This Article Abstract Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hui, S. L. Articles by Johnston, C. C. Search for Related Content PubMed PubMed Citation Articles by Hui, S. L. Articles by Johnston, C. C., Jr. Pubmed/NCBI databases Substance via MeSH

Difference in Bone Mass between Black and White American Children: Attributable to Body Build, Sex Hormone Levels, or Bone Turnover?

Departments of Medicine (S.L.H., M.P., R.M., C.C.J.) and Pediatrics (L.A.D.), Indiana University School of Medicine, Indianapolis, Indiana 46202; Regenstrief Institute, Inc., and Indiana University Center on Aging Research (S.L.H., A.J.P.), Indianapolis, Indiana 46202; and Departments of Obstetrics and Gynecology and Medicine (C.L.), University of Massachusetts Medical School, Worcester, Massachusetts 01655

Address all correspondence and requests for reprints to: Siu L. Hui, Ph.D., Regenstrief Institute, Inc., Indiana University School of Medicine, 1050 Wishard Boulevard, RG6, Indianapolis, Indiana 46202. E-mail: shui{at}iupui.edu.

	Abstract

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
A cross-sectional study of 232 healthy children, with about equal numbers of boys and girls and blacks and whites, aged 4 to 16 yr, was conducted to investigate the racial differences in bone mineral. Bone mineral content (BMC) by dual x-ray absorptiometry was found to be similar between blacks and whites at the spine after controlling for age and Tanner stage. However, total body BMC was higher in blacks, compared with whites of the same age and Tanner stage. Height and weight alone reduced the racial difference in BMC from 152 g to 66 g in girls and from 163 g to 105 g in boys, in whom the difference was further reduced to 66 g after accounting for lean and fat body mass and subscapular skinfold. The only significant sex hormone was androstenedione, which explained another 4–5 g of the racial difference in total body BMC for both boys and girls. Among the biochemical variables, only 25OH vitamin D reduced the residual racial difference in total body BMC to 39 g in girls, whereas serum PTH, urine free deoxypyridinoline ratio, and 1,25(OH)₂ vitamin D reduced the residual difference to 25 g in boys. The residual racial differences in bone mass were not statistically significant.

	Introduction

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
BLACKS HAVE HIGHER axial and appendicular bone mineral content and density than whites of comparable ages and body weights (1, 2, 3). This is associated with a lower incidence of fractures in black adults than in whites (4, 5, 6).

Several studies have indicated that the increased bone mineral density (BMD) in blacks dates from infancy (7, 8) and is present through childhood (9, 10), but the etiology of this observable difference remains unclear. Although part of the difference can be attributed to the racial differences in skeletal size (11, 12), recent investigations implicate hormonal differences (13, 14), which could have major effects on bone growth around puberty.

Skeletal maturation, measured by the presence of ossification centers, is more advanced in black infants and children than whites (15). Physical signs of puberty also appear earlier in black children than in whites, although there is no evidence that the subsequent rate of progression through the stages of puberty differs between the races (16). The variability in pubertal and skeletal maturation in determining eventual differences in adult BMD is not yet quantified.

The goal of this study was to investigate whether the average bone mass was higher in black, compared with white, children of the same age and the same stage of sexual maturation, and how much of any difference between the races could be explained by body size and composition. We hypothesized that racial difference in serum levels of sex hormones during growth could contribute to black/white differences in bone mass. Other researchers have reported racial differences in bone metabolism, suggesting that these might contribute to differences in bone mass (17). Hence, this study also investigated whether sex hormone levels and biochemical variables related to bone metabolism could explain some of the observed racial differences in bone mass between black and white children.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
Subjects were 232 healthy children, 4–16 yr old, recruited through various means, including advertising on campus, churches, and newspapers. The children had no history of bone disease or growth problems and had not taken medications known to affect bone. Their self-reported race and other demographics were recorded. Approximately equal numbers of white and black boys and girls were recruited. These children were studied on the General Clinical Research Center after informed consent was given by the children’ parents or guardians with assent from children over the age of five. The study was approved by the Institutional Review Board at Indiana University.

