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At least 19 recordsLinked to original sources

PubMed2002

Differences in bone mineral density, bone mineral content, and bone areal size in fracturing and non-fracturing women, and their interrelationships at the spine and hip.

Osteoporotic fractures are a major public health problem, particularly in women. Bone mineral density (BMD), bone mineral content (BMC), and bone size have been regarded as important determinants of osteoporotic fractures. In 1449 women over age 30 years, we studied the detailed relationship, at the spine and hip, between BMD, BMC, and bone areal size (all measured by dual-energy X-ray absorptiometry) and compared their relative magnitudes in fracturing and non-fracturing individuals. We find that, (1) BMD and BMC are significantly higher at the spine and hip in non-fracturing women. Bone areal size is significantly larger at the spine in non-fracturing women; however, the significance disappears when adjustment is made for the significant difference of height (stature) between fracturing and non-fracturing women. In contrast to the spine, bone areal size is always significantly largerin fracturing women at the hip. (2) The relationship among BMD, BMC, and bone areal size is different at the spine and hip. Specifically, at the spine, BMD increases with bone areal size linearly. At the hip, BMD has a quadratic relationship with bone areal size, so that BMD increases at lower bone areal sizes, then (after an intermediate zone of values) decreases with increasing bone areal size. However, BMD adjusted for BMC always decreases with increasing bone areal size, as expected by the definition of BMD. With no adjustment for BMC, the increase in BMD with bone areal size is due to a more rapid increase of BMC than increasing bone areal size, thus explaining the observations of association of both larger BMD and larger bone areal size with stronger bone. (3) At the spine, 86.2% of BMD variation is attributable to BMC and 12.6% to bone areal size. At the hip, 98.0% of BMD variation is due to BMC and 1.1% due to bone areal size. The current study may be important in understanding the relationship among BMD, BMC, and bone size as risk determinants of osteoporotic fractures.

Absorptiometry, Photon↗

PubMed2004

Effects of long-term intervention with Lactobacillus helveticus-fermented milk on bone mineral density and bone mineral content in growing rats.

BACKGROUND: Lactobacillus helveticus-fermented milk has been shown to increase calcium absorption compared to ordinary sour milk. In the present study the possible effect of L. helveticus-fermented milk on bone was studied in growing rats. METHODS: Spontaneously hypertensive male rats, which develop an osteoporotic bone disorder with age, were randomized into 5 groups (n = 10) receiving milk fermented with L. helveticus 16H and, as reference drinks, milk fermented with L. helveticus and Saccharomyces cerevisiae, sour milk, skim milk or water, for 14 weeks. After the intervention bone mineral density and bone mineral content were measured by dual-energy X-ray absorptiometry. The femur weight, length and volume were measured before ashing. From the ashes the weight and mineral content were assessed. RESULTS: As the body weight gain differed significantly between the groups, the results were related to the body weight. The L. helveticus-fermented milk intervention significantly increased the bone mineral density and bone mineral content compared to the sour milk, skim milk and water interventions. The mean values of the bone mineral density and bone mineral content were higher in the L. helveticus-fermented milk group compared to the Saccharomyces-fermented milk group but the difference was not statistically significant. CONCLUSION: L. helveticus-fermented milk increases bone mineral density and bone mineral content in relation to body weight in the long-term feeding of growing rats. The mechanism of L. helveticus remains to be discovered.

Absorptiometry, Photon↗

PubMed2004

Effect of supplementation of calcium and vitamin D on bone mineral density and bone mineral content in peri- and post-menopause women; a double-blind, randomized, controlled trial.

