–47. [PubMed: 32286516]

20.

Angeli A, Guglielmi G, Dovio A, Capelli G, de Feo D, Giannini S. High prevalence of asymptomatic vertebral fractures in post-menopausal women receiving chronic glucocorticoid therapy: a cross-sectional outpatient study. Bone. 2006;39:253–9. [PubMed: 16574519]

21.

Vestergaard P, Rejnmark L, Mosekilde L. Fracture risk associated with systemic and topical corticosteroids. J Intern Med. 2005;257:374–84. [PubMed: 15788008]

22.

Van Staa TP, Leufkens HGM, Cooper C. Use of inhaled corticosteroids and risk of fractures. J Bone Miner Res. 2001;16:581–8. [PubMed: 11277277]

23.

van Staa TP, Leufkens HGM, Cooper C. Bone loss and inhaled glucocorticoids. N Engl J Med. 2002;346:533–5. [PubMed: 11858218]

24.

Hubbard RB, Smith CJP, Smeeth L, Harrison TW, Tattersfield AE. Inhaled corticosteroids and hip fractures: a population-based case-control study. Am J Respir Crit Care Med. 2002;166:1563–6. [PubMed: 12406825]

25.

de Vries F, Pouwels S, Lammers JW, Leufkens HG, Bracke M, Cooper C. Use of inhaled and oral glucocorticoids, severity of inflammatory disease and risk of hip/femur fracture: a population-based case-control study. J Intern Med. 2007;261:170–7. [PubMed: 17241182]

26.

Buehring B, Viswanathan R, Binkley N, Busse W. Glucocorticoid-induced osteoporosis: an update on effects and management. J Allergy Clin Immunol. 2013 Nov;132(5):1019–30. [PubMed: 24176682]

27.

Mazziotti G, Giustina A, Canalis E, Bilezikian JP. Glucocorticoid-induced Osteoporosis: clinical and therapeutic aspects. Arq Bras Endocrinol Metab. 2007;51:1404–12. [PubMed: 18209880]

28.

van Hogezand RA, Hamdy NA. Skeletal morbidity in inflammatory bowel disease. Scan J Gastroenterol. 2006;243:S59–S64. [PubMed: 16782623]

29.

Romas E. Bone loss in inflammatory arthritis: mechanisms and therapeutic approaches with bisphosphonates. Best Pract Res Clin Rheumatol. 2005;19:1065–79. [PubMed: 16301197]

30.

Lekamwasam S, Trivedi DP, Khaw KT. An association between respiratory function an bone mineral density in women from the general community: a cross sectional study. Osteoporos Int. 2002;13:710–5. [PubMed: 12195534]

31.

Sin DD, Man JP, Man SF. The risk of osteoporosis in Caucasian men and women with obstructive airways disease. Am J Med. 2003;114:10–4. [PubMed: 12543283]

32.

Dykman TR, Gluck OS, Murphy WA, Hahn TJ, Hahn BH. Evaluation of factors associated with glucocorticoid-induced osteopenia in patients with rheumatic diseases. Arthritis Rheum. 1985 Apr;28(4):361–8. [PubMed: 3872664]

33.

Hofbauer LC, Brueck CC, Singh SK, Dobnig H. Osteoporosis in patients with diabetes mellitus. J Bone Miner Res. 2007;22:1317–28. [PubMed: 17501667]

34.

Nicodemus KK, Folsom AR. Type 1 and type 2 diabetes and incident hip fractures in postmenopausal women. Diabetes Care. 2001;24:1192–7. [PubMed: 11423501]

35.

Zhukouskaya VV, Shepelkevich AP, Chiodini I. Bone Health in Type 1 Diabetes: Where We Are Now and How We Should Proceed. Advances in Endocrinology. 2014;DOI: 10.1155/2014/982129. [CrossRef]

36.

Botushanov NP, Orbetzova MM. Bone mineral density and fracture risk in patients with type 1 and type 2 diabetes mellitus. Folia Med (Plovdiv). 2009;51:12–7. [PubMed: 20232652]

37.

Prentice A. Diet, nutrition and the prevention of osteoporosis. Public Health Nutr. 2004;7:227–43. [PubMed: 14972062]

38.

Heaney RP. Effects of caffeine on bone and the calcium economy. Food and Chemical Toxicology. 2002 2002/9;40(9):1263-70. [PubMed: 12204390]

39.

Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003 2003 November 1;78(5):912–9. [PubMed: 14594776]

40.

Packard PT, Heaney RP. Medical Nutrition Therapy for Patients with Osteoporosis. J Am Diet Assoc. 1997 1997/4;97:414-7. [PubMed: 9120196]

41.

Eastell R, Hannon RA, Cuzick J, Dowsett M, Clack G, Adams JE. Effect of an aromatase inhibitor on BMD and bone turnover markers: 2-years results of the anastrozole, tamoxifen, alone or in combination (ATAC) trial. J Bone Miner Res. 2006;21:1215–23. [PubMed: 16869719]

42.

Ebeling PR. Osteoporosis in men. N Engl J Med. 2008;358:1474–82. [PubMed: 18385499]

43.

Coates PS, Fernstrom JD, Fernstrom MH, Schauer PR, Greenspan SL. Gastric bypass surgery for a morbid obesity leads to an increase in bone turnover and a decrease in bone mass. J Clin Endocrinol Metab. 2004;89:1061–5. [PubMed: 15001587]

44.

Bachelot A, Chakhtoura Z, Samara-Boustani D, Dulon J, Touraine P, Polak M. Bone health should be an important concern in the care of patients affected by 21 hydroxylase deficiency. Int J Pediatr Endocrinol. 2010;2010:326275. [PMC free article: PMC2948879] [PubMed: 20936142]

45.

King JA, Wisniewski AB, Bankowski BJ, Carson KA, Zacur HA, Migeon CJ. Long-term corticosteroid replacement and bone mineral density in adult women with classical congenital adrenal hyperplasia. J Clin Endocrinol Metab. 2006 Mar;91(3):865–9. [PubMed: 16278269]

46.

Cizza G, Ravn P, Chrousos GP, Gold PW. Depression: a major, unrecognized risk factor for osteoporosis? Trends Endocrinol Metab. 2001 Jul;12(5):198–203. [PubMed: 11397644]

47.

Thompson JM, Modin GW, Arnaud CD, Lane NE. Not all postmenopausal women on chronic steroid and estrogen treatment are osteoporotic: predictors of bone mineral density. Calcif Tissue Int. 1997 Nov;61(5):377–81. [PubMed: 9351878]

48.

Varonos S, Ansell BM, Reeve J. Vertebral collapse in juvenile chronic arthritis: its relationship with glucocorticoid therapy. Calcif Tissue Int. 1987 Aug;41(2):75–8. [PubMed: 3115548]

49.

Rizzato G, Tosi G, Mella C, Montemurro L, Zanni D, Sisti S. Prednisone-induced bone loss in sarcoidosis: a risk especially frequent in postmenopausal women. Sarcoidosis. 1988 Sep;5(2):93–8. [PubMed: 3227194]

50.

Rich GM, Mudge GH, Laffel GL, LeBoff MS. Cyclosporine A and prednisone-associated osteoporosis in heart transplant recipients. J Heart Lung Transplant. 1992 Sep-Oct;11(5):950–8. [PubMed: 1420244]

51.

Shane E, Rivas MC, Silverberg SJ, Kim TS, Staron RB, Bilezikian JP. Osteoporosis after cardiac transplantation. Am J Med. 1993 Mar;94(3):257–64. [PubMed: 8452149]

52.

Komori T. Glucocorticoid Signaling and Bone Biology. Horm Metab Res. 2016 Nov;48(11):755–63. [PubMed: 27871116]

53.

Martin CS, Cooper MS, Hardy RS. Endogenous Glucocorticoid Metabolism in Bone: Friend or Foe. Front Endocrinol (Lausanne). 2021;12:733611. [PMC free article: PMC8429897] [PubMed: 34512556]

54.

Peng CH, Lin WY, Yeh KT, Chen IH, Wu WT, Lin MD. The molecular etiology and treatment of glucocorticoid-induced osteoporosis. Tzu Chi Med J. 2021 Jul-Sep;33(3):212–23. [PMC free article: PMC8323641] [PubMed: 34386357]

55.

Jensen PR, Andersen TL, Hauge EM, Bollerslev J, Delaisse JM. A joined role of canopy and reversal cells in bone remodeling--lessons from glucocorticoid-induced osteoporosis. Bone. 2015 Apr;73:16–23. [PubMed: 25497571]

56.

Katagiri T, Takahashi N. Regulatory mechanisms of osteoblast and osteoclast differentiation. Oral Dis. 2002 May;8(3):147–59. [PubMed: 12108759]

57.

Xavier A, Toumi H, Lespessailles E. Animal Model for Glucocorticoid Induced Osteoporosis: A Systematic Review from 2011 to 2021. Int J Mol Sci. 2021 Dec 29;23(1) [PMC free article: PMC8745049] [PubMed: 35008803]

58.

Ehrlich PJ, Lanyon LE. Mechanical strain and bone cell function: a review. Osteoporos Int. 2002 Sep;13(9):688–700. [PubMed: 12195532]

59.

Laan RF, Buijs WC, van Erning LJ, Lemmens JA, Corstens FH, Ruijs SH, et al. Differential effects of glucocorticoids on cortical appendicular and cortical vertebral bone mineral content. Calcif Tissue Int. 1993 Jan;52(1):5–9. [PubMed: 8453505]

60.

Reid IR, Heap SW. Determinants of vertebral mineral density in patients receiving long-term glucocorticoid therapy. Arch Intern Med. 1990 Dec;150(12):2545–8. [PubMed: 2244770]

61.

Reid IR, Evans MC, Stapleton J. Lateral spine densitometry is a more sensitive indicator of glucocorticoid-induced bone loss. J Bone Miner Res. 1992 Oct;7(10):1221–5. [PubMed: 1456089]

62.

Yao W, Dai W, Jiang JX, Lane NE. Glucocorticoids and osteocyte autophagy. Bone. 2013 Jun;54(2):279–84. [PMC free article: PMC3784314] [PubMed: 23356984]

63.

