help button home button Endocrine Society JCEM JCEM Call for Nominations for EIC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ferrari, S.
Right arrow Articles by Bonjour, J.-P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ferrari, S.
Right arrow Articles by Bonjour, J.-P.
The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 2 358-361
Copyright © 1998 by The Endocrine Society

Original Studies

Familial Resemblance for Bone Mineral Mass Is Expressed before Puberty1

S. Ferrari, R. Rizzoli, D. Slosman and J.-P. Bonjour

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


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
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.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
PEAK BONE mineral mass, which is virtually achieved by the end of puberty at sites like the lumbar spine and femoral neck (1), is a major determinant of the risk of osteoporosis. Thus, optimizing peak bone mineral mass might decrease the prevalence of osteoporotic fractures (2). A few trials have indicated that calcium supplements and physical exercise may improve bone mineral mass accrual during childhood, mostly during pre- and early pubertal years (3, 4, 5). Numerous studies comparing bone mineral mass in mono- and dizygotic twins, or in parents and offsprings, have shown a predominant genetic effect on peak bone mineral mass (see Ref. 6 for review). Twin models, however, carry an important risk of overestimating bone mineral mass heritability, because of shared life-style and environmental covariates in these groups (7). Correlations for bone mineral mass between parents and their adult offspring also have been shown to decrease when common life-style factors are taken into account (8). How early and to what extent genetic factors may actually affect bone mineral mass is thus presently unknown (9).

We investigated familial resemblance for bone mineral content (BMC), density, and bone size before pubertal growth spurt occurs. For this purpose, BMC, bone area (BA), areal bone mineral density (aBMD), and volumetric bone mineral apparent density (BMAD) were compared between 138 prepubertal daughters and their premenopausal mothers. These girls were then remeasured after 1 and 2 yr, to examine a possible tracking of bone traits during this period.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Healthy Caucasian prepubertal girls, 6.6–11.1 yr old, and their mothers were recruited through the Public Health Youth Service of the Geneva district. All the girls previously had participated in a study on bone mineral density measurements (1) or in a calcium intervention trial on bone mineral mass growth (5). After obtaining parental informed consent, clinical examination was conducted by a senior pediatrician, who established the pubertal stage according to Tanner’s criteria (1). Reasons for exclusion were a height/weight ratio above the 97th or below the 3rd percentile according to local reference values, physical signs of puberty, chronic disease, gastrointestinal disease susceptible to induce malabsorption, congenital or acquired bone disease, or regular medication use. Bone and body size parameters were measured in 138 prepubertal daughters and their mothers at entry. These measurements and pubertal status assessment were repeated in the 138 girls after 1 yr and in 128 girls again after 2 yr. By that time, 47 girls (37%) had begun puberty (Tanner’s stage 2).

BMC (g), BA (cm2) and aBMD (g/cm2) were measured at L2-L4 vertebrae (LS) in anteroposterior view, as well as at the femoral neck (FN) and midfemoral diaphysis (FS) by dual x-ray absorptiometry using a Hologic QDR-2000 instrument (Waltham, Massachusetts). Coefficients of variation of repeated measurements at these sites varied from 1–1.6% for aBMD and from 0.3–3% for BMC and BA. An estimate of volumetric bone mineral density (BMAD, g/cm3) was calculated as previously described (10, 11). Dietary calcium intake was estimated through frequency food questionnaires administered by a trained dietitian at entry and after 6, 12, and 24 months.

Statistical analysis

Resemblance, for body size and bone traits, between the mothers and their daughters was evaluated by Pearson’s correlation coefficients (r) using linear regressions, after adjustment for age (Z-scores). For this purpose, mean values ± SD were calculated at yearly intervals in the children population and at 5-yr intervals in the adult population. Individual measurements were expressed as a number of SD differences from these means (Z-scores). Heritability by maternal descent, 1/2 h2 (%), i.e. half the additive genetic variance of the trait, can be estimated as the slope of the regression (regression coefficient, ß) for body size or bone traits (Z-scores) between mothers and daughters, which is the proportion of the total variance for the trait among the mothers explained by the covariance of the trait between daughters and mothers (12). To estimate heritability of bone traits independently of the genetic effects on body size and the dietary calcium intake, adjusted bone parameter residuals were calculated by multiple regression analysis [including height (Z-scores), weight (Z-scores), and calcium intake (mg/day)] and then regressed between mothers and daughters (8).