BACKGROUND: Osteoporosis is a serious global health problem for the future, that is why improving diagnostic methods and prevention of this disease could be helpful. OBJECTIVES: To assess the effects of calcium supplementations combined with Vitamin D on bone mineral density (BMD) and bone mineral content (BMC) in a representative sample of peri- and post-menopausal women in a double-blind, a randomized, controlled trial was untaken. DESIGN: A total of 120 women aged over 45 were included in a randomised placebo-controlled, double-blind trial on the effect of a daily dietary supplementation of calcium and Vitamin D on bone mineral density and bone mineral content; over a 30-month period. METHODS: Dietary intake assessment; dual-energy X-ray absorptiometry to measure total body and segmental bone mineral density and bone mineral content at beginning of the study and every 15 months were undertaken. RESULTS: There was no significant change in dietary calcium or Vitamin D intakes in either of the treatment groups during the 30-month intervention period. The change in total BMD in the calcium group was significantly different from that in the placebo group (P <0.005). The placebo group lost a total BMD at a rate of about 0.4% per year. There was an inverse correlation between BMD and age. CONCLUSIONS: The effect of calcium and Vitamin D supplementation on bone mineral density of calcium has been demonstrated in this group of young adult women. Our results showed the positive effect of calcium and Vitamin D supplementation in women both peri- and post-menopausal status; for this reason a supplementation of calcium and Vitamin D should be recommended as a strategic option in helping to prevent early postmenopausal bone loss.

Analysis of Variance↗

PubMed1995

[Effect of vitamin D receptor gene polymorphism and lifestyle on bone mineral density and bone mineral density decrement rate].

The effects of genetic and environmental factors on bone mineral density (BMD) were investigated in 108 healthy Japanese women. Of the 108 subjects, BMD (from the second to forth lumbar vertebrae) was measured in 1992 in 103, in 1993 in 100, and in both years in 95 by dual energy X-ray absorptiometry. Vitamin D receptor (VDR) gene polymorphism in intron 8 was used as a genetic marker. Information on menstruation, health status, lifestyle, quantities of nutrient intake and frequencies of food intake was obtained by questionnaire. The frequency of allele B (825bp), whose polymerase chain reaction (PCR) products cannot be cut with BsmI, was 0.259 and the frequency of allele b (650bp), whose PCR products can be cut with BsmI, was 0.741. The subjects in our study obeyed the Hardy-Weinberg law. While the frequency of allele B was 0.448 in European whites as reported by Morrison et al, it was 0.259 in our Japanese subjects, suggesting a racial difference. Z score values (average value 0, standard deviation 1) increased in the order BB, Bb and bb. This result indicates that allele B is associated with the lower BMD in Japanese, as in European whites. The BMD decrement rate increased in the order bb, Bb and BB, indicating that VDR gene polymorphism may be a regulatory factor for losing BMD. Most of lifestyle variables, calcium intake and vitamin D intake were not correlated with BMD, but the food frequency score (which was defined as values weighted in each of three food categories obtained by factor analysis) was significantly correlated with BMD. Multiple regression analysis showed significant influences of years after menopause, the food frequency score and VDR genotype on BMD. VDR genotype and years after menopause influenced the BMD decrement rate significantly in multiple regression analysis. Neither a relationship between BMD and calcium intake nor between BMD and vitamin D intake by VDR genotype was found. These results suggest that the VDR gene is a genetic factor in BMD and the BMD decrement rate in Japanese.

Adult↗

PubMed2004

Methylenetetrahydrofolate reductase polymorphism interacts with riboflavin intake to influence bone mineral density.

Bone mineral density is a complex trait regulated by an interaction between genetic and environmental factors. Recent studies have identified a functional polymorphism affecting codon 677 of the methylenetetrahydrofolate reductase (MTHFR) gene that is associated with reduced bone mineral density (BMD) in Japanese and Danish postmenopausal women and increased risk of fracture in elderly Danish women. Since dietary B vitamins can influence circulating homocysteine (tHcy) levels, we examined the relationship among MTHFR genotype, B complex vitamins (folate, vitamin B12, vitamin B6 and riboflavin), BMD, and rate of change in BMD in a longitudinal study of 1241 Scottish women aged 45-54 years, at the time of initial study, who were followed up for a mean (SD) of 6.6 (0.7) years. There was no significant association between BMD and either MTHFR genotype or B complex vitamins when examined separately. However, we detected a significant interaction among quartile of energy-adjusted riboflavin intake, MTHFR 'TT' genotype, and BMD (P = 0.01 for baseline FN BMD, P = 0.02 for follow-up FN BMD). Increasing dietary riboflavin intake correlated with LS BMD and FN BMD in homozygotes for the MTHFR 'T' allele, which remained significant for FN after adjustment for confounders (r = 0.192, P = 0.036 for baseline; r = 0.186, P = 0.043 at follow-up) but not in the other genotypes. This raises the possibility that riboflavin intake and MTHFR genotype might interact to regulate BMD. Further work is required to determine if this association holds true for other populations and ethnic groups.

