At the onset of the study, the participants had a mean bone age of 12 years (range, 6.5–17) and mean chronological age of 12 years (range, 6.9–16.6). Bone age and chronological age did not differ (mean difference = –0.03 ± 0.1 years). Thirty-six girls were prepubertal, with a bone age of 9.3 years (range, 6.3–12) and a chronological age of 9.4 years (range, 6.9–11.9); 26 girls were peripubertal, with a bone age 11.8 years (range, 9.6–15) and a chronological age of 12.0 years (range, 10.1–15.1); 36 girls were postpubertal, with a bone age of 14.9 years (range, 12–17) and a chronological age of 14.6 years (range, 11.4–16.6). Five girls refused assessment of pubertal status.
Growth in bone length and bone mass.
Table shows the absolute values for anthropometric and bone mass measurements. Figure shows the results expressed as a percentage of the predicted adult value versus bone age. The shaded region in Figure represents pubertal growth from Tanner stage 2 to menarche. In prepubertal girls with a bone age of 7 years, height, sitting height, and region lengths were approximately 80% of the predicted adult value; total and regional BMC were approximately 40% of the predicted adult value. At menarche (12.7 ± 0.1 years), bone lengths were within 3% of their adult peak; total and regional BMC were 15–20% below their predicted peak.
Height, sitting height, appendicular segment lengths, total and regional bone mineral content in 109 girls aged 7 to 17 years (mean ± SEM)
Height, regional lengths, and total body and regional BMC expressed as a percentage of the predicted young adult peak value versus bone age. The shaded area represents the pubertal growth period (Tanner stage 2 to menarche).
Figure shows that the variance in the age-adjusted BMC residuals increased with advancing bone age, whereas age-adjusted residuals for bone length did not. The pre-, peri-, and postpubertal BMC residuals (g2) increased, being, respectively, 174 ± 34.6, 626 ± 139, and 1,838 ± 381 (spine, P < 0.001), and 4,777 ± 1729, 8,775 ± 2,229, and 27,237 ± 5,539 (legs, P < 0.05 to 0.001). The respective pre-, peri-, and postpubertal length residuals (cm2) did not increase significantly and were 6.1 ± 1.3, 12.9 ± 2.7, 9.7 ± 1.9 (sitting height), and 9.6 ± 1.7, 17.5 ± 10.6, 17.3 ± 3.7 (leg length).
Figure 2 The bone-age adjusted residuals for spine and leg BMC increased with advancing age, whereas the bone age adjusted residuals for sitting height and leg length did not. Prepubertal (open circles), peripubertal (filled circles), and postpubertal (filled (more ...)
Figure shows the prospectively derived rates of total and regional growth in bone size and BMC versus bone age. Growth velocity of sitting height slowed before puberty, accelerated, and then decelerated at approximately 12 years. Growth velocity of the legs was more rapid than that of sitting height before puberty. In contrast to the spine, the legs showed no significant acceleratory phase before decelerating rapidly at approximately 11 years. There was no detectable increase in sitting height after 14 years of age or in leg length after 16 years of age.
Rates of growth in regional bone length (centimeters per month) and bone mass (grams per month) versus bone age (mean ± SEM). The shaded area represents the pubertal growth period (Tanner stage 2 to menarche).
At approximately 7 years, mineral accrual at the legs was higher than at the spine (5.1 ± 0.6 versus 0.8 ± 0.5 g/month). At approximately 12 years, mineral accrual was higher in the legs than spine (10.8 ± 0.8 versus 3.8 ± 0.6 g/month, respectively) despite growth in leg and spine lengths being similar (~0.3 cm/month). Deceleration in mineral accrual occurred 1 year later than deceleration in bone length at both sites. Bone mass accrual continued at the spine and legs until 16 years of age.
Between 7 and 17 years, 1,491 g of mineral was accrued: 42% (630 g) in the legs; 25% (376 g) in the ribs, sternum, pectoral, and pelvic girdles; 12% (176 g) in the arms; 11% (157 g) in the skull; and 10% (156 g) in the spine. Between the 7–11 years (prepuberty), 11–14 years (puberty), and 14–17 years (postpuberty), the increases in spine BMC were 38, 72, and 46 g, respectively. The corresponding increases in leg BMC were 240, 241, and 149 g.
Growth in BMC and vBMD.
Midshaft metacarpal and femoral cortical widths were approximately 70% of the predicted adult peak in prepubertal girls (Tanner stage 1). As shown in Figure , periosteal diameter increased at both sites with little change in endocortical diameter. Thus, cortical width increased, particularly when endocortical diameter contracted at Tanner stage 3 at the metacarpal, and after menarche at the femur. Of final cortical width, endocortical contraction contributed 13% at the metacarpal and 7% at the femur.
Midshaft metacarpal and femoral dimensions and femoral midshaft vBMD and cortical true BMD as a function of pubertal status.
Bone mass measurements were available for the femur, not metacarpal. As shown in Figure , as periosteal and endocortical diameters of the femoral midshaft increased comparably, cortical width remained constant between Tanner stage 4 and menarche. Despite this, femoral midshaft vBMD increased, presumably because true BMD of the cortex increased (lighter shaded column). After menarche, periosteal diameter increased and endocortical (medullary) diameter decreased resulting in an increase in cortical width (Figure , darkly shaded column). Despite the increasing femoral midshaft cortical width, vBMD remained unchanged, perhaps because true BMD of the cortex decreased.
As shown in Figure , BMC at the femoral midshaft increased across age by 50%, or 3.4 SD. This was 4 times the increase of 0.86 SD in femoral midshaft vBMD. L3 BMC increased across age by 150%; a 3.7 SD increase, 1.5 times the increase of 2.6 SD in vBMD.
BMC and vBMD at the femoral midshaft and third lumbar vertebra versus bone age.
Biochemical and hormonal measurements.
Biochemical measures of bone remodeling and serum E2 increased, reached a peak at bone age approximately 12 years (Tanner stage 4) and then decreased at menarche at a serum E2 of 200–400 pmol/mL (Table ; Figures and ). Change in total bone mass (grams per month) correlated with alkaline phosphatase (r = 0.20), osteocalcin (r = 0.38), P1CP (r = 0.32), and CrossLaps (r = 0.24) (all P < 0.02). Serum E2 accounted for 28% of the variance in leg BMC accrual in the accelerating phase of growth, 19% of the variance in the spine BMC accrual, and 49% of the variance in cortical width in the decelerating phase of growth (both, P < 0.05). IGF-1 accounted for 21% of the variance in the spine BMC in the accelerating phase of growth and for 14% of the variance in endocortical diameter (both P < 0.03). Bone age was the only independent predictor of leg bone mass accrual accounting for 35% of the variance (P < 0.005).
GH, IGF-1, serum estradiol, testosterone, androstenedione and, DHEAS according to Tanner stage (mean ± SEM)
Figure 6 Serum bone specific alkaline phosphatase, osteocalcin, collagen propeptide of type I collagen (PICP), and urinary type I C-telopeptide breakdown products (CrossLaps) versus bone age. Prepubertal (filled circles), peripubertal (open circles), and postpubertal (more ...)
Figure 7 Serum bone specific alkaline phosphatase, osteocalcin, collagen propeptide of type I collagen (PICP), and urinary type I C-telopeptide breakdown products (CrossLaps) versus estradiol. Numbers denote maturational stages; 1 (Tanner stage 1), 2 (includes (more ...)