	Bone measurements

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
Dual-energy x-ray absorptiometry (DXA) measurements of bone mineral content (BMC) were made at the spine and total body using a DPXL machine (Lunar Corp., Madison, WI). In adults, the short-term reproducibility is 1% for total body BMC (TBMC) and 0.8% for spine BMC (SBMC) in our laboratory. Long-term quality control is assured by consistency of daily scans of standard external phantoms.

	Body size and composition

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
Standing height was measured with a wall-mounted stadiometer that was calibrated weekly and weight with an electronic digital scale. Body composition was measured as total lean mass and total fat mass from the DXA total body scan. Anthropometric measurements obtained using steel measuring tapes and calipers included biacromial width, subscapular skinfold, and calf circumference.

	Tanner staging

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
Sexual development of the children was measured by Tanner stage, which ranges from I (prepubertal) to V (fully mature) (18). Using a gender-specific questionnaire, the children reported their Tanner stage by comparing their own physical development to the five stages in standard sets of diagrams. A parent or the research coordinator then reviewed the results with the children to make sure they understood the questionnaire. When an individual reported discordant stages of pubic hair and breast or genital development, the higher of the two stages was used.

	Sex hormones

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
We measured the serum levels of estrone (E1), estrone sulfate, estradiol (E2), testosterone (T), androstenedione (4-A), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), and SHBG. E1 was measured using kits from Diagnostic Systems Laboratories, Inc. (DSL; Webster, TX). The sensitivity was 1.2 pg/ml and inter- and intraassay coefficients of variation (CV) were 11.1% and 5.6%, respectively. E2 was measured using kits from DSL. The sensitivity was 2.0 pg/ml and the inter- and intraassay CV were 8.9% and 7.5%, respectively. Estrone sulfate was measured by RIA as estrone following extraction of estrone, hydrolysis of the spent plasma, solvent extraction, and Celite chromatography as described (19). The inter- and intraassay CV were 9.7% and 3.5%. T was measured by RIA using a kit supplied by Diagnostic Products (Los Angeles, CA). The inter- and intraassay CV were 10% and 5.1%. The 4-A and DHEA were measured by RIA using kits supplied by Diagnostic Systems Laboratory. The inter- and intraassay CV were 8.8% and 8.7% for 4-A, and 9.6% and 2.8% for DHEA. DHEAS was measured by RIA using a kit supplied by Diagnostic Products. The inter- and intraassay CV were 8.6% and 6.2%. SHBG was measured by immunoradiometric assay using a kit from DSL. The inter- and intraassay CV were 4.9% and 2.0%. All CV refer to the ranges found in children.

	Biochemical assays

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
Random nonfasting blood and urine samples were collected at each visit when subjects arrived at the General Clinical Research Center. Urine samples were collected, aliquoted, and stored at -70 C until analyzed. The serum samples were collected and processed after clotting at room temperature for 30 min. They were then aliquoted and stored at -80 C until analyzed. Calcium (Ca), creatinine (Cr), and free deoxypyridinoline (FdPd) were measured in all urine samples. Serum samples were analyzed for bone-specific alkaline phosphatase (BAP), osteocalcin (OC), intact 1–84 PTH, 25OH vitamin D (25D), and 1,25(OH)₂vitamin D(1,25D).

Urine Ca and Cr were analyzed on the Cobas Mira (Roche Diagnostics, Indianapolis, IN). All CV reported for biochemical assays are interassay CV. Urine Ca (CV, 3.7% at 12.2 mg/dl) was analyzed using the Arsenazo III method. Urine Cr (CV, 3.3% at 226.6 mg/dl) was analyzed using the Jaffe Kinetic method. FdPd (CV, 10.9% at 17.5 nmol/liter) was assayed after 1:20 dilution using an ELISA assay supplied by Quidel (formerly Metra Biosystems, Mountain View, CA). Urine Ca and FdPd were divided by the corresponding Cr to yield Ca/Cr ratio and FdPd/Cr ratio.

