Glucocorticoid-induced osteopenia in the mouse as assessed by histomorphometry, microcomputed tomography, and biochemical markers

McLaughlin, Fiona; Mackintosh, J.; Hayes, Brad; McLaren, Andrew; Uings, Iain; Salmon, Phil; Humphreys, John; Meldrum, E.; Farrow, Stuart N.

doi:10.1016/s8756-3282(02)00737-8

Cited by 105 publications

(92 citation statements)

References 44 publications

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“…Furthermore, GC has been shown to stimulate osteoclast formation in bone marrow cultures in the mouse (Shuto et al 1994) and to extend the life span of preexisting osteoclasts in murine osteoclast cultures (Weinstein et al 2002). In another model, the dog, as in the mouse, a significant decrease of trabecular bone volume was observed in vivo after treatment with GC (Altman et al 1992, Quarles 1992, Weinstein et al 1998, McLaughlin et al 2002. Our present study indicates that GC-induced osteoclastic (nZ8 eels/group).…”

Section: Cortisol-induced Osteoclastic Resorptionsupporting

confidence: 62%

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Sbaihi

Rousseau

Baloche

et al. 2009

Journal of Endocrinology

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Endogenous excess cortisol and glucocorticoid (GC) therapy are a major cause of secondary osteoporosis in humans. Intense bone resorption can also be observed in other vertebrates such as migratory teleost fish at the time of reproductive migration and during fasting when large amounts of calcium and phosphate are required. Using a primitive teleost, the European eel, as a model, we investigated whether cortisol could play an ancestral role in the induction of vertebral skeleton demineralization. Different histological and histomorphometric methods were performed on vertebral samples of control and cortisoltreated eels. We demonstrated that cortisol induced a significant bone demineralization of eel vertebrae, as shown by significant decreases of the mineral ratio measured by incineration, and the degree of mineralization measured by quantitative microradiography of vertebral sections. Histology and image analysis of ultrathin microradiographs showed the induction by cortisol of different mechanisms of bone resorption, including periosteocytic osteolysis and osteoclastic resorption. Specificity of cortisol action was investigated by comparison with the effects of sex steroids. Whereas, testosterone had no effect, estradiol induced vertebral skeleton demineralization, an effect related to the stimulated synthesis of vitellogenin (Vg), an oviparous specific phospho-calciolipoprotein. By contrast, the cortisol demineralization effect was not related to any stimulation of Vg. This study demonstrates GC-induced bone demineralization in an adult non-mammalian vertebrate, which undergoes natural bone resorption during its life cycle. Our data suggest that the stimulatory action of cortisol on bone loss may represent an ancestral and conserved endocrine regulation in vertebrates.

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Section: Cortisol-induced Osteoclastic Resorptionsupporting

confidence: 62%

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Sbaihi

Rousseau

Baloche

et al. 2009

Journal of Endocrinology

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“…It was shown recently in vivo, in animals and in humans, that glucocorticoidinduced osteoporosis has been linked to leptin production. 34,35 In view of the known properties of leptin on bone metabolism, it is tempting to speculate that corticosteroid exposure, leptin production and demineralization are linked events. Accordingly, the blockade of the leptin production would be favorable.…”

Section: Discussionmentioning

confidence: 99%

Genistein induces adipogenesis but inhibits leptin induction in human synovial fibroblasts

