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The Journal of Clinical Endocrinology & Metabolism 89(4):1698 –1703
Copyright © 2004 by The Endocrine Society
doi: 10.1210/jc.2003-031113
Relationship of Sex Hormones to Bone Geometric
Properties and Mineral Density in Early Pubertal Girls
QINGJU WANG, PATRICK H. F. NICHOLSON, MIIA SUURINIEMI, ARJA LYYTIKÄINEN,
ERKKI HELKALA, MARKKU ALEN, HARRI SUOMINEN, AND SULIN CHENG
University of Jyväskylä (Q.W., P.H.F.N., M.S., A.L., E.H., H.S., S.C.) and LIKES-Foundation for Sport and Health Sciences
(Q.W., M.S., A.L.), Jyväskylä Fin-40014; and Peurunka-Medical Rehabilitation Center (M.A.), Jyväskylä Fin-41340, Finland
This study aimed to evaluate the associations among serum
17␤-estradiol (E2), testosterone (T), sex hormone-binding
globulin (SHBG), bone geometric properties, and mineral density in 248 healthy girls between the ages of 10 and 13 yr old.
The left tibial shaft was measured by peripheral quantitative
computed tomography (Stratec XCT-2000; Stratec Medizintechnik, GmbH, Pforzheim, Germany). The cortical bone and
marrow cavity areas were expressed as proportions of the
total tibial cross-sectional area (CSA). Cortical thickness and
total volumetric bone mineral density (vBMD) were also determined. These tibial geometric and densitometric measures
were correlated against the serum sex hormone concentrations after controlling for age and body size. The results
showed that E2 was negatively associated with marrow cavity
proportion (r ⴝ ⴚ0.19, P ⴝ 0.003) and positively associated
S
EX HORMONES PLAY a major role in bone development during adolescence and bone maintenance in later
life. However, their effects on bone development in pubertal
girls in terms of bone cross-sectional geometric properties
and mineral density are far from clearly understood. Most of
the evidence from animal studies and comparative studies in
bone morphology between males and females indicates that
17␤-estradiol (E2) exerts its effects on the long bone shaft
during growth by suppressing bone formation at the pericortical surface and bone resorption at the endocortical surface (1– 4). E2 is the most potent and abundant estrogen
during puberty and throughout the fertile life of females.
However, few studies have been performed in children to
investigate the relationship of bone cross-sectional properties to E2 levels. In a cross-sectional study, Neu et al. (5)
showed that, although the total bone diameter of proximal
radius of girls increased until approximately 15 yr of age, the
diameter of the marrow cavity did not change during the
early pubertal period.
Testosterone (T) has profound effects on longitudinal bone
growth, but its effects on bone calcium accrual or crosssectional development have been investigated even less extensively than the effect of E2. It is believed that T also exerts
its effect in adult men by suppressing bone turnover and that
Abbreviations: CSA, Cross-sectional area; E2, 17␤-estradiol; pQCT,
peripheral quantitative computed tomography; SHBG, sex hormonebinding globulin; T, testosterone; vBMD, volumetric bone mineral
density.
JCEM is published monthly by The Endocrine Society (http://www.
endo-society.org), the foremost professional society serving the endocrine community.
with cortical proportion and thickness and with total vBMD
(r ⴝ 0.26, P < 0.001; r ⴝ 0.25, P < 0.001; and r ⴝ 0.23, P < 0.001,
respectively). However, T was not associated with these bone
variables. On the other hand, SHBG was positively associated
with marrow cavity proportion (r ⴝ 0.17, P ⴝ 0.007) and negatively associated with cortical proportion and thickness and
with total vBMD (r ⴝ ⴚ0.14, P ⴝ 0.029; r ⴝ ⴚ0.16, P ⴝ 0.010; and
r ⴝ ⴚ0.18, P ⴝ 0.005, respectively). Total bone CSA did not
correlate with E2, T, or SHBG. These results suggest that E2
has a positive effect on bone geometric and densitometric
development by suppressing bone turnover at the endocortical surface during the early pubertal period, that SHBG plays
an opposite role to E2, and that T has no detectable effect.
(J Clin Endocrinol Metab 89: 1698 –1703, 2004)
the effects may be mediated by the estrogen pathway (6).
Some of the studies in adult females also indirectly confirmed that the effect of T on bone mass and its change are
mediated by E2 (7, 8).