Tracking for body size and bone traits in the daughters was examined by calculating absolute Z-score differences between measurements performed at the start and after 1 yr, and between measurements performed after one and 2 yr, as well as by correlations between Z-scores at entry and after 2 yr. Mother-daughter correlations also were reevaluated during follow-up.

P < 0.05 was considered the level of statistical significance for r values and for heritability estimates, i.e. for the regression coefficient ß of mother-daughter pair correlations.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Baseline body size and bone parameters in 138 healthy Caucasian prepubertal girls and their premenopausal mothers are shown in Table 1Go. When daughters’ values were expressed as percentages of their mothers’ values (i.e. peak body size and bone values), body height and weight by the age of 8 yr were 78% and 44% of adult height and weight, respectively, whereas great disparities appeared in the maturity of the various bone traits. BMC in the daughters was the lowest, as compared with their mothers (33% to 43%, depending on the skeletal site), BMAD the highest (75–105%), and aBMD and BA were in the intermediate range (59–78% and 47–69%, respectively) (Table 1Go).


View this table:
[in this window]
[in a new window]
  		Table 1. Clinical characteristics of prepubertal daughters and their premenopausal mothers

 
Age-adjusted body size and bone trait Z-scores were significantly correlated between mothers and daughters (r: 0.22–0.36, P < 0.01), without major differences across bone sites or traits (except FS BMAD, for which no significant correlation was found) (Table 2Go). Heritability by maternal descent (i.e. half the additive genetic variance of the traits, as estimated for height and weight after adjustment for dietary calcium intake, and for bone traits after adjustment for body size and dietary calcium intake) varied from 18% (FS aBMD) to 38% (height) (Table 2Go).


View this table:
[in this window]
[in a new window]
  		Table 2. Mother-daughter correlations and heritability estimates

 
Body size and bone measurement changes could be evaluated in the 138 prepubertal girls after 1 yr and in 128 girls again after two yr. By that time, mean age (± SD) was 10.0 ± 0.5 yr. During this period, bone mineral mass and bone size increased at all skeletal sites, as expected, with the largest increase found at the level of FS (Table 3Go). In contrast, BMAD changed little or not at all, at any site.


View this table:
[in this window]
[in a new window]
  		Table 3. Yearly body size and bone parameters changes in prepubertal girls

 
To examine the possibility of tracking for body size and bone traits during prepubertal and early pubertal years, absolute Z-score differences between measurements performed at 1-yr intervals were calculated (Table 3Go). It is noteworthy that Z-score changes were less than 0.5 for any bone trait and site over these years. Moreover, when Z-scores at baseline and 2 yr later were compared by linear regression, a high degree of correlation was found at each skeletal site with r values between 0.76 and 0.91 (P < 0.0001) (Table 3Go). The correlations between the various LS variables are shown in Fig. 1Go. Accordingly, Pearson’s correlation coefficients for mother-daughter comparisons performed at 1- and 2-yr follow-ups remained unchanged, as compared with baseline (data not shown).



View larger version (33K):
[in this window]
[in a new window]
  		Figure 1. Z-score correlations at the level of LS, between measurements performed at baseline and after 2 yr, in 128 prepubertal girls [BMC (r: 0.91), BA (r: 0.92), aBMD (r: 0.90), and volumetric BMAD (r: 0.83)]. All correlations were significant at P < 0.0001.

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
In this study, we investigated, for the first time, familial resemblance for bone mineral mass at the lumbar spine and femur before pubertal bone growth spurt occurred. By comparing 138 healthy Caucasian prepubertal daughters and their premenopausal mothers, we first observed that BMAD (g/cm3), which is an evaluation of volumetric bone density (10, 11), was close to complete achievement (LS, FS) or had already achieved peak values (FN) by the age of 8 yr, whereas BMC (g) was only about one third of peak BMC. These results were consistent with 2 recent reports showing little, if any, changes in BMAD during puberty (13, 14) and with assessments of volumetric bone mineral density in childhood by quantitative computed tomography (15). Thus, bone mineral mass accrual during growth is mainly caused by changes in bone size, without significant changes of the "amount of bone in bone".

