Relevant bibliographies by topics / Bone mineral density

Academic literature on the topic 'Bone mineral density'

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Published: 4 June 2021
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Journal articles on the topic "Bone mineral density"

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Marquezan, Mariana, Thiago Chon Leon Lau, Claudia Trindade Mattos, Amanda Carneiro da Cunha, Lincoln Issamu Nojima, Eduardo Franzotti Sant'Anna, Margareth Maria Gomes de Souza, and Mônica Tirre de Souza Araújo. "Bone mineral density." Angle Orthodontist 82, no. 1 (July 20, 2011): 62–66. http://dx.doi.org/10.2319/031811-192.1.

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Abstract Objective: To verify whether bone mineral density (BMD) of cortical bone, trabecular bone, and total bone influence the primary stability of orthodontic miniscrews and to verify whether there is a correlation between the measurement of BMD by cone-beam computed tomography (CBCT) and central dual-energy x-ray absorptiometry (DEXA). Materials and Methods: Twenty bovine bone sections were extracted from the pubic and iliac bones from regions with cortical thicknesses of approximately 1 mm. The BMD of the total bone block was evaluated using two methods: CBCT and DEXA. The BMD of cortical, trabecular, and total bone in the region of interest (ROI) were also evaluated by CBCT. After scanning the bone blocks, 20 self-drilling miniscrews (INP®) 1.4 mm in diameter and 6 mm long were inserted into them. The peak implant insertion torque (IT) was registered. After this, the pull-out test (PS) was performed and the maximum force registered. The Pearson correlation test was applied to verify the correlations between variables. Results: The BMD of the total bone block verified by CBCT and DEXA showed a positive and strong correlation (r = 0.866, P = .000). The BMD of the ROI for cortical bone influenced the IT (r = 0.518, P = .40) and the PS of miniscrews (r = 0.713, P = .001, Table 2). However, the total bone BMD (verified by CBCT and DEXA) and trabecular bone BMD presented weak and not statistically significant correlations with primary stability. Conclusions: There was a positive correlation between total bone block BMD measured by DEXA and CBCT. The cortical BMD influenced the IT and PS.
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Littrell, T. R., and C. M. Snow. "BONE MINERAL DENSITY." Medicine & Science in Sports & Exercise 35, Supplement 1 (May 2003): S19. http://dx.doi.org/10.1097/00005768-200305001-00090.

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Almeida Paz, ICL, and LDG Bruno. "Bone mineral density: review." Revista Brasileira de Ciência Avícola 8, no. 2 (June 2006): 69–73. http://dx.doi.org/10.1590/s1516-635x2006000200001.

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Perry, Wayne. "Bone Mineral Density Measurement." Journal of the Royal Society of Medicine 89, no. 10 (October 1996): 599. http://dx.doi.org/10.1177/014107689608901030.

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Hurley, MD, Daniel L. "BONE MINERAL DENSITY MEASUREMENT." Endocrine Practice 4, no. 2 (March 1998): 120–22. http://dx.doi.org/10.4158/ep.4.2.120b.

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Aberg, Judith A., and Grace McComsey. "Low Bone Mineral Density." Infectious Diseases in Clinical Practice 15, no. 3 (May 2007): 139–40. http://dx.doi.org/10.1097/01.idc.0000269900.59661.5a.

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Gallagher, J. Christopher. "Bone mineral density measurements." Menopause 22, no. 6 (June 2015): 581–83. http://dx.doi.org/10.1097/gme.0000000000000477.

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Sweeney, Ann T., Alan O. Malabanan, Michael A. Blake, Janice Weinberg, Adrian Turner, Patricia Ray, and Michael F. Holick. "Bone Mineral Density Assessment." Journal of Clinical Densitometry 5, no. 1 (March 2002): 57–62. http://dx.doi.org/10.1385/jcd:5:1:057.

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Chon, Mi-Young, Hye-Won Jeon, and Myoung-Hee Kim. "Bone Mineral Density and Factors influencing Bone Mineral Density in College Women." Korean Journal of Women Health Nursing 18, no. 3 (2012): 190. http://dx.doi.org/10.4069/kjwhn.2012.18.3.190.

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Parvaneh, Kolsoom, Rosita Jamaluddin, Golgis Karimi, and Reza Erfani. "Effect of Probiotics Supplementation on Bone Mineral Content and Bone Mass Density." Scientific World Journal 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/595962.

