Estrogen therapy for postmenopausal osteoporosis

Fitzpatrick, Lorraine A.

doi:10.1590/s0004-27302006000400016

Cited by 50 publications

(30 citation statements)

References 68 publications

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“…Osteoporosis has become a public health issue threatening a large portion of the population over 50 years of age [1,2] . Estrogen replacement therapy (ERT) is effective in reducing or reversing postmenopausal bone loss [3] . In addition to its use for the treatment of postmenopausal symptoms, potential benefits of ERT include a reduction in the risk of osteoarthritis [4][5][6] and prevention of cardiovascular disease and dementia [7] .…”

Section: Introductionmentioning

confidence: 99%

Dose-dependent effects of genistein on bone homeostasis in rats' mandibular subchondral bone

Xing

Wang

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate the effect of genistein on bone homeostasis in mandibular subchondral bone of rats. Methods: Female SD rats were administered with genistein (10 and 50 mg/kg) or placebo by oral gavage for 6 weeks. Then the animals were sacrificed, and histomorphology and micro-structure of mandibular condyle were examined using HE staining and micro-CT analysis, respectively. The expression levels of alkaline phosphatase (ALP), osteocalcin (OC), osteoprotegerin (OPG), the receptor activator of nuclear factor κB ligand (RANKL) and estrogen receptors (ERs) in mandibular condyle were detected using real-time PCR. Cultured osteoblasts were prepared from rat mandibular condyle for in in vitro study. The cells were treated with genistein (10 -7 or 10 -4 mol/L) for 48 h. The expression of the bone homeostasis-associated factors and estrogen receptors (ERs) was detected using realtime PCR, and ER silencing was performed. Results: At both the low-and high-doses, genistein significantly increased the bone mineral density (BMD) and bone volume, and resulted in thicker subchondral trabecular bone in vivo. In both in vivo and in vitro study, the low-dose genistein significantly increased the expression of ALP, OC and OPG, but decreased the expression of RANKL and the RANKL/OPG ratio. The high-dose genistein decreased the expression of all these bone homeostasis-associated factors. Both the low and high doses of genistein significantly increased the expression of ERβ, while ERα expression was increased by the low dose genistein and decreased by the high dose genistein. ERβ silencing abrogated most of the effects of genistein treatment. Conclusion: In rat mandibular condylar subchondral bone, low-dose genistein increases bone formation and inhibit bone resorption, while excess genistein inhibits both bone formation and resorption. The effects of genistein were predominantly mediated through ERβ.

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Section: Introductionmentioning

confidence: 99%

Dose-dependent effects of genistein on bone homeostasis in rats' mandibular subchondral bone

Xing

Wang

et al. 2011

Acta Pharmacol Sin

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“…Hormone replacement therapy (HRT), if started soon after the onset of menopause, is effective for reducing or reversing postmenopausal bone loss (Lindsay et al 1976, Fitzpatrick 2006. Besides its use for treatment of postmenopausal symptoms, potential benefits of HRT include the prevention of cardiovascular disease and dementia (Stevenson 2004).…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor subtype-specific effects on markers of bone homeostasis

Hertrampf

Schleipen

Velders

et al. 2008

Molecular and Cellular Endocrinology

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Please cite this article as: Hertrampf, T., Schleipen, B., Velders, M., Laudenbach, U., Fritzemeier, K.H., Diel, P., Estrogen receptor subtype-specific effects on markers of bone homeostasis, Molecular and Cellular Endocrinology (2007), doi:10.1016/j.mce.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractTo further elucidate the processes involved in the physiology of bone-protection by estrogens, ovariectomized (OVX) rats were treated subcutaneously with 17-estradiol, the ER-specific agonist (16-LE2) and the ER-specific agonist (8-VE2).OVX and intact animals served as controls. Biomarkers of bone-formation (osteocalcin (OC), osteopontin (OPN)) and bone-resorption (telopeptides of collagen type I (CTx), pyridinoline cross-links (Pyd)) were quantified. Bone mineral density was measured by computed tomography.OVX-induced bone loss could be antagonized by subcutaneous administration of 17-estradiol and 16-LE2. Serum levels of CTx, OC and OPN were significantly elevated in OVX compared to intact animals and reduced by 17-estradiol and 16-LE2. Treatment of OVX rats with 8-VE2 did not affect BMD or bone-marker serum levels.Taken together, the complex expression pattern of bone-markers in OVX rats following subcutaneous administration of ER subtype-specific agonists indicates that 17-estradiol exerts its bone-protective effects by modulating the activity of osteoclasts and osteoblasts via ERα.

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“…Moreover, the prevalence of arterial calcification such as Mönkeberg's sclerosis particularly localized to the media mainly in women with ageing (8,9). Since estrogen has been well known to play a crucial role for inhibition of both bone loss (10) and arterial calcification (11), it is suggested that estrogen deficiency might be involved in a possible mechanism of the occurrences of both bone loss and arterial calcification in postmenopausal women.…”

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confidence: 99%

The Effect of Different Amounts of Calcium Intake on Bone Metabolism and Arterial Calcification in Ovariectomized Rats

Agata

Park

Hattori

et al. 2013

J Nutr Sci Vitaminol

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Summary Low calcium (Ca) intake is the one of risk factors for both bone loss and medial elastocalcinosis in an estrogen deficiency state. To examine the effect of different amounts of Ca intake on the relationship between bone mass alteration and medial elastocalcinosis, 6-wk-old female SD rats were randomized into ovariectomized (OVX) control or OVX treated with vitamin D3 plus nicotine injection (VDN) groups. The OVX treated with VDN group was then divided into 5 groups depending on the different Ca content in their diet, 0.01%, 0.1%, 0.6%, 1.2%, and 2.4% Ca intakes. After 8 wk of experimentation, the low Ca intake groups of 0.01% and 0.1% showed a low bone mineral density (BMD) and bone properties significantly different from those of the other groups, whereas the high Ca intake groups of 1.2% and 2.4% showed no difference compared with the OVX control. Only in the 0.01% Ca intake group, a significantly higher Ca content in the thoracic artery was found compared with that of the OVX control. Arterial tissues of the 0.01% Ca intake group showed an increase of bone-specific alkaline phosphatase (BAP) activity, a marker of bone mineralization, associated with arterial Ca content. However, the high Ca intake did not affect arterial Ca content nor arterial BAP activity. These results suggested that a low Ca intake during periods of rapid bone loss caused by estrogen deficiency might be one possible cause for the complication of both bone loss and medial elastocalcinosis.

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Estrogen therapy for postmenopausal osteoporosis

Cited by 50 publications

References 68 publications

Dose-dependent effects of genistein on bone homeostasis in rats' mandibular subchondral bone

Dose-dependent effects of genistein on bone homeostasis in rats' mandibular subchondral bone

Estrogen receptor subtype-specific effects on markers of bone homeostasis

The Effect of Different Amounts of Calcium Intake on Bone Metabolism and Arterial Calcification in Ovariectomized Rats

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