Parents-offspring and monozygotic/dizygotic twins comparisons have shown a strong genetic effect on peak bone mineral mass (6). In turn, peak bone mineral mass heritability at the level of lumbar spine and proximal femur, which is the proportion of the bone mineral mass variance attributable to genetic factors, was estimated to be 60–80%, depending on the model applied (parents-offspring vs. twins) and the evaluation for life-style and environmental covariates (7, 8). By comparing mother-daughter bone traits before daughters had begun puberty, we intended both to determine whether genetic factors governing bone mineral mass were expressed before pubertal growth spurt, and to estimate heritability for bone mineral mass before environmental and hormonal factors exert a durable influence on the skeleton. Significant correlations were observed between mothers and their prepubertal daughters for BMC and bone size at both the lumbar spine and femur. Moreover, remarkable heritability estimates were found for most bone traits, but for FS aBMD and BMAD. Heritability for all LS parameters and for FN aBMD and BMAD was close to heritability for height (38%), a trait known to be under strong genetic determination. It is noteworthy that heritability, by maternal descent, might provide a realistic view of the direct influence of genetic factors on bone traits, given that correlations were adjusted for body size and dietary calcium intake, and also because prepubertal daughters were unlikely to share with their mother life-style factors such as smoking or alcohol consumption. Thus, our results further suggested potential differences in the genetic influence on cortical (compact) vs. trabecular bone (6, 9), the latter being more directly dependent on genetic factors and less affected by body size determinants or the dietary calcium intake. This actually may help us to understand why LS seems to be less responsive to calcium supplementation than diaphysis of the appendicular skeleton in prepubertal girls (5).

We last examined the possibility of tracking for bone traits during prepubertal and early pubertal years. Tracking is a well-known phenomenon for body height, for instance, indicating that once familial resemblance for the trait is expressed, healthy subjects maintain their phenotype up to adulthood, unless major changes occur in their health status or environment. Our findings of only minor bone trait Z-score changes and high correlations between these Z-scores over a 2-yr period were compatible with tracking for BMC, aBMD, and volumetric bone mineral density, a well as for bone size. Further studies are needed to ascertain whether tracking for bone traits is maintained up to peak bone mineral mass achievement. However, the remarkable stability of mother-daughter correlations during the study period and the close similarity between our correlation coefficients and those previously reported between adult family members (6, 8, 12), strongly suggest that tracking is likely to last during the entire period of bone growth. Nevertheless, it should be emphasized that these results do not preclude that tracking for most bone traits may be definitely altered by changing environmental factors, such as dietary calcium intake (3, 4, 5). Rather, they further suggest that osteoporosis prevention trials should start in early childhood and last for several years.

In conclusion, familial resemblance for bone mineral mass was clearly detectable in prepubertal girls, particularly at sites of prevailing trabecular bone. Despite spontaneous changes in life-style and endogenous factors occurring during puberty, bone mineral mass is likely to track from childhood up to peak bone mineral mass achievement, suggesting that susceptibility genes for osteoporosis might be identified in the young child population (16).


   Acknowledgments
 
We are indebted to Dr. G. Theintz and Mrs. S. Gardiol for subjects management, clinical assessment, and collection of dietary calcium data; and to Mrs. M. Perez for secretarial assistance.


   Footnotes
 
1 This work was supported by the Swiss National Science Research Foundation (Grant No. 31–40758.94). Back

Received August 12, 1997.

Revised October 17, 1997.