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A few studies in animals and a study in humans showed a positive effect of probiotic on bone metabolism and bone mass density. Most of the investigated bacteria wereLactobacillusandBifidobacterium. The positive results of the probiotics were supported by the high content of dietary calcium and the high amounts of supplemented probiotics. Some of the principal mechanisms include (1) increasing mineral solubility due to production of short chain fatty acids; (2) producing phytase enzyme by bacteria to overcome the effect of mineral depressed by phytate; (3) reducing intestinal inflammation followed by increasing bone mass density; (4) hydrolysing glycoside bond food in the intestines byLactobacillusandBifidobacteria. These mechanisms lead to increase bioavailability of the minerals. In conclusion, probiotics showed potential effects on bone metabolism through different mechanisms with outstanding results in the animal model. The results also showed that postmenopausal women who suffered from low bone mass density are potential targets to consume probiotics for increasing mineral bioavailability including calcium and consequently increasing bone mass density.
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Dissertations / Theses on the topic "Bone mineral density"

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Vaughan, Tanya, and n/a. "Identifying Genes Influencing Bone Mineral Density." Griffith University. School of Health Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040430.161453.

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Bone mineral density (BMD) is a reflection of the action of osteoblasts compared to osteoclasts. An imbalance in the activity of osteoblasts or osteoclasts, results in bone disease such as osteoporosis caused by overactive osteoclasts. BMD is influenced by genetic and environmental factors as demonstrated through twin studies, association studies and linkage analysis (Ralston, 1999). Several polymorphisms involved in the determination of BMD have been identified, with Vitamin D receptor and Collagen Type 1 showing reproducible associations. To identify genes influencing BMD two distinct strategies have been employed: 1) To determine if DNA polymorphism within the runt related transcription factor (RUNX2) gene is a determinant of BMD and fracture in women. 2) The identification of RANKL target genes in osteoclastogenesis. RUNX2 is a runt domain transcription factor (Werner et al., 1999) essential for osteoblast differentiation (Lee et al., 1997). RUNX2 gene knock-out mice have no osteoblasts due to a failure in osteoblast differentiation and consequently unmineralised skeletons, (Komori et al., 1997; Otto et al., 1997). In humans, mutations in RUNX2 cause cleidocranial dysplasia (CCD), a disorder characterised by hypoplasia or aplasia of the clavicles, short stature, supernumerary teeth, patent fontanelles and other changes in skeletal patterning and growth (Mundlos et al., 1997). RUNX2 contains a poly-glutamine poly-alanine (polyQ/polyA) repeat where mutations causing cleidocranial dysplasia have been observed. BMD has not been routinely examined in CCD, two studies have identified CCD patients with lower BMD with one fracture case identified (Quack et al., 1999; Bergwitz et al., 2001). The central role of RUNX2 in determining osteoblast differentiation makes RUNX2 a prime candidate gene for regulating adult bone density. To determine if polymorphism was present in the polyQ/polyA tract the repeat was amplified within the upper and lower deciles of femoral neck (FN) BMD in the Geelong Osteoporosis study (GOS). The upper and lower deciles of FN BMD acted as a surrogate for genotyping the entire cohort. This study identified two common variants within the polyA repeat: an 18 base pair deletion (11Ala) and a synonymous alanine codon polymorphism with alleles, GCA and GCG (noted as A and G alleles, respectively). The 11Ala and SNP polymorphism are found on codon 64 and 66 respectively (RUNX2 MRIPV variant). A allele frequencies were significantly different in a comparison of the upper and lower deciles of FN BMD (p=0.019). In 495 randomly selected women of the Geelong Osteoporosis Study (GOS), the A allele was associated with higher BMD at all sites tested. The association was maximal at the ultra-distal radius (p=0.001). In a separate fracture study, the A allele was significantly protective against Colles' fracture in elderly women but not spine and hip fracture. The 11Ala polymorphism was not related to BMD in GOS. To further decipher the role of the RUNX2 A allele we genotyped 992 women from a Scottish cohort. The alleles of RUNX2 within the glutamine/alanine repeat were determined by MspA1I restriction digest. To examine the possible influence on estrogen related therapies or estrogen status on the potential genetic effect conferred by RUNX2, we divided the cohort by menopausal and hormone replacement therapy status. Within postmenopausal Scottish women the RUNX2 A allele was associated with significantly higher FN BMD (p=0.028, n=312) but not lumbar spine (LS) BMD. The A allele was associated with higher FN BMD (p=0.035) within a postmenopausal subgroup of the population (n=312). To investigate the effect of weight on the RUNX2 alleles the Scottish cohort was segregated into thin/normal (BMI ≥ 25 kg/m2) and overweight /obese (BMI > 25 kg/m2). RUNX2 A allele showed a stronger effect on FN BMD in postmenopausal women above the median BMI. The 11Ala RUNX2 deletion allele was significantly associated with decreased LS BMD (p=0.018) within overweight/obese women (n=546). The 11Ala allele was significantly associated with increased levels of pyridinoline (p=0.014) and deoxypyridinoline (p=0.038) in the HRT treated subgroup of the population (n=492). Glutamine variants and an alanine insertion were identified within the group. These data suggest that the RUNX2 11Ala and A alleles exert differing affects on BMD showing preference for different skeletal sites in a weight dependent manner. We genotyped 78 individuals from an osteoarthritic population to elucidate the role of the RUNX2 alleles on markers of bone turnover and inflammation. The RUNX2 11Ala allele was significantly associated with decreased osteocalcin (OC) serum levels (p = 0.01). The RUNX2 A allele was significantly related to reduced tumor necrosis factor alpha (TNF-alpha) serum levels (p = 0.004). RUNX2 is known to bind to the OC promoter. An OC promoter polymorphism is found 7bp upstream from a putative RUNX2 binding site. We hypothesized that OC polymorphism may effect the RUNX2 transactivation of the OC gene and thus affect OC serum levels. OC promoter polymorphism was not related to OC serum levels (n=78). These data present a novel link between RUNX2 alleles and OC and TNF serum levels, providing putative mechanisms of action for the RUNX2 alleles. Further studies in larger populations are required to confirm these findings. Ten individuals within