Reid IR, Evans MC, Wattie DJ, Ames R, Cundy TF. Bone mineral density of the proximal femur and lumbar spine in glucocorticoid-treated asthmatic patients. Osteoporos Int. 1992 Mar;2(2):103–5. [PubMed: 1536979]

64.

Sambrook P, Birmingham J, Kempler S, Kelly P, Eberl S, Pocock N, et al. Corticosteroid effects on proximal femur bone loss. J Bone Miner Res. 1990 Dec;5(12):1211–6. [PubMed: 2075834]

65.

Lane NE. An update on glucocorticoid-induced osteoporosis. Rheum Dis Clin North Am. 2001 Feb;27(1):235–53. [PubMed: 11285998]

66.

Saag KG. Glucocorticoid-induced osteoporosis. Endocrinol Metab Clin North Am. 2003 Mar;32(1):135–57. [PubMed: 12699296]

67.

Adinoff AD, Hollister JR. Steroid-induced fractures and bone loss in patients with asthma. N Engl J Med. 1983 Aug 4;309(5):265–8. [PubMed: 6866051]

68.

Dempster DW. Bone histomorphometry in glucocorticoid-induced osteoporosis. J Bone Miner Res. 1989 Apr;4(2):137–41. [PubMed: 2658477]

69.

Hahn TJ, Boisseau VC, Avioli LV. Effect of chronic corticosteroid administration on diaphyseal and metaphyseal bone mass. J Clin Endocrinol Metab. 1974 Aug;39(2):274–82. [PubMed: 4418482]

70.

Aaron JE, Francis RM, Peacock M, Makins NB. Contrasting microanatomy of idiopathic and corticosteroid-induced osteoporosis. Clin Orthop. 1989 Jun;(243):294–305. [PubMed: 2721071]

71.

Hartmann K, Koenen M, Schauer S, Wittig-Blaich S, Ahmad M, Baschant U, et al. Molecular Actions of Glucocorticoids in Cartilage and Bone During Health, Disease, and Steroid Therapy. Physiol Rev. 2016 Apr;96(2):409–47. [PubMed: 26842265]

72.

Bamberger CM, Schulte HM, Chrousos GP. Molecular determinants of glucocorticoid receptor function and tissue sensitivity to glucocorticoids. Endocr Rev. 1996 Jun;17(3):245–61. [PubMed: 8771358]

73.

Vottero A, Chrousos GP. Glucocorticoid Receptor beta: View I. Trends Endocrinol Metab. 1999 Oct;10(8):333–8. [PubMed: 10481166]

74.

Beavan S, Horner A, Bord S, Ireland D, Compston J. Colocalization of glucocorticoid and mineralocorticoid receptors in human bone. J Bone Miner Res. 2001 Aug;16(8):1496–504. [PubMed: 11499872]

75.

Masera RG, Dovio A, Sartori ML, Racca S, Angeli A. Interleukin-6 upregulates glucocorticoid receptor numbers in human osteoblast-like cells. Z Rheumatol. 2000;59 Suppl 2:II/103-7. [PubMed: 11155789]

76.

Dovio A, Masera RG, Sartori ML, Racca S, Angeli A. Autocrine up-regulation of glucocorticoid receptors by interleukin-6 in human osteoblast-like cells. Calcif Tissue Int. 2001 Nov;69(5):293–8. [PubMed: 11768200]

77.

Dovio A, Sartori ML, Masera RG, Ceoloni B, Reimondo G, Prolo P, et al. Autocrine down-regulation of glucocorticoid receptors by interleukin-11 in human osteoblast-like cell lines. J Endocrinol. 2003 Apr;177(1):109–17. [PubMed: 12697042]

78.

Angeli A, Dovio A, Sartori ML, Masera RG, Ceoloni B, Prolo P, et al. Interactions between glucocorticoids and cytokines in the bone microenvironment. Ann N Y Acad Sci. 2002 Jun;966:97–107. [PubMed: 12114264]

79.

Piemontese M, Onal M, Xiong J, Wang Y, Almeida M, Thostenson JD, et al. Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone. Bone. 2015 Jun;75:18–26. [PMC free article: PMC4387016] [PubMed: 25700544]

80.

Weinstein RS, Jilka RL, Michael Parfitt A, 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(2):274–82. [PMC free article: PMC508885] [PubMed: 9664068]

81.

O'Brien CA, Jia D, Plotkin LI, Bellido T, Powers CC, Stewart SA, et al. Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength. Endocrinology. 2004;145:1835–41. [PubMed: 14691012]

82.

Toth M, Grossman A. Glucocorticoid-induced osteoporosis: lessons from Cushing's syndrome. Clin Endocrinol (Oxf). 2013 Jul;79(1):1–11. [PubMed: 23452135]

83.

Webster JM, Fenton CG, Langen R, Hardy RS. Exploring the Interface between Inflammatory and Therapeutic Glucocorticoid Induced Bone and Muscle Loss. Int J Mol Sci. 2019 Nov 16;20(22) [PMC free article: PMC6888251] [PubMed: 31744114]

84.

Manolagas SC. Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocr Rev. 2000 Apr;21(2):115–37. [PubMed: 10782361]

85.

Shi J, Wang L, Zhang H, Jie Q, Li X, Shi Q, et al. Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy. Bone. 2015 Oct;79:222–32. [PubMed: 26115910]

86.

Sato AY, Tu X, McAndrews KA, Plotkin LI, Bellido T. Prevention of glucocorticoid induced-apoptosis of osteoblasts and osteocytes by protecting against endoplasmic reticulum (ER) stress in vitro and in vivo in female mice. Bone. 2015 Apr;73:60–8. [PMC free article: PMC4336847] [PubMed: 25532480]

87.

Stromstedt PE, Poellinger L, Gustafsson JA, Carlstedt-Duke J. The glucocorticoid receptor binds to a sequence overlapping the TATA box of the human osteocalcin promoter: a potential mechanism for negative regulation. Mol Cell Biol. 1991 Jun;11(6):3379–83. [PMC free article: PMC360193] [PubMed: 2038339]

88.

Heinrichs AA, Bortell R, Rahman S, Stein JL, Alnemri ES, Litwack G, et al. Identification of multiple glucocorticoid receptor binding sites in the rat osteocalcin gene promoter. Biochemistry. 1993 Oct 26;32(42):11436–44. [PubMed: 8218210]

89.

Jonat C, Rahmsdorf HJ, Park KK, Cato AC, Gebel S, Ponta H, et al. Antitumor promotion and antiinflammation: down-modulation of AP-1 (Fos/Jun) activity by glucocorticoid hormone. Cell. 1990 Sep 21;62(6):1189–204. [PubMed: 2169351]

90.

Morrison N, Eisman J. Role of the negative glucocorticoid regulatory element in glucocorticoid repression of the human osteocalcin promoter. J Bone Miner Res. 1993 Aug;8(8):969–75. [PubMed: 8213259]

91.

Raisz LG. Pathogenesis of osteoporosis: concepts, conflicts, and prospects. J Clin Invest. 2005 Dec;115(12):3318–25. [PMC free article: PMC1297264] [PubMed: 16322775]

92.

Ohnaka K, Tanabe M, Kawate H, Nawata H, Takayanagi R. Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts. Biochem Biophys Res Commun. 2005 Apr 1;329(1):177–81. [PubMed: 15721290]

93.

Weinstein RS. Glucocorticoid-induced bone disease. In: Rosen CJ, editor. Primer on the metabolic bone diseases and disorders of mineral metabolism. Ames, Iowa: John Wiley & Sons/American Society for Bone and Mineral Research; 2013. p. 473-81.

94.

Moutsatsou P, Kassi E, Papavassiliou AG. Glucocorticoid receptor signaling in bone cells. Trends Mol Med. 2012 Jun;18(6):348–59. [PubMed: 22578718]

95.

Rauch A, Seitz S, Baschant U, Schilling AF, Illing A, Stride B, et al. Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor. Cell Metab. 2010 Jun 9;11(6):517–31. [PubMed: 20519123]

96.

Derfoul A, Perkins GL, Hall DJ, Tuan RS. Glucocorticoids promote chondrogenic differentiation of adult human mesenchymal stem cells by enhancing expression of cartilage extracellular matrix genes. Stem Cells. 2006 Jun;24(6):1487–95. [PubMed: 16469821]

97.

Wood CL, Soucek O, Wong SC, Zaman F, Farquharson C, Savendahl L, et al. Animal models to explore the effects of glucocorticoids on skeletal growth and structure. J Endocrinol. 2018 Jan;236(1):R69–R91. [PubMed: 29051192]

98.

Kang H, Chen H, Huang P, Qi J, Qian N, Deng L, et al. Glucocorticoids impair bone formation of bone marrow stromal stem cells by reciprocally regulating microRNA-34a-5p. Osteoporos Int. 2016;27:1493–505. [PubMed: 26556739]

99.

Gronowicz G, McCarthy MB, Raisz LG. Glucocorticoids stimulate resorption in fetal rat parietal bones in vitro. J Bone Miner Res. 1990 Dec;5(12):1223–30. [PubMed: 2127506]

100.

Lowe C, Gray DH, Reid IR. Serum blocks the osteolytic effect of cortisol in neonatal mouse calvaria. Calcif Tissue Int. 1992 Feb;50(2):189–92. [PubMed: 1571836]

101.

Conaway HH, Grigorie D, Lerner UH. Differential effects of glucocorticoids on bone resorption in neonatal mouse calvariae stimulated by peptide and steroid-like hormones. J Endocrinol. 1997 Dec;155(3):513–21. [PubMed: 9487996]

102.

Bar-Shavit Z, Kahn AJ, Pegg LE, Stone KR, Teitelbaum SL. Glucocorticoids modulate macrophage surface oligosaccharides and their bone binding activity. J Clin Invest. 1984 May;73(5):1277–83. [PMC free article: PMC425148] [PubMed: 6715537]

103.

Teitelbaum SL, Bar-Shavit Z, Fallon MD, Imbimbo C, Malone JD, Kahn AJ. Glucocorticoids and bone resorption. Adv Exp Med Biol. 1984;171:121–9. [PubMed: 6372391]

104.

Liu YZ, Dvornyk V, Lu Y, Shen H, Lappe JM, Recker RR, et al. A novel pathophysiological mechanism for osteoporosis suggested by an in vivo gene expression study of circulating monocytes. J Biol Chem. 2005 Aug 12;280(32):29011–6. [PubMed: 15965235]

105.

