bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bone Loss in Patients with Untreated Chronic Obstructive Pulmonary Disease Is Mediated by an Increase in Bone Resorption Associated with Hypercapnia
Authors: Dimai Hans P. , Domej Wolfgang , Leb Georg , Lau K.-H. William 
Published: April 2006

Abstract
This study sought to determine whether the bone loss in untreated chronic obstructive pulmonary disease (COPD) is associated with hypercapnia and/or respiratory acidosis. Bone mineral density (BMD) measured at the distal forearm of the nondominant arm (with peripheral quantitative computed tomography [pQCT]) and serum markers of bone turnover were determined in 71 male patients with untreated COPD and 40 healthy male subjects who matched the patients in age, weight, and body mass index (BMI). The COPD patients, compared with controls, had reduced pulmonary functions, lower arterial pH, and elevated arterial partial pressure of CO2 (P CO 2). The BMD (in T score) was significantly lower in COPD patients than that in control subjects (−1.628 ± 0.168 vs. −0.058 ± 0.157; p &lt; 0.001). The BMD of COPD patients correlated positively with arterial pH (r = 0.582; p &lt; 0.001), negatively with P CO 2 (r = −0.442; p &lt; 0.001), and negatively with serum cross-linked telopeptide of type I collagen (ICTP), a bone resorption marker (r = −0.444; p &lt; 0.001) but not with serum osteocalcin, a bone formation marker. Serum ICTP, but not osteocalcin, correlated with P CO 2 (r = 0.593; p &lt; 0.001) and arterial pH (r = −0.415; p &lt; 0.001). To assess the role of hypercapnia, COPD patients were divided into the hypercapnic (P CO 2 &gt; 45 mm Hg; n = 35) and eucapnic (P CO 2 = 35–45 mm Hg) group (n = 36). Patients with hypercapnia had lower BMD, lower arterial pH, and higher serum ICTP than did patients with eucapnia. Arterial pH and serum ICTP of eucapnic patients were not different from those of controls. To evaluate the role of uncompensated respiratory acidosis, COPD patients with hypercapnia were subdivided into those with compensatory respiratory acidosis (pH ≥ 7.35; n = 20) and those with uncompensated respiratory acidosis (pH &lt; 7.35; n = 15). The BMD and serum ICTP were not different among the two subgroups. In conclusion, this study presents the first associative evidence that the bone loss in COPD is at least in part attributed to an increased bone resorption that is associated primarily with hypercapnia rather than uncompensated respiratory acidosis.
Five-Week Intake of Short-Chain Fructo-Oligosaccharides Increases Intestinal Absorption and Status of Magnesium in Postmenopausal Women
Authors: Tahiri Maha , Tressol Jean C. , Arnaud Josiane , Bornet Francis , Bouteloup-Demange Corinne , Feillet-Coudray Christine , Ducros Véronique , Pépin Denise , Brouns Fred , Roussel Anne M. , Rayssiguier Yves , Coudray Charles 
Published: April 2006

Abstract
Fermentable carbohydrates have been shown to be nondigestible by human enzymes in the small intestine but are fermented extensively in the large bowel to short-chain fatty acids (SCFAs), which can increase mineral absorption. It has been shown that feeding such carbohydrates including short-chain fructo-oligosaccharides (sc-FOSs) increases intestinal magnesium (Mg) absorption in animals, but their beneficial impact on Mg absorption in humans still remains to be established. Therefore, this work aimed to investigate the effect of moderate daily doses of sc-FOSs (10 g/day) on the intestinal absorption and status of Mg in postmenopausal women without hormone replacement therapy (HRT). Eleven healthy postmenopausal women aged 59 ± 6 years (mean ± SD) received for 5 weeks sc-FOS or sucrose (placebo) treatments according to a randomized, double-blind, crossover design separated by a washout period of at least 3 weeks. Subjects ingested 87.5 mg of stable isotope25Mg together with a fecal marker. Subsequently, feces were collected for 5–7 days. An inductively coupled plasma mass spectrometer (ICP/MS) was used for25Mg stable isotope measurements in feces, urine, and blood. Mg levels were assessed also at the beginning and at the end of each treatment in plasma, erythrocytes, and urine. These measurements allowed for the determination of net intestinal Mg absorption and Mg status. The results show that the addition of 10 g sc-FOS to the diet increased Mg absorption by 12.3%, from 30.2 ± 5.0% (placebo treatment) to 33.9 ± 7.2% (sc-FOS treatment; mean ± SD; p &lt; 0.02). This increase in intestinal Mg absorption was accompanied by an increase in plasma25Mg level and led to a higher urinary25Mg excretion. This is the first time that such an effect is shown in humans. The overall conclusion of this work is that the ingestion of moderate doses of sc-FOS did improve intestinal Mg absorption and status in postmenopausal women. Because of the important role of Mg in many cellular functions, such Mg absorption improvement may be particularly interesting when the dietary intake of Mg is limited.
Perspective: Reconsidering the Effects of Antiresorptive Therapies in Reducing Osteoporotic Fracture
Authors: Chesnut C. H. , Rosen C. J. 
Published: April 2006