the GOS and the Scottish cohort were found to carry rare mutations of the polyQ/polyA repeat. All polyQ variants had a normal polyA repeat (17 amino acids) and were heterozygous for a normal 23Q/17A allele. Variants observed were 15, 16, 24 and 30Q. One individual was observed with an extended polyA repeat (24A). Patient records indicated otherwise unremarkable clinical history except for fracture in 4/10 individuals from GOS (hip and spine). BMD data from the LS and the FN were expressed as T-scores, a measure that relates BMD in terms of standard deviations below the young normal value. In addition, BMD data were also expressed as Z-scores around the age-mean. Under the null hypothesis, where RUNX2 Q repeat variation has no effect on BMD, Z scores would be expected to be distributed around a mean of zero. However, when all variants were pooled the BMD was significantly lower than expected. This effect persisted when deletion variants were considered alone. The effect was stronger on FN BMD (p=0.001) rather than LS BMD (p=0.096), reflecting either difference in precision of BMD measurements at these sites or perhaps a differential genetic effect on different skeletal sites. These data suggest that polyQ and polyA variants are associated with significantly lower BMD, and may be an important determinant for fracture. Glutamine variants exist at high frequency (~0.7%): this rate of mutation could be important when considering large populations at risk of age related osteoporosis. Considering that these subjects are heterozygous for a normal allele, it suggests that a more severe phenotype might be expected in rare subjects homozygous for glutamine repeat variants. In summary, this study investigated the role of novel polymorphisms and rare variants of the RUNX2 gene in influencing BMD, fracture and markers of bone turnover. Two common polymorphisms were identified within the polyA repeat: an 18 base pair deletion and a synonymous alanine codon polymorphism with alleles, A and G. The A allele was associated with increased BMD and was protective against a common form of osteoporotic fracture within a Geelong population. To verify these findings the RUNX2 alleles were genotyped in 992 women from a Scottish cohort. The magnitude and the direction of the effect of the A allele was maintained in the Scottish cohort. Interestingly, the A allele was shown to exert a menopause specific effect, with postmenopausal women showing the strongest effect. On re-analysis of the GOS data the post-menopausal women were found to drive the significance identified in the cohort. The magnitude of the effect of the A allele on BMD was greater in overweight/obese postmenopausal women indicating a gene-weight interaction for RUNX2. The RUNX2 11Ala allele showed a significant relationship with decreased LS BMD in overweight/obese Scottish women. The 11Ala allele was also associated with higher levels of urinary PYD and DPD in women treated with HRT, indicating higher levels of bone turnover in carriers of the 11Ala allele. In contrast to the Scottish cohort, no significant association with heterozygous carriers of 11Ala was observed in GOS, although a significant association was detected for homozygous carriers and LS BMAD. The 11 Ala RUNX2 allele was significantly associated with decreased serum osteocalcin levels and the A allele was significantly associated with TNF in OA patients. Glutamine variants and an alanine insertion were identified within Geelong and Scottish cohorts, which showed low Z and T scores suggesting that RUNX2 variants may be related to genetic effects on BMD and osteoporosis. Polymorphism of the polyQ/polyA region of RUNX2 were identified within this study were shown to associate with significant differences in BMD. The A allele showed a significant association with increased BMD in postmenopausal women from a Geelong and Scottish cohort, with a decreased frequency of the A allele observed in Colles' fracture patients from Geelong. The 11Ala deletion allele was significantly associated with decreased LS BMD and increases in markers of bone turnover in the Scottish cohort. A significant decrease in OC serum levels was observed in OA patients suggesting a direct effect of the allele on the transactivation of the RUNX2 gene. Rare variants of RUNX2 were identified which showed low BMD. These studies have provided insight into the role of RUNX2 in influencing BMD, further studies are required to verify the role of the A allele on BMD and fracture, the role of the rare variants and to identify the precise mechanisms behind the observed changes in BMD. - 2) The identification of RANKL target genes in osteoclastogenesis. Osteoclastogenesis is regulated in vivo by the action of osteoblast/stromal cells that express membrane bound, receptor activator of NF-kB ligand (RANKL). Monocytes treated in vitro with a soluble form of RANKL and macrophage colony stimulating factor (M-CSF) differentiate to osteoclasts, whereas monocytes treated with M-CSF alone differentiate to macrophage-like cells. The gene expression profile of human osteoclasts has not been extensively explored. Genes highly expressed by rabbit osteoclasts were identified through random sequencing of an osteoclast cDNA library (Sakai et al., 1995). Differential gene expression of mouse osteoclastogenesis was elucidated by array analysis (Cappellen et al., 2002). To identify genes important for human osteoclastogenesis, total RNA was isolated from monocytes treated for three weeks with either M-CSF alone or with RANKL and M-CSF. RANKL treatment for 3 weeks and 12 hours was investigated in this study, to complement previous data. Differential display was performed on RNA (12 hour treatment with RANKL) and differential gene expression profiles examined. The differential display products were pooled to generate a probe for screening a gene array system derived from a human osteoclast cDNA library. cDNA (3 week treatment with RANKL) hybridisation experiments against the array revealed additional regulated genes. Gene clones that showed significant regulation in M-CSF and RANKL treated cells compared M-CSF treated cells represent genes that are targets for RANKL-specific regulation. Osteopontin, creatine kinase and various mitochondrial genes were up regulated by the treatment of RANKL. Changes in gene expression observed in the array data were confirmed with real-time PCR using mRNA derived from in vitro induced osteoclasts. Cathepsin K gene expression was more than 300 fold greater in osteoclasts compared to macrophage-like cells after one week treatment with RANKL and M-CSF. Cystatin C expression showed a six-fold induction at two weeks of RANKL and M-CSF treatment and cystatin B showed a steady increase in expression. Some of these regulated genes may provide useful targets for influencing BMD.
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Koay, M. A. "LRP5 ploymorphisms and bone mineral density." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414229.