Biomarkers↗

PubMed2005

The roles of bone mineral density, bone turnover, and other properties in reducing fracture risk during antiresorptive therapy.

Osteoporosis is a skeletal disorder characterized by compromised bone strength and increased risk of fracture. Properties related to bone strength include rate of bone turnover, bone mineral density, geometry, microarchitecture, and mean degree of mineralization. These properties (with or without bone density) are sometimes collectively referred to as bone quality. Antiresorptive agents may reduce fracture risk by several separate but interrelated effects on these individual properties. For example, antiresorptive agents have been reported to reduce bone turnover, stabilize or increase bone density, preserve or improve microarchitecture, reduce the number or size of resorption sites, and improve mineralization. Although changes in bone architecture and mineralization are not currently measurable in clinical practice, bone turnover is assessed easily in vivo and affects the other bone properties. Moreover, antiresorptive therapies that produce larger decreases in bone turnover markers together with larger increases in bone mineral density are associated with greater reductions in fracture risk, especially at sites primarily composed of cortical bone such as the hip. Reductions in fracture risk are the most convincing evidence of good bone quality. Data from well-designed randomized clinical trials with up to 10 years of continuous antiresorptive therapy have shown that certain antiresorptive agents effectively reduce fracture risk and (together with extensive preclinical data) suggest no deleterious effects on bone quality.

Bone Density↗

PubMed2002

Evidence for a major gene for bone mineral density/content in human pedigrees identified via probands with extreme bone mineral density.

Bone mineral content (BMC) and/or bone mineral density (BMD, i.e. BMC scaled by bone size) are major determinants for osteoporosis, which is a serious health problem. The major determinant of variation in BMD/BMC is genetic. The few studies now available are inconsistent in the identification and/or even in the existence of major gene(s) for BMD/BMC. In 51 human pedigrees with 941 individuals (526 measured for phenotypes) identified via probands with extreme BMD values, we performed complex segregation analyses to test the existence of a genetic locus with a major effect on BMD/BMC variation. We analyzed BMD and BMC at the spine, hip and wrist jointly by employing, as the study phenotype, factor scores (FS) of the principle component that explains approximately 75% of the total BMD/BMC variation at the three sites. The results indicate that a major gene exists with a codominant effect that is responsible for approximately 16% of the FS variation when adjusted for significant effects of sex, body weight and age. A significant genotype-x-sex-x-age interaction was found, which may explain approximately 14% of the FS variation after adjusting for body weight. Testing of various models did not provide support for shared familial environmental effects but suggested the existence of residual polygenic effects, which may explain approximately 50% of the FS variation when adjusting for sex, body weight and age. This study indicates a promising aspect of studies to identify a major gene for BMD/BMC variation in our pedigrees identified via extreme probands.

Bone Density↗

PubMed1993

Influence of birth weight on adult bone mineral density.

Bone mineral density (BMD) increases during growth until a peak is reached at maturity. The risk of development of postmenopausal osteoporosis depends on the peak bone density and the rate of its subsequent loss. To identify whether low weight at birth could affect the peak bone density, we measured BMD at both the lumbar spine and femoral neck using dual energy X-ray absorptiometry (DXA) in a group of women who had low weight at birth and in a control group of normal birth weight. There was no significant correlation between the weight at birth and the adult BMD. It appears, therefore, that low weight at birth does not influence the peak bone density and that prematurity is not a risk factor for osteoporosis.