Abstract
Concepts of what constitutes osteoporosis have evolved from the single criterion of low bone mass to a more inclusive consideration of bone strength, based on both quantity and quality. The evidence driving this shift is drawn from many sources. For example, recent studies of bone geometry have shown what engineers have always known: material properties and structural strength are inseparable. Genetic factors also argue against a one-dimensional (1D) view of osteoporosis. Large-scale family studies present a strong case for genetic influences on bone mass and predisposition to fracture. The contribution of aging to fracture risk has long been known, but we are only now beginning to understand what happens to bone remodeling and microstructure in an aging skeleton. The recognition that osteoporosis is far more complex than previously thought suggests that factors in addition to bone mineral density (BMD) may be useful for evaluating bone fragility and therapeutic effectiveness. Although assessment of BMD is noninvasive and widely available, the degree of increase in BMD alone fails to account for the broader effectiveness of antiresorptive agents in reducing the risk of fractures related to osteoporosis. Indeed, the very multiplicity of factors that determine fracture risk implies that response to therapy may be equally complex. Studies of response to antiresorptive agents and the cellular processes they induce are at best preliminary at this time. Although new technologies have been applied to studying bone microarchitecture, their invasive nature limits wide use. New methods are needed to provide insight into the causes and effects of bone fragility. The definition of osteoporosis, meanwhile, must still be considered a work in progress.
Parathyroid Hormone-Related Protein Is Required for Normal Intramembranous Bone Development
Authors: Suda Naoto , Baba Otto , Udagawa Nobuyuki , Terashima Tatsuo , Kitahara Yutaka , Takano Yoshiro , Kuroda Takayuki , Senior Paul V. , Beck Felix , Hammond Vicki E. 
Published: April 2006

Abstract
It is well established that parathyroid hormone-related protein (PTHrP) regulates chondrocytic differentiation and endochondral bone formation. Besides its effect on cartilage, PTHrP and its major receptor (type I PTH/PTHrP receptor) have been found in osteoblasts, suggesting an important role of PTHrP during the process of intramembranous bone formation. To clarify this issue, we examined intramembranous ossification in homozygous PTHrP-knockout mice histologically. We also analyzed phenotypic markers of osteoblasts and osteoclasts in vitro and in vivo. A well-organized branching and anastomosing pattern was seen in the wild-type mice. In contrast, marked disorganization of the branching pattern of bone trabeculae and irregularly aligned osteoblasts were recognized in the mandible and in the bone collar of the femur of neonatal homozygous mutant mice. In situ hybridization showed that most of the osteoblasts along the bone surfaces of the wild-type mice and some of the irregularly aligned osteoblastic cells in the homozygous mice expressed osteocalcin. Alkaline phosphatase (ALP) activity and expression of osteopontin messenger RNA (mRNA) in primary osteoblastic cells did not show significant differences between cultures derived from the mixture of heterozygous mutant and wild-type mice (+/? mice) and those from homozygous mutant mice. However, both mRNA and protein levels of osteocalcin in the osteoblastic cells of homozygous mutant mice were lower than those of +/? mice, and exogenous PTHrP treatment corrected this suppression. Immunohistochemical localization of characteristic markers of osteoclasts and ruffled border formation did not differ between genotypes. Cocultures of calvarial osteoblastic cells and spleen cells of homozygous mutant mice generated an equivalent number of tartrate-resistant acid phosphatase-positive (TRAP+) mononuclear and multinucleated cells and of pit formation to that of +/? mice, suggesting that osteoclast differentiation is not impaired in the homozygous mutant mice. These results suggest that PTHrP is required not only for the regulation of cartilage formation but also for the normal intramembranous bone development.
Generation of Bone-Resorbing Osteoclasts from B220+ Cells: Its Role in Accelerated Osteoclastogenesis due to Estrogen Deficiency
Authors: Sato Takuya , Shibata Takeshi , Ikeda Kyoji , Watanabe Ken 
Published: April 2006