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Vaughan, Tanya. "Identifying Genes Influencing Bone Mineral Density." Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366470.

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In summary, this study investigated the role of novel polymorphisms and rare variants of the RUNX2 gene in influencing BMD, fracture and markers of bone turnover. Two common polymorphisms were identified within the polyA repeat: an 18 base pair deletion and a synonymous alanine codon polymorphism with alleles, A and G. The A allele was associated with increased BMD and was protective against a common form of osteoporotic fracture within a Geelong population. To verify these findings the RUNX2 alleles were genotyped in 992 women from a Scottish cohort. The magnitude and the direction of the effect of the A allele was maintained in the Scottish cohort. Interestingly, the A allele was shown to exert a menopause specific effect, with postmenopausal women showing the strongest effect. On re-analysis of the GOS data the post-menopausal women were found to drive the significance identified in the cohort. The magnitude of the effect of the A allele on BMD was greater in overweight/obese postmenopausal women indicating a gene-weight interaction for RUNX2. The RUNX2 11Ala allele showed a significant relationship with decreased LS BMD in overweight/obese Scottish women. The 11Ala allele was also associated with higher levels of urinary PYD and DPD in women treated with HRT, indicating higher levels of bone turnover in carriers of the 11Ala allele. In contrast to the Scottish cohort, no significant association with heterozygous carriers of 11Ala was observed in GOS, although a significant association was detected for homozygous carriers and LS BMAD. The 11 Ala RUNX2 allele was significantly associated with decreased serum osteocalcin levels and the A allele was significantly associated with TNF in OA patients. Glutamine variants and an alanine insertion were identified within Geelong and Scottish cohorts, which showed low Z and T scores suggesting that RUNX2 variants may be related to genetic effects on BMD and osteoporosis. Polymorphism of the polyQ/polyA region of RUNX2 were identified within this study were shown to associate with significant differences in BMD. The A allele showed a significant association with increased BMD in postmenopausal women from a Geelong and Scottish cohort, with a decreased frequency of the A allele observed in Colles’ fracture patients from Geelong. The 11Ala deletion allele was significantly associated with decreased LS BMD and increases in markers of bone turnover in the Scottish cohort. A significant decrease in OC serum levels was observed in OA patients suggesting a direct effect of the allele on the transactivation of the RUNX2 gene. Rare variants of RUNX2 were identified which showed low BMD. These studies have provided insight into the role of RUNX2 in influencing BMD, further studies are required to verify the role of the A allele on BMD and fracture, the role of the rare variants and to identify the precise mechanisms behind the observed changes in BMD.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sciences
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Bergström, Ingrid. "Effects of gonadal hormone deficiency on bone mineral density : can physical activity increase bone mineral density in women? /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-833-9/.

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Degtyar, M. A. "Regional mineral density of the bone tissue." Thesis, Sumy State University, 2017. http://essuir.sumdu.edu.ua/handle/123456789/53961.

