[Postmenopausal bone loss. Role of estrogens].
Menopause is attended by an increase in bone remodelling, predominantly resorption, resulting in a trabecular and cortical bone loss which can be prevented by administration of oestrogens. This indicates that oestrogen deficiency is one of the major physiopathological elements of postmenopausal osteoporosis. The mechanism of action of oestrogens has not yet been fully elucidated. The recent finding of functional oestrogen receptors in osteoblasts suggests that oestrogens might have a direct action on bone cells, side by side with their action on the activity or production of calcitropic hormones. The antiresorptive effect of oestrogens might be due to the osteoblasts producing one or several local factors that modulate the differentiation and/or recruitment of osteoclasts. Moreover, animal studies have provided arguments in favour of a direct action of oestrogens on bone formation.
Trémollières
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F
UF Maladies osseuses et métaboliques, CHU Purpan, Toulouse.
Pouilles
J M
JM
Ribot
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C
D000368:Aged; D002116:Calcitonin / Q000172:deficiency; D004958:Estradiol / Q000172:deficiency / Q000494:pharmacology; D004967:Estrogens / Q000172:deficiency* / Q000494:pharmacology; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis; D008875:Middle Aged; D010006:Osteoblasts / Q000187:drug effects / Q000378:metabolism; D015663:Osteoporosis, Postmenopausal / Q000209:etiology*; D010281:Parathyroid Hormone / Q000172:deficiency; D013002:Somatomedins / Q000096:biosynthesis; D015291:Transforming Growth Factors / Q000187:drug effects; D014808:Vitamin D Deficiency / Q000209:etiology
D004967:Estrogens; D007375:Interleukin-1; D010281:Parathyroid Hormone; D013002:Somatomedins; D004958:Estradiol; D015291:Transforming Growth Factors; D002116:Calcitonin