Takuma A, Kaneda T, Sato T, Ninomiya S, Kumegawa M, Hakeda Y. Dexamethasone enhances osteoclast formation synergistically with transforming growth factor-beta by stimulating the priming of osteoclast progenitors for differentiation into osteoclasts. J Biol Chem. 2003 Nov 7;278(45):44667–74. [PubMed: 12944401]

106.

Heymann D, Guicheux J, Gouin F, Passuti N, Daculsi G. Cytokines, growth factors and osteoclasts. Cytokine. 1998 Mar;10(3):155–68. [PubMed: 9576060]

107.

Rifas L. Bone and cytokines: beyond IL-1, IL-6 and TNF-alpha. Calcif Tissue Int. 1999 Jan;64(1):1–7. [PubMed: 9868276]

108.

Horowitz MC, Xi Y, Wilson K, Kacena MA. Control of osteoclastogenesis and bone resorption by members of the TNF family of receptors and ligands. Cytokine Growth Factor Rev. 2001 Mar;12(1):9–18. [PubMed: 11312114]

109.

Hofbauer LC, Heufelder AE. Clinical review 114: hot topic. The role of receptor activator of nuclear factor-kappaB ligand and osteoprotegerin in the pathogenesis and treatment of metabolic bone diseases. J Clin Endocrinol Metab. 2000 Jul;85(7):2355–63. [PubMed: 10902778]

110.

Pfeilschifter J, Seyedin SM, Mundy GR. Transforming growth factor beta inhibits bone resorption in fetal rat long bone cultures. J Clin Invest. 1988 Aug;82(2):680–5. [PMC free article: PMC303563] [PubMed: 3165385]

111.

Ake Y, Saegusa Y, Matsubara T, Mizuno K. Cultured osteoblast synthesize nitric oxide in response to cytokines and lipopolysaccharide. Kobe J Med Sci. 1994 Aug;40(3-4):125–37. [PubMed: 7739201]

112.

Vidal NO, Brandstrom H, Jonsson KB, Ohlsson C. Osteoprotegerin mRNA is expressed in primary human osteoblast-like cells: down-regulation by glucocorticoids. J Endocrinol. 1998;159:191–5. [PubMed: 9795357]

113.

Bornefalk E, Dahlen I, Johannsson G, Ljunggren O, Ohlsson C. Serum levels of osteoprotegerin: effects of glucocorticoids and growth hormone. Bone. 1998;23:S486.

114.

Hofbauer LC, Gori F, Riggs BL, Lacey DL, Dunstan CR, Spelsberg TC, 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 Oct;140(10):4382–9. [PubMed: 10499489]

115.

Hock JM, Centrella M, Canalis E. Insulin-like growth factor I has independent effects on bone matrix formation and cell replication. Endocrinology. 1988 Jan;122(1):254–60. [PubMed: 3335207]

116.

Canalis E, Rydziel S, Delany AM, Varghese S, Jeffrey JJ. Insulin-like growth factors inhibit interstitial collagenase synthesis in bone cell cultures. Endocrinology. 1995 Apr;136(4):1348–54. [PubMed: 7895645]

117.

Delany AM, Durant D, Canalis E. Glucocorticoid suppression of IGF I transcription in osteoblasts. Mol Endocrinol. 2001 Oct;15(10):1781–9. [PubMed: 11579210]

118.

Bennett A, Chen T, Feldman D, Hintz RL, Rosenfeld RG. Characterization of insulin-like growth factor I receptors on cultured rat bone cells: regulation of receptor concentration by glucocorticoids. Endocrinology. 1984 Oct;115(4):1577–83. [PubMed: 6090106]

119.

Rydziel S, Canalis E. Cortisol represses insulin-like growth factor II receptor transcription in skeletal cell cultures. Endocrinology. 1995 Oct;136(10):4254–60. [PubMed: 7664643]

120.

Rechler MM. Insulin-like growth factor binding proteins. Vitam Horm. 1993;47:1–114. [PubMed: 7680510]

121.

Okazaki R, Riggs BL, Conover CA. Glucocorticoid regulation of insulin-like growth factor-binding protein expression in normal human osteoblast-like cells. Endocrinology. 1994 Jan;134(1):126–32. [PubMed: 7506203]

122.

Gabbitas B, Pash JM, Delany AM, Canalis E. Cortisol inhibits the synthesis of insulin-like growth factor-binding protein-5 in bone cell cultures by transcriptional mechanisms. J Biol Chem. 1996 Apr 12;271(15):9033–8. [PubMed: 8621551]

123.

Andress DL, Birnbaum RS. Human osteoblast-derived insulin-like growth factor (IGF) binding protein-5 stimulates osteoblast mitogenesis and potentiates IGF action. J Biol Chem. 1992 Nov 5;267(31):22467–72. [PubMed: 1385400]

124.

Mehls O, Himmele R, Homme M, Kiepe D, Klaus G. The interaction of glucocorticoids with the growth hormone-insulin-like growth factor axis and its effects on growth plate chondrocytes and bone cells. J Pediatr Endocrinol Metab. 2001;14:1475–82. [PubMed: 11837502]

125.

Pereira RC, Blanquaert F, Canalis E. Cortisol enhances the expression of mac25/insulin-like growth factor-binding protein-related protein-1 in cultured osteoblasts. Endocrinology. 1999 Jan;140(1):228–32. [PubMed: 9886829]

126.

Wong SC, Dobie R, Altowati MA, Werther GA, Farquharson C, Ahmed SF. Growth and the Growth Hormone-Insulin Like Growth Factor 1 Axis in Children With Chronic Inflammation: Current Evidence, Gaps in Knowledge, and Future Directions. Endocrine Reviews. 2016;37(1):62–110. [PubMed: 26720129]

127.

Canalis E, Pash J, Varghese S. Skeletal growth factors. Crit Rev Eukaryot Gene Expr. 1993;3(3):155–66. [PubMed: 8241601]

128.

Gurlek A, Kumar R. Regulation of osteoblast growth by interactions between transforming growth factor-beta and 1alpha,25-dihydroxyvitamin D3. Crit Rev Eukaryot Gene Expr. 2001;11(4):299–317. [PubMed: 12067069]

129.

Alliston T, Choy L, Ducy P, Karsenty G, Derynck R. TGF-beta-induced repression of CBFA1 by Smad3 decreases cbfa1 and osteocalcin expression and inhibits osteoblast differentiation. Embo J. 2001 May 1;20(9):2254–72. [PMC free article: PMC125448] [PubMed: 11331591]

130.

Centrella M, McCarthy TL, Canalis E. Glucocorticoid regulation of transforming growth factor beta 1 activity and binding in osteoblast-enriched cultures from fetal rat bone. Mol Cell Biol. 1991 Sep;11(9):4490–6. [PMC free article: PMC361319] [PubMed: 1875934]

131.

Oursler MJ, Riggs BL, Spelsberg TC. Glucocorticoid-induced activation of latent transforming growth factor-beta by normal human osteoblast-like cells. Endocrinology. 1993 Nov;133(5):2187–96. [PubMed: 8404670]

132.

Fuller K, Owens J, Chambers TJ. The effect of hepatocyte growth factor on the behaviour of osteoclasts. Biochem Biophys Res Commun. 1995 Jul 17;212(2):334–40. [PubMed: 7626045]

133.

Sato T, Hakeda Y, Yamaguchi Y, Mano H, Tezuka K, Matsumoto K, et al. Hepatocyte growth factor is involved in formation of osteoclast-like cells mediated by clonal stromal cells (MC3T3-G2/PA6). J Cell Physiol. 1995 Jul;164(1):197–204. [PubMed: 7790391]

134.

Grano M, Galimi F, Zambonin G, Colucci S, Cottone E, Zallone AZ, et al. Hepatocyte growth factor is a coupling factor for osteoclasts and osteoblasts in vitro. Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):7644–8. [PMC free article: PMC38800] [PubMed: 8755529]

135.

Ferracini R, Di Renzo MF, Scotlandi K, Baldini N, Olivero M, Lollini P, et al. The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit. Oncogene. 1995 Feb 16;10(4):739–49. [PubMed: 7862451]

136.

Hock JM, Canalis E. Platelet-derived growth factor enhances bone cell replication, but not differentiated function of osteoblasts. Endocrinology. 1994 Mar;134(3):1423–8. [PubMed: 8119182]

137.

Raines EW, Lane TF, Iruela-Arispe ML, Ross R, Sage EH. The extracellular glycoprotein SPARC interacts with platelet-derived growth factor (PDGF)-AB and -BB and inhibits the binding of PDGF to its receptors. Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1281–5. [PMC free article: PMC48433] [PubMed: 1311092]

138.

Ng KW, Manji SS, Young MF, Findlay DM. Opposing influences of glucocorticoid and retinoic acid on transcriptional control in preosteoblasts. Mol Endocrinol. 1989 Dec;3(12):2079–85. [PubMed: 2628742]

139.

Raisz LG. Prostaglandins and bone: physiology and pathophysiology. Osteoarthr Cartilage. 1999 Jul;7(4):419–21. [PubMed: 10419786]

140.

Chyun YS, Raisz LG. Stimulation of bone formation by prostaglandin E2. Prostaglandins. 1984 Jan;27(1):97–103. [PubMed: 6584942]

141.

Canalis E. The hormonal and local regulation of bone formation. Endocr Rev. 1983 Winter;4(1):62–77. [PubMed: 6299718]

142.

Kenkre JS, Bassett JHD. The bone remodelling cycle. Annals of Clinical Biochemistry. 2017 [PubMed: 29368538] [CrossRef]

143.

Raisz LG, Dietrich JW, Canalis EM. Factors influencing bone formation in organ culture. Isr J Med Sci. 1976 Feb;12(2):108–14. [PubMed: 1262198]

144.

Raisz LG, Fall PM. Biphasic effects of prostaglandin E2 on bone formation in cultured fetal rat calvariae: interaction with cortisol. Endocrinology. 1990 Mar;126(3):1654–9. [PubMed: 2155107]

145.

Hughes-Fulford M. Prostaglandin regulation of gene expression and growth in normal and malignant tissues. Adv Exp Med Biol. 1997;400A:269–78. [PubMed: 9547568]

146.

