Browsing by Subject "Bone mineral density"
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Item Alterations to maternal cortical and trabecular bone in multiparous middle-aged mice(Hylonome, 2017-12-01) Gu, A.; Sellamuthu, R.; Himes, E.; Childress, P.J.; Pelus, L.M.; Orschell, C.M.; Kacena, Melissa A.; Orthopaedic Surgery, School of MedicineOBJECTIVES: During the reproductive cycle, altered calcium homeostasis is observed due to variable demand for mineral requirements. This results in increased bone resorption during the time period leading up to parturition and subsequent lactation. During lactation, women will lose 1-3% of bone mineral density per month, which is comparable to the loss experienced on an annual basis post-menopausal. The purpose of this study was to determine the effect of parity on bone formation in middle-aged mice. METHODS: Mice were mated and grouped by number of parity and compared with age matched nulliparous controls. Measurements were taken of femoral trabecular and cortical bone. Calcium, protein and alkaline phosphatase levels were also measured. RESULTS: An increase in trabecular bone mineral density was observed when comparing mice that had undergone parity once to the nulliparous control. An overall decrease in trabecular bone mineral density was observed as parity increased from 1 to 5 pregnancies. No alteration was seen in cortical bone formation. No difference was observed when calcium, protein and alkaline phosphatase levels were assessed. CONCLUSIONS: This study demonstrates that number of parity has an impact on trabecular bone formation in middle-aged mice, with substantial changes in bone density seen among the parous groups.Item Association of Circulating Renin and Aldosterone With Osteocalcin and Bone Mineral Density in African Ancestry Families(American Heart Association, 2016-05) Kuipers, Allison L.; Kammerer, Candace M.; Pratt, J. Howard; Bunker, Clareann H.; Wheeler, Victor W.; Patrick, Alan L.; Zmuda, Joseph M.; Medicine, School of MedicineHypertension is associated with accelerated bone loss, and the renin-angiotensin-aldosterone system is a key regulator of blood pressure. Although components of this system are expressed in human bone cells, studies in humans are sparse. Thus, we studied the association of circulating renin and aldosterone with osteocalcin and bone mineral density. We recruited 373 African ancestry family members without regard to health status from 6 probands (mean family size: 62 and relative pairs: 1687). Participants underwent a clinical examination, dual-energy x-ray absorptiometry, and quantitative computed tomographic scans. Renin activity, aldosterone concentration, and osteocalcin were measured in fasting blood samples. Aldosterone/renin ratio was calculated as aldosterone concentration/renin activity. All models were analyzed using pedigree-based variance components methods. Full models included adjustment for age, sex, body composition, comorbidities, lifestyle factors, blood pressure, and antihypertensive medication. Higher renin activity was significantly associated with lower total osteocalcin and with higher trabecular bone mineral density (both P<0.01). There were also significant genetic correlations between renin activity and whole-body bone mineral density. There were no associations with aldosterone concentration in any model and results for aldosterone/renin ratio were similar to those for renin activity. This is the first study to report a significant association between renin activity and a marker of bone turnover and bone mineral density in generally healthy individuals. Also, there is evidence for significant genetic pleiotropy and, thus, there may be a shared biological mechanism underlying both the renin-angiotensin-aldosterone system and bone metabolism that is independent of hypertension.Item Associations of Low Vitamin D and Elevated Parathyroid Hormone Concentrations With Bone Mineral Density in Perinatally HIV-Infected Children(Wolters Kluwer, 2017-09-01) Jacobson, Denise L.; Stephensen, Charles B.; Miller, Tracie L.; Patel, Kunjal; Chen, Janet S.; Van Dyke, Russell B.; Mirza, Ayesha; Schuster, Gertrud