Sex hormones are mainly stored and transported in serum
by binding to their sex hormone-binding globulin (SHBG),
which is an important regulator of the bioavailability of sex
hormones. Studies in old women have shown that SHBG
levels are negatively associated with bone mass and its
change and that the association is independent of serum E2
level (9 –11), which indicates that an extra pathway exists for
SHBG to exert its effect on bone mass. Such a phenomenon
has not been investigated in growing girls.
In the present study, we measured the midshaft of the
tibia using peripheral quantitative computed tomography
(pQCT), a technique capable of separately analyzing cortical
bone, trabecular bone, and marrow cavity compartments.
Our aim was to investigate whether levels of E2, T, or SHBG
were associated with the geometric and densitometric properties of the tibia.
Subjects and Methods
Subjects
The subjects consisted of 248 Finnish girls aged 10 –13 yr. To be
eligible for the study, the participants had to have no history of disease
or medication known to affect bone metabolism. None of the participants had menarche. The physical maturational stage was determined
by the developmental patterns of breast and pubic hair assessed by a
public nurse according to the Tanner grade system (12). If there was a
disagreement between breast and pubic hair development, the final
decision was made based on the development of breast. The numbers
of girls at each maturational stage were 126, 109, and 13 at Tanner stages
1698
Wang et al. • Sex Hormones and Bone Geometry and Density
I, II, and III, respectively. All participants provided written consents by
themselves and their guardians also provided consent in accordance
with the ethical committees of University of Jyväskylä, the Central
Hospital of Central Finland, and the Finnish National Agency of
Medicines.
Anthropometric assessments
Body weight was measured using an electronic scale and recorded to
the 0.1 kg with subjects wearing light clothes and no shoes. Height was
determined with stadiometer to the nearest 0.5 cm.
Sex hormone assessments
Serum T, E2, and serum SHBG were assessed using time-resolved
fluoroimmunoassays (Delfia; Wallac Oy, Turku, Finland). Blood was
drawn in the morning between 0700 and 0900 after an overnight fast.
Inter- and intraassay coefficients of variation were 5.2% and 5.1% for E2,
9.2% and 9.4% for T, and 1.1% and 1.1% for SHBG, respectively. The free
E2 was calculated as: free E2 (pmol/liter) ⫽ E2 (pmol/liter)/[K ⴱ SHBG
(nmol/liter) ⫹1], and the free T was calculated as: free T (pmol/liter) ⫽
T (nmol/liter) ⴱ 1000/[K ⴱ SHBG (nmol/liter) ⫹ 1], according to Ekins
(13), where K for E2 and T binding to SHBG are the equilibrium constants
(0.68 ⴱ 109 liter/mol and 1.6 ⴱ 109 liter/mol, respectively).
There were 22 girls with the serum T concentration under detectable
level, and therefore, they were excluded from the analysis of the association between T and other variables.
Bone densitometric and geometric measurements
A pQCT device (XCT-2000; Stratec Medizintechnik, GmbH, Pforzheim, Germany) was used to scan the left tibial shaft of the participants.
A 2-mm thick single tomographic slice with pixel size of 0.59 mm was
taken from the transverse plane 60% of lower leg length up from the
lateral malleolus. The lower leg length was defined as the distance
between the lateral condyle of tibia and lateral malleolus and measured
when the participant was in sitting position with the knee at a 90° angle.
The pQCT device was calibrated once a week using a standard phantom
and once a month using a cone phantom provided by the manufacture.
The results were analyzed using Bonalyse 1.3 software (Bonalyse Oy,
Jyväskylä, Finland). The outer-bone border was determined using a
specified threshold of 280 mg/cm3. The total cross-sectional area (CSA)
of the tibial shaft was then defined as the area enclosed within the
outer-bone border. The total CSA was separated into three parts, the
cortex, subcortex, and medullary cavity, based on the following two
thresholds: 711 mg/cm3 to distinguish cortex and subcortex, and 100
mg/cm3 to separate subcortex and medullary cavity. The areas of these
three compartments were then expressed as percentages relative to the
total bone CSA. The volumetric bone mineral density (vBMD, mg/cm3)
of the total and cortical bone was also obtained. Cortical thickness was
obtained from the Stratec software version 5.4 (Stratec Medizintechnik)
using the circular ring model in which the cortical thickness was calculated as follows: (total bone CSA/␲)0.5 ⫺ [(total bone CSA ⫺ cortical
bone CSA)/␲]0.5. The coefficients of variation were 1% for CSA and less
than 1% for vBMD and cortical thickness.