Hughes-Fulford M, Appel R, Kumegawa M, Schmidt J. Effect of dexamethasone on proliferating osteoblasts: inhibition of prostaglandin E2 synthesis, DNA synthesis, and alterations in actin cytoskeleton. Exp Cell Res. 1992 Nov;203(1):150–6. [PubMed: 1426038]

147.

Kimberg DV, Baerg RD, Gershon E, Graudusius RT. Effect of cortisone treatment on the active transport of calcium by the small intestine. J Clin Invest. 1971 Jun;50(6):1309–21. [PMC free article: PMC292062] [PubMed: 4325312]

148.

Fuller K, Chambers TJ. Effect of arachidonic acid metabolites on bone resorption by isolated rat osteoclasts. J Bone Miner Res. 1989 Apr;4(2):209–15. [PubMed: 2499165]

149.

Klein DC, Raisz LG. Prostaglandins: stimulation of bone resorption in tissue culture. Endocrinology. 1970 Jun;86(6):1436–40. [PubMed: 4315103]

150.

Bellido T, Hill Gallant KM. Hormonal Effects on Bone Cells. In: Burr DB, Allen MR, editors. Basic and Applied Bone Biology. London: Elsevier; 2014. p. 299-314.

151.

Wajchenberg BL, Pereira VG, Kieffer J, Ursic S. Effect of dexamethasone on calcium metabolism and 47Ca kinetics in normal subjects. Acta Endocrinol (Copenh). 1969 May;61(1):173–92. [PubMed: 4890968]

152.

Morris HA, Need AG, O'Loughlin PD, Horowitz M, Bridges A, Nordin BE. Malabsorption of calcium in corticosteroid-induced osteoporosis. Calcif Tissue Int. 1990 May;46(5):305–8. [PubMed: 2110853]

153.

Binder HJ. Effect of dexamethasone on electrolyte transport in the large intestine of the rat. Gastroenterology. 1978 Aug;75(2):212–7. [PubMed: 149689]

154.

Sjoberg HE. Retention of orally administered 47-calcium in man under normal and diseased conditions studied with a whole-body counter technique. Acta Med Scand Suppl. 1970;509:1–28. [PubMed: 5273461]

155.

Lee DB. Unanticipated stimulatory action of glucocorticoids on epithelial calcium absorption. Effect of dexamethasone on rat distal colon. J Clin Invest. 1983 Feb;71(2):322–8. [PMC free article: PMC436870] [PubMed: 6822667]

156.

Hahn TJ, Halstead LR, Strates B, Imbimbo B, Baran DT. Comparison of subacute effects of oxazacort and prednisone on mineral metabolism in man. Calcif Tissue Int. 1980;31(2):109–15. [PubMed: 6770974]

157.

Lekkerkerker JF, Van Woudenberg F, Doorenbos H. Influence of low dose of steroid therapy on calcium absorption. Acta Endocrinol (Copenh). 1972 Mar;69(3):488–96. [PubMed: 5067013]

158.

Aloia JF, Semla HM, Yeh JK. Discordant effects of glucocorticoids on active and passive transport of calcium in the rat duodenum. Calcif Tissue Int. 1984 May;36(3):327–31. [PubMed: 6432296]

159.

Shultz TD, Bollman S, Kumar R. Decreased intestinal calcium absorption in vivo and normal brush border membrane vesicle calcium uptake in cortisol-treated chickens: evidence for dissociation of calcium absorption from brush border vesicle uptake. Proc Natl Acad Sci U S A. 1982 Jun;79(11):3542–6. [PMC free article: PMC346457] [PubMed: 6954501]

160.

Kimura S, Rasmussen H. Adrenal glucocorticoids, adenine nucleotide translocation, and mitochondrial calcium accumulation. J Biol Chem. 1977 Feb 25;252(4):1217–25. [PubMed: 190224]

161.

Suzuki Y, Ichikawa Y, Saito E, Homma M. Importance of increased urinary calcium excretion in the development of secondary hyperparathyroidism of patients under glucocorticoid therapy. Metabolism. 1983 Feb;32(2):151–6. [PubMed: 6298567]

162.

Nielsen HK, Thomsen K, Eriksen EF, Charles P, Storm T, Mosekilde L. The effects of high-dose glucocorticoid administration on serum bone gamma carboxyglutamic acid-containing protein, serum alkaline phosphatase and vitamin D metabolites in normal subjects. Bone Miner. 1988 Apr;4(1):105–13. [PubMed: 3263890]

163.

Adams JS, Wahl TO, Lukert BP. Effects of hydrochlorothiazide and dietary sodium restriction on calcium metabolism in corticosteroid treated patients. Metabolism. 1981 Mar;30(3):217–21. [PubMed: 7207196]

164.

Au WY. Cortisol stimulation of parathyroid hormone secretion by rat parathyroid glands in organ culture. Science. 1976 Sep 10;193(4257):1015–7. [PubMed: 948759]

165.

Cosman F, Nieves J, Herbert J, Shen V, Lindsay R. High-dose glucocorticoids in multiple sclerosis patients exert direct effects on the kidney and skeleton. J Bone Miner Res. 1994 Jul;9(7):1097–105. [PubMed: 7942157]

166.

Freiberg JM, Kinsella J, Sacktor B. Glucocorticoids increase the Na+-H+ exchange and decrease the Na+ gradient-dependent phosphate-uptake systems in renal brush border membrane vesicles. Proc Natl Acad Sci U S A. 1982 Aug;79(16):4932–6. [PMC free article: PMC346799] [PubMed: 6956901]

167.

Heersche JN, Jez DH, Aubin J, Sodek J. Regulation of hormone responsiveness of bone in vitro by corticosteroids, PTH, PGE2, and calcitonin. In: Talmage RV, Cohn DV, Mathews JL, editors. Hormonal control of calcium metabolism. Amsterdam: Excerpta Medica; 1981. p. 157-62.

168.

Fucik RF, Kukreja SC, Hargis GK, Bowser EN, Henderson WJ, Williams GA. Effect of glucocorticoids on function of the parathyroid glands in man. J Clin Endocrinol Metab. 1975 Jan;40(1):152–5. [PubMed: 1112874]

169.

Lukert BP, Adams JS. Calcium and phosphorus homeostasis in man. Effect of corticosteroids. Arch Intern Med. 1976 Nov;136(11):1249–53. [PubMed: 185973]

170.

Bonadonna S, Burattin A, Nuzzo M, Bugari G, Rosei EA, Valle D, et al. Chronic glucocorticoid treatment alters spontaneous pulsatile parathyroid hormone secretory dynamics in human subjects. Eur J Endocrinol. 2005 Feb;152(2):199–205. [PubMed: 15745926]

171.

Lukert BP, Stanbury SW, Mawer EB. Vitamin D and intestinal transport of calcium: effects of prednisolone. Endocrinology. 1973 Sep;93(3):718–22. [PubMed: 4352809]

172.

Hahn TJ, Halstead LR, Haddad JG Jr. Serum 25-hydroxyvitamin D concentrations in patients receiving chronic corticosteroid therapy. J Lab Clin Med. 1977 Aug;90(2):399–404. [PubMed: 886226]

173.

Chesney RW, Mazess RB, Hamstra AJ, DeLuca HF, O'Reagan S. Reduction of serum-1, 25-dihydroxyvitamin-D3 in children receiving glucocorticoids. Lancet. 1978 Nov 25;2(8100):1123–5. [PubMed: 82684]

174.

Zerwekh JE, Emkey RD, Harris ED Jr. Low-dose prednisone therapy in rheumatoid arthritis: effect on vitamin D metabolism. Arthritis Rheum. 1984 Sep;27(9):1050–2. [PubMed: 6383408]

175.

Seeman E, Kumar R, Hunder GG, Scott M, Heath H 3rd, Riggs BL. Production, degradation, and circulating levels of 1,25-dihydroxyvitamin D in health and in chronic glucocorticoid excess. J Clin Invest. 1980 Oct;66(4):664–9. [PMC free article: PMC371639] [PubMed: 7419714]

176.

Colette C, Monnier L, Pares Herbute N, Blotman F, Mirouze J. Calcium absorption in corticoid treated subjects effects of a single oral dose of calcitriol. Horm Metab Res. 1987 Jul;19(7):335–8. [PubMed: 3623424]

177.

Luton JP, Thieblot P, Valcke JC, Mahoudeau JA, Bricaire H. Reversible gonadotropin deficiency in male Cushing's disease. J Clin Endocrinol Metab. 1977 Sep;45(3):488–95. [PubMed: 198424]

178.

Sakakura M, Takebe K, Nakagawa S. Inhibition of luteinizing hormone secretion induced by synthetic LRH by long-term treatment with glucocorticoids in human subjects. J Clin Endocrinol Metab. 1975 May;40(5):774–9. [PubMed: 1092709]

179.

Hsueh AJ, Erickson GF. Glucocorticoid inhibition of FSH-induced estrogen production in cultured rat granulosa cells. Steroids. 1978 Dec;32(5):639–48. [PubMed: 734698]

180.

Swift AD, Crighton DB. The effects of certain steroid hormones on the activity of ovine hypothalamic luteinizing hormone-releasing hormone (LH-RH)-degrading enzymes. FEBS Lett. 1979 Apr 1;100(1):110–2. [PubMed: 374114]

181.

Dubey AK, Plant TM. A suppression of gonadotropin secretion by cortisol in castrated male rhesus monkeys (Macaca mulatta) mediated by the interruption of hypothalamic gonadotropin-releasing hormone release. Biol Reprod. 1985 Sep;33(2):423–31. [PubMed: 3929850]

182.

Sapolsky RM. Stress-induced suppression of testicular function in the wild baboon: role of glucocorticoids. Endocrinology. 1985 Jun;116(6):2273–8. [PubMed: 2986942]

183.

Crilly R, Cawood M, Marshall DH, Nordin BE. Hormonal status in normal, osteoporotic and corticosteroid-treated postmenopausal women. J R Soc Med. 1978 Oct;71(10):733–6. [PMC free article: PMC1436218] [PubMed: 712726]

184.

Montecucco C, Caporali R, Caprotti P, Caprotti M, Notario A. Sex hormones and bone metabolism in postmenopausal rheumatoid arthritis treated with two different glucocorticoids. J Rheumatol. 1992 Dec;19(12):1895–900. [PubMed: 1294736]

185.

