Bone Parameters (bone + parameter)

Distribution by Scientific Domains
Medical Sciences92%

Selected Abstracts

Increased bone density and resistance to ovariectomy-induced bone loss in FoxP3-transgenic mice based on impaired osteoclast differentiation

ARTHRITIS & RHEUMATISM, Issue 8 2010
Mario M. Zaiss
Objective Immune activation triggers bone loss. Activated T cells are the cellular link between immune activation and bone destruction. The aim of this study was to determine whether immune regulatory mechanisms, such as naturally occurring Treg cells, also extend their protective effects to bone homeostasis in vivo. Methods Bone parameters in FoxP3-transgenic (Tg) mice were compared with those in their wild-type (WT) littermate controls. Ovariectomy was performed in FoxP3-Tg mice as a model of postmenopausal osteoporosis, and the bone parameters were analyzed. The bones of RAG-1,/, mice were analyzed following the adoptive transfer of isolated CD4+CD25+ T cells. CD4+CD25+ T cells and CD4+ T cells isolated from FoxP3-Tg mice and WT mice were cocultured with monocytes to determine their ability to suppress osteoclastogenesis in vitro. Results FoxP3-Tg mice developed higher bone mass and were protected from ovariectomy-induced bone loss. The increase in bone mass was found to be the result of impaired osteoclast differentiation and bone resorption in vivo. Bone formation was not affected. Adoptive transfer of CD4+CD25+ T cells into T cell,deficient RAG-1,/, mice also increased the bone mass, indicating that Treg cells directly affect bone homeostasis without the need to engage other T cell lineages. Conclusion These data demonstrate that Treg cells can control bone resorption in vivo and can preserve bone mass during physiologic and pathologic bone remodeling. [source]

Murine TNF,ARE Crohn's disease model displays diminished expression of intestinal Ca2+ transporters

INFLAMMATORY BOWEL DISEASES, Issue 6 2008
Sylvie Huybers MSc
Abstract Background: Patients suffering from Crohn's disease (CD) show increased incidence of low bone mineral density. Investigating this complication is difficult because the exact etiology of CD remains elusive. Mice carrying a deletion in the tumor necrosis factor (TNF) AU-rich elements (ARE) are reported as a model for human CD and are characterized by elevated TNF-, levels and inflammations in the terminal ileum. To evaluate whether these mice have a Ca2+ handling problem, this study analyzed the Ca2+ homeostasis in heterozygous TNF,ARE mice (TNF,ARE/+) in comparison to wildtype littermates. Methods: Beside serum Ca2+ and vitamin D levels, the expression of Ca2+ transporters was analyzed in intestine, kidney and bone using quantitative real-time PCR, Western blot and immunohistochemistry. Bone scans were performed to measure bone parameters. Results: Ca2+ transporters in duodenum (TRPV6, calbindin-D9K, PMCA1b) and kidney (TRPV5, calbindin-D28K, NCX1) showed significantly reduced mRNA expression levels in TNP,ARE/+ mice, except for renal TRPV5. In bone, only calbindin-D9K mRNA displayed a significant down-regulation. These findings were supported by declined duodenal calbindin-D9K and renal calbindin-D28K protein values. Likely, this down-regulation of Ca2+ transporters in TNP,ARE/+ mice is mediated by the 58 ± 9% reduction in serum 1,25(OH)2D3 levels. Diminished expression of Ca2+ transporters combined with unchanged serum Ca2+ levels assumes Ca2+ loss from bone to compensate for the body's overall Ca2+ shortage. Indeed, microcomputed tomography scanning demonstrated reduced trabecular and corticol bone thickness and volume in TNF,ARE/+ mice. This finding is further supported by increased total deoxypyridinoline in serum. Conclusions: Our results imply that TNF,ARE/+ mice have a disturbed Ca2+ homeostasis characterized by reduced duodenal and renal Ca2+ transporters, diminished 1,25(OH)2D3 levels, and increased bone resorption associated with profound bone abnormalities. (Inflamm Bowel Dis 2008) [source]