Abstract
Estrogen deficiency stimulates both osteoclastic bone resorption and pre-B lymphopoiesis, the interrelationships between which remain unknown. To investigate the involvement of an increase in the number of B220+ cells in accelerated osteoclastogenesis after estrogen deficiency, we first examined whether ovariectomy (OVX) increased the frequency of clonogenic osteoclast precursors in bone marrow. The results were that after OVX, the frequency of clonogenic osteoclast precursors is increased in bone marrow, suggesting that accumulated osteoclast precursors contribute to accelerated osteoclastogenesis. Further, we found that cocultures of B220+ cells purified from bone marrow cells and stromal ST2 cells in the presence of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] gave rise to osteoclasts that can resorb bone and express calcitonin receptors. When the frequencies of clonogenic osteoclast precursors in the purified B220+ and B220− cell fractions were compared, it was found that the fractions gave rise to osteoclasts at similar frequencies, which rules out the possibility of cross-contamination and suggests that the two fractions contain comparable numbers of osteoclast precursors. Furthermore, we identified cells that are positive for both tartrate-resistant acid phosphatase (TRAP) and B220, not only in cocultures of B220+ and ST2 cells, but also in freshly isolated unfractionated bone cells. Therefore, it is concluded that at least a subfraction of B220+ cells are capable of generating osteoclasts and that the increase in the number of B220+ cells caused by estrogen deficiency may contribute to accelerated bone resorption by this novel osteoclastogenesis pathway.
Conditional Ablation of the Osteoblast Lineage in Col2.3Δtk Transgenic Mice
Authors: Visnjic D. , Kalajzic I. , Gronowicz G. , Aguila H. L. , Clark S. H. , Lichtler A. C. , Rowe D. W. 
Published: April 2006

Abstract
Two transgenic mouse lines were generated with a DNA construct bearing a 2.3-kilobase (kb) fragment of the rat α1 type I collagen promoter driving a truncated form of the herpes thymidine kinase gene (Col2.3Δtk). Expression of the transgene was found in osteoblasts coincident with other genetic markers of early osteoblast differentiation. Mice treated with ganciclovir (GCV) for 16 days displayed extensive destruction of the bone lining cells and decreased osteoclast number. In addition, a dramatic decrease in bone marrow elements was observed, which was more severe in the primary spongiosum and marrow adjacent to the diaphyseal endosteal bone. Immunostaining for transgene expression within the bone marrow was negative and marrow stromal cell cultures developed normally in the presence of GCV until the point of early osteoblast differentiation. Our findings suggest that the early differentiating osteoblasts are necessary for the maintenance of osteoclasts and hematopoiesis. Termination of GCV treatment produced an exaggerated response of new bone formation in cortical and trabecular bone. The Col2.3Δtk mouse should be a useful model to define the interrelation between bone and marrow elements as well as a model to analyze the molecular and cellular events associated with a defined wave of osteogenesis on termination of GCV treatment.
Arthrodesis of Lumbar Spine Transverse Processes Using Nacre in Rabbit
Authors: Lamghari Meriem , Antonietti Pierre , Berland Sophie , Laurent Alex , Lopez Evelyne 
Published: April 2006

Abstract
This study compares the osteogenic effects of nacre and autogenous bone grafts in a rabbit model of lumbar spine transverse process arthrodesis. A total of 15 rabbits were processed for arthrodesis between the fifth and sixth lumbar vertebrae using nacre powder mixed with autologous blood or autogenous iliac crest bone. Control rabbits were sham operated. Sample vertebrae were removed from the nacre-implanted rabbits at 2, 5, and 11 weeks postsurgery. The autogenous bone graft and sham-operated groups were processed for histological study 11 weeks postsurgery. The results for the three groups were compared at 11 weeks. The nacre-implanted samples taken at 2 weeks showed that the nacre was well tolerated by the host tissue. Endochondral bone formation was seen in the region of the dissolving nacre particles by 5 weeks. The newly formed bone formed a solid fusion between the transverse processes in one-third of the rabbits. There was still new bone formation at 11 weeks at the nacre implant site. Two-thirds of the rabbits had formed a solid fusion. Light microscopy also showed new bone formation 11 weeks after the autologous bone graft. All rabbits had a solid fusion. This initial study indicates that nacre can induce spinal fusion in an acceptable percentage of cases.
Identification of the Calcium-Sensing Receptor in the Developing Tooth Organ
Authors: Mathias Robert S. , Mathews Catharina H. E. , Gao Cen , Machule Darren , Li Wu , Denbesten Pamela K. 
Published: April 2006