U.; Hazra, Rohan; Ellis, Angela; Brummel, Sean S.; Geffner, Mitchell E.; Silio, Margarita; Spector, Stephen A.; DiMeglio, Linda A.; Pediatrics, School of MedicineBACKGROUND: Perinatally HIV-infected (PHIV) children have, on average, lower bone mineral density (BMD) than perinatally HIV-exposed uninfected (PHEU) and healthy children. Low 25-hydroxy vitamin D [25(OH)D] and elevated parathyroid hormone (PTH) concentrations may lead to suboptimal bone accrual. METHODS: PHIV and PHEU children in the Pediatric HIV/AIDS Cohort Study had total body (TB) and lumbar spine (LS) BMD and bone mineral content (BMC) measured by dual-energy x-ray absorptiometry; BMD z-scores (BMDz) were calculated for age and sex. Low 25(OH)D was defined as ≤20 ng/mL and high PTH as >65 pg/mL. We fit linear regression models to estimate the average adjusted differences in BMD/BMC by 25(OH)D and PTH status and log binomial models to determine adjusted prevalence ratios of low 25(OH)D and high PTH in PHIV relative to PHEU children. RESULTS: PHIV children (n = 412) were older (13.0 vs. 10.8 years) and more often black (76% vs. 64%) than PHEU (n = 207). Among PHIV, children with low 25(OH)D had lower TB-BMDz [SD, -0.38; 95% confidence interval (CI), -0.60 to -0.16] and TB-BMC (SD, -59.1 g; 95% CI, -108.3 to -9.8); high PTH accompanied by low 25(OH)D was associated with lower TB-BMDz. Among PHEU, children with low 25(OH)D had lower TB-BMDz (SD, -0.34; 95% CI, -0.64 to -0.03). Prevalence of low 25(OH)D was similar by HIV status (adjusted prevalence ratio, 1.00; 95% CI, 0.81 to 1.24). High PTH was 3.17 (95% CI, 1.25 to 8.06) times more likely in PHIV children. CONCLUSIONS: PHIV and PHEU children with low 25(OH)D may have lower BMD. Vitamin D supplementation trials during critical periods of bone accrual are needed.Item Bone Density in Children with Single Ventricle Physiology(Springer, 2015-04) Bendaly, Edgard A.; DiMeglio, Linda A.; Fadel, William F.; Hurwitz, Roger A.; Department of Pediatrics, Indiana University School of MedicineBackground Children with chronic diseases are at risk for low bone mineral density (BMD). There are no studies of BMD in children with congenital heart disease and particularly SV. Children with this defect are often treated with warfarin, suspected to negatively impact BMD in adults. We assessed BMD in patients with single ventricle (SV) physiology and compared the BMD of subjects taking warfarin to those who were not. Methods Subjects 5-12 years with SV were included. BMD z-scores by dual-energy X-ray absorptiometry (DXA) of the spine and total body less head (TBLH) were obtained. Calcium intake, activity level, height, and Tanner stage were assessed. Linear regression models and t-tests were used to investigate differences between participants and normative data as well as between subjects' subgroups. Results Twenty six subjects were included; 16 took warfarin. Mean BMD z-score at the spine was significantly lower than expected at -1.0±0.2 (p<0.0001), as was the BMD z-score for TBLH at - 0.8±0.2 (p<0.0001). Those results remained significant after adjusting for height. Subjects who were on warfarin tended to have lower BMD at both the spine and TBLH than those who were not, with a z-score difference of 0.6±0.46 at the spine (p=0.106) and a difference of 0.4±0.34 at TBLH (p=0.132). Conclusions BMD is significantly reduced in children with SV. Warfarin appears to lower BMD but the effect is less conclusive. Continued evaluation is recommended for these patients at risk for reduced bone density. Evaluation of other cardiac patients on warfarin therapy should also be considered.Item Bone Quality in Chronic Kidney Disease: Definitions and Diagnostics(Springer, 2017-06) McNerny, Erin M.B.; Nickolas, Thomas L.; Medicine, School of MedicinePURPOSE OF REVIEW: In this paper, we review the epidemiology, diagnosis, and pathogenesis of fractures and renal osteodystrophy. RECENT FINDINGS: The role of bone quality in the pathogenesis of fracture susceptibility in chronic kidney disease (CKD) is beginning to be elucidated. Bone quality refers to bone material properties, such as cortical and trabecular