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Treatment of Postmenopausal Osteoporosis - Essay Example

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Treatment of Postmenopausal Osteoporosis

mechanism of action of estrogen in estropryvic osteoporosis can be reconstructed as

decrease of numbers of OC by decreased OC formation and increased OC natural death

or apoptosis, induction of deceased OC activity by suppression of T cell-mediated

production of inflammatory cytokines by decreased RANK ligand (RANKL) expression

and thereby down-regulation of cytokines, such as, IL-1, IL-6, TNF-, granulocyte-

macrophage colony stimulating factor, macrophage colony stimulating factor, and

prostaglandin E2, and simultaneous stimulation of estrogen (E) receptors on osteoblasts

leading to increased calcium incorporation and increased bone production6. Since

osteoclasts exhibit substantial nitric oxide (NO) synthetase activity, and it has been

observed that increased bone turnover is related to estrogen-dependent increase in

endothelial NO formation in the osteoclasts, it was investigated to be found that estrogen

in these women reduces receptor-mediated superoxide anion production that would

have enhanced biologic activity of endothelial NO (eNO)7.

The apparently easy treatment of osteoporosis is plagued by a serious problem.

Estrogen replacement therapy directed to menopausal women proved effective to increase

bone mass, so it was accepted to be a standard replacement therapy in menopausal

women, but it was implicated in increased incidence of breast and endometrial cancer in

this population. It was not irrational since estrogen has long been known to be a promoter

of breast growth. Discovery of receptors of estrogen in breast malignancy specimens and

responsiveness of estrogen-receptor positive cancers of the breast to tamoxifen, both led

to objections against hormone replacement therapy (HRT) and solved...
Estradiol and Selective Estrogen Receptor Modulators Differentially Regulate Target Genes with Estrogen Receptors and ; Molecular Biology of the Cell, Vol. 15, pp. 1262-1272. ...Show more

Summary

Simoncini, T. and Genazzani, A.R., (2000). Raloxifene Acutely Stimulates Nitric Oxide Release From Human Endothelial Cells Via An Activation Of Endothelial Nitric Oxide Synthase. Journal of Clinical Endocrinology and Metabolism, 85:pp. 2966-2969.
Tee, M.K., Rogatsky, I., Tzagarakis-Foster, C., Cvoro, A., An, J., Christy, R.J., Yamamoto, K.R., and Leitman, D.C., (2004)…
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