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In healthy human subjects, bone mineral mass follows a trajectory from birth on to attain a maximal value, the so-called peak bone mass (PBM), by the end of the second or the beginning of the third decade, according to both gender and skeletal sites examined . Later menarcheal age was shown to be a risk Etomidate factor for reduced bone mineral mass in postmenopausal women [2–7] and increased prevalence of fragility fractures at several sites of the skeleton [8–11]. The negative influence of later menarcheal age on bone mineral mass observed in postmenopausal women is already expressed
long before menopause as it was observed in middle-age premenopausal women with mean age 45 years, and in healthy young adult females in their very early twenties . Furthermore, this influence of pubertal timing on peak bone mass was found to be predetermined before the onset of pubertal maturation in a prospective follow-up study from age 8 to 20 years . This suggested that both pubertal timing and bone traits may be under the influence of common genetic factors . The risk of hip fracture is dependent upon the amount of areal bone mineral density (aBMD) or bone mineral content (BMC) as assessed by osteodensitometry at the level of proximal femur, particularly in the femoral neck (FN). Longitudinal studies of women ranging from 20 to 94 years with follow-up periods from 16 to 22 years showed that the average annual rate of bone loss was relatively constant and tracked well within individuals [15, 16].