OC was assayed by RIA (CV, 8.9% at 26.9 ng/ml) using a rabbit polyclonal antiserum raised against bovine OC. Intact PTH was assayed (CV, 9.7% at 17.5 pg/ml) by an immunoradiometric assay (Nichols Institute, San Juan Capistrano, CA). BAP (CV, 7.3% at 12.4 ng/ml) was assayed by an ELISA assay (Quidel).

The 25D (CV, 11.4% at 11.4 ng/ml) was assayed using the vitamin D-binding protein after extraction and purification on HPLC. Serum 1,25 D (CV, 10.6% at 41.6 pg/ml) was assayed using the vitamin D receptor protein purified from calf thymus after extraction and purification on HPLC.

	Statistical methods

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
We chose to measure BMC on each subject using TBMC and at SBMC for two reasons. First, these two sites have well-defined anatomical boundaries, so the analysis of scans does not require the operator to decide on comparable regions of interest, a difficult task when the areas of bone scans vary greatly among children of different ages. Second, we chose BMC over BMD (BMC divided by area) because a change in BMC reflects simply the change in bone mass, whereas a change in BMD is affected by the growth in both bone mass and bone area. If the growth spurt of the bone area is asynchronous with the growth spurt of bone mineral, the change in BMD might be difficult to interpret. Using BMC circumvents the problem of choosing an appropriate method to normalize the bone mass for different sizes (20, 21, 22). However, we also investigated the growth in skeletal size by comparing the total body bone area (TAREA) and spine area (SAREA) between black and white children.

Descriptive statistics for different Tanner stages were calculated for the four groups of black and white boys and girls. Tanner stages II and III were combined, as were Tanner stages IV and V, to provide adequate sample sizes for reliable estimates of means and SDs for the various measurements. Multiple regression analysis was used to test for differences in all measurements between races and between sexes while controlling for age and Tanner stage. The primary interest was in estimating and testing the black/white difference separately for TBMC and SBMC while controlling for sex, age, and Tanner stage. If there were significant interactions between any two of the four factors, separate analyses were conducted for subgroups of children. When racial differences were found, height and weight were added to the model to test whether the racial differences could be explained by body size. To explain any residual racial difference in bone mass, three sets of possible factors were added in stepwise fashion. The first set included anthropometric measurements and body composition variables (total lean and fat mass) from DXA. The second set included serum levels of sex hormones, and the third set consisted of biochemical variables. After each set of variables was added to the model, backward elimination was performed to remove the nonsignificant predictors from that set, and the difference in bone mass between black and white children was estimated. Because separate models for boys and girls gave significantly better fit once the anthropometric variables were added, the final results were reported for boys and girls separately.

	Results

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
The numbers of subjects were approximately equal in the four subgroups of black and white boys and girls (Table 1). About 40% of the children were in Tanner stage I, 35% in Tanner stages II or III, and 25% in Tanner stages IV or V. The age distributions by Tanner stage are also displayed within each of the four subgroups. Overall, black children were 0.6 yr younger than white children of the same sex and at the same Tanner stage, and girls were 0.7 yr younger than boys of the same race and the same Tanner stage (P < 0.01 for both comparisons).

View larger version (60K): [in this window] [in a new window]   Figure 1. Mean TBMC (A) and mean SBMC (B) plotted against Tanner stages for black and white boys and girls.

Tests for sex differences in Table 2C were based on comparisons of means of boys in Table 2A with corresponding means of girls in Table 2B (with black and white children combined), and controlling for age, Tanner stage, and race. Boys were significantly higher in total body BMC, areas of the total body and spine, and most anthropometrics. The T and E1 levels differed between sexes as expected. DHEAS was slightly higher in boys but 4-A was slightly higher in girls. DHEA and SHBG did not differ between sexes. Of all the biochemical variables, only BAP was higher in boys.