Statistical analysis
Descriptive statistics were used to present the background and bone
information. All the hormone values were first transformed into normal
or approximately normal distribution by applying a logarithm or square
root transform before further analysis. Body weight and height were
highly correlated with each other, and therefore, they were reduced to
one body size index using principal components factor analysis, and this
index was used for adjustment instead of body weight and height. The
correlations between age, body weight and height, sex hormones, and
bone geometric and densitometric properties were assessed using the
Pearson product moment correlation. Partial correlation analysis was
used to evaluate the relationship of bone geometric properties and
vBMD to hormone variables, controlling for age and body size index. To
explore the E2-independent effect of SHBG on bone density and geometric properties, partial correlation analysis was used, adjusting for
total E2, age, and body size. A P ⬍ 0.05 was considered statistically
J Clin Endocrinol Metab, April 2004, 89(4):1698 –1703 1699
significant. Statistical analysis was carried out using SPSS version 11.0
for Windows (SPSS Inc., Chicago, IL).
Results
Descriptive characteristics of age, body height and weight,
sex hormones and SHBG levels, and bone geometric and
densitometric variables are given in Table 1.
Age, body weight and height, sex hormones, tibial total
bone CSA, and cortical thickness were associated positively
with each other (P ⬍ 0.001; Table 2). Age did not correlate
with cortical, subcortical, or marrow proportions, or with
total vBMD of tibial shaft, but it did correlate positively with
cortical vBMD (P ⫽ 0.001). Body weight was positively associated with cortical proportion and negatively associated
with subcortical proportion (P ⫽ 0.009 and P ⬍ 0.001, respectively), but it was not associated with either tibial total
or cortical vBMD. Body height was negatively correlated
with subcortical proportion (P ⬍ 0.001), but it was not associated with tibial total or cortical vBMD or cortical
proportion.
E2 was positively correlated with total and cortical vBMD,
as well as with cortical proportion (P ⬍ 0.001, P ⫽ 0.018, and
P ⬍ 0.001, respectively; Fig. 1), and negatively correlated
with subcortical and marrow proportions (P ⫽ 0.007 and P ⫽
0.013, respectively). Free E2 had similar results to E2.
T and free T were negatively associated with subcortical
proportion but not with either bone vBMD or cortical proportion. SHBG correlated negatively with age, body weight
and height, sex hormones (except for E2), bone CSA, and
cortical thickness (P ⬍ 0.014), as well as with total vBMD and
cortical proportion (P ⫽ 0.014 and P ⫽ 0.008, respectively),
and SHBG correlated positively with subcortical proportion
(P ⫽ 0.042).
After controlling for age and body size, the results showed
that E2 correlated positively with total vBMD, as well as with
cortical thickness and proportion (P ⬍ 0.001, Table 3), and
negatively with marrow proportion (P ⫽ 0.003, Table 3), but
E2 did not correlate with either total CSA or cortical vBMD
TABLE 1. The mean ⫾ SD or median (5–95 percentile) of
anthropometric, tibial, and sex hormonal variables
Variables
Age (yr)
Height (cm)
Weight (kg)
SHBG (nmol/liter)
E2 (nmol/liter)a
Free E2 (pmol/liter)a
T (nmol/liter)a,b
Free T (pmol/liter)a,b
Left tibia shaft
Total CSA (mm2)
Cortical CSA (mm2)
Cortical thickness (mm)
Cortical proportion (%)
Marrow proportion (%)
Subcortical proportion (%)
Total vBMD (mg/cm3)
Cortical vBMD (mg/cm3)
Mean ⫾
SD
11.2 ⫾ 0.7
145.3 ⫾ 7.8
38.8 ⫾ 8.3
82.7 ⫾ 34.9
0.089 (0.039 – 0.242)
1.941 (0.566 –5.589)
0.407 (0.049 –1.378)
3.620 (0.380 –23.256)
364 ⫾ 54
198 ⫾ 31
3.45 ⫾ 0.40
55.5 ⫾ 4.3
24.1 ⫾ 4.2
20.4 ⫾ 2.5
665 ⫾ 48
1042 ⫾ 54
a
For E2, free E2, T, and free T, the median and 5–95 percentile
were given.
b
Only girls with detectable T were included.
