bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of High-Impact Exercise on Ultrasonic and Biochemical Indices of Skeletal Status: A Prospective Study in Young Male Gymnasts
Authors: Daly Robin M. , Rich Peter A. , Klein Rudi , Bass Shona 
Published: April 2006

Abstract
Physical activity has been proposed as one strategy to enhance bone mineral acquisition during growth. The aim of this study was to determine whether frequent impact loading associated with gymnastics training confers a skeletal benefit on pre- and peripubertal male gymnasts. We measured broadband ultrasonic attenuation (BUA, dB/MHz) at the calcaneus (CBUA); ultrasound velocity (m/s) at the calcaneus (CVOS), distal radius (RVOS) and phalanx (PVOS); serum osteocalcin (OC); total alkaline phosphatase (ALP) and insulin-like growth factor-I (IGF-I) every 3–4 months over an 18-month period in elite male gymnasts and matched normoactive controls (pubertal stage ≤2). Ground reaction forces of common gymnastics maneuvers were determined using a force platform and loading histories of the upper and lower extremities approximated from video recordings. Ultrasound results were expressed as a standardized score (Z score) adjusted for age, height, and weight. At baseline, no differences were detected between the gymnasts (n = 31) and controls (n = 50) for CBUA, although ultrasound velocity at each site was higher in the gymnasts (0.6–1.5 SD) than the predicted mean in controls (p ≤ 0.001). Over 18 months, CBUA Z scores increased significantly in the gymnasts from baseline (0.3 vs. 1.0, p &lt; 0.05, n = 18). In contrast, ultrasound velocity did not increase in either group, although CVOS and RVOS remained significantly higher in gymnasts compared with controls (range p &lt; 0.01 and &lt; 0.001). No differences between groups were found for OC, ALP, or IGF-I at any time. Gymnastics training was associated with on average 102 and 217 impacts per session on the upper and lower extremities, respectively, with peak magnitudes of 3.6 and 10.4 times body weight. These results suggest that frequent high-impact, weight-bearing exercise during the pre and peripubertal period may enhance the mechanical competence of the skeleton, perhaps offering an important strategy for osteoporosis prevention if the benefits are maintained.
Long-Term Recreational Gymnastics, Estrogen Use, and Selected Risk Factors for Osteoporotic Fractures
Authors: Uusi-Rasi Kirsti , Sievänen Harri , Vuori Ilkka , Heinonen Ari , Kannus Pekka , Pasanen Matti , Rinne Marjo , Oja Pekka 
Published: April 2006

Abstract
The purpose of this cross-sectional study was to examine whether long-term participation in recreational gymnastics or folk dancing or estrogen replacement therapy (ERT) is associated with mechanically more competent bones and improved muscular strength and body balance. One hundred and seventeen healthy, female postmenopausal recreational gymnasts (mean age 62.1 [SD 4.7] years) and 116 sedentary controls (mean age 61.5 [4.6] years) were enrolled in the study. Bone mineral content (BMC) of the distal radius, femoral neck, and trochanter were measured with dual-energy X-ray absorptiometry. BMC of the midshaft and distal tibia and trabecular density (TrD) of the distal tibia were measured with peripheral computed quantitative tomography. Maximal isometric strength, muscular power, cardiorespiratory fitness, and body balance of the participants were also assessed. The cardiorespiratory fitness, muscular strength, and dynamic balance of the recreational gymnasts and folk dancers combined were significantly better than those of the controls, the average group difference ranging from 7.5% (95% confidence interval 5.0–9.9%) in dynamic balance to 12.8% (6.6–19.4%) in dynamic muscular power. ERT was not associated with the fitness indicators, muscular power, or balance, but was significantly associated with the BMC at all the measured bone sites, the mean group difference between estrogen users and nonusers ranging from 6.5% (3.7–9.3%) for the tibial shaft to 11.8% (6.4–17.0%) for the distal radius. Recreational gymnastics, in turn, was significantly associated with higher BMC at the tibia only, the mean group difference being 3.9% (0.9–6.9%) for the tibial shaft and 7.7% (3.7–11.9%) for the distal tibia. Recreational gymnastics was also associated with higher TrD at the distal tibia (5.2%; 1.2–9.2%), whereas estrogen usage did not show such association. The results indicate that ERT seems especially effective in preventing postmenopausal bone loss, whereas recreational gymnastics and folk dancing improve muscular performance and body balance in addition to increased bone mass and bone size in the tibia. All these factors are essential in prevention of fall-related fractures of the elderly.
A Chimeric Form of Osteoprotegerin Inhibits Hypercalcemia and Bone Resorption Induced by IL-1β, TNF-α, PTH, PTHrP, and 1,25(OH)2D3
Authors: Morony Sean , Capparelli Casey , Lee Richard , Shimamoto Grant , Boone Thomas , Lacey David L. , Dunstan Colin R. 
Published: April 2006

Abstract
Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation and activity and appears to be a critical regulator of bone mass and metabolism. In the current study, mice were challenged with various cytokines and hormones (interleukin-1β, tumor necrosis factor-α, parathyroid hormone, parathyroid hormone-related protein, and 1α,25-dihydroxyvitamin D3) that are known to increase bone resorption and cause hypercalcemia and treated concurrently with either a recombinant chimeric Fc fusion form of human OPG, with enhanced biological activity (cOPG) (2.5 mg/kg/day) or vehicle. Mice receiving these bone-resorbing factors became hypercalcemic by day 3 after commencing treatment and had increased bone resorption as evidenced by elevated osteoclast numbers on day 5. Concurrent cOPG treatment prevented hypercalcemia (p &lt; 0.05) and maintained osteoclast numbers in the normal range (p &lt; 0.001). The demonstration that cOPG can inhibit bone resorption suggests that this molecule may be useful in the treatment of diseases including hyperparathyroidism, humoral hypercalcemia of malignancy, osteoporosis, and inflammatory bone disease, which are characterized, in part, by increases in osteoclastic bone resorption.
Expression of Osteoprotegerin (Osteoclastogenesis Inhibitory Factor) in Cultures of Human Dental Mesenchymal Cells and Epithelial Cells
Authors: Sakata Masatoshi , Shiba Hideki , Komatsuzawa Hitoshi , Fujita Tsuyoshi , Ohta Kouji , Sugai Motoyuki , Suginaka Hidekazu , Kurihara Hidemi 
Published: April 2006

Abstract
Osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF) inhibits osteoclast differentiation, activity, and survival; therefore OPG/OCIF may regulate the resorption of dental hard tissues, such as alveolar bone, cementum, and dentin. To investigate this issue, reverse transcriptase-polymerase chain reaction using specific primers for OPG/OCIF was performed with total RNAs isolated from human gingival keratinocytes (HGKs), human gingival fibroblasts (HGFs), human periodontal ligament cells (HPDLs), and human pulp cells (HPCs) in culture. PCR products were found in HGFs, HPDLs, and HPCs, but not in HGKs, and the DNA sequence of these products was 100% identical to the reported sequence of the OPG gene. Northern blot analyses also showed that HGFs, HPDLs, and HPCs, but not HGKs, expressed OPG/OCIF transcripts of ∼2.5 kb. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) increased OPG/OCIF mRNA levels in a dose-and time-dependent manner in HPDL. After 12 h of treatment, IL-1β at 3 ng/ml and TNF-α at 3 ng/ml increased OPG/OCIF mRNA expression by 190% and 110%, respectively, with a maximal effect. The stimulatory effects of IL-1β and TNF-α were also seen in HPC. However, IL-6 and transforming growth factor-β had little effect on OPG/OCIF mRNA levels in HPDL. These findings suggest that OPG/OCIF synthesized by dental mesenchymal cells locally regulates the resorption of dental hard tissues through cytokines.
Anabolic or Catabolic Responses of MC3T3-E1 Osteoblastic Cells to Parathyroid Hormone Depend on Time and Duration of Treatment
Authors: Schiller Paul C. , D'Ippolito Gianluca , Roos Bernard A. , Howard Guy A. 
Published: April 2006