Adult↗

PubMed1998

Vitamin D and bone mineral density.

Bone mineral density (BMD) at the lumbar spine and the neck of femur and serum concentrations of 25-hydroxyvitamin D (25OHD), intact parathyroid hormone (PTH), alkaline phosphatase, calcium, albumin, creatinine and phosphate were measured in a group of 166 postmenopausal women (30-79 years) attending a bone clinic for bone density measurements. Four subjects with suspected primary hyperparathyroidism were excluded from analysis. BMD at the lumbar spine was correlated with body mass index (BMI) (r = 0.278, p = 0.0003), age (r = -0.194, p = 0.0134) and serum 25OHD (r = 0.188, p = 0.0167). BMD at the neck of femur correlated with BMI (r = 0.391, p < 0.0001), age (r = -0.356, p < 0.0001), PTH (r = -0.156, p = 0.047) and serum 25OHD (r = 0.231, p = 0.0031). Stepwise multiple regression analysis showed that age, BMI and serum 25OHD contributed to the variation in BMD at lumbar spine. At the neck of femur, PTH was an additional contributor. We conclude that serum 25OHD makes a contribution to BMD a lumbar spine and neck of femur.

Adult↗

PubMedDate not supplied

Senile diabetes and bone mineral density.

Bone mineral density was determined in a series of 67 elderly diabetics (38 males and 29 females) and 40 non-diabetic elderly subjects (20 males and 20 females) at the third medial and tenth ultradistal of the non-dominating radius using an X-ray densitometer (DEXA). Bone metabolism markers (Ct, PTH, HOP, UCA, AP, Vit-25-OH-D, BGP) were also measured. Our results indicate that there is no significant difference in values of BMD and the bone metabolism markers studied between diabetic and non-diabetic elderly subjects. We believe that senile diabetes is not a risk factor of onset and maintenance of senile osteoporosis.

Journal Article↗

PubMed2002

Tests of linkage and/or association of genes for vitamin D receptor, osteocalcin, and parathyroid hormone with bone mineral density.

Bone mineral density (BMD) is a major determinant of osteoporotic fractures (OFs). The heritability of BMD ranges from 50% to 90% in human populations. Extensive molecular genetic analyses have been performed through traditional linkage or association approaches to test and identify genes or genomic regions underlying BMD variation. The results, particularly those concerning the vitamin D receptor (VDR) gene, have been inconsistent and controversial. In this study, we simultaneously test linkage and/or association of the genes for VDR, osteocalcin (also known as bone Gla protein [BGP]), and parathyroid hormone (PTH) with BMD in 630 subjects from 53 human pedigrees. Each of these pedigrees was ascertained through a proband with an extreme BMD value at the hip or spine (Z score < or = -1.28). For the raw BMD values, adjusting for significant covariate effects of age, sex, and weight, we performed tests for linkage alone, association alone, and then both linkage and association. For the spine BMD, at the two markers (ApaI and FokI) inside the VDR gene we found evidence for linkage (p < 0.05) and for both linkage and association by the transmission disequilibrium test (TDT; p < 0.05); association was detected (p < 0.07) with regular statistical testing by analyses of variance (ANOVA). In addition, significant results were found for association alone (p < 0.05), linkage alone (p = 0.0005), and for linkage and association (p = 0.0019) for the intragenic marker HindIII of the BGP gene for the hip BMD. Through testing for association, linkage, and linkage and association simultaneously, our data support the VDR gene as a quantitative trait locus (QTL) underlying spine BMD variation and the BGP gene as a QTL underlying hip BMD variation. However, our data do not support the PTH gene as a QTL underlying hip or spine BMD variation. This is the first study in the broad field of bone genetics that tests candidate genes as QTLs for BMD by testing simultaneously for association alone, for linkage alone, and for association and linkage (via the TDT).