Accepted November 3, 1997.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Bonjour JP, Theintz G, Buchs B, Slosman D, Rizzoli R. 1991 Critical years and stages of puberty for spinal and femoral bone mass accumulation during adolescence. J Clin Endocrinol Metab. 73:555–563.[Abstract]
  2. Bonjour JP, Rizzoli R. 1996 Bone acquisition in adolescence. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego: Academic Press; 465–476.
  3. Johnston Jr CC, Miller JZ, Slemenda CW, et al. 1992 Calcium supplementation and increases in bone mineral density in children. N Engl J Med. 327:82–86.[Abstract]
  4. Lloyd T, Martel K, Rollings N, et al. 1996 The effect of calcium supplementation and Tanner stage on bone density, content and area in teenage women. Osteoporos Int. 6:276–283.[Medline]
  5. Bonjour JP, Carrie AL, Ferrari S, et al. 1997 Calcium-enriched foods and bone mass growth in prepubertal girls: a randomized, double-blind, placebo-controlled trial. J Clin Invest. 99:1287–1294.[Medline]
  6. Kelly PJ, Morrison NA, Sambrook PN, Nguyen TV, Eisman JA. 1995 Genetic influences on bone turnover, bone density and fracture. Eur J Endocrinol. 133:265–271.[Medline]
  7. Slemenda CW, Christian JC, Williams CJ, Norton JA, Johnston Jr CC. 1991 Genetic determinants of bone mass in adult women: a reevaluation of the twin model and the potential importance of gene interaction on heritability estimates. J Bone Miner Res. 6:561–567.[Medline]
  8. Krall EA, Dawson-Hughes B. 1993 Heritable and life-style determinants of bone mineral density. J Bone Miner Res. 8:1–9.[Medline]
  9. Kelly PJ, Harris M. 1995 Genetic regulation of peak bone mass. Acta Paediatr. [Suppl]411:24–29.
  10. Katzman DK, Bachrach LK, Carter DR, Marcus R. 1991 Clinical and anthropometric correlates of bone mineral acquisition in healthy adolescent girls. J Clin Endocrinol Metab. 73:1332–1339.[Abstract]
  11. Carter DR, Bouxsein ML, Marcus R. 1992 New approaches for interpreting projected bone densitometric data. J Bone Miner Res. 7:137–145.[Medline]
  12. Tylavsky FA, Bortz AD, Hancock RL, Anderson JJB. 1989 Familial resemblance of radial bone mass between premenopausal mothers and their college-age daughters. Calcif Tissue Int. 45:265–272.[Medline]
  13. Lu PW, Cowell CT, Lloyd-Jones SA, Briody JN, Howman-Giles R. 1996 Volumetric bone mineral density in normal subjects, aged 5–27 years. J Clin Endocrinol Metab. 81:1586–1590.[Abstract]
  14. Haapasalo H, Kannus P, Sievänen H, et al. 1996 Development of mass, density, and estimated mechanical characteristics of bones in Caucasian females. J Bone Miner Res. 11:1751–1760.[Medline]
  15. Gilsanz V, Gibbens DT, Roe TF, et al. 1988 Vertebral bone density in children: effect of puberty. Radiology. 166:847–850.[Abstract/Free Full Text]
  16. Ferrari SL, Rizzoli R, Manen D, Slosman DO, Eisman J, Bonjour JP. 1996 Vitamin D receptor allelic polymorphisms and bone mass in females: influence of age and calcium supplementation. Osteoporos Int. [Suppl 1]6:160.



This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
L. Richert, T. Chevalley, D. Manen, J.-P. Bonjour, R. Rizzoli, and S. Ferrari
Bone Mass in Prepubertal Boys Is Associated with a Gln223Arg Amino Acid Substitution in the Leptin Receptor
J. Clin. Endocrinol. Metab., November 1, 2007; 92(11): 4380 - 4386.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
N. Ashton, S. H. Al-Wasil, H. Bond, J. L. Berry, J. Denton, and A. J. Freemont
The effect of a low-protein diet in pregnancy on offspring renal calcium handling
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2007; 293(2): R759 - R765.
[Abstract] [Full Text] [PDF]

Home page
 PediatricsHome page
V. Gilsanz and T. Wren
Assessment of Bone Acquisition in Childhood and Adolescence
Pediatrics, March 1, 2007; 119(Supplement_2): S145 - S149.
[Abstract] [Full Text] [PDF]

Home page
 IBMS BoneKEyHome page
J.-P. Bonjour and T. Chevalley
Pubertal Timing, Peak Bone Mass and Fragility Fracture Risk
IBMS BoneKEy, February 1, 2007; 4(2): 30 - 48.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
S. A. Abrams, I. J. Griffin, K. M. Hawthorne, and L. Liang
Height and Height Z-Score Are Related to Calcium Absorption in Five- to Fifteen-Year-Old Girls
J. Clin. Endocrinol. Metab., September 1, 2005; 90(9): 5077 - 5081.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
A. Arabi, H. Tamim, M. Nabulsi, J. Maalouf, H. Khalife, M. Choucair, R. Vieth, and G. El-Hajj Fuleihan
Sex differences in the effect of body-composition variables on bone mass in healthy children and adolescents
Am. J. Clinical Nutrition, November 1, 2004; 80(5): 1428 - 1435.
[Abstract] [Full Text] [PDF]

Home page
 PediatricsHome page
M. Horlick, J. Wang, R. N. Pierson Jr., and J. C. Thornton
Prediction Models for Evaluation of Total-Body Bone Mass With Dual-Energy X-Ray Absorptiometry Among Children and Adolescents
Pediatrics, September 1, 2004; 114(3): e337 - e345.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. GenomicsHome page
Q.-Y. Huang, F.-H. Xu, H. Shen, H.-Y. Deng, T. Conway, Y.-J. Liu, Y.-Z. Liu, J.-L. Li, M.-X. Li, K. M. Davies, et al.
Genome scan for QTLs underlying bone size variation at 10 refined skeletal sites: genetic heterogeneity and the significance of phenotype refinement
Physiol Genomics, May 19, 2004; 17(3): 326 - 331.
[Abstract] [Full Text] [PDF]

