By Rene Rizzoli
René Rizzoli Menopause is the time in a woman’s existence whilst reproductive means ends. Ovaries lessen their job and the construction of intercourse hormones ceases. this era should be linked to a wide number of signs affecting the cardiovascular and urogenital structures, in addition to pores and skin, hair and bone. Bone capital is gathered through the tip of the second one decade and is still kind of consistent as much as the time of menopause. intercourse hormone deficiency results in sped up bone turnover, a damaging stability and microarchitectural deterioration, which compromises bone power, thereby expanding bone fragility and, therefore, fracture chance. by means of the age of eighty, it really is envisioned that fifty% of trab- ular bone could have been misplaced. normal menopause happens among the a long time of forty five and fifty four years around the globe. This age doesn't seem to have replaced considerably over the centuries. by contrast, because the heart of the nineteenth century, lifestyles expectancy, rather in girls, has elevated significantly, with most girls residing to the age of eighty years or extra in lots of areas of the area. which means on the age of fifty years, a girl will stay for greater than 30 years with no bone safeguard by means of intercourse hormones. This r- resents greater than one-third of a woman’s existence. on the age of fifty years, the lifetime probability to event a fracture is set 50% (ie, one out of 2 ladies may have a fracture in this period).
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Extra resources for Atlas of Postmenopausal Osteoporosis, 3rd Edition
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Estrogen-deficiency also prompts apoptosis of osteocytes. Reproduced with permission from Ferrari S. Cellular and molecular mechanisms of osteoporosis. In: Innovation in skeletal medicine. Edited by JY Reginster and R Rizzoli. Issy-Les-Moulineaux: Elsevier Masson, 2008c; 19–46. 23. This model illustrates the effect of estrogen (respectively estrogen deficiency) on the intricate crosstalk between immune cells and bone cells by modulating cytokine production in the bone marrow environment. Normally, estrogen supresses (E−) osteoclastogenesis, and induces osteoclast apoptosis (E+) by exerting a direct effect on osteoclasts, bone marrow stromal cells/osteoblasts, monocytes/macrophages and T cells.
A) This figure illustrates the percentage loss of trabecular bone microachitecture over one year in placebo-treated postmenopausal women, as evaluated by micro-computed tomography of iliac crest bone biopsies. 3% loss of spine bone mineral density (BMD), there was a disproportionate loss of trabecular number and volume, with a marked increase in the space between trabeculae. The insets illustrate the loss of horizontal struts leading to mechanical failure, as seen in vertebrae or distal radius.