Adult↗

PubMed2006

Assessment of linkage and association of 13 genetic loci with bone mineral density.

Bone mineral density (BMD), an important risk factor for osteoporosis, is a complex trait likely affected by multiple genes. The linkage and/or association of 13 polymorphic loci of seven candidate genes (estrogen receptor alpha [ERalpha] and beta [ERbeta], calcium-sensing receptor, vitamin D receptor, collagen type 1alpha1, low-density lipoprotein [LDL] receptor-related protein 5 [LRPS], and transforming growth factor beta1) were evaluated in 177 southern Chinese pedigrees of 674 subjects, with each pedigree identified through a proband having a BMD Z score of -1.28 or less at the hip or spine. A suggestive linkage was detected between the IVS1-351A/G polymorphism of ERalpha and spine BMD, and between the 1082G/A, 1730G/A, and D14S1026 polymorphisms of ERbeta and BMD at both spine and hip. The quantitative transmission disequilibrium test (QTDT) detected total family association between 1730G/A of ERbeta and BMD at spine and hip; between D14S1026 of ERbeta and hip BMD; and between the 266A/G and 2220C/T polymorphisms of LRP5 and hip BMD. Similar total family associations were detected when only the females were analyzed. In addition, the IVS1-397T/C polymorphism of ERalpha was associated with spine BMD, and the 266A/G and 2220C/T polymorphisms of LRP5 were associated with femoral neck BMD in the females. A within-family association was detected with the IVS1-397T/C polymorphism of ERalpha, and the 266A/G and 2220C/T polymorphisms of LRP5 in the females. The effect of each polymorphism on BMD variance ranged from 1% to 4%. In conclusion, ERalpha, ERbeta and LRP5 are important candidate genes determining BMD variation, especially in females.

Adult↗

PubMed1992

Growth hormone deficiency during puberty reduces adult bone mineral density.

Bone mineral density (BMD) was evaluated by dual energy x ray absorptiometry in 60 adults (33 males, 27 females; aged 50, range 23-76 years) who were growth hormone deficient from various causes for 10.4 (1-31) years. Adult patients who had acquired growth hormone deficiency before completion of puberty had significantly reduced mean (SEM) BMD compared with age matched healthy controls at the lumbar spine: 0.87 (0.09) v 1.20 (0.03) g/cm2, femoral neck: 0.81 (0.06) v 1.08 (0.04) g/cm2, and Ward's triangle: 0.68 (0.07) v 1.04 (0.05) g/cm2. These values were also reduced compared with those of patients who had received human growth hormone during puberty. Untreated growth hormone deficiency when present during puberty results in reduced adult bone density.

Absorptiometry, Photon↗

PubMed1998

[The effect of treatment method for tibial fracture on tibial bone mineral density].

Bone mineral density (BMD) has been measured above malleolar fracture site and within femoral neck in 17 patients treated conservatively and in 17 patients treated surgically. The BMD was taken 3 months after injury. BMD at the fracture site decreased in patients treated conservatively by 20 +/- 3% and by 17 +/- 4% in those operated on. BMD within the femoral neck of the extremity involved decreased by 5% regardless of the mode of treatment. The results achieved indicate no significant difference in BMD in both groups of patients.

Adult↗

PubMed1978

Melorheostosis. A case report with special reference to bone mineral density, bone circulation and bone scan.

A new case of melorheostosis is presented. Bone mineral density, and bone circulation were determined and bone scan carried out in the patient. The bone mineral density measured by photon absorption in the region of the distal radius of the patient's left forearm was found to be within normal limits, the bone blood circulation determined by Xc-133 clearance method was better in the affected side, and an area of increased uptake of Tc99m was found by bone scanning in the affected extremity.

Adult↗

PubMed2005

Effects of exemestane administered for 2 years versus placebo on bone mineral density, bone biomarkers, and plasma lipids in patients with surgically resected early breast cancer.

