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Original Studies |
Department of Radiology (M.L.L., V.G.) and Division of Endocrinology and Metabolism (T.F.R., F.R.K.), Childrens Hospital Los Angeles, Los Angeles, California 90027; Department of Biostatistics (J.S.), University of CaliforniaLos Angeles, School of Medicine, Los Angeles, California 90027; and Department of Preventive Medicine (M.I.G.), University of Southern California, Los Angeles, California 90033
Address correspondence and requests for reprints to: Vicente Gilsanz, M.D., Ph.D., Childrens Hospital Los Angeles, Department of Radiology, MS #81, 4650 Sunset Boulevard, Los Angeles, California 90027. E-mail: gilsanz{at}hsc.usc.edu
The amount of bone that is gained during adolescence is the main contributor to peak bone mass, which, in turn, is a major determinant of osteoporosis and fracture risk in the elderly. We examined whether computed tomography measurements for the density and the volume of bone in the axial and the appendicular skeletons could be tracked through puberty in 40 healthy white children (20 girls and 20 boys). Longitudinal measurements of the cross-sectional area and cancellous bone density of the vertebral bodies and the cross-sectional and cortical bone areas of the femurs at the beginning of puberty accounted for 6292% of the variations seen at sexual maturity; on average, 3 yr later. When baseline values for these bone traits were divided into quartiles, a linear relation across Tanner stages of sexual development was observed for each quartile in both girls and boys. The regression lines differed among quartiles for each trait, paralleled each other, and did not overlap. Thus, we are now in a position to identify those children who are genetically prone to develop low values for peak bone mass and toward whom osteoporosis prevention trials should be geared.
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