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The objective of this research was to define influence of a 6-month power training of all body (Century) from the general and regional mineral density of a bone tissue (MDBT) and the mineral maintenance of a bone (MMB) at groups of persons with different gender and century characteristics.
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Pretorius, S. M. "Feedback to patients with low bone mineral density after bone densitometry." Thesis, Bloemfontein : Central University of Technology, Free State, 2006. http://hdl.handle.net/11462/70.

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Thesis (M. Tech.) -- Central University of Technology, Free State, 2006
Osteoporosis is defined as a skeletal disorder characterised by low bone mass and micro-architectural deterioration of bone tissue, with the overall focus on bone quality. It affects more than 75 million people worldwide, and cause people to become bedridden with life threatening secondary complications. An estimated 10 million South Africans, out of a population of 43 million people, are at high risk of developing osteoporosis. In South Africa osteoporosis affects one in three women over 50 and one in five men. Within one year after a hip fracture, up to 20% of the people die, 15-20% needs to be institutionalised and 50% of the remainder will not be able to lead an independent life. The number of fractures is two to three times higher in women than in men due to the hormonal changes that occur after menopause. The prevalence of osteoporosis increases markedly with age and, based on the bone mineral density at the femoral neck of the hip, approximately 30% of Caucasian women, by age of 75 years will be classified as having osteoporosis. Dual-Energy X-ray Absorptiometry (DEXA) is the preferred method for measuring BMD. The results of the DEXA scan are scored in comparison with the BMD of young, healthy individuals, resulting in a measurement called a T-score. A T-score of –2.5 or lower is considered to be osteoporosis and T-scores between –0.1 and –2.5 are generally considered to show osteopenia. The aim of the study was to examine communication between referring physicians and patients who had been referred for a DEXA scan. A total of fifty patients were included in the study group. This was much smaller than was anticipated. The ideal would have been a much bigger sample group for a bigger representation of the population. Patients, who complied with the inclusion criteria and also gave their consent, were recruited between January 2004 and November 2004. Not all the patients referred for a DEXA scan had the required low BMD. Bone scans were performed on the HOLOGIC 4500 QDR, a multiple detector, fan beam, Dual Energy X-ray Densitometer. The Hologic 4500 QDR Bone Densitometer estimates the Bone Mineral Content (BMC) in grams, and the BMD in grams per cm2. The QDR 4500 uses a low level of X-rays with two different energies to estimate BMC and BMD. The radiation exposure at a distance of two metres from the equipment is less than one mR/hour. The age distribution of the study group ranged between 14 and 84 years (average age was 57,2 years). Out of the total of 50 patients, only one was male and the entire patient population was Caucasian. This may be due to the small sample size and inclusion/exclusion criteria. Concerning the references of the patient population, Universitas Academic Hospital (UAH) referred more than half of the patients (64%), while the other points of care referred only 36%. In this study, it was found that BMD results do influence the management of osteopenia/osteoporosis in the majority of patients and the test has a positive impact on the management of patients with this condition. There was however 22% of patients that did not receive feedback concerning the results of the DEXA and the necessary treatment. These findings also highlighted the fact that communication between physician and patient is a very important component in using the information provided by this test to its full potential. The ideal is to identify a low BMD early enough to stop the damaging consequences thereof, but this is not always feasible due to the high costs involved in a DEXA scan. Access to treatment and care is also not readily available to a large section of the population and, in State Hospitals; the availability of drugs to treat osteoporosis is limited due to the high costs.
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Welsh, Linda Jane. "The effects of exercise on bone mineral density." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338834.

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Anderson, Simon Hamish Charles. "Silicon: a treatment for low bone mineral density." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414415.

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Kemp, John Peter. "Genetic determinants of bone mineral density and osteoporosis." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.682725.