1700
J Clin Endocrinol Metab, April 2004, 89(4):1698 –1703
Wang et al. • Sex Hormones and Bone Geometry and Density
TABLE 2. Pearson moment product correlation coefficient of age, body weight and height, sex hormones, SHBG, and bone variables
Weight
Height
E2
Free E2
T
Free T
SHBG
Total CSA
Cortical thickness
Cortical proportion
Subcortical proportion
Marrow proportion
Total vBMD
Cortical vBMD
Age
Weight
Height
E2
Free E2
T
Free T
SHBG
0.311c
0.554c
0.411c
0.400c
0.303c
0.214c
⫺0.208b
0.373c
0.212c
⫺0.004
⫺0.013
0.006
0.028
0.209c
0.718c
0.250c
0.545c
0.376c
0.509c
⫺0.579c
0.751c
0.583c
0.165b
⫺0.244c
⫺0.032
0.057
0.007
0.397c
0.527c
0.412c
0.403c
⫺0.418c
0.732c
0.536c
0.105
0.336c
0.080
0.020
0.089
0.697c
0.372c
0.254c
⫺0.109
0.257c
0.359c
0.260c
⫺0.171b
⫺0.157a
0.228c
0.150a
0.362c
0.547c
⫺0.582c
0.413c
0.490c
0.267c
⫺0.209b
⫺0.148a
0.226c
0.094
0.742c
⫺0.139a
0.344c
0.231c
0.039
⫺0.131a
0.023
0.022
0.094
⫺0.367c
0.398c
0.292c
0.082
⫺0.142a
⫺0.012
0.031
0.031
⫺0.381c
⫺0.408c
⫺0.169b
0.129a
0.100
⫺0.156a
⫺0.057
a
Correlation is significant at the 0.05 level (two-tailed).
Correlation is significant at the 0.01 level (two-tailed).
c
Correlation is significant at the 0.001 level (two-tailed).
b
of tibia shaft. Free E2 showed similar associations with these
bone geometric and densitometric properties as total E2.
However, T and free T did not show any relationship with
these bone variables. SHBG correlated negatively with total
vBMD, as well as with cortical thickness and proportion, and
positively with marrow proportion (P ⫽ 0.005, P ⫽ 0.010, P ⫽
0.029, and P ⫽ 0.007, respectively; Table 3). When further
controlled for the total E2 level, the negative correlation
between SHBG and total vBMD, cortical thickness, and cortical proportion, and the positive correlation between SHBG
and marrow proportion remained (P ⫽ 0.003, P ⫽ 0.021, P ⫽
0.038, and P ⫽ 0.014, respectively).
Discussion
FIG. 1. Scatterplot of bone geometric and densitometric properties
against E2 level transformed by natural logarithm. The best-fit linear
regression lines are also shown.
The present study showed that serum E2 was significantly
and positively associated with total vBMD, cortical thickness, and cortical proportion of the tibial shaft and was
negatively correlated with the marrow proportion. These
associations were independent of age and body size. However, serum T was not associated with these bone geometric
properties and vBMD after controlling for age and body size.
SHBG had the opposite association with bone geometric
properties and density of that seen for E2, even after controlling for total E2 level.
During early puberty, body height increases by 0.5–1.0 cm
per month; therefore, even a half year’s difference in age can
elicit large differences in bone size. To evaluate the association of E2 and bone geometric properties, the confounding
effect of age and body height and weight must be controlled
for.
In the present study, we divided the total CSA of tibial
shaft into three compartments (cortex, subcortex, and marrow cavity) and expressed them as proportions to the total
CSA and found that no correlation existed between any of the
three proportions and chronological age. Because the total
CSA was not correlated with E2 after adjustment for age and
body size, the larger cortical proportion and the thickening
of the cortex relating to higher E2 level cannot be attributed
to periosteal expansion but can only be due to reduction, or
relatively less expansion, of the marrow cavity. Our results
indicate that E2 may not influence the total CSA, but rather,
E2 acts to constrict the marrow cavity or suppress bone
Wang et al. • Sex Hormones and Bone Geometry and Density
J Clin Endocrinol Metab, April 2004, 89(4):1698 –1703 1701
TABLE 3. The correlations coefficients of bone geometric and density variables and sex hormones and their binding globulin after
adjustment for age and body size index formed by body weight and height
Total CSA
Cortical thickness
Cortical proportion
Subcortical proportion
Marrow proportion
Total vBMD
Cortical vBMD
E2
Free E2
T
Free T
SHBG
SHBGa
⫺0.029
0.250d
0.261d
⫺0.131
⫺0.191c
0.233d
0.064
⫺0.108
0.254d
0.251d
⫺0.082
⫺0.207d
0.269d
0.067
0.002
⫺0.018
0.000
⫺0.026
0.008
0.007
0.037
0.028
⫺0.014
0.004
0.013
⫺0.017
⫺0.006
⫺0.017
0.086
⫺0.161c
⫺0.137b
⫺0.059
0.167c
⫺0.177c
⫺0.037
0.101
⫺0.148b
⫺0.132b
⫺0.048
0.156b
⫺0.187c
⫺0.054
a
Indicates correlations between SHBG and bone variables adjusted for total E2 level, age and body size.
