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“Introduction

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 [1]. Later menarcheal age was shown to be a risk PAK6 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 [12]. 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 [13]. This suggested that both pubertal timing and bone traits may be under the influence of common genetic factors [14]. 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 Blasticidin S mouse 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].