Table 3 presents the models for predicting total body BMC and area, first using sex, age, Tanner stage, and race (model 1). The model shows both BMC and area of the total body are higher in blacks than in white, in boys than in girls and that they increase with age and Tanner stage. Compared with white children of the same sex, age, and Tanner stage, the estimated TBMC of black children was higher by 138 g (10%, P < 0.0001), and their total body area was greater by 82 cm² (5.3%, P = 0.0001). To investigate how much of the racial difference could be explained by body size, height and weight were added to the model (model 2). After adjustments for height and weight, the mean TBMC remained higher in black children, but the difference was reduced to 80 g (5.5%, P = 0.0004). The total bone area was still greater in blacks by 40 cm² (2.6%, P = 0.004). These six demographic and developmental characteristics accounted for 92% of the variation in total body BMC and 95% of the variation in total body area, with no significant interactions between any two variables. These findings on both TBMC and area were very consistent across boys and girls when separate models were fitted to the two groups (results not shown).

To investigate whether sex hormone levels could explain the residual racial difference, the sex hormones were added to the separate models for boys and girls. Among the boys, only 4-A showed a significant positive correlation with TBMC. Despite minimal improvement in model fit, the addition of 4-A reduced the estimated racial difference from 65 g to 61 g. In girls, both 4-A and E2 were positive predictors of TBMC (P < 0.05), reducing the estimated racial difference from 66 g to 61 g. With the subsequent addition of biochemical variables, however, 4-A remained the only significant predictor in both boys and girls.

When the biochemical variables were added to the model in boys, PTH, free FdPd/Cr, and 1,25D together reduced the boys’ racial difference in mean TBMC from 61 g to 25 g (still higher in blacks), which was not statistically significant (P > 0.32). Among the girls, 25D was the only biochemical variable that marginally improved the fit of the model. Its inclusion reduced the estimated racial difference from 61 g to 39 g, again no longer statistically significant (P > 0.14).

	Discussion

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 
In this study, we examined the difference in bone mass between black and white children. For children at the same age and Tanner stage, we found no difference in BMC or area at the lumbar spine between blacks and whites. The lack of black/white difference in BMC agrees with Wang et al. (23), although they found BMD to be higher in blacks than a combined group of whites, Asians, and Hispanics in subsequent follow-up (24), but differs from at least two other studies on children. Bell et al. (10) found that black children between the ages of 7 and 12 yr have higher spine BMD after adjusting for sex, age, and weight. Because black children are usually more sexually advanced than white children of the same age (as reflected by the lower ages for black children, compared with whites in the same Tanner stage in Table 1), not controlling for Tanner stage in our data also resulted in an apparently higher spine BMD in blacks. In another study, Gilsanz et al. (9, 25) showed a sizable divergence in trabecular bone density by quantitative computed tomography (QCT) as black and white children reached Tanner stages IV and V. QCT measures only trabecular bone, but anteroposterior DXA scans in our study included the cortical envelope and posterior processes of the spine. Because we did not show a racial difference in spine BMC, the racial difference may be primarily in trabecular rather than cortical bone. This speculation is consistent with data from adult studies. In normal women aged 55–75 yr, the percent difference between blacks and whites is much larger in QCT than in BMD measurements of the spine (26). The racial difference in adult spine BMD, also reported by others (27), could be due to a longer period of postpubertal growth in blacks because they reach Tanner stage V at an earlier age.

The higher TBMC in our black children appears to be in all Tanner stages, which means that it exists already in prepubertal children as previously reported (7, 8, 9, 10). Nevertheless, despite the lack of power to detect a significant interaction between race and Tanner stage, the raw data in Fig. 1 suggest that the racial difference might become more pronounced when girls reach Tanner stage III and boys reach Tanner stage IV. This pattern would be similar to that observed in trabecular density of the spine (9, 25).

The racial difference in TBMC could be partially explained by the larger body size (weight more than height) of black children. Age, sex, Tanner stage, and body size together explain over 92% of the variation of total body BMC and area (>85% for spine) in children between the ages of 4 and 16 yr. Each factor tends to have similar effects on BMC and its corresponding area. Thus, our findings agree with most studies that conclude that racial/ethnic difference may be largely accounted for by differences in bone size (14, 28).