MacAdams MR, White RH, Chipps BE. Reduction of serum testosterone levels during chronic glucocorticoid therapy. Ann Intern Med. 1986 May;104(5):648–51. [PubMed: 3083749]

186.

Urban RJ, Veldhuis JD. Endocrine control of steroidogenesis in granulosa cells. Oxf Rev Reprod Biol. 1992;14:225–62. [PubMed: 1331938]

187.

Buyon JP, Dooley MA, Meyer WR, Petri M, Licciardi F. Recommendations for exogenous estrogen to prevent glucocorticoid-induced osteoporosis in premenopausal women with oligo- or amenorrhea: comment on the American College of Rheumatology recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Rheum. 1997 Aug;40(8):1548–9. [PubMed: 9259444]

188.

Goulding A, Gold E. Effects of chronic prednisolone treatment on bone resorption and bone composition in intact and ovariectomized rats and in ovariectomized rats receiving beta-estradiol. Endocrinology. 1988 Feb;122(2):482–7. [PubMed: 3338411]

189.

Ohlsson C, Bengtsson BA, Isaksson OG, Andreassen TT, Slootweg MC. Growth hormone and bone. Endocr Rev. 1998 Feb;19(1):55–79. [PubMed: 9494780]

190.

Giustina A, Bussi AR, Jacobello C, Wehrenberg WB. Effects of recombinant human growth hormone (GH) on bone and intermediary metabolism in patients receiving chronic glucocorticoid treatment with suppressed endogenous GH response to GH-releasing hormone. J Clin Endocrinol Metab. 1995 Jan;80(1):122–9. [PubMed: 7829600]

191.

Manelli F, Carpinteri R, Bossoni S, Burattin A, Bonadonna S, Agabiti Rosei E, et al. Growth hormone in glucocorticoid-induced osteoporosis. Front Horm Res. 2002;30:174–83. [PubMed: 11892265]

192.

King AP, Tseng MJ, Logsdon CD, Billestrup N, Carter-Su C. Distinct cytoplasmic domains of the growth hormone receptor are required for glucocorticoid- and phorbol ester-induced decreases in growth hormone (GH) binding. These domains are different from that reported for GH-induced receptor internalization. J Biol Chem. 1996 Jul 26;271(30):18088–94. [PubMed: 8663346]

193.

Pratt WB, Aronow L. The effect of glucocorticoids on protein and nucleic acid synthesis in mouse fibroblasts growing in vitro. J Biol Chem. 1966 Nov 25;241(22):5244–50. [PubMed: 5928001]

194.

Leibovich SJ, Ross R. The role of the macrophage in wound repair. A study with hydrocortisone and antimacrophage serum. Am J Pathol. 1975 Jan;78(1):71–100. [PMC free article: PMC1915032] [PubMed: 1109560]

195.

Afifi AK, Bergman RA, Harvey JC. Steroid myopathy. Clinical, histologic and cytologic observations. Johns Hopkins Med J. 1968 Oct;123(4):158–73. [PubMed: 5681186]

196.

Pleasure DE, Walsh GO, Engel WK. Atrophy of skeletal muscle in patients with Cushing's syndrome. Arch Neurol. 1970 Feb;22(2):118–25. [PubMed: 4243379]

197.

Rebuffe-Scrive M, Krotkiewski M, Elfverson J, Bjorntorp P. Muscle and adipose tissue morphology and metabolism in Cushing's syndrome. J Clin Endocrinol Metab. 1988 Dec;67(6):1122–8. [PubMed: 3142910]

198.

Wang L, Luo GJ, Wang JJ, Hasselgren PO. Dexamethasone stimulates proteasome- and calcium-dependent proteolysis in cultured L6 myotubes. Shock. 1998 Oct;10(4):298–306. [PubMed: 9788663]

199.

Auclair D, Garrel DR, Chaouki Zerouala A, Ferland LH. Activation of the ubiquitin pathway in rat skeletal muscle by catabolic doses of glucocorticoids. Am J Physiol. 1997 Mar;272(3 Pt 1):C1007–16. [PubMed: 9124503]

200.

Danneskiold-Samsoe B, Grimby G. The influence of prednisone on the muscle morphology and muscle enzymes in patients with rheumatoid arthritis. Clin Sci (Lond). 1986 Dec;71(6):693–701. [PubMed: 3791871]

201.

Askari A, Vignos PJ Jr, Moskowitz RW. Steroid myopathy in connective tissue disease. Am J Med. 1976 Oct;61(4):485–92. [PubMed: 973643]

202.

Ruegsegger P, Medici TC, Anliker M. Corticosteroid-induced bone loss. A longitudinal study of alternate day therapy in patients with bronchial asthma using quantitative computed tomography. Eur J Clin Pharmacol. 1983;25(5):615–20. [PubMed: 6662161]

203.

Huizenga NA, Koper JW, De Lange P, Pols HA, Stolk RP, Burger H, 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 Jan;83(1):144–51. [PubMed: 9435432]

204.

van Rossum EF, Lamberts SW. Polymorphisms in the glucocorticoid receptor gene and their associations with metabolic parameters and body composition. Recent Prog Horm Res. 2004;59:333–57. [PubMed: 14749509]

205.

White PC, Mune T, Agarwal AK. 11 beta-Hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess. Endocr Rev. 1997 Feb;18(1):135–56. [PubMed: 9034789]

206.

Tomlinson JW, Walker EA, Bujalska IJ, Draper N, Lavery GG, Cooper MS. 11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response. Endocr Rev. 2004;25:31–66. [PubMed: 15466942]

207.

Tannin GM, Agarwal AK, Monder C, New MI, White PC. The human gene for 11 beta-hydroxysteroid dehydrogenase. Structure, tissue distribution, and chromosomal localization. J Biol Chem. 1991 Sep 5;266(25):16653–8. [PubMed: 1885595]

208.

Stewart PM, Krozowski ZS. 11 beta-Hydroxysteroid dehydrogenase. Vitam Horm. 1999;57:249–324. [PubMed: 10232052]

209.

Cooper MS, Walker EA, Bland R, Fraser WD, Hewison M, Stewart PM. Expression and functional consequences of 11beta-hydroxysteroid dehydrogenase activity in human bone. Bone. 2000 Sep;27(3):375–81. [PubMed: 10962348]

210.

Arampatzis S, Pasch A, Lippuner K, Mohaupt M. Primary male osteoporosis is associated with enhanced glucocorticoid availability. Rheumatology (Oxford). 2013 Nov;52(11):1983–91. [PubMed: 23882110]

211.

Cooper MS, Bujalska I, Rabbit E, Walker EA, Bland R, Sheppard MC. Modulation of 11beta-hydroxysteroid dehydrogenase isoenzymes by proinflammatory cytokines in osteoblasts: an autocrine switch from glucocorticoid inactivation to activation. J Bone Mineral Res. 2001;16:1037–44. [PubMed: 11393780]

212.

Williams LJ, Lyons V, MacLeod I, Rajan V, Darlington GJ, Poli V. C/EBP regulates hepatic transcription of 11beta-hydroxysteroid dehydrogenase type 1. A novel mechanism for cross-talk between the C/EBP and glucocorticoid signaling pathways. J Biol Chem. 2000;275:30232–9. [PubMed: 10906322]

213.

Escher G, Galli I, Vishwanath BS, Frey BM, Frey FJ. Tumor necrosis factor alpha and interleukin 1beta enhance the cortisone/cortisol shuttle. J Exp Med. 1997 Jul 21;186(2):189–98. [PMC free article: PMC2198986] [PubMed: 9221748]

214.

Cooper MS, Rabbit EH, Goddard PE, Bartlett WA, Hewison M, Stewart PM. Osteoblastic 11beta-hydroxysteroid dehydrogenase type 1 activity increases with age and glucocorticoid exposure. J Bone Mineral Res. 2002;17:979–86. [PubMed: 12054173]

215.

Mundell L, Lindemann R, Douglas J. Monitoring long-term oral corticosteroids. BMJ Open Quality. 2017;6(2) [PMC free article: PMC5699140] [PubMed: 29450303]

216.

Gonnelli S, Rottoli P, Cepollaro C, Pondrelli C, Cappiello V, Vagliasindi M, et al. Prevention of corticosteroid-induced osteoporosis with alendronate in sarcoid patients. Calcif Tissue Int. 1997;61:382–5. [PubMed: 9351879]

217.

Adler RA, Hochberg MC. Suggested Guidelines for Evaluation and Treatment of Glucocorticoid-Induced Osteoporosis for the Department of Veterans Affairs. Arch Intern Med. 2003 2003 November 24;163(21):2619–24. [PubMed: 14638562]

218.

Anonymous Consensus development conference: diagnosis, prophylaxis, and treatment of osteoporosis. Am J Med. 1993 Jun;94(6):646–50. [PubMed: 8506892]

219.

Anonymous Osteoporosis prevention, diagnosis, and therapy. JAMA. 2001 Feb 14;285(6):785–95. [PubMed: 11176917]

220.

Anonymous Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis: 2001 update. American College of Rheumatology Ad Hoc Committee on Glucocoritcoid-Induced Osteoporosis. Arthritis Rheum. 2001 Jul;44(7):1496–503. [PubMed: 11465699]

221.

Eastell R, Reid DM, Compston J, Cooper C, Fogelman I, Francis RM, et al. A UK Consensus Group on management of glucocorticoid-induced osteoporosis: an update. J Intern Med. 1998 Oct;244(4):271–92. [PubMed: 9797491]

222.

Lukert BP, Higgins JC, Stoskopf MM. Serum osteocalcin is increased in patients with hyperthyroidism and decreased in patients receiving glucocorticoids. J Clin Endocrinol Metab. 1986 May;62(5):1056–8. [PubMed: 3485650]

223.

Ekenstam E, Stalenheim G, Hallgren R. The acute effect of high dose corticosteroid treatment on serum osteocalcin. Metabolism. 1988 Feb;37(2):141–4. [PubMed: 3257542]

224.

Prummel MF, Wiersinga WM, Lips P, Sanders GT, Sauerwein HP. The course of biochemical parameters of bone turnover during treatment with corticosteroids. J Clin Endocrinol Metab. 1991 Feb;72(2):382–6. [PubMed: 1991808]

225.