Correlation is significant at the 0.05 level (two-tailed).
c
Correlation is significant at the 0.01 level (two-tailed).
d
Correlation is significant at the 0.001 level (two-tailed).
b
resorption at the endosteal surface. Libanati et al. (14) reported a decrease in marrow diameter of the second metacarpal bone in girls with more advanced puberty, which is
consistent with our finding. On the other hand, they did not
find any correlation between E2 and second metacarpal indices, such as total bone thickness, cortical thickness, or marrow diameter. However, the authors reported that both
the E2 level and total metacarpal thickness increased with the
increase of the maturational stages, which indicated that the
sample size might not be big enough to show the slight
correlation between E2 and marrow diameter. Many studies
have demonstrated that serum E2 levels are negatively associated with both bone formation and resorption markers
during the growth or postmenopausal periods (15–21),
which indicates that E2 at physiological levels might exert its
suppressing effect on both bone formation and resorption,
which are coupled. A study by Plato and Purifoy (22) showed
that postmenopausal women who were currently using estrogen had significantly smaller medullary cavity and larger
cortical area of the second metacarpal bone compared with
estrogen nonusers measured using radiographic morphometry. Using the same method, Horsman et al. (23) also demonstrated that a high dose of E2 up to 25 mg/d could completely inhibit bone resorption at the endosteal surface.
Although the physiological conditions are different between
postmenopausal women and growing girls, the effect of E2
on bone resorption at the endosteal surface is evident in the
two different populations. Therefore, we could propose that
the negative relationship of E2 with the marrow cavity proportion found in our study is mainly due to the suppressing
effect of E2 on the bone resorption and not from new bone
formation.
Total vBMD measured by pQCT is defined as the mass of
mineral contained in the bone slice per volume of the slice.
It is mainly determined by the following three elements:
mean mineral density, the porosity of solid components, and
the structural compartmentalization of total CSA. The pQCT
provides us with a possibility to separately analyze the trabecular, subcortical, and cortical bone compartments. No
correlation was found between serum E2 level and cortical
vBMD of tibial shaft in our study. This implies that physiological E2 levels do not influence the mineralization or the
porosity of the cortical bone. This view is supported by
ovariectomized young animal studies in which the cortical
vBMD at long bone shaft did not differ over experimental
period (24, 25). The positive association between cortical
vBMD and age found in this study, which is consistent with
a cross-sectional study by Schoenau et al. (26) showing that
cortical vBMD increases until adulthood, may not be related
to changes in E2 level over the growing and fertile period but,
instead, may be related to other factors. Naturally, it is conceivable that the positive correlation between E2 and total
vBMD, with or without adjustment for age and body size, is
due to the smaller proportion of marrow cavity of the total
CSA of tibial shaft associated with high E2 levels.
Bone size and mass are determined by many factors such
as heredity, body size, aging, disease, diet, physical activity,
medication, and alcohol and tobacco use. Evidence from twin
and family studies suggests that genetic factors account for
up to 85% of the variance in peak BMD and other bone
properties. Although epidemiological and experimental
studies have identified estrogen deficiency as an important
risk factor for osteoporosis and E2 as a vital determinant of
sexual skeletal dimorphism, estrogen exposure is not necessarily required for the normal occurrence of the major
functions of the skeleton, which has been exhibited in sexually immature and hypogonadal individuals. Few studies
have reported the amount of the variance explained by E2 in
bone mass during puberty. In the present study, E2 was
found to account for only 5.2% of the variance in total vBMD,
6.7% in cortical proportion of total tibial CSA, and 2.5% in
marrow proportion. We have not found any comparable
studies with which to confirm our results.