The course of some bone remodelling plasma metabolites in healthy horses and in horses offered a calcium-deficient diet

JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 3-4 2003
V. De Behr
Summary An inquiry was carried out to assess the concentrations of plasma metabolites related to bone remodelling in 21 saddle horses of Warmblood breed aged 4,26 years, five draught horses of Ardennes breed aged 4,10 years, and 10 Ardennes foals aged 9,11 months. They were fed according to normal feeding practice in Belgium. The changes in some bone remodelling plasma metabolite concentrations were studied when an unbalanced diet was offered and later corrected for four Warmblood horses. Bone formation was evaluated by bone alkaline phosphatase (BALP), total alkaline phosphatase (TALP) and osteocalcin (bone gla-protein, OC). Bone resorption was assessed by hydroxyproline (HYP). Total calcium, ionized calcium, phosphorus (P) and 25-hydroxyvitamin D3 [25-(OH)D] concentrations were more or less constant. The comparison of four bone remodelling factors between the Ardennes and Warmblood horses showed higher concentrations in the Ardennes breed. Bone marker concentrations decreased according to age. The correction of the unbalanced Ca : P diet induced inconsistent effects at plasma level. The interpretation of the different bone parameters appeared to be difficult if not associated with other parameters such as a complete anamnesis and clinical examination of the animal in addition to dietary evaluation. Zusammenfassung Verlauf verschiedener Knochenmarker bei gesunden Pferden und bei Pferden, welche mit einer in Bezug auf Kalzium unausgewogenen Ration gefüttert wurden Eine Studie zur Erfassung der Konzentrationen von Knochenmarkern wurde bei 21 Warmblütern im Alter von 4 bis 26 Jahren, fünf Ardenner Kaltblütern im Alter von 4 bis 10 Jahren und 10 Ardenner Kaltblutfohlen im Alter von 9 bis 11 Monaten durchgeführt. Die Pferde wurden gemäss der normalen Fütterungpraxis in Belgien gefüttert. Der Verlauf der Knochenmarkerkonzentrationen wurde auch bei vier Pferden gemessen, die zunächst mit einer unausgewogenen Ration in Bezug auf Kalzium und dann mit einer korrigierenden Ration gefüttert wurden. Der Knochenaufbau wurde anhand der Aktivität der knochenspezifischen alkalischen Phosphatase (BALP), der totalen alkalischen Phosphatasen (TALP) und anhand des Osteocalcin (bone gla-proteine, OC) gemessen. Der Knochenabbau wurde anhand des Hydroxyprolins (HYP) gemessen. Die Konzentrationen des totalen Kalziums, ionisierten Kalziums, Phosphors (P), und 25-Hydroxyvitamin D3 [25(OH)D] waren unverändert. Beim Vergleich der vier gemessenen Knochenmakerkonzentrationen bei den Ardenner Kaltblütern mit den Warmblutpferden konnte gezeigt werden, dass die Kaltblüter deutlich höhere Konzentrationen hatten als die Warmblüter. Die Konzentrationen der Marker nahmen mit steigendem Alter der Pferde ab. Die Korrektur der unausgewogenen Ca:P Ration ergab nicht eindeutige Veränderungen der Plasmakonzentrationen der verschiedenen Marker. Die Interpretation der verschiedenen Knochenmarker erscheint schwierig, wenn nicht andere Parameter, wie eine komplette Anamnese und eine klinische Untersuchung, sowie eine Auswertung der Ration hinzugezogen werden. [source]

