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The worldwide incidence of fragility fractures has been exponentially growing, with significant impact on quality of life, mortality and social burden. Although up to 40% of fragility fractures affect men, male osteoporosis remains underdiagnosed and undertreated. Therefore, it would be crucial to identify new mediators for male bone fragility. Recent data suggest a direct effect of follicle stimulating hormone (FSH) on the skeletal metabolism. High FSH levels have been found to correlate with impaired bone health in females, whereas evidence in males is still poor and conflicting. Intriguingly, men with primary (high FSH levels) and central (low/normal FSH levels) hypogonadism might represent a novel study model in this setting. Thus, 119 men were enrolled in this cross-sectional observational study at the time of the first diagnosis of hypogonadism (whether primary or central). Bone mineral density and prevalence of fragility fractures were assessed. Our results indicate a potential negative effect of FSH excess on the male bone mass, especially at spine. The duration of exposure to high serum FSH may also play a part in this context.
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