Reid IR, Chapman GE, Fraser TR, Davies AD, Surus AS, Meyer J, et al. Low serum osteocalcin levels in glucocorticoid-treated asthmatics. J Clin Endocrinol Metab. 1986 Feb;62(2):379–83. [PubMed: 3484482]

226.

Hall GM, Spector TD, Delmas PD. Markers of bone metabolism in postmenopausal women with rheumatoid arthritis. Effects of corticosteroids and hormone replacement therapy. Arthritis Rheum. 1995 Jul;38(7):902–6. [PubMed: 7612039]

227.

Reeve J, Loftus J, Hesp R, Ansell BM, Wright DJ, Woo PM. Biochemical prediction of changes in spinal bone mass in juvenile chronic (or rheumatoid) arthritis treated with glucocorticoids. J Rheumatol. 1993 Jul;20(7):1189–95. [PubMed: 8371216]

228.

Ton FN, Gunawardene SC, Lee H, Neer RM. Effects of low-dose prednisone on bone metabolism. J Bone Miner Res. 2005;20:464–70. [PubMed: 15746991]

229.

Lems WF, Gerrits MI, Jacobs JW, van Vugt RM, van Rijn HJ, Bijlsma JW. Changes in (markers of) bone metabolism during high dose corticosteroid pulse treatment in patients with rheumatoid arthritis. Ann Rheum Dis. 1996 May;55(5):288–93. [PMC free article: PMC1010164] [PubMed: 8660101]

230.

Gennari C, Imbimbo B, Montagnani M, Bernini M, Nardi P, Avioli LV. Effects of prednisone and deflazacort on mineral metabolism and parathyroid hormone activity in humans. Calcif Tissue Int. 1984 May;36(3):245–52. [PubMed: 6432287]

231.

Baran DT, Faulkner KG, Genant HK, Miller PD, Pacifici R. Diagnosis and management of osteoporosis: guidelines for the utilization of bone densitometry. Calcif Tissue Int. 1997;61:433–40. [PubMed: 9383266]

232.

Guglielmi G, Lang TF. Quantitative computed tomography. Semin Musculoskelet Radiol. 2002;6:219–27. [PubMed: 12541199]

233.

Hui SL, Slemenda CW, Johnston CC Jr. Baseline measurement of bone mass predicts fracture in white women. Ann Intern Med. 1989 Sep 1;111(5):355–61. [PubMed: 2764403]

234.

Blake GM, Fogelman I. Applications of bone densitometry for osteoporosis. Endocrinol Metab Clin North Am. 1998 Jun;27(2):267–88. [PubMed: 9669138]

235.

Finkelstein JS, Cleary RL, Butler JP, Antonelli R, Mitlak BH, Deraska DJ, et al. A comparison of lateral versus anterior-posterior spine dual energy x-ray absorptiometry for the diagnosis of osteopenia. J Clin Endocrinol Metab. 1994 Mar;78(3):724–30. [PubMed: 8126149]

236.

Sandru F, Carsote M, Dumitrascu MC, Albu SE, Valea A. Glucocorticoids and Trabecular Bone Score. J Med Life. 2020 Oct-Dec;13(4):449–53. [PMC free article: PMC7803323] [PubMed: 33456590]

237.

Kobza AO, Herman D, Papaioannou A, Lau AN, Adachi JD. Understanding and Managing Corticosteroid-Induced Osteoporosis. Open Access Rheumatol. 2021;13:177–90. [PMC free article: PMC8259736] [PubMed: 34239333]

238.

Van Staa TP, Laan RF, Barton IP, Cohen S, Reid DM, Cooper C. Bone density threshold and other predictors of vertebral fracture in patients receiving oral glucocorticoid therapy. Arthritis Rheum. 2003;48:3224–9. [PubMed: 14613287]

239.

Kanis JA, Johannsson H, Oden A. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19:893–9. [PubMed: 15125788]

240.

Kanis JA, Torgerson D, Cooper C. Comparison of the European and USA practice guidelines for Osteoporosis. Trends Endocrinol Metab. 2000 Jan-Feb;11(1):28–32. [PubMed: 10652503]

241.

Park SY, Gong HS, Kim KM, Kim D, Kim HY, Jeon CH, et al. Korean Guideline for the Prevention and Treatment of Glucocorticoid-induced Osteoporosis. J Bone Metab. 2018 Nov;25(4):195–211. [PMC free article: PMC6288607] [PubMed: 30574464]

242.

Adler GS, Shatto A. Screening for osteoporosis and colon cancer under Medicare. Health Care Financ Rev. 2002 Summer;23(4):189–200. [PMC free article: PMC4194763] [PubMed: 12500479]

243.

Weinstein RS. Glucocorticoid-induced osteoporosis and osteonecrosis. Endocrinol Metab Clin North Am. 2012 Sep;41(3):595–611. [PMC free article: PMC3417039] [PubMed: 22877431]

244.

Kanis JA, Johansson H, Oden A, McCloskey EV. Guidance for the adjustment of FRAX according to the dose of glucocorticoids. Osteoporosis Int. 2011 [PubMed: 21229233] [CrossRef]

245.

Buckley L, Guyatt G, Fink HA, Cannon M, Grossman J, Hansen KE, et al. 2017 American College of Rheumatology Guideline for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis. Arthritis Rheumatol. 2017 Aug;69(8):1521–37. [PubMed: 28585373]

246.

Lee TH, Song YJ, Kim H, Sung YK, Cho SK. Intervention Thresholds for Treatment in Patients with Glucocorticoid-Induced Osteoporosis: Systematic Review of Guidelines. J Bone Metab. 2020 Nov;27(4):247–59. [PMC free article: PMC7746480] [PubMed: 33317228]

247.

Grossman JM, Gordon R, Ranganath VK, Deal C, Caplan L, Chen W, et al. American College of Rheumatology 2010 recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Care Res (Hoboken). 2010;62:1515–26. [PubMed: 20662044]

248.

Devogelaer JP, Goemaere S, Boonen S, Body JJ, Kaufman JM, Reginster JY, et al. Evidence-based guidelines for the prevention and treatment of glucocorticoid-induced osteoporosis: a consensus document of the Belgian Bone Club. Osteoporos Int. 2006 Jan;17(1):8–19. [PubMed: 16217586]

249.

Gluck OS, Murphy WA, Hahn TJ, Hahn B. Bone loss in adults receiving alternate day glucocorticoid therapy. A comparison with daily therapy. Arthritis Rheum. 1981 Jul;24(7):892–8. [PubMed: 7259801]

250.

Avgerinos PC, Cutler GB Jr, Tsokos GC, Gold PW, Feuillan P, Gallucci WT, et al. Dissociation between cortisol and adrenal androgen secretion in patients receiving alternate day prednisone therapy. J Clin Endocrinol Metab. 1987 Jul;65(1):24–9. [PubMed: 3034956]

251.

Martinati LC, Bertoldo F, Gasperi E, Fortunati P, Lo Cascio V, Boner AL. Longitudinal evaluation of bone mass in asthmatic children treated with inhaled beclomethasone dipropionate or cromolyn sodium. Allergy. 1998 Jul;53(7):705–8. [PubMed: 9700040]

252.

Briot K, Roux C. Glucocorticoid-induced osteoporosis. RMD Open. 2015;1(1):e000014. [PMC free article: PMC4613168] [PubMed: 26509049]

253.

Frediani B, Falsetti P, Bisogno S, Baldi F, Acciai C, Filippou G, et al. Effects of high dose methylprednisolone pulse therapy on bone mass and biochemical markers of bone metabolism in patients with active rheumatoid arthritis: a 12-month randomized prospective controlled study. J Rheumatol. 2004;31:1083–7. [PubMed: 15170918]

254.

Nielsen HK, Charles P, Mosekilde L. The effect of single oral doses of prednisone on the circadian rhythm of serum osteocalcin in normal subjects. J Clin Endocrinol Metab. 1988;67:1025–30. [PubMed: 3263379]

255.

Richy F, Bousquet J, Ehrlich GE, Meunier PJ, Israel E, Morii H, et al. Inhaled corticosteroids effects on bone in asthmatic and COPD patients: a quantitative systematic review. Osteoporos Int. 2003;14:179–90. [PubMed: 12730758]

256.

Bootsma GP, Dekhuijzen PN, Festen J, Mulder PG, Swinkels LM, van Herwaarden CL. Fluticasone propionate does not influence bone metabolism in contrast to beclomethasone dipropionate. Am J Respir Crit Care Med. 1996 Mar;153(3):924–30. [PubMed: 8630574]

257.

Luengo M, del Rio L, Pons F, Picado C. Bone mineral density in asthmatic patients treated with inhaled corticosteroids: a case-control study. Eur Respir J. 1997 Sep;10(9):2110–3. [PubMed: 9311512]

258.

Ebeling PR, Erbas B, Hopper JL, Wark JD, Rubinfeld AR. Bone mineral density and bone turnover in asthmatics treated with long-term inhaled or oral glucocorticoids. J Bone Miner Res. 1998 Aug;13(8):1283–9. [PubMed: 9718197]

259.

Aris R, Donohue JF, Ontjes D. Inhaled corticosteroids and fracture risk: having our cake and eating it too. Chest. 2005 Jan;127(1):5–7. [PubMed: 15653953]

260.

van Staa TP, Bishop N, Leufkens HG, Cooper C. Are inhaled corticosteroids associated with an increased risk of fracture in children? Osteoporos Int. 2004;15:785–91. [PubMed: 14985948]

261.

Pennisi P, Trombetti A, Rizzoli R. Glucocorticoid-induced osteoporosis and its treatment. Clin Orthop Relat Res. 2006 Feb;(443):39–47. [PubMed: 16462424]

262.

Boonen S, inventor IOF, assignee. Corticosteroid-induced osteoporosis. Geneva2011 February 1-3, 2011.

263.

Prestwood KM, Raisz LG. Prevention and treatment of osteoporosis. Clin Cornerstone. 2002;4:31–41. [PubMed: 12739329]

264.

Adami G, Rahn EJ, Saag KG. Glucocorticoid-induced osteoporosis: from clinical trials to clinical practice. Ther Adv Musculoskelet Dis. 2019;11:1759720X19876468. [PMC free article: PMC6755635] [PubMed: 31565078]

265.

