Cited by 201Bone health and osteoporosis researchBone Metabolism and DiseasesEstrogen and related hormone effects

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Molecular mechanisms of glucocorticoid-induced osteoporosis.

Patschan, D., Loddenkemper, K., Buttgereit, F.·2001·Bone

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Abstract

Bone loss resulting from long-term glucocorticoid therapy is common and clinically relevant. A number of different glucocorticoid-mediated effects are responsible for the reduction in bone density: (i) glucocorticoid-induced direct impairment of osteoblast, osteocyte, and osteoclast function leads to reduced bone remodeling and diminished repair of microdamage in bone; (ii) the effects of parathyroid hormone (PTH) might be more pronounced in the presence of glucocorticoids, whereas vitamin D plays a lesser role in the pathogenesis of steroid-induced osteoporosis; (iii) glucocorticoids antagonize gonadal function and inhibit the osteoanabolic action of sex steroids; and (iv) increased renal elimination and reduced intestinal absorption of calcium lead to a negative calcium balance that has been suggested to promote secondary hyperparathyroidism. From a mechanistic point of view, all of the aforementioned effects have long been considered to be mediated at the molecular level exclusively by genomic actions. However, there is now increasing evidence for the existence of rapid glucocorticoid effects that are incompatible with this classical mode of action. These rapid effects, termed nongenomic effects, are mediated by glucocorticoid interactions with biological membranes, either through binding to membrane receptors or by physicochemical interactions. It is possible, but has yet to be shown, that these effects play a role in the pathogenesis of glucocorticoid-induced osteoporosis.

