In addition to predicting adolescent fracture, maternal bone mass was also an independent predictor of adolescent BA and BMC. Twin- and family-based studies have indicated that 60–85 % LY2874455 in vivo of the variance in BMD is genetically determined [1, 22–24, 31]. All of these studies indicate that the bone mass of pre- and post-menarche daughters is Geneticin datasheet related to the BMD of their mothers. Most workers have found correlations between 0.22 and 0.58 in parent/children pairs or mother/children pairs [1, 29]. We found similar heritability

rates (approximately 30 %) by maternal descent in pre-pubertal and early pubertal South African children [9], indicating that genetics plays an important role in determining bone mass in black, white and mixed ancestry South African children. The pattern of differences in fracture prevalence

between ethnic groups was similar in the biological mothers to that of their adolescent offspring, with the white mothers and adolescents reporting the highest prevalence of fractures (white mothers 31 % vs. blacks 6 % vs. MA 16 %). Quisinostat chemical structure It is likely that the actual prevalence is higher than that recorded as the fractures were historic, occurred during childhood and had no means of verification. However, these figures are higher than those reported by an older group of men and women (>50 years of age) participating in the European Prospective Osteoporosis Study (EPOS). They reported a fracture prevalence between the ages of 8 and 18 years of 8.9 % in men and 4.5 % in women [32]. We were unable to show any association between the history of childhood/adolescent fractures in mothers and the prevalence of fractures in their adolescent offspring within each ethnic group (data not shown). The findings support those of Ma and Jones who did not observe any association between the prevalence of childhood fractures in offspring and maternal fracture history (but the number of participants was small) [33]. However, we did show an association within the same family, as the prevalence of sibling fractures was significantly higher in families who had adolescents who had fractures

(23 %) than in families whose adolescents had no fractures (14 %). Similar evidence of fracture association among siblings Buspirone HCl has been reported from Poland, where more than 50 % of adolescents with multiple fractures indicated that at least one family member had sustained a fracture, while only 29 % of the adolescents who had no fractures had a family member who had fracture(s) [34]. We were unable to show an association between the risk of childhood fractures and bone mass measurements at 17/18 years of age for the entire group. There are conflicting results concerning the association between childhood fractures and bone mass around the time of peak bone mass attainment. Several studies have found that childhood fractures are associated with low adult BMD [35],[36], but this was not confirmed by Kawalilak et al. [37].