Effect of Osteoblast-Targeted Expression of Bcl-2 in Bone: Differential Response in Male and Female Mice,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2005
Alexander G Pantschenko
Abstract Transgenic mice (Col2.3Bcl-2) with osteoblast-targeted human Bcl-2 expression were established. Phenotypically, these mice were smaller than their wildtype littermates and showed differential effects of the transgene on bone parameters and osteoblast activity dependent on sex. The net effect was an abrogation of sex differences normally observed in wildtype mice and an inhibition of bone loss with age. Ex vivo osteoblast cultures showed that the transgene had no effect on osteoblast proliferation, but decreased bone formation. Estrogen was shown to stimulate endogenous Bcl-2 message levels. These studies suggest a link between Bcl-2 and sex regulation of bone development and age-related bone loss. Introduction: Whereas Bcl-2 has been shown to be an important regulator of apoptosis in development, differentiation, and disease, its role in bone homeostasis and development is not well understood. We have previously showed that the induction of glucocorticoid-induced apoptosis occurred through a dose-dependent decrease in Bcl-2. Estrogen prevented glucocorticoid-induced osteoblast apoptosis in vivo and in vitro by preventing the decrease in Bcl-2 in osteoblasts. Therefore, Bcl-2 may be an important regulator of bone growth through mechanisms that control osteoblast longevity and function. Materials and Methods: Col2.3Bcl-2 mice were developed carrying a 2.3-kb region of the type I collagen promoter driving 1.8 kb of human Bcl-2 (hBcl-2). Tissue specific expression of hBcl-2 in immunoassays validated the transgenic animal model. Histomorphometry and DXA were performed. Proliferation, mineralization, and glucocorticoid-induced apoptosis were examined in ex vivo cultures of osteoblasts. The effect of estrogen on mouse Bcl-2 in ex vivo osteoblast cultures was assayed by RT-PCR and Q-PCR. Results and Conclusions: Two Col2.3Bcl-2 (tg/+) founder lines were established and appeared normal except that they were smaller than their nontransgenic wildtype (+/+) littermates at 1, 2, and 6 months of age, with the greatest differences at 2 months. Immunohistochemistry showed hBcl-2 in osteoblasts at the growth plate and cortical surfaces. Nontransgenic littermates were negative. Western blots revealed hBcl-2 only in type I collagen-expressing tissues. Histomorphometry of 2-month-old mice showed a significant decrease in tg/+ calvaria width with no significant differences in femoral trabecular area or cortical width compared with +/+. However, tg/+ males had significantly more trabecular bone than tg/+ females. Female +/+ mice showed increased bone turnover with elevated osteoblast and osteoclast parameters compared with +/+ males. Col2.3Bcl-2 mice did not show such significant differences between sexes. Male tg/+ mice had a 76.5 ± 1.5% increase in ObS/BS with no significant differences in bone formation rate (BFR) or mineral apposition rate (MAR) compared with male +/+ mice. Transgenic females had a significant 48.4 ± 0.1% and 20.1 ± 5.8% decrease in BFR and MAR, respectively, compared with +/+ females. Osteoclast and osteocyte parameters were unchanged. By 6 months, femurs from female and male +/+ mice had lost a significant amount of their percent of trabecular bone compared with 2-month-old mice. There was little to no change in femoral bone in the tg/+ mice with age. Ex vivo cultures of osteoblasts from +/+ and Col2.3Bcl-2 mice showed a decrease in mineralization, no effect on proliferation, and an inhibition of glucocorticoid-induced apoptosis in Col2.3Bcl-2 cultures. Estrogen was shown to increase mouse Bcl-2 transcript levels in osteoblast cultures of wildtype mice, supporting a role for Bcl-2 in the sex-related differences in bone phenotype regulated by estrogen. Therefore, Bcl-2 differentially affected bone phenotype in male and female transgenic mice, altered bone cell activity associated with sex-related differences, and decreased bone formation, suggesting that apoptosis is necessary for mineralization. In addition, Bcl-2 targeted to mature osteoblasts seemed to delay bone development, producing a smaller transgenic mouse compared with wildtype littermates. These studies suggest that expression of Bcl-2 in osteoblasts is important in regulating bone mass in development and in the normal aging process of bone. [source]