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Bone mineral density (BMD) is a highly heritable trait, indicating that genetic elements are partly responsible for variation in osteoporosis risk. To further understand the genetic variation underlying osteoporosis, I performed genome-wide association (GWA) studies using designs that have largely not been performed in osteoporosis literature to date. Three strategies were used: i) a selected sample of postmenopausal women with high (z ~ 1.5, n = 1,055) or low (z≥1.5, n = 900) hip BMD [as measured by Dual-energy X-ray absorptiometry (DXA)] were used for GWA, followed by replication in an unselected sample of 20,898 adults, ii) a GW A meta-analysis on unselected children from the Avon Longitudinal Study of Parents and Children [ALSPAC (n = 5,330)] and the Generation R study [GEN-R (n = 4,098)], using DXA derived total-body less head BMD (TBLH-BMD) measures, iii) refining total-body BMD measures in children by subregional analysis: i.e. quantifying the genetic and environmental correlation between paediatric BMD measures [ALSPAC (n≥5,299)] of the skull (S-BMD), lower limb (LL-BMD) and upper limb (UL-BMD) using genome-wide complex trait analysis (GCT A) and thereafter performing a GWA meta-analysis on each site using subjects from ALSPAC and GEN-R (n ~ 9,300). The role of bone resorption in bone growth and accrual was investigated via a cross-sectional analysis of 1,130 adolescents from ALSPAC using serum measures of ,β-C-telopeptides of type I collagen (CTX) and quantitative computed tomography (pQCT) measures of the mid-tibia. Two novel BMD associated loci were identified using the selective genotyping strategy: GALNTJ (rs6710518, P = 1.4x lO· 10) and RSP03 (rsI3204965, P = 3.0x lO· 10). Association studies of paediatric TBLH-BMD identified a novel variant in RlN3 (rs754388, P = 3.0x 10.9) and replicated 31 adult BMD associated loci, with six reaching the GWA threshold of association (P < 5.0x 10·R). Sub-regional GCT A analysis indicated that appendicular sites shared a greater proportion of genetic architecture (LL-/UL-BMD rg=0.78, P = 1 x 10.7) when compared to the skull [(UL-/SBMD rg = 0.58, P = 9x l0·7) and (LL-/S-BMD rg = 0.43, P = l x lO'~)]. GWA meta-analysis echoed these findings by identifying twelve known BMD-associated variants that differed in the strength of their association and magnitude of effect with each sub-region. In particular, variants at the WNTl6 and RSP03 showed considerable site-specificity as indicated by strong association with S-BMD and/or UL-BMD, but not with LL-BMD. An investigation into the role of bone resorption in adolescent bone suggested that CTX was positively related to periosteal circumference (PC) [,8 = 0.19 (0 .13, 0.24)] (coefficient = SD change per SD increase in CTX, 95% Cl)], but inversely associated with cortical BMD [,8 = -0.46 (-0.52, -0.40)] and positively related to bone strength as reflected by the strength-strain index (SSI) [,8 = 0.09 (0 .03 , 0.14)]. These relationships were replicated using genetic proxies for bone resorption . . These results suggest that the selective sampling GWA strategy represents an efficient alternative to conventional random sampling designs. However the real world feasibility of selective sampling is questionable, as it requires extensive phenotyping in order to ensure adequate sample size and study power is obtained. BMD measures of children are well suited for GW A, however the replication of adult BMD associated SNPs implies that many of the BMD associated loci identified operate throughout the life course. Whether this strategy enriches for genetic factors involved in bone modelling remains to be seen. BMD at different skeletal sites appears to be influenced by distinct genetic and environmental influences, suggesting that phenotypic refinement of BMD may represent a superior GW A strategy, when compared to using heterogeneous BMO measures (i .e TBLH-BMO). Finally, bone resorption might play an important role in paediatric bone growth, accrual and strength.
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Farrell, Vanessa. "Nutrients and Bone Mineral Density in Postmenopausal Women." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/195768.

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This dissertation’s three studies investigated the short and long-term relationships of bone-related nutrient intakes with bone mineral density (BMD) in postmenopausal women. This dissertation compared the equivalency of dietary intakes assessed by eight days of diet records (DR) and the Arizona Food Frequency Questionnaire (AFFQ) at one year. It also determined the association of one year (DR) and the average of four-year (AFFQ) dietary intakes with cross-sectional BMD. The dietary intake associations with BMD were further investigated by hormone therapy (HT). Participant’s BMD was measured at the lumbar spine (L2-L4), femur trochanter, femur neck, Ward's triangle and total body using dual energy X-ray absorptiometry. Separate multiple linear regression analysis (p≤0.05), controlled for various covariates, were used to examine the associations between dietary intakes and regional and total body BMD. In study number one (n=266), significant correlations (r=0.30-0.70, p≤0.05) between dietary assessment methods were found with all dietary intake variables. Iron, magnesium, zinc, dietary calcium, phosphorous, potassium, total calcium, and fiber intakes were positively associated with BMD at three or more of the same bone sites regardless of the dietary assessment method at one year. In study number two (n=266), femur trochanter, lumbar spine, and total body BMD had mostly significant inverse associations with dietary polyunsaturated fatty acid (PUFA) intake at one year. In the HT group (n=136), inverse associations with dietary PUFA intake were seen in the spine and total body BMD. In study number three (n=130), average dietary intake of selected bone-related nutrients, were significantly inversely associated with lumbar spine BMD and total body BMD at year four. In the HT group (n=92), inverse associations with dietary PUFA intake were seen in the spine and total body BMD. The DR and AFFQ are acceptable dietary tools used to determine the associations of particular nutrients and BMD sites in healthy postmenopausal women at one year. At one and four year, dietary PUFA intakes had mostly inverse associations with lumbar spine and total body BMD. When categorized by HT use the associations remained significant only in the HT groups, suggesting that HT may influence dietary intake associations with BMD.
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Books on the topic "Bone mineral density"

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Erlichman, Martin. Dual photon absorptiometry for measuring bone mineral density. Rockville, MD: National Center for Health Services Research and Health Care Technology Assessment, U.S. Dept. of Health and Human Services, Public Health Service, 1987.

