title: Commentary-FSH and bone 2010: evolving evidence.
abstract: Bone loss due to menopause, natural or artificial, has been attributed solely to low estrogen. However, in a woman's life, the most precipitous bone loss begins 2 years prior to the last menstrual period, during which time estrogen levels are unperturbed whereas FSH is elevated. Our cell-based and mouse genetic studies have shown that FSH stimulates bone resorption by osteoclasts directly in a pituitary-bone axis, independently of the estrogen effect. On the basis of this and evolving clinical and scientific evidence, we propose that elevated FSH contributes to bone loss across the menopausal transition, particularly during late perimenopause. In the current issue of the European Journal of Endocrinology, Rendina et al. strengthen the view for a primary role of FSH signaling in the regulation of bone mass and bone remodeling in humans by demonstrating that an 'activating' polymorphism AA rs6166 causes low bone mass and high bone turnover.
authors.affiliation: The Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, New York, USA.
authors.forename: Jameel
authors.initials: J
authors.lastname: Iqbal
authors.forename: Li
authors.initials: L
authors.lastname: Sun
authors.forename: Mone
authors.initials: M
authors.lastname: Zaidi
mesh_terms: D000818:Animals; D001862:Bone Resorption / Q000139:chemically induced / Q000378:metabolism; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D005640:Follicle Stimulating Hormone / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D008954:Models, Biological; D010024:Osteoporosis / Q000378:metabolism / Q000473:pathology
chemical_list: D005640:Follicle Stimulating Hormone