Ovariectomy-Induced Bone Loss Varies Among Inbred Strains of Mice,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2005
Mary L Bouxsein PhD
Abstract There is a subset of women who experience particularly rapid bone loss during and after the menopause. However, the factors that lead to this enhanced bone loss remain obscure. We show that patterns of bone loss after ovariectomy vary among inbred strains of mice, providing evidence that there may be genetic regulation of bone loss induced by estrogen deficiency. Introduction: Both low BMD and increased rate of bone loss are risk factors for fracture. Bone loss during and after the menopause is influenced by multiple hormonal factors. However, specific determinants of the rate of bone loss are poorly understood, although it has been suggested that genetic factors may play a role. We tested whether genetic factors may modulate bone loss subsequent to estrogen deficiency by comparing the skeletal response to ovariectomy in inbred strains of mice. Materials and Methods: Four-month-old mice from five inbred mouse strains (C3H/HeJ, BALB/cByJ, CAST/EiJ, DBA2/J, and C57BL/6J) underwent ovariectomy (OVX) or sham-OVX surgery (n = 6-9/group). After 1 month, mice were killed, and ,CT was used to compare cortical and trabecular bone response to OVX. Results: The effect of OVX on trabecular bone varied with mouse strain and skeletal site. Vertebral trabecular bone volume (BV/TV) declined after OVX in all strains (,15 to ,24%), except for C3H/HeJ. In contrast, at the proximal tibia, C3H/HeJ mice had a greater decline in trabecular BV/TV (,39%) than C57BL/6J (,18%), DBA2/J (,23%), and CAST/EiJ mice (,21%). OVX induced declines in cortical bone properties, but in contrast to trabecular bone, the effect of OVX did not vary by mouse strain. The extent of trabecular bone loss was greatest in those mice with highest trabecular BV/TV at baseline, whereas cortical bone loss was lowest among those with high cortical bone parameters at baseline. Conclusions: We found that the skeletal response to OVX varies in a site- and compartment-specific fashion among inbred mouse strains, providing support for the hypothesis that bone loss during and after the menopause is partly genetically regulated. [source]

,-Arrestin2 Regulates the Differential Response of Cortical and Trabecular Bone to Intermittent PTH in Female Mice,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 4 2005
Mary L Bouxsein PhD
Abstract Cytoplasmic arrestins regulate PTH signaling in vitro. We show that female ,-arrestin2,/, mice have decreased bone mass and altered bone architecture. The effects of intermittent PTH administration on bone microarchitecture differed in ,-arrestin2,/, and wildtype mice. These data indicate that arrestin-mediated regulation of intracellular signaling contributes to the differential effects of PTH at endosteal and periosteal bone surfaces. Introduction: The effects of PTH differ at endosteal and periosteal surfaces, suggesting that PTH activity in these compartments may depend on some yet unidentified mechanism(s) of regulation. The action of PTH in bone is mediated primarily by intracellular cAMP, and the cytoplasmic molecule ,-arrestin2 plays a central role in this signaling regulation. Thus, we hypothesized that arrestins would modulate the effects of PTH on bone in vivo. Materials and Methods: We used pDXA, ,CT, histomorphometry, and serum markers of bone turnover to assess the skeletal response to intermittent PTH (0, 20, 40, or 80 ,g/kg/day) in adult female mice null for ,-arrestin2 (,-arr2,/,) and wildtype (WT) littermates (7-11/group). Results and Conclusions: ,-arr2,/, mice had significantly lower total body BMD, trabecular bone volume fraction (BV/TV), and femoral cross-sectional area compared with WT. In WT females, PTH increased total body BMD, trabecular bone parameters, and cortical thickness, with a trend toward decreased midfemoral medullary area. In ,-arr2,/, mice, PTH not only improved total body BMD, trabecular bone architecture, and cortical thickness, but also dose-dependently increased femoral cross-sectional area and medullary area. Histomorphometry showed that PTH-stimulated periosteal bone formation was 2-fold higher in ,-arr2,/, compared with WT. Osteocalcin levels were significantly lower in ,-arr2,/, mice, but increased dose-dependently with PTH in both ,-arr2,/, and WT. In contrast, whereas the resorption marker TRACP5B increased dose-dependently in WT, 20-80 ,g/kg/day of PTH was equipotent with regard to stimulation of TRACP5B in ,-arr2,/,. In summary, ,-arrestin2 plays an important role in bone mass acquisition and remodeling. In estrogen-replete female mice, the ability of intermittent PTH to stimulate periosteal bone apposition and endosteal resorption is inhibited by arrestins. We therefore infer that arrestin-mediated regulation of intracellular signaling contributes to the differential effects of PTH on cancellous and cortical bone. [source]