The addition of other anthropometric measurements besides height and weight did not further explain the racial difference in TBMC in girls. In contrast, inclusion of height and weight alone explained less of the racial difference in boys. The further inclusion of total lean and fat body mass and sc fat was necessary to reduce the boys’ racial difference in TBMC to a level similar to that observed in girls.

Although we had hypothesized that differences in sex hormone levels might have led to higher bone mass in blacks, the data in Table 2 did not show any systematic differences in hormone levels between blacks and whites in the same Tanner stages. Furthermore, only 4-A appeared to have a consistent, albeit small, effect on TBMC after adjusting for age, Tanner stage, and body size and composition, explaining a few grams of the residual racial difference in TBMC in both sexes. However, this does not mean that sex hormone levels are unimportant in determining bone mass. Most of the effects of sex hormones on TBMC could have been mediated through their effects on sexual maturation (Tanner stage) and body size (height, weight, lean mass), which explain the majority of the variation in TBMC. It has been hypothesized that some of the racial difference in BMD is related to differences in serum E1 (13). Estrogens may mediate their effect on BMD by increasing GH secretion, leading to GH-induced increases in bone mass (14). However, we did not find significant differences in E1 or E2 levels between whites and blacks at the same Tanner stage. We did not examine direct or indirect measures of GH secretion.

We (29) previously reported that lower bone turnover in black children might explain their higher bone mass. This more carefully designed study shows that there might be a differential effect between boys and girls. Consistent with previous studies (17), we found racial differences in 25D, 1,25D, and Ca/Cr. Additionally, we found FdPd/Cr to be higher in whites. In boys, adding 1,25D, PTH, and FdPd/Cr to the model reduced the residual racial difference in TBMC by 60%, making it statistically nonsignificant. In girls, however, only 25D entered the model, reducing the residual racial difference by 36%. Therefore biochemical variables related to bone metabolism appear to account for a nontrivial part of the racial difference in TBMC despite the large variations in their measurements caused by both biological fluctuations and assay result variability.

In summary, black children on average have higher total body BMC than white children. Over half of this difference can be explained by differences in the body size and composition of the two races. A substantial portion of the residual differences can be explained by bone metabolism and, to a much smaller extent, by sex hormone levels, leaving only 2% of the difference between the races unexplained.

	Acknowledgments

 
We thank Diane Cornner for recruiting the children and coordinating the study, and Charlene Franz for measuring the sex hormones.

	Footnotes

 
This work was partially supported by NIH grants AG05793, AG18397, and M01-RR750.

Abbreviations: 1,25D, 1,25(OH)₂ vitamin D; 4-A, androstenedione; 25D, 25OH vitamin D; BAP, bone-specific alkaline phosphatase; BMC, bone mineral content; BMD, bone mineral density; Ca, calcium; Cr, creatinine; CV, coefficient(s) of variation; DHEAS, dehydroepiandrosterone sulfate; DXA, dual-energy x-ray absorptiometry; E1, estrone; E2, estradiol; FdPd; free deoxypyridinoline; OC, osteocalcin; QCT, quantitative computed tomography; SAREA, spine area; SBMC, spine BMC; T, testosterone; TAREA, total body bone area; TBMC, total body BMC.

Received April 26, 2002.

Accepted November 3, 2002.

	References

Top Abstract Introduction Subjects and Methods Bone measurements Body size and composition Tanner staging Sex hormones Biochemical assays Statistical methods Results Discussion References

 