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Background
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“Bone loss is one of the most devastating side effects of glucocorticoids because they inhibit calcium transport, cause secondary hyperparathyroidism, hypogonadism, and impairment of osteoblast function (Patschan et al., 2001, Rackoff and Rosen 1998).”
Background
Animal Models of Osteoporosis
Hayashi, K., & Fotovati, A. (2002) · CRC Press eBooks · doi:10.1201/b14228-7 · Cited by 32
Alendronate sodium in the management of osteoporosis
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“…gut and increased renal losses, may lead to low-grade secondary hyperparathyroidism with further increased osteoclast activity (Cosman et al 1994; Patschan et al 2001; Weinstein 2001; Canalis et al 2004) Several studies investigated the efficiency of alendronate for the prevention and treatment…”
Effects of salvianolate on bone metabolism in glucocorticoid-treated lupus-prone B6.MRL-Faslpr/J mice
Liu, Y., Cui, Y., Zhang, X., Gao, X., Su, Y., Xu, B., Wu, T., Chen, W., & Cui, L. (2016) · Drug Design Development and Therapy · doi:10.2147/dddt.s110125 · Cited by 31
“22 These effects indirectly lead to osteoporosis.”
Tactile/kinesthetic stimulation (TKS) increases tibial speed of sound and urinary osteocalcin (U-MidOC and unOC) in premature infants (29–32weeks PMA)
Haley, S., BEACHY, J. C., Ivaska, K. K., Slater, H., Smith, S. L., & Moyer‐Mileur, L. J. (2012) · Bone · doi:10.1016/j.bone.2012.07.016 · Cited by 29
“suppression and development of insulin-like growth factor 1 (IGF1) resistance[57].”
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Cannabinoid Receptors as Target for Treatment of Osteoporosis: A Tale of Two Therapies
Idris, A. I. (2010) · Current Neuropharmacology · doi:10.2174/157015910792246173 · Cited by 29
“Osteoclast formation and activity is controlled by the combined action of receptor activator of nuclear factor kappa-B ligand (RANKL) [40], osteoprotegerin (OPG) [41] and monocyte colony forming factor (M-CSF) [42] produced by cells of the osteoblastic lineage.”
BackgroundInfluential
Compared clinical efficacy and bone metabolic effects of low-dose deflazacort and methyl prednisolone in male inflammatory arthropathies: a 12-month open randomized pilot study
Saviola, G., Abdì-Alì, L., Eddin, S. S., Coppini, A., Cavalieri, F., Campostrini, L., Sacco, S., Bucci, M., Cirino, G., & Rossini, M. (2007) · Lara D. Veeken · doi:10.1093/rheumatology/kem030 · Cited by 29
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“Finally, increased excretion of urinary calcium and reduced intestinal absorption of calcium lead to a negative calcium balance that has been suggested to promote secondary hyperparathyroidism (Reid, 1997; Patschan et al. 2001).”
Background
The treatment of glucocorticoid-induced osteoporosis
Cohen, D., & Adachi, J. D. (2004) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2004.01.003 · Cited by 29
The protective role of bone morphogenetic protein-8 in the glucocorticoid-induced apoptosis on bone cells
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A Study to Evaluate the Cause of Bone Demineralization in Gynecological Cancer Survivors
Stavraka, C., Maclaran, K., Gabra, H., Agarwal, R., Ghaem‐Maghami, S., Taylor, A., Dhillo, W. S., Panay, N., & Blagden, S. P. (2013) · The Oncologist · doi:10.1634/theoncologist.2012-0416 · Cited by 27
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Immunocytochemical Evidence on the Effects of Glucocorticoids on Type I Collagen Synthesis in Human Osteoblastic Cells
Hernández, M. V., Guañabens, N., Álvarez, L., Monegal, A., Peris, P., Riba, J., Ercilla, G., de Osaba, M. J. M., & Muñoz-Gómez, J. (2003) · Calcified Tissue International · doi:10.1007/s00223-002-1095-5 · Cited by 25
“The effects of glucocorticoids on bone mineral metabolism have been extensively analyzed [1].”
Background
Design and development of glucocorticoid receptor modulators
Buttgereit, F., Elling, C., & Jakob, F. (2025) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2025.06.005 · Cited by 25
Self-citation
Therapeutic interactions between mesenchymal stem cells for healing medication-related osteonecrosis of the jaw
Matsuura, Y., Atsuta, I., Ayukawa, Y., Yamaza, T., Kondo, R., Takahashi, A., Ueda, N., Oshiro, W., Tsukiyama, Y., & Koyano, K. (2016) · Stem Cell Research & Therapy · doi:10.1186/s13287-016-0367-3 · Cited by 25
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Result
Siglec-15-targeting therapy protects against glucocorticoid-induced osteoporosis of growing skeleton in juvenile rats
Sato, D., Takahata, M., Ota, M., Fukuda, C., Hasegawa, T., Yamamoto, T., Amizuka, N., Tsuda, E., Okada, A., Hiruma, Y., et al. (2020) · Bone · doi:10.1016/j.bone.2020.115331 · Cited by 24
Association of genetic variations of genes encoding thrombospondin, type 1, domain-containing 4 and 7A with low bone mineral density in Japanese women with osteoporosis