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Erlichman, Martin. Radiographic absorptiometry for measuring bone mineral density. Rockville, MD: U.S. Dept. of Health and Human Services, Public Health Service, 1988.

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National Center for Health Services Research and Health Care Technology Assessment (U.S.), ed. Radiographic absorptiometry for measuring bone mineral density. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service, 1988.

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Erlichman, Martin. Single photon absorptiometry for measuring bone mineral density. Rockville, MD: National Center for Health Services Research and Health Care Technology Assessment, U.S. Dept. of Health and Human Services, Public Health Service ; Springfield, VA : Available from National Technical Information Service, 1986.

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Wright, Charlotte Eleanor. Lifestyle factors affecting bone mineral density during youth. [s.l: The Author], 1999.

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Stronach, Ian Michael. Bone mineral density measurement techniques: Evaluation and application. Birmingham: University of Birmingham, 1992.

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Total body bone area, bone mineral content, and bone mineral density for individuals aged 8 years and over: United States, 1999-2006. Hyattsville, Maryland: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics, 2013.

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1998), Bath Conference on Osteoporosis and Bone Mineral Measurement (6th. Current research in osteoporosis and bone mineral measurement V: 1998: Proceedings of the Sixth Bath Conference on Osteoporosis and Bone Mineral Measurement, Bath, 22-26 June 1998. London: British Institute of Radiology, 1998.

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Bath Conference on Osteoporosis and Bone Mineral Measurement (5th 1996). Current research in osteoporosis and bone mineral measurement IV, 1996: Proceedings of the Fifth Bath Conference on Osteoporosis and Bone Mineral Measurement, Bath, 24-26 June 1996. London: British Institute of Radiology, 1996.

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National Center for Health Statistics (U.S.) and National Health and Nutrition Examination Survey (U.S.), eds. Lumbar spine and proximal femur bone mineral density, bone mineral content, and bone area, United States, 2005-2008: Data from the National Health and Nutrition Examnination Survey (NHANES). Hyattsville, Md: U.S. Dept. of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics, 2012.

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Book chapters on the topic "Bone mineral density"

1

Hill, Keith, Tom Baranowski, Walter Schmidt, Nicole Prommer, Michel Audran, Philippe Connes, Ramiro L. Gutiérrez, et al. "Bone Mineral Density." In Encyclopedia of Exercise Medicine in Health and Disease, 138–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_31.

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Guglielmi, Giuseppe, Fabio Ferrari, and Alberto Bazzocchi. "Bone Mineral Density and Quantitative Imaging." In Pitfalls in Diagnostic Radiology, 109–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44169-5_6.

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Miyashita, Hirotaka, Se-Min Kim, and John G. Graham. "Hypercalcemia and High Bone Mineral Density." In A Case-Based Guide to Clinical Endocrinology, 243–49. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-84367-0_27.

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Trevisan, C., and S. Ortolani. "Periprosthetic Bone Mineral Density and Other Orthopedic Applications." In Bone Densitometry and Osteoporosis, 541–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80440-3_28.

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Fukunaga, M., and R. Morita. "Bone Mineral Density in Chronic Renal Failure." In New Actions of Parathyroid Hormone, 455–58. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0567-5_54.

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Lenchik, Leon, Scott Wuertzer, and Thomas C. Register. "Clinical and Research Applications of Bone Mineral Density Examinations." In Nutrition and Bone Health, 81–102. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2001-3_6.

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Hay, S. M. "Use of Bone Mineral Density Measurement in Orthopaedic Practice." In Manual of Bone Densitometry Measurements, 147–70. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0759-0_8.

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Brown, P. "Use of Bone Mineral Density Measurement in Primary Care." In Manual of Bone Densitometry Measurements, 171–98. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-0759-0_9.

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Bartl, Reiner, and Bertha Frisch. "Bone Mineral Density (BMD): The Crucial Diagnostic Parameter." In Osteoporosis, 58–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-09163-0_7.

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Haeck, Inge, Sara van Velsen, Marjolein de Bruin-Weller, and Carla Bruijnzeel-Koomen. "Bone Mineral Density in Patients with Atopic Dermatitis." In New Trends in Allergy and Atopic Eczema, 96–99. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000331893.

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Conference papers on the topic "Bone mineral density"

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Nishi, SP, MR Gupta, GA Lombard, SG LaPlace, L. Seaone, GS Dhillon, and VG Valentine. "Bone Mineral Density in Lung Transplantation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4601.