1. Nelson DA, Simpson PM, Johnson CC, Barondess DA, Kleerekoper M 1997 The accumulation of whole body skeletal mass in third- and fourth-grade children: effects of age, gender, ethnicity, and body composition. Bone 20:73–78[Medline]
2. Wang J, Horlick M, Thornton JC, Levine LS, Heymsfield SB, Pierson Jr RN 1999 Correlations between skeletal muscle mass and bone mass in children 6–18 years: influences of sex, ethnicity, and pubertal status. Growth Dev Aging 63:99–109[Medline]
3. Trotter M, Peterson RR 1970 Weight of the skeleton during postnatal development. Am J Phys Anthropol 33:313–323[CrossRef][Medline]
4. Farmer ME, White LR, Brody JA, Bailey KR 1984 Race and sex differences in hip fracture incidence. Am J Public Health 74:1374–1380[Abstract/Free Full Text]
5. Griffin MR, Ray WA, Fought RL, Melton LJ, III 1992 Black-white differences in fracture rates. Am J Epidemiol 136:1378–1385.[Abstract/Free Full Text]
6. Baron JA, Barrett JA, Karagas MR 1996 The epidemiology of peripheral fractures. Bone 18(Suppl 3):209S–213S
7. Li JY, Specker BL, Ho ML, Tsang RC 1989 Bone mineral content in black and white children 1 to 6 years of age. Early appearance of race and sex differences. Am J Dis Child 143:1346–1349[Abstract/Free Full Text]
8. Rupich RC, Specker BL, Lieuw AF, Ho M 1996 Gender and race differences in bone mass during infancy. Calcif Tissue Int 58:395–397[Medline]
9. Gilsanz V, Roe TF, Mora S, Costin G, Goodman WG 1991 Changes in vertebral bone density in black girls and white girls during childhood and puberty. N Engl J Med 325:1597–1600[Abstract]
10. Bell NH, Shary J, Stevens J, Garza M, Gordon L, Edwards J 1991 Demonstration that bone mass is greater in black than in white children. J Bone Miner Res 6:719–723[Medline]
11. Taner J1978 Physical growth and development. In: Forfar J, Arnell C, eds. Textbook of pediatrics. Edinburgh: Churchill Livingstone; 249–303
12. Hamill PVV, Johnson FE, Lemeshow S 1973 Body weight, stature, and sitting height: white and Negro youths 12–17 years. No. 126. Rockville, MD: U.S. Department of Health, Education, and Welfare. DHEW publications HRA. Vital and Health Statistics Series 11
13. Cauley JA, Gutai JP, Kuller LH, Scott J, Nevitt MC 1994 Black-white differences in serum sex hormones and bone mineral density. Am J Epidemiol 139:1035–1046[Abstract/Free Full Text]
14. Wright NM, Renault J, Willi S, Veldhuis JD, Pandey JP, Gordon L, Key LL, Bell NH 1995 Greater secretion of growth hormone in black than in white men: possible factor in greater bone mineral density—a clinical research center study. J Clin Endocrinol Metab 80:2291–2297[Abstract]
15. Garn SM, Sandusky ST, Nagy JM, McCann MB 1972 Advanced skeletal development in low-income Negro children. J Pediatr 80:965–969[CrossRef][Medline]
16. Herman-Giddens ME, Slora EJ, Wasserman RC, Bourdony CJ, Bhapkar MV, Koch GG, Hasemeier CM 1997 Secondary sexual characteristics and menses in young girls seen in office practice: a study from the Pediatric Research in Office Settings network. Pediatrics 99:505–512[Abstract/Free Full Text]
17. Bell NH, Yergey AL, Vieira NE, Oexmann MJ, Shary JR 1993 Demonstration of a difference in urinary calcium, not calcium absorption, in black and white adolescents. J Bone Miner Res 8:1111–1115[Medline]
18. Tanner JM, Whitehouse RH 1976 Clinical longitudinal standards for height, weight, height velocity, weight velocity, and stages of puberty. Arch Dis Child 51:170–179[Abstract/Free Full Text]
19. Franz C, Watson D, Longcope C 1979 Estrone sulfate and dehydroepiandrosterone sulfate concentrations in normal subjects and men with cirrhosis. Steroids 34:563–573[CrossRef][Medline]
20. Carter DR, Bouxsein ML, Marcus R 1992 New approaches for interpreting projected bone densitometry data. J Bone Miner Res 7:137–145[Medline]
21. Seeman E 1997 From density to structure: growing up and growing old on the surfaces of bone. J Bone Miner Res 12:509–521[CrossRef][Medline]
22. Nevill AM, Holder RL, Maffulli NA, Cheung JCY, Leung SF, Lee WTK, Lau JTF 2002 Adjusting bone mass for differences in projected bone area and other confounding variables: an allometric perspective. J Bone Miner Res 17:703–708[CrossRef][Medline]
23. Wang MC, Aguirre M, Bhudhikanok GS, Kendall CG, Kirsch S, Marcus R, Bachrach LK 1997 Bone mass and hip axis length in healthy Asian, black, Hispanic, and white American youths. J Bone Miner Res 12:1922–1935[CrossRef][Medline]
24. Bachrach LK, Hastie T, Wang MC, Narasimhan B, Marcus R 1999 Bone mineral acquisition in healthy Asian, Hispanic, black, and Caucasian youth: a longitudinal study. J Clin Endocrinol Metab 84:4702–4712[Abstract/Free Full Text]
25. Gilsanz V, Skaggs DL, Kovanlikaya A, Sayre J, Loro ML, Kaufman F, Korenman SG 1998 Differential effect of race on the axial and appendicular skeletons of children. J Clin Endocrinol Metab 83:1420–1427[Abstract/Free Full Text]
26. Kleerekoper M, Nelson DA, Peterson EL, Flynn MJ, Pawluszka AS, Jacobsen G, Wilson P 1994 Reference data for bone mass, calciotropic hormones, and biochemical markers of bone remodeling in older (55–75) postmenopausal white and black women. J Bone Miner Res 9:1267–1276[Medline]
27. Ettinger B, Sidney S, Cummings SR, Libanati C, Bikle DD, Tekawa IS, Tolan K, Steiger P 1997 Racial differences in bone density between young adult black and white subjects persist after adjustment for anthropometric, lifestyle, and biochemical differences. J Clin Endocrinol Metab 82:429–434[Abstract/Free Full Text]
28. Bhudhikanok GS, Wang MC, Eckert K, Matkin C, Marcus R, Bachrach LK 1996 Differences in bone mineral in young Asian and Caucasian Americans may reflect differences in bone size. J Bone Miner Res 11:1545–1556[Medline]
29. Slemenda CW, Peacock M, Hui S, Zhou L, Johnston CC 1997 Reduced rates of skeletal remodeling are associated with increased bone mineral density during the development of peak skeletal mass. J Bone Miner Res 12:676–682[CrossRef][Medline]