Liu Z, Zhang M, Shen Z, Ke J, Zhang D, Yin F. Efficacy and safety of 18 anti-osteoporotic drugs in the treatment of patients with osteoporosis caused by glucocorticoid: A network meta-analysis of randomized controlled trials. PLoS One. 2020;15(12):e0243851. [PMC free article: PMC7743932] [PubMed: 33326444]

266.

Buckley LM, Leib ES, Cartularo KS, Vacek PM, Cooper SM. 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 Dec 15;125(12):961–8. [PubMed: 8967706]

267.

Adachi JD, Bensen WG, Bianchi F, Cividino A, Pillersdorf S, Sebaldt RJ, et al. Vitamin D and calcium in the prevention of corticosteroid induced osteoporosis: a 3 year followup. J Rheumatol. 1996 Jun;23(6):995–1000. [PubMed: 8782129]

268.

Reginster JY, Kuntz D, Verdickt W, Wouters M, Guillevin L, Menkes CJ, et al. Prophylactic use of alfacalcidol in corticosteroid-induced osteoporosis. Osteoporos Int. 1999;9(1):75–81. [PubMed: 10367032]

269.

Amin S, LaValley MP, Simms RW, Felson DT. The role of vitamin D in corticosteroid-induced osteoporosis: a meta-analytic approach. Arthritis Rheum. 1999 Aug;42(8):1740–51. [PubMed: 10446876]

270.

Homik J, Suarez-Almazor ME, Shea B, Cranney A, Wells G, Tugwell P. Calcium and vitamin D for corticosteroid-induced osteoporosis. Cochrane Database Syst Rev. 2000;(2):CD000952. [PMC free article: PMC7046131] [PubMed: 10796394]

271.

Fuji N, Hamano T, Mikami S, Nagasawa Y, Isaka Y, Moriyama T, et al. Risedronate, an effective treatment for glucocorticoid-induced bone loss in CKD patients with or without concomitant active vitamin D (PRIUS-CKD). Nephrol Dial Transplant. 2007;22:1601–7. [PubMed: 17124283]

272.

Dechant KL, Goa KL. Calcitriol. A review of its use in the treatment of postmenopausal osteoporosis and its potential in corticosteroid-induced osteoporosis. Drugs Aging. 1994;5:300–17. [PubMed: 7827399]

273.

Adverse Drug Reactions Advisory Committee A. Calcitriol and hypercalcaemia. Aust Adv Drug React Bull. 1997;16:2.

274.

LaCroix AZ, Wienpahl J, White LR, Wallace RB, Scherr PA, George LK, et al. Thiazide diuretic agents and the incidence of hip fracture. N Engl J Med. 1990 Feb 1;322(5):286–90. [PubMed: 2296269]

275.

Felson DT, Sloutskis D, Anderson JJ, Anthony JM, Kiel DP. Thiazide diuretics and the risk of hip fracture. Results from the Framingham Study. JAMA. 1991 Jan 16;265(3):370–3. [PubMed: 1984536]

276.

Cauley JA, Cummings SR, Seeley DG, Black D, Browner W, Kuller LH, et al. Effects of thiazide diuretic therapy on bone mass, fractures, and falls. The Study of Osteoporotic Fractures Research Group. Ann Intern Med. 1993 May 1;118(9):666–73. [PubMed: 8489642]

277.

Rodan GA, Fleisch HA. Bisphosphonates: mechanisms of action. J Clin Invest. 1996 Jun 15;97(12):2692–6. [PMC free article: PMC507360] [PubMed: 8675678]

278.

Sambrook PN. How to prevent steroid induced osteoporosis. Ann Rheum Dis. 2005 Feb;64(2):176–8. [PMC free article: PMC1755379] [PubMed: 15647424]

279.

Compston J, Bowring C, Cooper A, Cooper C, Davies C, Francis R, et al. Diagnosis and management of osteoporosis in postmenopausal women and older men in the UK: National Osteoporosis Guideline Group (NOGG) update 2013. Maturitas. 2013 Aug;75(4):392–6. [PubMed: 23810490]

280.

Lekamwasam S, Adachi JD, Agnusdei D, Bilezikian J, Boonen S, Borgstrom F, et al. A framework for the development of guidelines for the management of glucocorticoid-induced osteoporosis. Osteoporos Int. 2012 Sep;23(9):2257–76. [PubMed: 22434203]

281.

Adachi JD, Saag KG, Delmas PD, Liberman UA, Emkey RD, Seeman E, et al. Two-year effects of alendronate on bone mineral density and vertebral fracture in patients receiving glucocorticoids: a randomized, double-blind, placebo-controlled extension trial. Arthritis Rheum. 2001 Jan;44(1):202–11. [PubMed: 11212161]

282.

de Nijs RN, Jacobs JW, Lems WF, Laan RF, Algra A, Huisman AM, et al. Alendronate or alfacalcidol in glucocorticoid-induced osteoporosis. N Engl J Med. 2006 Aug 17;355(7):675–84. [PubMed: 16914703]

283.

Shane E, Addesso V, Namerow PB, McMahon DJ, Lo SH, Staron RB, et al. Alendronate versus calcitriol for the prevention of bone loss after cardiac transplantation. N Engl J Med. 2004;350:767–76. [PubMed: 14973216]

284.

Wang YK, Zhang YM, Qin SQ, Wang X, Ma T, Guo JB, et al. Effects of alendronate for treatment of glucocorticoid-induced osteoporosis: A meta-analysis of randomized controlled trials. Medicine (Baltimore). 2018 Oct;97(42):e12691. [PMC free article: PMC6211897] [PubMed: 30334952]

285.

Reid DM, Hughes RA, Laan RF, Sacco-Gibson NA, Wenderoth DH, Adami S, et al. Efficacy and safety of daily risedronate in the treatment of corticosteroid-induced osteoporosis in men and women: a randomized trial. European Corticosteroid-Induced Osteoporosis Treatment Study. J Bone Miner Res. 2000 Jun;15(6):1006–13. [PubMed: 10841169]

286.

Reid IR, Brown JP, Burckhardt P, Horowitz Z, Richardson P, Trechsel U, et al. Intravenous Zoledronic Acid in Postmenopausal Women with Low Bone Mineral Density. N Engl J Med. 2002 2002 February 28;346(9):653–61. [PubMed: 11870242]

287.

Reid IR. Bisphosphonates: new indications and methods of administration. Curr Opin Rheumatol. 2003 Jul;15(4):458–63. [PubMed: 12819475]

288.

Theriault RL. Zoledronic acid (Zometa) use in bone disease. Expert Rev Anticancer Ther. 2003 Apr;3(2):157–66. [PubMed: 12722875]

289.

Biskobing DM. Novel therapies for osteoporosis. Expert Opin Investig Drugs. 2003 Apr;12(4):611–21. [PubMed: 12665416]

290.

Biskobing DM, Novy AM, Downs R Jr. Novel therapeutic options for osteoporosis. Curr Opin Rheumatol. 2002 Jul;14(4):447–52. [PubMed: 12118183]

291.

Doggrell SA. Zoledronate once-yearly increases bone mineral density--implications for osteoporosis. Expert Opin Pharmacother. 2002 Jul;3(7):1007–9. [PubMed: 12083999]

292.

Reid DM, Devogelaer JP, Saag K, Roux C, Lau CS, Reginster JY, 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. [PubMed: 19362675]

293.

Ward LM. Glucocorticoid-Induced Osteoporosis: Why Kids Are Different. Front Endocrinol (Lausanne). 2020;11:576. [PMC free article: PMC7772619] [PubMed: 33391179]

294.

Teitelbaum SL, Seton MP, Saag KG. Should bisphosphonates be used for long-term treatment of glucocorticoid-induced osteoporosis? Arthritis and rheumatism. 2011;63(2):325–8. [PMC free article: PMC3069536] [PubMed: 21279986]

295.

Bultink IE, Baden M, Lems WF. Glucocorticoid-induced osteoporosis: an update on current pharmacotherapy and future directions. Expert Opin Pharmacother. 2013 Feb;14(2):185–97. [PubMed: 23317448]

296.

Dore RK, Cohen SB, Lane NE, Palmer W, Shergy W, Zhou L, et al. Effects of denosumab on bone mineral density and bone turnover in patients with rheumatoid arthritis receiving concurrent glucocorticoids or bisphosphonates. Ann Rheum Dis. 2010;69:872–5. [PMC free article: PMC6909937] [PubMed: 19734132]

297.

Akashi K, Nishimura K, Kageyama G, Ichikawa S, Shirai T, Yamamoto Y, et al. FRI0553 The efficacy of 2-years denosumab treatment for glucocorticoid-induced osteoporosis (GIOP). Annals of the Rheumatic Diseases. 2017;76 Suppl 2:699.

298.

Denosumab for glucocorticoid-induced osteoporosis. Birmingham, UK: NIHR Horizon Scanning Centre, University of Birmingham2014.

299.

Amgen. FDA Accepts Supplemental Biologics License Application For Prolia® (Denosumab) In Glucocorticoid-Induced Osteoporosis. 2017 [February 17, 2018]; Available from: https://www​.amgen.com/media/news-releases​/2017/10​/fda-accepts-supplemental-biologics-license-application-for-prolia-denosumab-in-glucocorticoidinduced-osteoporosis/.

300.

Yanbeiy ZA, Hansen KE. Denosumab in the treatment of glucocorticoid-induced osteoporosis: a systematic review and meta-analysis. Drug Des Devel Ther. 2019;13:2843–52. [PMC free article: PMC6698580] [PubMed: 31616133]

301.

Yamaguchi Y, Morita T, Kumanogoh A. The therapeutic efficacy of denosumab for the loss of bone mineral density in glucocorticoid-induced osteoporosis: a meta-analysis. Rheumatol Adv Pract. 2020;4(1):rkaa008. [PMC free article: PMC7197806] [PubMed: 32373775]

302.

Saag KG, McDermott MT, Adachi J, Lems W, Lane NE, Geusens P, et al. The Effect of Discontinuing Denosumab in Patients With Rheumatoid Arthritis Treated With Glucocorticoids. Arthritis Rheumatol. 2021 Sep 17; [PMC free article: PMC9305881] [PubMed: 34535967]

303.