microarchitecture, mineralization, turnover, microdamage, and collagen content and structure. Recent data has added to our understanding of the effects of CKD on alterations to bone quality, emerging data on the role of abnormal collagen structure on bone strength, the potential of non-invasive methods to inform our knowledge of bone quality, and how we can use these methods to inform strategies that protect against bone loss and fractures. However, more prospective data is required. CKD is associated with abnormal bone quality and strength which results in high fracture incidence.Item Current Analysis of Skeletal Phenotypes in Down Syndrome(Springer, 2021) Thomas, Jared R.; Roper, Randall J.; Biology, School of SciencePurpose: Down syndrome (DS) is caused by trisomy 21 (Ts21) and results in skeletal deficits including shortened stature, low bone mineral density, and a predisposition to early onset osteoporosis. Ts21 causes significant alterations in skeletal development, morphology of the appendicular skeleton, bone homeostasis, age-related bone loss, and bone strength. However, the genetic or cellular origins of DS skeletal phenotypes remain unclear. Recent findings: New studies reveal a sexual dimorphism in characteristics and onset of skeletal deficits that differ between DS and typically developing individuals. Age-related bone loss occurs earlier in the DS as compared to general population. Perturbations of DS skeletal quality arise from alterations in cellular and molecular pathways affected by the overexpression of trisomic genes. Sex-specific alterations occur in critical developmental pathways that disrupt bone accrual, remodeling, and homeostasis and are compounded by aging, resulting in increased risks for osteopenia, osteoporosis, and fracture in individuals with DS.Item Foreword: Calcified Tissue International and Musculoskeletal Research Special Issue: Bone Material Properties and Skeletal Fragility.(Springer, 2015-09) Burr, David B.; Allen, Matthew R.; Department of Anatomy & Cell Biology, IU School of MedicineItem In Vivo Quantitative Imaging Biomarkers of Bone Quality and Mineral Density using Multi-Band-SWIFT Magnetic Resonance Imaging(Elsevier, 2021) Surowiec, Rachel K.; Ram, Sundaresh; Idiyatullin, Djaudat; Goulet, Robert; Schlecht, Stephen H.; Galban, Craig J.; Kozloff, Kenneth M.; Radiology and Imaging Sciences, School of MedicineBone is a composite biomaterial of mineral crystals, organic matrix, and water. Each contributes to bone quality and strength and may change independently, or together, with disease progression and treatment. Even so, there is a near ubiquitous reliance on ionizing x-ray-based approaches to measure bone mineral density (BMD) which is unable to fully characterize bone strength and may not adequately predict fracture risk. Characterization of treatment efficacy in bone diseases of altered remodeling is complicated by the lack of imaging modality able to safely monitor material-level and biochemical changes in vivo. To improve upon the current state of bone imaging, we tested the efficacy of Multi Band SWeep Imaging with Fourier Transformation (MB-SWIFT) magnetic resonance imaging (MRI) as a readout of bone derangement in an estrogen deficient ovariectomized (OVX) rat model during growth. MB-SWIFT MRI-derived BMD correlated significantly with BMD measured using micro-computed tomography (μCT). In this rodent model, growth appeared to overcome estrogen deficiency as bone mass continued to increase longitudinally over the duration of the study. Nonetheless, after 10 weeks of intervention, MB-SWIFT detected significant changes consistent with estrogen deficiency in cortical water, cortical matrix organization (T1), and marrow fat. Findings point to MB-SWIFT's ability to quantify BMD in good agreement with μCT while providing additive quantitative outcomes about bone quality in a manner consistent with estrogen deficiency. These results indicate MB-SWIFT as a non-ionizing imaging strategy with value for bone imaging and may be a promising technique to progress to the clinic for monitoring and clinical management of patients with bone diseases such as osteoporosis.Item Resonance in the mouse tibia