PURPOSE: To evaluate potential detrimental effects of exemestane on bone and lipid metabolism. PATIENTS AND METHODS: Postmenopausal women with early breast cancer were randomly assigned to exemestane 25 mg daily or placebo for 2 years in a double-blind setting. Primary objective was to evaluate the effect of exemestane on bone mineral density. Secondary objectives were effects on bone biomarkers, plasma lipids, coagulation factors, and homocysteine. Planned size was 128 patients. RESULTS: One hundred forty-seven patients were enrolled. All patients completed their 24-month visit except for those discontinuing treatment at an earlier stage. The mean annual rate of bone mineral density loss was 2.17% v 1.84% in the lumbar spine (P = .568) and 2.72% v 1.48% in the femoral neck (P = .024) in the exemestane and placebo arm, respectively. The mean change in T-score after 2 years was -0.21 for exemestane and -0.11 on placebo in the hip, and -0.30 and -0.21, respectively, in the lumbar spine. Exemestane significantly increased serum level and urinary excretion of bone resorption, but also bone formation markers. Except for a modest reduction in high-density lipoprotein cholesterol (P < .001) and apolipoprotein A1 (P = .004), exemestane had no major effect on lipid profile, homocysteine levels, or coagulation parameters. CONCLUSION: Exemestane modestly enhanced bone loss from the femoral neck without significant influence on lumbar bone loss. Except for a 6% to 9% drop in plasma high-density lipoprotein cholesterol, no major effects on serum lipids, coagulation factors, or homocysteine were recorded. Bone mineral density should be assessed according to the US Preventive Services Task Force guidelines.

Aged↗

PubMed2005

Effect of prepubertal ovariohysterectomy on bone mineral density and bone mineral content in puppies.

In this study, dual energy X-ray absorptiometry (DXA) was performed on the calcaneus (CAL) and accessory carpal bone (ACB) of early-age neutered (n = 11) and sham-operated puppies (n = 10) to investigate changes in bone mineral density (BMD) and bone mineral content (BMC) over time. Prepubertal ovariohysterectomy and sham surgery were performed at 10 weeks, while BMD and BMC were measured at 12, 16, 20 and 24 weeks of age. BMD and BMC of CAL and ACB of ovariohysterectomised puppies were found to be higher. The differences between the groups were statistically unimportant; however, the fourth measurement of the ACB showed a significant (P < 0.05) difference. Sexually intact puppies weighed less than gonadectomised puppies in all measurements. Because of the positive correlations between body weight and bone mineral density, BMD and BMC of early-age neutered puppies were found to be higher. These results suggest that BMD and BMC are not affected by prepubertal ovariohysterectomy until six months of age in mixed-breed puppies.

Animals↗

PubMed2000

Relationships between serum leptin level and regional bone mineral density, bone metabolic markers in healthy women.

BACKGROUND: Leptin might affect bone metabolism. This study was performed to investigate the relationship of leptin to bone metabolism in detail in premenopausal and postmenopausal healthy women. METHODS: The relationships between serum leptin level and bone mineral density of several regional sites of the body as well as whole body, along with bone metabolic markers, were examined in 47 premenopausal and 29 postmenopausal healthy women. RESULTS: Serum leptin level was weakly correlated with bone mineral density of pelvis (Pearson's correlation coefficient r=0.39, p<0.05) and left leg (r=0.41, p<0.01) in the premenopausal women, although the correlation decreased after adjustment for BMI. There was no significant relationship between serum leptin level and whole body bone mineral density both in the premenopausal and postmenopausal women. Serum leptin level was correlated with serum alkaline phosphatase (r=0.56, p<0.001) and urinary deoxypyridinoline/cr (r=-0.32, p<0.05) by Pearson's correlation test in the premenopausal women; the relationships were maintained even after adjustment for BMI (r=0.50 and -0.48, respectively). CONCLUSIONS: Leptin is not a key regulator of bone metabolism, although it may have some effects on bone metabolic markers and BMD regionally in premenopausal women.

Adult↗