Relić

Zeddou

Desoroux

et al. 2009

Laboratory Investigation

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It was shown recently that synovial fibroblast transformation into adipocytes reduced the expression of interleukin-6 (IL-6) and IL-8. However, the synovial fibroblast adipogenesis was inhibited in inflammatory conditions induced by the tumor necrosis factor-a (TNF-a). Furthermore, adipogenesis is often accompanied by leptin production, a proinflammatory adipokine in rheumatic diseases. In this study, we tested the phytohormone genistein for adipogenic and anti-inflammatory properties on human synovial fibroblasts. Results showed that genistein was able to transform synovial fibroblasts into adipocytes that expressed perilipin-A and produced adiponectin, but not leptin. Furthermore, genistein enhanced glucocorticoid-mediated synovial fibroblast adipogenesis and, in parallel, downregulated glucocorticoid-induced leptin and leptin receptor. Endogenous and TNF-a-induced expressions of IL-6, IL-8, p38, p65 and C/EBP-b were also downregulated by genistein, showing its anti-inflammatory properties. Peroxisome proliferatoractivated receptor-g (PPAR-g) agonist, rosiglitazone, had a synergic effect on genistein-induced adipogenesis, whereas the non-active tyrosine kinase inhibitor, daidzein, had a significantly inferior adipogenic activity than genistein. The Janus kinase-2 tyrosine kinase inhibitor, AG 490, mimicked the anti-leptin effect of genistein. These results showed that genistein-induced adipogenesis involves PPAR-g induction and tyrosine kinase inhibition. In conclusion, genistein, alone or coupled with glucocorticoids, have both adipogenic and anti-inflammatory effects on synovial fibroblasts.

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“…Microarchitecture of the femoral, tibial, and L 4 vertebrae trabecular bone was investigated using a microcomputed tomograph (CT; Skyscan 1072; Skyscan, Aartselaar, Belgium). The characteristics and methods have already been described elsewhere (McLaughlin et al, 2002). The X-ray source was set at 75 kV and 100 A, with a pixel size at 11 m. Four hundred projections were acquired over an angular range of 180°(angular step of 0.45°).…”

Section: Methodsmentioning

confidence: 99%

Dose Effects of Propranolol on Cancellous and Cortical Bone in Ovariectomized Adult Rats

Bonnet

Laroche²,

Vico³

et al. 2006

J Pharmacol Exp Ther

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Animal studies suggest that bone remodeling is under ␤-adrenergic control via the sympathetic nervous system. The purpose of this study was to examine the preventive effect of different doses of nonspecific ␤-blockers (propranolol) on trabecular and cortical bone envelopes in ovariectomized rats. Six-month-old female Wistar rats were ovariectomized (OVX, n ϭ 60) or shamoperated (n ϭ 15). Then, OVX rats were subcutaneously injected with 0.1 (n ϭ 15), 5 (n ϭ 15), or 20 (n ϭ 15) mg/kg propranolol or vehicle (n ϭ 15) for 10 weeks. Tibial and femoral bone mineral density (BMD) were analyzed longitudinally by dual-energy X-ray absorptiometry. At death, the left tibial metaphysis and L 4 vertebrae were removed, and microcomputed tomography (Skyscan 1072; Skyscan, Aartselaar, Belgium) was performed for trabecular bone structure investigation. Histomorphometry analysis was performed on the right proximal tibia to assess bone cell activities. After 10 weeks, OVX rats had decreased BMD and trabecular parameters and increased bone turnover, as well as cortical porosity compared with the sham group (p Ͻ 0.001). Bone architecture alteration was preserved by 0.1 mg/kg propranolol due to higher trabecular number and thickness (ϩ50.35 and ϩ6.81%, respectively, than OVX; p Ͻ 0.001) and lower cortical pore number (Ϫ52.38% than OVX; p Ͻ 0.001). Animals treated by 0.1 mg/kg propranolol had a lower osteoclast surface and a higher osteoblast activity compared with OVX. Animals treated by 20 mg of propranolol did not significantly differ from OVX rats. Animals treated by 5 mg of propranolol have been partially preserved from the ovariectomy. These results showed a dose effect of ␤-blockers. The lower the dose of propranolol breeding, the better the preventive effect against ovariectomy.

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Glucocorticoid-induced osteopenia in the mouse as assessed by histomorphometry, microcomputed tomography, and biochemical markers

Cited by 105 publications

References 44 publications

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Genistein induces adipogenesis but inhibits leptin induction in human synovial fibroblasts

Dose Effects of Propranolol on Cancellous and Cortical Bone in Ovariectomized Adult Rats

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