Compared with E2, the effects of T on bone mineralization
and cross-sectional development appear insignificant after
controlling for body size. Very few studies have investigated
the effects of T on development of bone CSA in pubertal girls
to date. One study from Libanati et al. (14) reported that free
serum T level positively related to cortical thickness and total
bone thickness of the second metacarpal bone in girls at
Tanner stage II–IV. These findings are in agreement with our
results that T level positively correlated with cortical thickness and total bone CSA of tibia shaft when body size was
not controlled (see Table 2). However, the significant correlations between T and cortical thickness and bone CSA of the
tibia shaft disappeared when the difference of body size
between individuals was adjusted. This indicates that the
effect of growth plays a critical role in the relationship between T and bone size in growing girls, which suggests that
it is improper to leave the body size ignored when assessing
the relationship between sex hormones and bone size at the
growing period. It is believed that the effects of androgens
1702
J Clin Endocrinol Metab, April 2004, 89(4):1698 –1703
on bone mineralization are mediated by estrogens. This is
supported by results in men, which showed that destructive
mutation in the ER gene (estrogen resistance) or in the CYP19
gene (aromatase deficiency) is associated with low BMD
despite adequate or even well above normal androgen levels
(27–30). Men with aromatase deficiency respond to estrogen
therapy with marked increases in bone mass, whereas T
treatment has no effect on bone mass (27–30). In the present
study, no significant correlation was found between T and
either vBMD or cortical and marrow proportion. This is in
agreement with some previous studies in which T showed
less association with bone mineral density (31, 32).
SHBG modulates the bioavailability of sex steroids by
decreasing their serum free levels. We found that SHBG was
negatively associated with bone variables, which was consistent with previous studies in older women (9, 10). One
study even showed that SHBG was superior to sex hormone
levels for predicting the occurrence of postmenopausal fracture (11). Another explanation for our finding could be that
SHBG actually has a more complex role than simply acting
as a transporter and bioavailability modulator of sex steroids
in the circulatory system (33, 34). An inhibiting effect of
SHBG on the E2 induction of cell proliferation through SHBG
receptor and cAMP was also found in estrogen-dependent
breast cancer (35). It is conceivable that the SHBG/SHBGreceptor system, if it exists in bone tissue, may also exert an
antiestrogen effect on the skeletal system through this mechanism. Our results support this view.
Compared with chronological age, biological age is a more
relevant and reliable measurement for monitoring the stage
of bone growth during puberty. In this study, we were not
able to determine the biological age of the bone because of
the study protocol. Another shortcoming is that we only
measured the serum E2 level, which fluctuates diurnally,
once for every girl. It is possible that a single measurement
did not give us a representative indicator of E2 exposure.
Nevertheless, in clinical settings, a single measurement from
serum sample drawn in the early morning is commonly used
and acceptable.
In summary, we conclude that, in early pubertal girls, E2
levels are associated positively with vBMD, cortical thickness, and proportion of cortical bone relative to total CSA and
negatively with medullary area proportion, and are not associated with total bone CSA. SHBG showed precisely the
opposite pattern of associations with bone properties as
those seen with E2, and T was not associated at all with bone
properties. Our results indicate that E2 influences bone crosssectional development mainly by suppressing bone resorption at endocortical surface and provide new insights into the
effects of sex hormones on bone in early pubertal girls.
Acknowledgments
Received June 30, 2003. Accepted December 30, 2003.
Address all correspondence and requests for reprints to: Sulin Cheng,
Department of Health Sciences, P.O. Box 35 (LL), Fin-40014 University
of Jyväskylä, Finland. E-mail: [email protected].
This work was supported by the Finish Ministry of Education and the
Academy of Finland.
Wang et al. • Sex Hormones and Bone Geometry and Density
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Relaxin 2004
Fourth International Conference on Relaxin and Related Peptides
September 5–10, 2004
Grand Teton National Park
Jackson Hole, Wyoming, USA
This conference will present recent advances on the chemistry, physiology, and pharmacology of relaxin,
related peptides, and their receptors. Information about registration, lodging, abstract, and activities has been
added to the website. For information, visit the conference website at http://www.life.uiuc.edu/relaxin2004/
or contact [email protected].
JCEM is published monthly by The Endocrine Society (http://www.endo-society.org), the foremost professional society serving the
endocrine community.