An In Vitro Study of the Ultrasonic Axial Transmission Technique at the Radius: 1-MHz Velocity Measurements Are Sensitive to Both Mineralization and Intracortical Porosity,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2004
Emmanuel Bossy
Abstract The ultrasonic axial transmission technique allows for investigating skeletal sites such as the cortical layer of long bones (radius, tibia, phalanges). Using synchrotron radiation ,CT, we investigated, in vitro, the relationships between 1-MHz axial transmission SOS measurements at the radius and site-matched measurements of C.Th, POR, MIN, and vBMD. Introduction: The ultrasonic axial transmission technique allows for investigating skeletal sites such as the cortical layer of long bones (radius, tibia, phalanges). Materials and Methods:Using synchrotron radiation ,CT, we investigated, in vitro, the relationships between 1-MHz axial transmission speed of sound (SOS) measurements at the radius and site-matched measurements of cortical thickness (C.Th), intracortical porosity (POR), tissue mineralization (MIN), and volumetric BMD (vBMD). SOS measurements were based on bidirectional axial transmission and were performed with a 1-MHz proprietary probe on 39 excised human radii. Results: The highest correlations between SOS values and bone parameters (R2SOS/POR = 0.28, p < 10,3; R2SOS/MIN = 0.38, p < 10,4; R2SOS/vBMD = 0.57, p < 10,3) were found for bone parameters assessed in a 1-mm-thick periosteal region of the cortex rather than throughout the whole cortex. The observed moderate correlation between SOS and C.Th values (R2SOS/C.Th = 0.20, p < 10,2) disappeared when controlled for other variables. The two best multilinear predictive models, including either BMD alone or the pair of dependent variables MIN and POR (all assessed in the periosteal cortex), were equally accurate in predicting SOS values (R2SOS/(POR,MIN) = 0.59, p < 10,5; R2SOS/vBMD = 0.57, p < 10,5). Conclusion: For the first time, the respective adjusted contributions of POR (,24 m/s%,1) and tissue mineralization (+3.5 m/s/mg/cm,3) to SOS values were assessed. These results suggest potential sensitivity of axial transmission SOS values to changes in cortical bone status under different pathological conditions or treatments affecting POR and/or tissue mineralization. [source]

Female Estrogen Receptor ,,/, Mice Are Partially Protected Against Age-Related Trabecular Bone Loss

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2001
Sara H. Windahl
Abstract Recently, it has been shown that inactivation of estrogen receptor , (ER-,) by gene targeting results in increased cortical bone formation in adolescent female mice. To study the possible involvement of ER-, in the regulation of the mature skeleton, we have extended the analyses to include 1-year-old ER-, knockout mice (ER-,,/,). Male ER-,,/, mice did not express any significant bone phenotypic alterations at this developmental stage. However, the increase in cortical bone parameters seen already in the adolescent female ER-,,/, mice was maintained in the older females. The aged female ER-,,/, mice further exhibited a significantly higher trabecular bone mineral density (BMD) as well as increased bone volume/total volume (BV/TV) compared with wild-type (wt) mice. This was caused by a less pronounced loss of trabecular bone during adulthood in female ER-,,/, mice. The growth plate width was unaltered in the female ER-,,/, mice. Judged by the expression of the osteoclast marker tartrate-resistant acid phosphatase (TRAP) and cathepsin K (cat K; reverse-transcription-polymerase chain reaction [RT-PCR]) as well as the serum levels of C-terminal type I collagen cross-linked peptide, bone resorption appeared unaffected. However, an increase in the messenger RNA (mRNA) expression levels of the osteoblast marker core-binding factor ,1 (Cbfa1) suggested an anabolic effect in bones of old female ER-,,/, mice. In addition, the mRNA expression of ER-, was augmented, indicating a role for ER-, in the development of this phenotype. Taken together, the results show that ER-, is involved in the regulation of trabecular bone during adulthood in female mice and suggest that ER-, acts in a repressive manner, possibly by counteracting the stimulatory action of ER-, on bone formation. [source]

