76** 0.63–0.91 Odds ratios are adjusted for all other variables in the table and for adolescent–mother pair heights and adolescent TB BA and BMC LS lumbar spine, BMC bone mineral content *p < 0.001, **p < 0.01, ***p < 0.05 Discussion To our knowledge, this is the first paper to describe the familial patterns

of fracture risk in adolescents and its relationship with bone mass measurements in adolescent–biological mother pairs of different ethnic backgrounds. The main findings of this study were that an adolescent’s risk of fracture was decreased if his/her mother had a greater lumbar spine BMC (24 % reduction in fracture risk for every SD increase in maternal BMC), but was increased if a sibling had a history of fracture or if the adolescent was white or male. Adolescent height and weight, maternal BA and IWP-2 chemical structure BMC, males and white ethnicity were positive predictors of adolescent bone mass. Lastly, there was a higher prevalence of fractures in white mothers prior to 18 years of age compared

to the other ethnic groups, a pattern similar to that of their adolescent children, which we have reported previously [19]. However, we were unable to show any association between a maternal history of childhood/adolescent fractures and the prevalence of fractures in their adolescent offspring. Maternal influences such as gestational height, adiposity and vitamin D status Phospholipase D1 have been postulated to be important in intrauterine programming

and in the tracking of skeletal development and body composition STA-9090 cost from infancy to adulthood [20, 21]. These maternal influences are beyond the scope of this paper, but it will be important to determine if these factors predict or influence fracture risk and bone mass in adolescents from the different ethnic buy Entinostat groups in South Africa. Although the positive relationship between the mother’s bone mass and her offspring’s has been researched and documented worldwide [1, 22–24], the finding that maternal bone mass might influence her offspring’s fracture prevalence during childhood and adolescence has not been reported previously. Intuitively, this association should not be surprising as several studies, although not all [25–28], have shown that children who had fracture(s) tend to have reduced BMC and BA compared to their peers who had no fractures, and genetic inheritance (maternal and paternal bone mass) plays a large role in determining childhood BMC, BA and peak bone mass [29]. However, in our earlier study of the Bt20 cohort [30], we did not find an inverse association between fracture history prevalence and bone mass at two time points during childhood and adolescence. In fact, in white males, there was a positive association between fracture risk and bone mass [30], possibly associated with increased contact sport participation [19].