This article has been cited by other articles:

				A. Fausto-Sterling The bare bones of race. Social Studies of Science, October 1, 2008; 38(5): 657 - 694. [Abstract] [PDF]

				C. M. Weaver, L. D. McCabe, G. P. McCabe, M. Braun, B. R. Martin, L. A. DiMeglio, and M. Peacock Vitamin D Status and Calcium Metabolism in Adolescent Black and White Girls on a Range of Controlled Calcium Intakes J. Clin. Endocrinol. Metab., October 1, 2008; 93(10): 3907 - 3914. [Abstract] [Full Text] [PDF]

				M. Braun, C. Palacios, K. Wigertz, L. A Jackman, R. J Bryant, L. D McCabe, B. R Martin, G. P McCabe, M. Peacock, and C. M Weaver Racial differences in skeletal calcium retention in adolescent girls with varied controlled calcium intakes Am. J. Clinical Nutrition, June 1, 2007; 85(6): 1657 - 1663. [Abstract] [Full Text] [PDF]

				M. Braun, B. R Martin, M. Kern, G. P McCabe, M. Peacock, Z. Jiang, and C. M Weaver Calcium retention in adolescent boys on a range of controlled calcium intakes. Am. J. Clinical Nutrition, August 1, 2006; 84(2): 414 - 418. [Abstract] [Full Text] [PDF]

				K. Wigertz, C. Palacios, L. A Jackman, B. R Martin, L. D. McCabe, G. P McCabe, M. Peacock, J H. Pratt, and C. M Weaver Racial differences in calcium retention in response to dietary salt in adolescent girls Am. J. Clinical Nutrition, April 1, 2005; 81(4): 845 - 850. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hui, S. L. Articles by Johnston, C. C. Search for Related Content PubMed PubMed Citation Articles by Hui, S. L. Articles by Johnston, C. C., Jr. Pubmed/NCBI databases Substance via MeSH