In vivo ultra-high-field magnetic resonance imaging of trabecular bone microarchitecture at 7 T

JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2008
Roland Krug PhD
Abstract Purpose To investigate the feasibility of 7T magnetic resonance imaging (MRI) to visualize and quantify trabecular bone structure in vivo by comparison with 3T MRI and in vivo three-dimensional (3D) high-resolution peripheral quantitative computed tomography (HR-pQCT). Materials and Methods The distal tibiae of 10 healthy volunteers were imaged. Therefore, fully balanced steady state free precession (bSSFP) and spin-echo (bSSSE) pulse sequences were implemented and optimized for 7T. Structural bone parameters, such as apparent bone-volume over total-volume fraction (app.BV/TV), apparent trabecular plate separation (app.TbSp), apparent trabecular plate thickness (app.TbTh), and apparent trabecular plate number (app.TbN), were derived. Results All structural trabecular bone parameters correlated well (r > 0.6) between 7T and 3T, and between 7T and HR-pQCT (r > 0.69), with the exception of app.TbTh, which correlated modestly (r = 0.41) between field strengths and very low with HR-pQCT (r < 0.16). Regarding absolute values, app.TbN varied only 4% between field strengths, and only 0.6% between 7T and HR-pQCT. App.TbSp correlated best between 7T and HR-pQCT (r = 0.89). Using bSSSE, significant smaller trabecular thickness and significant higher trabecular number were found compared to bSSFP. Conclusion We concluded that imaging and quantification of the trabecular bone architecture at 7T is feasible and preferably done using bSSSE. There exists great potential for ultra-high-field (UHF) MRI applied to trabecular bone measurements. J. Magn. Reson. Imaging 2008;27:854,859. © 2008 Wiley-Liss, Inc. [source]

Morphometric and hormonal changes during the Chimpanzee menstrual cycle

JOURNAL OF MEDICAL PRIMATOLOGY, Issue 6 2006
Ivo H. Machatschke
Abstract Background, Sex steroids affect many peripheral tissue sites in female mammals. Receptors for these hormones have been found in skin, fat, and bone. In women, these tissues can show morphological changes during the menstrual cycle that may be directly related to steroid secretion. Methods The present study was done on chimpanzees to document morphometric markers associated with these tissues (anogenital swelling volume, skin fold thickness as indicator of subcutaneous fat, bony diameters of mandible, wrist, and elbow) and to compare them with cyclic patterns of estradiol, progesterone, testosterone, gonadotropins, and prolactin. Results, Swelling volume changed significantly over the menstrual cycle. All other morphometric parameters showed variation without statistical significance. Skin folds were thickest during the luteal phase. Bony diameters displayed similar but less distinctive changes. Testosterone correlated positively with diameter sites, inversely with subcutaneous fat. No relationships with either estradiol or progesterone were found. We assume that subcutaneous fat and morphometric bone parameters exhibit cycle-dependent changes that may be caused by changes in steroid secretion. [source]

Increased bone density and resistance to ovariectomy-induced bone loss in FoxP3-transgenic mice based on impaired osteoclast differentiation