Mori, S., Kou, I., Sato, H., Emi, M., Ito, H., Hosoi, T., & Ikegawa, S. (2008) · Journal of Human Genetics · doi:10.1007/s10038-008-0300-4 · Cited by 23
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Background
Secondary Osteoporosis
Templeton, K. J. (2005) · Journal of the American Academy of Orthopaedic Surgeons · doi:10.5435/00124635-200511000-00007 · Cited by 23
Second generation sequencing of microRNA in Human Bone Cells treated with Parathyroid Hormone or Dexamethasone
Laxman, N., Rubin, C., Mallmin, H., Nilsson, O., Tellgren‐Roth, C., & Kindmark, A. (2015) · Bone · doi:10.1016/j.bone.2015.12.053 · Cited by 21
Bone response of broiler chickens (Gallus gallus domesticus) induced by corticosterone
Luo, J., Zhou, Z., Zhang, H., Ma, R., & Hou, J. F. (2012) · Comparative Biochemistry and Physiology Part A Molecular & Integrative Physiology · doi:10.1016/j.cbpa.2012.12.001 · Cited by 21
“The results of the earlier studies indicated that elevated CORT concentration led to reduction in bone mass and disturbed longitudinal bone growth in human and rodents (Li et al., 1996; Patschan et al., 2001; Bianchi, 2002).”
Result
Role of Serum- and Glucocorticoid-Inducible Kinase SGK1 in Glucocorticoid Regulation of Renal Electrolyte Excretion and Blood Pressure
Boini, K. M., Nammi, S., Grahammer, F., Oßwald, H., Kuhl, D., & Lang, F. J. W. (2008) · Kidney & Blood Pressure Research · doi:10.1159/000151666 · Cited by 21
“plasma Ca 2+ concentration. The increase of plasma Ca 2+ concentration may result in part from demineralization of bone [”
Background
Effects of Alfacalcidol on Mechanical Properties and Collagen Cross-Links of the Femoral Diaphysis in Glucocorticoid-Treated Rats
Saito, M., Marumo, K., Ushiku, C., Kato, S., Sakai, S., Hayakawa, N., Mihara, M., & Shiraishi, A. (2011) · Calcified Tissue International · doi:10.1007/s00223-011-9472-6 · Cited by 20
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Background
Alpinumisoflavone rescues glucocorticoid-induced apoptosis of osteocytes via suppressing Nox2-dependent ROS generation
Yin, J., Han, L., & Cong, W. (2017) · Pharmacological Reports · doi:10.1016/j.pharep.2017.11.001 · Cited by 20
Retracted
The utility of human dedifferentiated fat cells in bone tissue engineering in vitro
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Use of high-dose intermittent systemic glucocorticoids and the risk of fracture in patients with chronic obstructive pulmonary disease
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BackgroundInfluential
The efficacy of core decompression for steroid‐associated osteonecrosis of the femoral head in rabbits
Maruyama, M., Lin, T., Kaminow, N. I., Thio, T., Storaci, H. W., Pan, C., Yao, Z., Takagi, M., Goodman, S. B., & Yang, Y. (2020) · Journal of Orthopaedic Research® · doi:10.1002/jor.24888 · Cited by 18
The inhibitory mechanisms of losartan and vitamin D on amiodarone‐induced lung inflammation in rats: Role of mitogen‐activated protein kinases/activator protein‐1
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Background
Glucocorticoid-induced osteoporosis—from molecular mechanism to clinical practice
Hsu, C. H., Hsu, C. L., Langley, A., Wojcik, C., Iraganje, E., & Grygiel‐Górniak, B. (2024) · Drugs & Therapy Perspectives · doi:10.1007/s40267-024-01079-4 · Cited by 19
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Application of Large Language Models in Drug-Induced Osteotoxicity Prediction
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Authors: Patschan, D., Loddenkemper, K., & Buttgereit, F.
Affiliations: Humboldt-Universität zu Berlin (DE)
Corresponding author: Buttgereit, F.
ORCID: Patschan, D.
Buttgereit, F.
Venue: Bone
Publisher: Elsevier BV
Published: 2001-12
Volume: 29
Issue: 6
Pages: 498-505
ISSN: 1873-2763 (ISSN-L)
8756-3282
DOI: 10.1016/s8756-3282(01)00610-x
OpenAlex: W2005326563
Cited by: 201
References: 80
Citations by year: 2026: 2 · 2025: 7 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 11 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 6 · 2016: 8 · 2015: 9 · 2014: 8 · 2013: 6 · 2012: 6
FWCI: 8.19
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Bone (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Keywords: glucocorticoid-induced osteoporosis, bone loss, bone remodeling, osteoblast activity, osteoclast function, osteocyte function, parathyroid hormone, vitamin D, sex steroids, gonadal function, calcium balance, secondary hyperparathyroidism, glucocorticoid receptor signaling
MeSH terms: Calcium, Glucocorticoids, Humans, Intestinal Absorption, Kidney, Osteoblasts, Osteoclasts, Osteoporosis, Parathyroid Hormone, Gonadal Steroid Hormones, Vitamin D

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Molecular mechanisms of glucocorticoid-induced osteoporosis.

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