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Ruchi Kerketta, Shilpi, and Debalina Ghosh. "Microwave Analysis on Bone Mineral Density." In 2020 International Symposium on Antennas & Propagation (APSYM). IEEE, 2020. http://dx.doi.org/10.1109/apsym50265.2020.9350679.

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Sneha, K., C. Sridevi, B. Yazhini, and Amridha Lakshmi Venkkautaesh. "Multimodal Analysis of Bone Mineral Density Classification." In 2024 Tenth International Conference on Bio Signals, Images, and Instrumentation (ICBSII). IEEE, 2024. http://dx.doi.org/10.1109/icbsii61384.2024.10562389.

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Chuaychunu, N., Y. Pititheerapab, T. Chanwimalueang, P. Lertprasert, and C. Pintavirooj. "Bone mineral density and bone mineral content estimation using low-cost x-ray detector." In 2007 6th International Conference on Information, Communications & Signal Processing. IEEE, 2007. http://dx.doi.org/10.1109/icics.2007.4449744.

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Azmy, E., and R. N. Ibrahim. "MEASUREMENT OF BONE DENSITY AND BONE MINERAL CONTENT USING ULTRASONIC WAVES." In Proceedings of the Third Australasian Congress on Applied Mechanics. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812777973_0011.

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Sardella, Alberto, Federica Bellone, Carmen Giulia Lasco, Gabriella Martino, Nunziata Morabito, and Antonino Catalano. "AB0820 COGNITIVE IMPULSIVITY CORRELATES WITH BONE MINERAL DENSITY." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4257.

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Ugryumova, Nadya, Stephen J. Matcher, and Donald P. Attenburrow. "Estimation of bone-mineral density from OCT images." In Biomedical Optics 2004, edited by Valery V. Tuchin, Joseph A. Izatt, and James G. Fujimoto. SPIE, 2004. http://dx.doi.org/10.1117/12.530892.

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Ugryumova, Nadya, Stephen J. Matcher, and Don P. Attenburrow. "Optical studies of changes in bone mineral density." In Biomedical Optics 2003, edited by Alexander V. Priezzhev and Gerard L. Cote. SPIE, 2003. http://dx.doi.org/10.1117/12.479182.

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Brankovic, SC, NZ Pilipovic, and P. Vukojevic. "AB0192 Influence of exercise on bone mineral density." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.631.

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Atalay, A., S. Arslan, and R. Çeliker. "AB0179 Bone mineral density measurements in obese patients." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.618.

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Reports on the topic "Bone mineral density"

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Modugno, Francesmary. Bone Mineral Density, Sex Steroid Genes, Race, and Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada443083.

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Modugno, Francesmary. Bone Mineral Density, Sex Steroid Genes, Race and Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada430319.

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Kim, Hee-Ju, Seo-A. Choi, Min-Sun Gu, Seo-Yeong Ko, Jae-Hee Kwon, Ja-Young Han, Jae Hyun Kim, and Myeong Gyu Kim. Effects of glucagon-like peptide-1 receptor agonist on bone mineral density and bone turnover markers: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2024. http://dx.doi.org/10.37766/inplasy2024.6.0050.

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Shang, Xueyan, Hezhang Yun, Yaowei Sun, jing Wang, Bin Lu, and Wenbo Su. Impact of Resistance Training on Bone Mineral Density in Postmenopausal Women: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2024. http://dx.doi.org/10.37766/inplasy2024.5.0035.

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Sacco-Gibson, N., J. Abrams, S. Chaudhry, D. Hurst, D. Peterson, and M. Bhattacharyya. Osteoporotic-like effects of cadmium on bone mineral density and content in aged ovariectomized beagles. Office of Scientific and Technical Information (OSTI), December 1992. http://dx.doi.org/10.2172/10185066.

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Teng, Zhaowei, Yun Zhu, Lirong Yang, Qing Long, Yu Zhao, Qinggang Hao, Yirong Teng, et al. Interaction risk between sarcopenia and osteoporosis or low bone mineral density: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0110.

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Wu, Haiyang, Yiru Wang, Guowei Wen, Zhenyin Tang, Yiqun Yu, Jiren Zhang, Ping Liu, and Junhao Wu. Tai Chi on bone mineral density of postmenopausal osteoporosis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2020. http://dx.doi.org/10.37766/inplasy2020.7.0104.

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Liu, Shijie. Effect of Traditional Chinese Exercises on Bone Mineral Density in Postmenopausal Women: A Systematic Review and Network Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0030.

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Wang, Lin, Fei Dai, maolin Zhang, Hong Wang, and Zaiqing Chun. Effect of Mind-Body Exercise on Bone Mineral Density in Elderly Patients with Osteoporosis: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2024. http://dx.doi.org/10.37766/inplasy2024.1.0110.

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Chen, Tai-Li, Jing-Wun Lu, and Yu-Wen Huang. Bone mineral density and risk of fractures in adult patients with psoriasis or psoriatic arthritis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0106.

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