Glucocorticosteroid-induced spinal osteoporosis: scientific update on pathophysiology and treatment

Popp, Albrecht; Isenegger, Juerg; Buergi, Elizabeth M.; Buergi, Ulrich; Lippuner, Kurt

doi:10.1007/s00586-005-0056-x

Cited by 28 publications

(21 citation statements)

References 150 publications

(77 reference statements)

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“…GCs are potent osteopenic agents which disrupt the balance of calcium and bone density at many levels. The most significant adverse effects of GCs on bone formation or density are due to the direct inhibition of matrix synthesis by osteoblasts, the reduction in calcium absorption in both the gut and the renal tubule, and the production of hypogonadism, particularly in men (Nijenhuis et al 2004;Popp et al 2006). Bone loss resulting from GC therapy is a relatively common adverse effect, and has been linked to a decrease in intestinal calcium absorption, an increase in renal clearance of calcium, and sex steroid deficiency (Liu et al 2004;Patschan et al 2001;Prummel et al 1991).…”

Section: Discussionmentioning

confidence: 98%

The negative effect of dexamethasone on calcium-processing gene expressions is associated with a glucocorticoid-induced calcium-absorbing disorder

Kim¹,

Lee²,

Jung³

et al. 2009

Life Sciences

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Section: Discussionmentioning

confidence: 98%

The negative effect of dexamethasone on calcium-processing gene expressions is associated with a glucocorticoid-induced calcium-absorbing disorder

Kim¹,

Lee²,

Jung³

et al. 2009

Life Sciences

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“…18 It is of interest that a dual relationship between GC and CT is emerging, with the former being able to restore or retain CT receptor expression in osteoclasts 18 and the latter being effective in preventing GC-induced spine fractures. 19,20 No studies have yet addressed if and how GC and CT actions could converge on the RANKL system or the potential functional consequences on this interaction on bone cells, as well as in vivo, and this was the main aim of the present investigation.…”

mentioning

confidence: 99%

Calcitonin and Prednisolone Display Antagonistic Actions on Bone and Have Synergistic Effects in Experimental Arthritis

Mancini

Paul-Clark

Rosignoli

et al. 2007

The American Journal of Pathology

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We tested here the hypothesis that calcitonin and glucocorticoids, known to modulate bone metabolism, could have opposite actions on bone cells regulating expression of cytokine receptor activator of nuclear factor-〉 ligand (RANKL) and osteoprotegerin (OPG). In the U2OS osteosarcoma cell line, calcitonin (10 ؊11 to 10 ؊9 mol/L) reduced RANKL and augmented OPG both at the mRNA and protein levels. Cell incubation with prednisolone (10 ؊8 to 10 ؊6 mol/L), the glucocorticoid chosen for this study, produced opposite results. These molecular studies prompted more functional analyses whereby osteoclast bone resorptive activity was determined. Calcitonin (10 ؊10 mol/L) abrogated the stimulating effect of 10 ng/ml RANKL or 10 ؊9 mol/L prednisolone; similar results were obtained with OPG. Assessment of calcitonin and prednisolone effects in an in vivo model of rheumatoid arthritis revealed partially surprising results. In fact, calcitonin not only preserved bone morphology (as assessed on day 18) in rats subjected to arthritis and treated with prednisolone (0.8 to 4 mg/kg daily from day 13) but also synergized with the steroid to elicit its antiarthritic effects. These results suggest that calcitonin could be used as a novel cotreatment to augment efficacy and reduce side effects associated with the prolonged use of steroids. The receptor activator of nuclear factor-␤ ligand (RANKL) and its receptor RANK are key regulators of bone remodeling and are essential for osteoclast development and activation.

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“…The main component of steroids, glucocorticoid, inhibits bone matrix formation in childhood, which then results in a decrease in bone density 19) . On the other hand, etidronate used as a bisphosphonate reverses the decrease of bone density by inhibiting bone resorption 20,21) .…”

Section: Discussionmentioning

confidence: 99%

Biomechanical analysis of combined treatment of high calcium and bisphosphonate in tibia of steroid-treated growing-phase rats

Yokote

Kimura

et al. 2008

Dent. Mater. J.

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Childhood systemic diseases are commonly treated with steroids. Consequently, steroid-induced osteoporosis is often observed as a side effect of steroid therapy. However, osteoporosis of tibia resulting from steroid therapy has not been reported yet. Herein we constructed a steroid-induced osteoporosis in tibia of the growing phase rats to examine internal structural changes of the bone and tried to find out the effect of bisphosphonates as a new and early treatment method. Biomechanical analysis was performed using two-dimensional microdensitometry and three-dimensional pQCT method. In addition, the following evaluations were carried out: noninvasive bone strength measurements in steroid-induced osteoporotic rat tibiae; comparing the effectiveness of single high-calcium diet versus combined treatment of high calcium and bisphosphonate for osteoporosis; and quantitative measurement of four elements (Ca, P, Mg, Zn) in bone matrix. Our data suggested that a combined treatment of high calcium and bisphosphonate was an effective new method to improve and treat steroid-induced osteoporosis in childhood.

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Glucocorticosteroid-induced spinal osteoporosis: scientific update on pathophysiology and treatment

Cited by 28 publications

References 150 publications

The negative effect of dexamethasone on calcium-processing gene expressions is associated with a glucocorticoid-induced calcium-absorbing disorder

The negative effect of dexamethasone on calcium-processing gene expressions is associated with a glucocorticoid-induced calcium-absorbing disorder

Calcitonin and Prednisolone Display Antagonistic Actions on Bone and Have Synergistic Effects in Experimental Arthritis

Biomechanical analysis of combined treatment of high calcium and bisphosphonate in tibia of steroid-treated growing-phase rats

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