Hayes KN, Baschant U, Hauser B, Burden AM, Winter EM. When to Start and Stop Bone-Protecting Medication for Preventing Glucocorticoid-Induced Osteoporosis. Front Endocrinol (Lausanne). 2021;12:782118. [PMC free article: PMC8715727] [PubMed: 34975756]

304.

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 May;15(5):944–51. [PubMed: 10804025]

305.

Lane NE, Sanchez S, Modin GW, Genant HK, Pierini E, Arnaud CD. Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial. J Clin Invest. 1998 Oct 15;102(8):1627–33. [PMC free article: PMC509014] [PubMed: 9788977]

306.

Devogelaer JP, Adler RA, Recknor C, See K, Warner MR, Wong M, et al. Baseline glucocorticoid dose and bone mineral density response with teriparatide or alendronate therapy in patients with glucocorticoid-induced osteoporosis. J Rheumatol. 2010;37:141–8. [PubMed: 19918047]

307.

Saag KG, Zanchetta JR, Devogelaer JP, Adler RA, Eastell R, See K, et al. Effects of teriparatide versus alendronate for treating glucocorticoid-induced osteoporosis: thirty-six-month results of a randomized, double-blind, controlled trial. Arthritis Rheum. 2009;60:3346–55. [PubMed: 19877063]

308.

Summey BT, Yosipovitch G. Glucocorticoid-induced bone loss in dermatologic patients: an update. Arch Dermatol. 2006 Jan;142(1):82–90. [PubMed: 16415391]

309.

Hodsman AB, Bauer DC, Dempster D. Parathyroid hormone and teriparatide for the treatment of osteoporosis: a review of the evidence and suggested guidelines for its use. Endocr Rev. 2005;26:688–703. [PubMed: 15769903]

310.

Li W, Chen W, Lin Y. The Efficacy of Parathyroid Hormone Analogues in Combination With Bisphosphonates for the Treatment of Osteoporosis: A Meta-Analysis of Randomized Controlled Trials. Medicine. 2015;94(38):e1156. [PMC free article: PMC4635737] [PubMed: 26402797]

311.

Rittmaster RS, Bolognese M, Ettinger MP. Enhancement of bone mass in osteoporotic women with parathyroid hormone followed by alendronate. J Clin Endocrinol Metab. 2000;85:2129–34. [PubMed: 10852440]

312.

Lems WF, Jacobs WG, Bijlsma JW, Croone A, Haanen HC, Houben HH, et al. Effect of sodium fluoride on the prevention of corticosteroid-induced osteoporosis. Osteoporos Int. 1997;7(6):575–82. [PubMed: 9604055]

313.

Lems WF, Jacobs JW, Bijlsma JW, van Veen GJ, Houben HH, Haanen HC, et al. Is addition of sodium fluoride to cyclical etidronate beneficial in the treatment of corticosteroid induced osteoporosis? Ann Rheum Dis. 1997 Jun;56(6):357–63. [PMC free article: PMC1752400] [PubMed: 9227164]

314.

Adami S, Fossaluzza V, Rossini M, Bertoldo F, Gatti D, Zamberlan N, et al. The prevention of corticosteroid-induced osteoporosis with nandrolone decanoate. Bone Miner. 1991 Oct;15(1):73–81. [PubMed: 1747568]

315.

Grecu EO, Weinshelbaum A, Simmons R. Effective therapy of glucocorticoid-induced osteoporosis with medroxyprogesterone acetate. Calcif Tissue Int. 1990 May;46(5):294–9. [PubMed: 2140069]

316.

Lukert BP, Johnson BE, Robinson RG. Estrogen and progesterone replacement therapy reduces glucocorticoid-induced bone loss. J Bone Miner Res. 1992 Sep;7(9):1063–9. [PubMed: 1329440]

317.

Hall GM, Daniels M, Doyle DV, Spector TD. Effect of hormone replacement therapy on bone mass in rheumatoid arthritis patients treated with and without steroids. Arthritis Rheum. 1994 Oct;37(10):1499–505. [PubMed: 7945476]

318.

Rossouw JE, Anderson GL, Prentice RL, LaCroix AZ, Kooperberg C, Stefanick ML, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA. 2002 Jul 17;288(3):321–33. [PubMed: 12117397]

319.

Reid IR, Wattie DJ, Evans MC, Stapleton JP. Testosterone therapy in glucocorticoid-treated men. Arch Intern Med. 1996 Jun 10;156(11):1173–7. [PubMed: 8639011]

320.

Gruenewald DA, Matsumoto AM. Testosterone Supplementation Therapy for Older Men: Potential Benefits and Risks. J Am Geriatr Soc. 2003;51:101–15. [PubMed: 12534854]

321.

Oettel M. The endocrine pharmacology of testosterone therapy in men. Naturwissenschaften. 2004 Feb;91(2):66–76. [PubMed: 14991143]

322.

Hafez B, Hafez ES. Andropause: endocrinology, erectile dysfunction, and prostate pathophysiology. Arch Androl. 2004 Mar-Apr;50(2):45–68. [PubMed: 14761837]

323.

Rhoden EL, Morgentaler A. Risks of testosterone-replacement therapy and recommendations for monitoring. N Engl J Med. 2004 Jan 29;350(5):482–92. [PubMed: 14749457]

324.

Fritz PC, Ward WE, Atkinson SA, Tenenbaum HC. Tamoxifen attenuates the effects of exogenous glucocorticoid on bone formation and growth in piglets. Endocrinology. 1998 Aug;139(8):3399–403. [PubMed: 9681488]

325.

Buckley L, Guyatt G, Fink HA, Cannon M, Grossman J, Hansen KE, et al. 2017 American College of Rheumatology Guideline for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis. Arthritis Care Res (Hoboken). 2017 Aug;69(8):1095–110. [PubMed: 28585410]

326.

Delmas PD, Bjarnason NH, Mitlak BH, Ravoux AC, Shah AS, Huster WJ, et al. Effects of raloxifene on bone mineral density, serum cholesterol concentrations, and uterine endometrium in postmenopausal women. N Engl J Med. 1997 Dec 4;337(23):1641–7. [PubMed: 9385122]

327.

Ettinger B, Black DM, Mitlak BH, Knickerbocker RK, Nickelsen T, Genant HK, et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: results from a 3-year randomized clinical trial. Multiple Outcomes of Raloxifene Evaluation (MORE) Investigators. JAMA. 1999 Aug 18;282(7):637–45. [PubMed: 10517716]

328.

Rizzoli R, Biver E. Glucocorticoid-induced osteoporosis: who to treat with what agent? Nat Rev Rheumatol. 2015;11:98–109. [PubMed: 25385412]

329.

Radius. FDA Approves Radius Health's TYMLOS™ (abaloparatide), a Bone Building Agent for the Treatment of Postmenopausal Women with Osteoporosis at High Risk for Fracture. 2017 [February 17, 2018]; Available from: http://investors​.radiuspharm​.com/releasedetail​.cfm?releaseid=1023557.

330.

Shakeri A, Adanty C. Romosozumab (sclerostin monoclonal antibody) for the treatment of osteoporosis in postmenopausal women: A review. J Popul Ther Clin Pharmacol. 2020 Jan 6;27(1):e25–e31. [PubMed: 31922699]

331.

Brent MB. Abaloparatide: A review of preclinical and clinical studies. Eur J Pharmacol. 2021 Oct 15;909:174409. [PubMed: 34364879]

332.

Hauser B, Alonso N, Riches PL. Review of Current Real-World Experience with Teriparatide as Treatment of Osteoporosis in Different Patient Groups. J Clin Med. 2021 Apr 1;10(7) [PMC free article: PMC8037129] [PubMed: 33915736]

333.

Yao W, Dai W, Jiang L, Lay EYA, Zhong Z, Ritchie RO, et al. Sclerostin-antibody treatment of glucocorticoid-induced osteoporosis maintained bone mass and strength. Osteoporosis Int. 2016;27(1):283–94. [PMC free article: PMC4958115] [PubMed: 26384674]

334.

Devogelaer JP. New perspectives in the management of glucocorticoid-induced osteoporosis. European Musculuskeletal Review. 2010;5:40–3.

335.

Sundahl N, Bridelance J, Libert C, De Bosscher K, Beck IM. Selective glucocorticoid receptor modulation: New directions with non-steroidal scaffolds. Pharmacol Ther. 2015 Aug;152:28–41. [PubMed: 25958032]

336.

Resche-Rigon M, Gronemeyer H. Therapeutic potential of selective modulators of nuclear receptor action. Curr Opin Chem Biol. 1998 Aug;2(4):501–7. [PubMed: 9736923]

337.

Fardellone P, Séjourné A, Paccou J, Goëb V. Bone Remodelling Markers in Rheumatoid Arthritis. Mediators of Inflammation. 2014;2014:484280. [PMC free article: PMC4009257] [PubMed: 24839355]

338.

Gifre L, Ruiz-Gaspà S, Monegal A, Nomdedeu B, Filella X, Guañabens N, et al. Effect of glucocorticoid treatment on Wnt signalling antagonists (sclerostin and Dkk-1) and their relationship with bone turnover. Bone. 2013;57:272–6. [PubMed: 23981659]

339.

Leong GM, Mercado-Asis LB, Reynolds JC, Hill SC, Oldfield EH, Chrousos GP. The effect of Cushing's disease on bone mineral density, body composition, growth, and puberty: a report of an identical adolescent twin pair. J Clin Endocrinol Metab. 1996 May;81(5):1905–11. [PubMed: 8626856]

340.

Catargi B, Tabarin A, Basse-Cathalinat B, Ducassou D, Roger P. Ann Endocrinol (Paris). 1996;57(3):203–8. [Development of bone mineral density after cure of Cushing's syndrome] [PubMed: 8949415]

341.

Manning PJ, Evans MC, Reid IR. Normal bone mineral density following cure of Cushing's syndrome. Clin Endocrinol (Oxf). 1992 Mar;36(3):229–34. [PubMed: 1563076]

342.

Rizzato G, Montemurro L. Reversibility of exogenous corticosteroid-induced bone loss. Eur Respir J. 1993 Jan;6(1):116–9. [PubMed: 8425581]