as a predictor of frequencies and locations of loading-induced bone formation(Springer, 2014-01) Zhao, Liming; Dodge, Todd; Nemani, Arun; Yokota, Hiroki; Biomedical Engineering, School of Engineering and TechnologyTo enhance new bone formation for the treating of patients with osteopenia and osteoporosis, various mechanical loading regimens have been developed. Although a wide spectrum of loading frequencies is proposed in those regimens, a potential linkage between loading frequencies and locations of loading-induced bone formation is not well understood. In this study, we addressed a question: Does mechanical resonance play a role in frequency-dependent bone formation? If so, can the locations of enhanced bone formation be predicted through the modes of vibration? Our hypothesis is that mechanical loads applied at a frequency near the resonant frequencies enhance bone formation, specifically in areas that experience high principal strains. To test the hypothesis, we conducted axial tibia loading using low, medium, or high frequency to the mouse tibia, as well as finite element analysis. The experimental data demonstrated dependence of the maximum bone formation on location and frequency of loading. Samples loaded with the low-frequency waveform exhibited peak enhancement of bone formation in the proximal tibia, while the high-frequency waveform offered the greatest enhancement in the midshaft and distal sections. Furthermore, the observed dependence on loading frequencies was correlated to the principal strains in the first five resonance modes at 8.0-42.9 Hz. Collectively, the results suggest that resonance is a contributor to the frequencies and locations of maximum bone formation. Further investigation of the observed effects of resonance may lead to the prescribing of personalized mechanical loading treatments.Item Serum fibroblast growth factor 23, serum iron and bone mineral density in premenopausal women(Elsevier, 2016-05) Imel, Erik A.; Liu, Ziyue; McQueen, Amie K.; Acton, Dena; Acton, Anthony; Padgett, Leah R.; Peacock, Munro; Econs, Michael J.; Department of Medicine, IU School of MedicineFibroblast growth factor 23 (FGF23) circulates as active protein and inactive fragments. Low iron status increases FGF23 gene expression, and iron deficiency is common. We hypothesized that in healthy premenopausal women, serum iron influences C-terminal and intact FGF23 concentrations, and that iron and FGF23 associate with bone mineral density (BMD). Serum iron, iron binding capacity, percent iron saturation, phosphorus, and other biochemistries were measured in stored fasting samples from healthy premenopausal white (n=1898) and black women (n=994), age 20-55years. Serum C-terminal and intact FGF23 were measured in a subset (1631 white and 296 black women). BMD was measured at the lumbar spine and femur neck. Serum phosphorus, calcium, alkaline phosphatase and creatinine were lower in white women than black women (p<0.001). Serum iron (p<0.0001) and intact FGF23 (p<0.01) were higher in white women. C-terminal FGF23 did not differ between races. Phosphorus correlated with intact FGF23 (white women, r=0.120, p<0.0001; black women r=0.163, p<0.01). However, phosphorus correlated with C-terminal FGF23 only in black women (r=0.157, p<0.01). Intact FGF23 did not correlate with iron. C-terminal FGF23 correlated inversely with iron (white women r=-0.134, p<0.0001; black women r=-0.188, p<0.01), having a steeper slope at iron <50mcg/dl than ≥50mcg/dl. Longitudinal changes in iron predicted changes in C-terminal FGF23. Spine BMD correlated with iron negatively (r=-0.076, p<0.01) in white women; femur neck BMD correlated with iron negatively (r=-0.119, p<0.0001) in black women. Both relationships were eliminated in weight-adjusted models. BMD did not correlate with FGF23. Serum iron did not relate to intact FGF23, but was inversely related to C-terminal FGF23. Intact FGF23 correlated with serum phosphorus. In weight-adjusted models, BMD was not related to intact FGF23, C-terminal FGF23 or iron. The influence of iron on FGF23 gene expression is not important in determining bone density in healthy premenopausal women.