Abstract
Calcium (Ca2+) is a critical component of tooth enamel, dentin, and the surrounding extracellular matrix. Ca2+ also may regulate tooth formation, although the mechanisms for such action are poorly understood. The Ca2+-sensing receptor (CaR) that is expressed in the parathyroid gland, kidney, bone, and cartilage has provided a mechanism by which extracellular Ca2+ can regulate cell function. Because these tissues play an important role in maintaining mineral homeostasis and because Ca2+ is hypothesized to play a crucial role in tooth formation, we determined whether the CaR was present in teeth. In this study, using immunohistochemistry, CaR protein was detected in developing porcine molars localized in the predentin (pD), early secretory-stage ameloblasts, maturation-stage smooth-ended ameloblasts (SA), and certain cells in the stratum intermedium. CaR protein and messenger RNA (mRNA) were detected also in an immortalized ameloblast-like cell line (PABSo-E) using immunofluorescence, reverse-transcription polymerase chain reaction (RT-PCR), and Northern analysis. Based on the observation that the CaR is expressed in cultured ameloblasts, we determined whether increments in medium Ca2+ concentration could activate the intracellular Ca2+ signal transduction pathway. In PABSo-E cells, increasing extracellular Ca2+ in the medium from 0 (baseline) to 2.5mM or 5.0 mM resulted in an increase in intracellular Ca2+ above baseline to 534 ± 69 nM and 838 ± 86 nM, respectively. Taken together, these results suggest that the CaR is expressed in developing teeth and may provide a mechanism by which these cells can respond to alterations in extracellular Ca2+ to regulate cell function and, ultimately, tooth formation.
Measurement of Midfemoral Shaft Geometry: Repeatability and Accuracy Using Magnetic Resonance Imaging and Dual-Energy X-ray Absorptiometry
Authors: Woodhead Helen J. , Kemp Allan F. , Blimkie Cameron J. R. , Briody Julie N. , Duncan Craig S. , Thompson Madeleine , Lam Albert , Howman-Giles Robert , Cowell Christopher T. 
Published: April 2006

Abstract
Although macroscopic geometric architecture is an important determinant of bone strength, there is limited published information relating to the validation of the techniques used in its measurement. This study describes new techniques for assessing geometry at the midfemur using magnetic resonance imaging (MRI) and dual-energy X-ray absorptiometry (DXA) and examines both the repeatability and the accuracy of these and previously described DXA methods. Contiguous transverse MRI (Philips 1.5T) scans of the middle one-third femur were made in 13 subjects, 3 subjects with osteoporosis. Midpoint values for total width (TW), cortical width (CW), total cross-sectional area (TCSA), cortical cross-sectional area (CCSA), and volumes from reconstructed three-dimensional (3D) images (total volume [TV] and cortical volume [CVol]) were derived. Midpoint TW and CW also were determined using DXA (Lunar V3.6, lumbar software) by visual and automated edge detection analysis. Repeatability was assessed on scans made on two occasions and then analyzed twice by two independent observers (blinded), with intra- and interobserver repeatability expressed as the CV (CV ± SD). Accuracy was examined by comparing MRI and DXA measurements of venison bone (and Perspex phantom for MRI), against “gold standard” measures made by vernier caliper (width), photographic image digitization (area) and water displacement (volume). Agreement between methods was analyzed using mean differences (MD ± SD%). MRI CVs ranged from 0.5 ± 0.5% (TV) to 3.1 ± 3.1% (CW) for intraobserver and 0.55 ± 0.5% (TV) to 3.6 ± 3.6% (CW) for interobserver repeatability. DXA results ranged from 1.6 ± 1.5% (TW) to 4.4 ± 4.5% (CW) for intraobserver and 3.8 ± 3.8% (TW) to 8.3 ± 8.1% (CW) for interobserver variation. MRI accuracy was excellent for TV (3.3 ± 6.4%), CVol (3.5 ± 4.0%), TCSA (1.8 ± 2.6%), and CCSA (1.6 ± 4.2%) but not TW (4.1 ± 1.4%) or CW (16.4 ± 14.9%). DXA results were TW (6.8 ± 2.7%) and CW (16.4 ± 17.0%). MRI measures of geometric parameters of the midfemur are highly accurate and repeatable, even in osteoporosis. Both MRI and DXA techniques have limited value in determining cortical width. MRI may prove valuable in the assessment of surface-specific bone accrual and resorption responses to disease, therapy, and variations in mechanical loading.
Can Metacarpal Cortical Area Predict the Occurrence of Hip Fracture in Women and Men Over 3 Decades of Follow-Up? Results From the Framingham Osteoporosis Study
Authors: Kiel Douglas P. , Hannan Marian T. , Broe Kerry E. , Felson David T. , Cupples L. Adrienne 
Published: April 2006