Home page
 Arch Intern MedHome page
M. L. Gourlay and S. A. Brown
Clinical Considerations in Premenopausal Osteoporosis
Arch Intern Med, March 22, 2004; 164(6): 603 - 614.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
S. Arpadi, M. Horlick, and E. Shane
Metabolic Bone Disease in Human Immunodeficiency Virus-Infected Children
J. Clin. Endocrinol. Metab., January 1, 2004; 89(1): 21 - 23.
[Full Text] [PDF]

Home page
 Physiol. GenomicsHome page
M. Suuriniemi, A. Mahonen, V. Kovanen, M. Alen, and S. Cheng
Relation of PvuII site polymorphism in the COL1A2 gene to the risk of fractures in prepubertal Finnish girls
Physiol Genomics, August 15, 2003; 14(3): 217 - 224.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
D. Prie, V. Huart, N. Bakouh, G. Planelles, O. Dellis, B. Gerard, P. Hulin, F. Benque-Blanchet, C. Silve, B. Grandchamp, et al.
Nephrolithiasis and Osteoporosis Associated with Hypophosphatemia Caused by Mutations in the Type 2a Sodium-Phosphate Cotransporter
N. Engl. J. Med., September 26, 2002; 347(13): 983 - 991.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
M. Peacock, C. H. Turner, M. J. Econs, and T. Foroud
Genetics of Osteoporosis
Endocr. Rev., June 1, 2002; 23(3): 303 - 326.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
C. Baudoin, M. E. Cohen-Solal, J. Beaudreuil, and M. C. De Vernejoul
Genetic and Environmental Factors Affect Bone Density Variances of Families of Men and Women with Osteoporosis
J. Clin. Endocrinol. Metab., May 1, 2002; 87(5): 2053 - 2059.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
M. S Treuth, N. F Butte, K. J Ellis, L. J Martin, and A. G Comuzzie
Familial resemblance of body composition in prepubertal girls and their biological parents
Am. J. Clinical Nutrition, October 1, 2001; 74(4): 529 - 533.
[Abstract] [Full Text] [PDF]

Home page
 Drug Metab. Dispos.Home page
J. A. Eisman
Pharmacogenetics of the Vitamin D Receptor and Osteoporosis
Drug Metab. Dispos., April 1, 2001; 29(4): 505 - 512.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
M. Luiza Loro, J. Sayre, T. F. Roe, M. I. Goran, F. R. Kaufman, and V. Gilsanz
Early Identification of Children Predisposed to Low Peak Bone Mass and Osteoporosis Later in Life
J. Clin. Endocrinol. Metab., October 1, 2000; 85(10): 3908 - 3918.
[Abstract] [Full Text]

Home page
 Endocr. Rev.Home page
J. A. Eisman
Genetics of Osteoporosis
Endocr. Rev., December 1, 1999; 20(6): 788 - 804.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
S. Ferrari, D. Manen, J.-P. Bonjour, D. Slosman, and R. Rizzoli
Bone Mineral Mass and Calcium and Phosphate Metabolism in Young Men: Relationships with Vitamin D Receptor Allelic Polymorphisms
J. Clin. Endocrinol. Metab., June 1, 1999; 84(6): 2043 - 2048.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
G. I. Baroncelli, S. Bertelloni, C. Ceccarelli, and G. Saggese
Measurement of Volumetric Bone Mineral Density Accurately Determines Degree of Lumbar Undermineralization in Children with Growth Hormone Deficiency--Author's Response
J. Clin. Endocrinol. Metab., April 1, 1999; 84(4): 1490a - 1491.
[Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
J. Sainz, J. M. Van Tornout, J. Sayre, F. Kaufman, and V. Gilsanz
Association of Collagen Type 1 {alpha}1 Gene Polymorphism with Bone Density in Early Childhood
J. Clin. Endocrinol. Metab., March 1, 1999; 84(3): 853 - 855.
[Abstract] [Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ferrari, S.
Right arrow Articles by Bonjour, J.-P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ferrari, S.
Right arrow Articles by Bonjour, J.-P.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals