Download Atlas of Postmenopausal Osteoporosis by Serge Ferrari, Johann D Ringe (auth.), René Rizzoli (eds.) PDF

By Serge Ferrari, Johann D Ringe (auth.), René Rizzoli (eds.)

René Rizzoli Menopause is the time in a woman’s lifestyles whilst reproductive capability ends. Ovaries lessen their job and the construction of intercourse hormones ceases. this era should be linked to a wide number of indicators affecting the cardiovascular and urogenital structures, in addition to dermis, hair and bone. Bone capital is gathered via the tip of the second one decade and continues to be roughly consistent as much as the time of menopause. intercourse hormone deficiency results in sped up bone turnover, a detrimental stability and microarchitectural deterioration, which compromises bone energy, thereby expanding bone fragility and, hence, fracture possibility. through the age of eighty, it truly is envisioned that fifty% of trab- ular bone may have been misplaced. usual menopause happens among the a long time of forty five and fifty four years worldwide. This age doesn't seem to have replaced considerably over the centuries. by contrast, because the center of the nineteenth century, existence expectancy, relatively in girls, has elevated significantly, with most ladies residing to the age of eighty years or extra in lots of areas of the realm. which means on the age of fifty years, a girl will stay for greater than 30 years with no bone defense by way of intercourse hormones. This r- resents greater than one-third of a woman’s existence. on the age of fifty years, the lifetime possibility to event a fracture is ready 50% (ie, one out of 2 girls could have a fracture in this period).

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In certain circumstances, a low dietary calcium, or high urine sodium, can exacerbate these losses and induce further bone loss. Data from Riggs BL, Khosla S, Melton JL 3rd. Sex steroids and the construction and conservation of the adult skeleton. Endocr Rev 2002 23:279–302. 31. The effects of three approaches (exercise, exercise plus calcium supplementation, and exercise plus estrogen replacement therapy) were studied in 120 postmenopausal women who had low forearm bone mineral density. The results showed that in women less than 10 years after the menopause, calcium supplementation prevented forearm bone loss, but estrogen replacement increased bone mass slightly, and was more effective than calcium alone.

Ralston SH. Genetic control of susceptibility to osteoporosis. J Clin Endocrinol Metab 2002; 87:2460–6. Rauch F, Travers R, Glorieux FH. Cellular activity on the seven surfaces of iliac bone: a histomorphometric study in children and adolescents. J Bone Miner Res 2006; 21:513–9. Recker R, Lappe J, Davies KM et al. Bone remodeling increases substantially in the years after menopause and remains increased in older osteoporosis patients. J Bone Miner Res 2004; 19:1628–33. Riggs BL, Khosla S, Melton LJ 3rd.

Reproduced with permission from Lindsay R, Aitken JM, Anderson JB et al. Long-term prevention of postmenopausal osteoporosis by oestrogen: evidence for an increased bone mass after delayed onset of oestrogen treatment. Lancet 1976; 1:1038–41. 29. Glucocorticoid excess, either endogenously (such as in Cushing’s disease) or exogeneously (use of prednisone in inflammatory conditions), represents a major risk factor for osteoporosis. Glucocorticoids affect bone metabolism both systemically, by directly inhibiting intestinal calcium absorption (thereby competing with vitamin D) and suppressing the production of growth hormone GH/IGF-1 and gonadal steroids, and locally by directly inhibiting the function of osteoblasts and osteocytes while promoting osteoclastic bone resorption, the latter through an increase of RANKL/OPG ratio in the bone marrow environment.

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