Abstract
The purpose of this study was to determine if a single measurement of metacarpal cortical area could predict the subsequent risk of hip fracture over a long-term follow-up period. Thirteen hundred eighty-six women and 1014 men (mean age [±SD] 61 ± 8 years) underwent posteroanterior hand radiography between 1966 and 1970 as part of the Framingham Study. Measurements of cortical bone width (external width and medullary width) were made at the midpoint of the second metacarpal with a digital caliper to the nearest 0.1 mm. Hip fracture occurrence was ascertained on all survivors through December 1995. Surprisingly, in women, there was no significant increase in hip fracture according to metacarpal cortical area measurements (per SD decrease) in either age-adjusted (hazard ratio [HR] = 1.13; 95% CI, 0.94–1.35) or multivariate-adjusted models (HR = 1.06; 95% CI, 0.88–1.27). The same results were seen when considering only those women who were ≥65 years of age at the time of their X-ray or when considering only the first 10 years of follow-up. When the type of hip fracture was considered in women, after adjustment for other risk factors, there appeared to be an association between metacarpal cortical area and intertrochanteric fracture risk (HR = 1.24; 95% CI, 0.91–1.71) but not femoral neck fracture risk (HR = 0.93; 95% CI, 0.71–1.22). In men, the age-adjusted risk of hip fracture was increased modestly per SD decrease in metacarpal cortical area (HR = 1.38; 95% CI, 1.02–1.87), and this remained true after adjustment for potential confounders. In this prospective cohort study with up to 30 years of follow-up, metacarpal cortical area in men predicted hip fracture risk. In women, the only association between metacarpal cortical area and fracture risk was observed for intertrochanteric fractures and was not significant when adjusting for multiple potential confounders. We conclude that this peripheral measure of bone status is not a potent predictor of hip fracture over a long period of follow-up.
High Serum Retinyl Esters Are Not Associated with Reduced Bone Mineral Density in the Third National Health and Nutrition Examination Survey, 1988–1994
Authors: Ballew Carol , Galuska Deborah , Gillespie Cathleen 
Published: April 2006

Abstract
Hypervitaminosis A is sometimes associated with abnormalities of calcium metabolism and bone mineral status. A recent study found a negative association between reported dietary vitamin A intake and bone mineral density (BMD). Some segments of the U.S. population have high fasting serum retinyl ester concentrations, a physiological marker that may reflect high and possibly excessive vitamin A intake. We examined the association between fasting serum retinyl esters and BMD in the Third National Health and Nutrition Examination Survey, 1988–1994 (NHANES III), a large, nationally representative sample of the U.S. population. BMD was measured for the femoral neck, trochanter, intertrochanter, and total hip on all nonpregnant participants aged ≥20 years; 5790 participants also had complete data on fasting serum retinyl esters and covariates including age, body mass index (BMI), smoking, alcohol consumption, dietary supplement use, diabetes, physical activity, and, among women, parity, menopausal status, and the use of oral contraceptives or estrogen-replacement therapy. The sample included non-Hispanic white, non-Hispanic black, and Mexican American men and women. We examined the association between fasting serum retinyl esters and BMD at each site, controlling for covariates with multiple linear regression. We examined the association with osteopenia and osteoporosis with multiple logistic regression. Although the prevalences of high fasting serum retinyl esters concentration and low BMD were both substantial in this sample, there were no significant associations between fasting serum retinyl esters and any measure of bone mineral status.