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Division of Bone Diseases (S.F., R.R., J.-P.B.), WHO Center for Osteoporosis and Bone Diseases, Department of Internal Medicine, and Division of Nuclear Medicine (D.S.), Department of Radiology, University Hospital, 1211 Geneva 14, Switzerland
Address all correspondence and requests for reprints to: Dr René Rizzoli, M.D., Division of Bone Diseases, Department of Internal Medicine, University Hospital, 1211 Geneva 14, Switzerland. E-mail: rizzoli{at}cmu.unige.ch
Genetic factors are known to explain a major proportion of peak bone mineral mass variance. Whether the influence of these genetic factors is expressed before the pubertal bone mineral mass accrual and whether there is tracking of bone mineral mass during pubertal growth, however, are not clearly established. We prospectively investigated correlations for bone mineral content (BMC), density, and bone size between prepubertal daughters and their premenopausal mothers.
Height, weight, lumbar spine (LS), femoral neck (FN) and midfemoral diaphysis BMC, bone area (BA), areal bone mineral density (aBMD), and volumetric bone mineral apparent density (BMAD) were evaluated in 138 mothers (mean age ± SD, 40.0 ± 4.0 yr) and their daughters (8.1 ± 0.7 yr), who were then remeasured at yearly intervals for 2 yr.
Eight-year-old prepubertal daughters had reached 78% and 44% of their mothers’ height and weight, respectively. At the various skeletal sites, they had reached 33–43% of their mothers’ BMC, 47–69% of their BA, 59–78% of their aBMD, and 75–105% of their BMAD. All body size and bone traits (age-adjusted Z-scores) were significantly correlated between prepubertal daughters and their mothers (r: 0.22–0.36, P < 0.01), except midfemoral diaphysis BMAD. Heritability estimates (1/2 h2), after adjustment for body size and dietary calcium intake, showed that 18–37% of bone traits were directly determined by maternal descent. During the next 2 yr, growth was accompanied by a marked increase of BMC, aBMD, and BA, whereas BMAD changed very little. In contrast, during this period, there were only minor changes in body size or bone trait Z-scores (i.e. <0.5 Z-scores), which were thus highly correlated between consecutive measurements (r: 0.75–0.92, P < 0.0001). Accordingly, mother-daughter correlations remained unchanged over that period.
Although more than 60% of peak bone mineral mass is gained during puberty (mostly at the expense of an increase in bone size while volumetric bone density slightly changes), familial resemblance for most bone traits is already present between daughters and their mothers before puberty. In the girls, moreover, yearly measurements were highly correlated, suggesting tracking of bone traits during pubertal growth. These results indicate that genetic susceptibility to osteoporosis may already be detectable in early childhood.
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