ARTHRITIS & RHEUMATISM, Issue 8 2010
Mario M. Zaiss
Objective Immune activation triggers bone loss. Activated T cells are the cellular link between immune activation and bone destruction. The aim of this study was to determine whether immune regulatory mechanisms, such as naturally occurring Treg cells, also extend their protective effects to bone homeostasis in vivo. Methods Bone parameters in FoxP3-transgenic (Tg) mice were compared with those in their wild-type (WT) littermate controls. Ovariectomy was performed in FoxP3-Tg mice as a model of postmenopausal osteoporosis, and the bone parameters were analyzed. The bones of RAG-1,/, mice were analyzed following the adoptive transfer of isolated CD4+CD25+ T cells. CD4+CD25+ T cells and CD4+ T cells isolated from FoxP3-Tg mice and WT mice were cocultured with monocytes to determine their ability to suppress osteoclastogenesis in vitro. Results FoxP3-Tg mice developed higher bone mass and were protected from ovariectomy-induced bone loss. The increase in bone mass was found to be the result of impaired osteoclast differentiation and bone resorption in vivo. Bone formation was not affected. Adoptive transfer of CD4+CD25+ T cells into T cell,deficient RAG-1,/, mice also increased the bone mass, indicating that Treg cells directly affect bone homeostasis without the need to engage other T cell lineages. Conclusion These data demonstrate that Treg cells can control bone resorption in vivo and can preserve bone mass during physiologic and pathologic bone remodeling. [source]

Volumetric bone mineral density is an important tool when interpreting bone mineralization in healthy children

ACTA PAEDIATRICA, Issue 2 2009
Susanne Eriksson
Abstract In adults, it is well known that gender influences bone mass, but studies in children have shown contradictory results. Also, conflicting results have been reported regarding bone mineral density in obese children. Objective: To investigate bone parameters in healthy 8-year-old children and relate them to anthropometry and self-reported physical activity (PA). Design: Bone measurements were performed with dual X-ray absorptiometry in 96 children, and questionnaires were used to assess self-reported PA. Results: Bone mineral content and density differed by gender. Eighteen percent of the children were overweight/obese and they had higher bone mineral content and density than children with normal weight. Bone mineral apparent density (g/cm3) of the lumbar spine did not differ, since the vertebral size differed, as was also the case between genders. Self-reported weight-bearing PA influenced bone mass in the hip. Conclusion: PA influenced bone mineralization at this age. The differences in bone mineral content and density in healthy children would mainly be explained by the differences in bone size, reflected in body height and the width of the vertebrae. This indicates the importance of determining volumetric bone mineralization in children. [source]

Effects of 10 years of growth hormone (GH) replacement therapy in adult GH-deficient men

CLINICAL ENDOCRINOLOGY, Issue 3 2005
Lucia I. Arwert
Summary Objective, GH-deficient adults have changes in body composition, bone mineral density (BMD) and lipid profile that can be altered by GH substitution. However, long-term data on GH substitution (up to 10 years of follow-up) are limited. Design, The effects of 10 years of GH replacement therapy on BMD, body composition, bone parameters, serum lipids and glucose metabolism were studied. Patients, Twenty-three childhood-onset GH-deficient men (mean age at baseline 28·6 years) were studied during 10 years of GH substitution therapy. A group of 19 age-matched healthy men served as a control group for BMD measurements at baseline and after 10 years. Results, BMD of the lumbar spine increased during the 10 years of GH therapy. Bone markers and BMD in the hip increased during the first 5 years of GH therapy, but were not different from baseline after 10 years. BMD changes over time in the lumbar spine and femoral neck were significantly different in the patients compared to the controls. After 10 years the difference between the groups had decreased, but BMD was still higher in the controls than in the patients. Lipid profile had improved after 10 years of GH therapy, but body mass index (BMI), waist,hip ratio (WHR), fasting glucose and glycosylated haemoglobin (HbA1c) had increased compared to baseline. Conclusions, This long-term follow-up study found that 10 years of GH substitution in GH-deficient men causes sustained improvements in BMD in the lumbar spine and lipid profile but not in body composition. [source]