Abstract
We have investigated signaling (cAMP) and anabolic responses (mineralization of extracellular matrix [ECM]) to parathyroid hormone (PTH) in long-term (30 days) cultures of MC3T3-E1 cells, a murine model of osteoblast differentiation. Expression of PTH/PTH–related peptide receptor (PTH1R) mRNA is detected early and remains relatively constant for 2 weeks with somewhat higher levels observed during the second half of the culture period. In contrast to the relatively stable PTH1R mRNA expression, the cAMP response to PTH varies markedly with no response at day 5 and a marked response (80-fold versus control) by day 10. Responsiveness to PTH remains elevated with fluctuations of 30- to 80-fold stimulation throughout the remainder of the culture period. The timing and duration of PTH treatment to achieve in vitro mineralization of ECM was evaluated. When continuous PTH treatment was initiated before day 20, mineralization decreased. If continuous PTH treatment began on or after day 20, mineralization was unaffected. However, if treatment began on day 20 and then stopped on day 25, mineralization on day 30 was increased 5-fold. This mineralization response to intermittent PTH was confirmed in primary cultures of murine and human osteoblastic cells. These data provide a potential basis for understanding the differential responses to PTH (anabolic versus catabolic) and indicate the developmental temporal variance of anabolic and catabolic responses. Since cAMP signaling was relatively unchanged during this interval (day 10–30) and stimulation of adenylate cyclase only partially mimicked the PTH effect on increased mineralization, other signaling pathways are likely to be involved in order to determine the specific anabolic response to short-term PTH treatment during the differentiation process.
Low Cell Motility Induced by hsp27 Overexpression Decreases Osteolytic Bone Metastases of Human Breast Cancer Cells In Vivo
Authors: Lemieux Pierre , Harvey J. , Guise Theresa , Dallas Mark , Oesterreich Steffi , Yin Juan Juan , Selander Katri , Fuqua Suzanne 
Published: April 2006

Abstract
The mechanisms controlling the formation of osteolytic bone metastases in patients with breast cancer are still poorly understood. To explore the role of motility in the establishment of osteolytic bone metastases, we have used a model of bone metastasis in which MDA-MB-231 breast cancer cells exhibiting low (hsp27-transfectants) and high (control-transfectant) endogenous cell motility were compared. We found that MDA-MB-231 cells exhibiting low cell motility were less capable of establishing osteolytic lesions. The number and the area of the osteolytic lesions in mice inoculated with low motility cells were both significantly smaller. Histomorphometry of bone lesions also demonstrated less tumor area in mice bearing hsp27 transfectants although there was no difference in the osteoclast number per square millimeter of tumor–bone interface. These data suggest that cell motility may be an important mechanism in the metastatic cascade of breast cancer cells to the bone and that controlling cell motility may be a useful target to prevent the establishment of osteolytic bone metastases.
Trabecular Bone Turnover and Bone Marrow Cell Development in Tail-Suspended Mice
Authors: Sakata Takeshi , Sakai Akinori , Tsurukami Hiroshi , Okimoto Nobukazu , Okazaki Yuichi , Ikeda Satoshi , Norimura Toshiyuki , Nakamura Toshitaka 
Published: April 2006

Abstract
To clarify the relationship between the changes of trabecular bone turnover and bone marrow cell development during mechanical unloading and reloading, we performed experiments with tail-suspended mice. At 8 weeks of age, 150 male ddY mice were divided into three body weight-matched groups. Mice of group 1 were euthanized at the start of tail suspension (day 0) as a baseline control. The mice of group 2 were subjected to hindlimb unloading by tail suspension for 14 days and reloading for the subsequent 14 days. The mice of group 3 were normally loaded as age-matched controls. Mice of groups 2 and 3 were sacrificed at 7, 14, and 28 days after the start of the experiment. In the first experiment (histomorphometric study of tibiae), unloading for 7 and 14 days and reloading for the subsequent 14 days significantly decreased the bone volume compared with that in the age-matched controls, respectively. Unloading for 7 and 14 days also significantly reduced the bone formation rate (BFR/BS), respectively, but reloading for the subsequent 14 days restored BFR/BS to the control level. While the unloading for 7 and 14 days significantly increased both the osteoclast surface (Oc.S/BS) and the osteoclast number (Oc.N/BS), the reloading for the subsequent 14 days decreased Oc.S/BS and Oc.N/BS, respectively. In the second experiment (bone marrow cell culture study of tibiae), unloading for 7 and 14 days reduced the adherent stromal cell number, without significance. Unloading for 7 days significantly decreased the mineralized nodule formation. Reloading for the subsequent 14 days markedly increased the adherent stromal cell number and the mineralized nodule formation. Unloading for 7 days significantly increased the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. These data clearly demonstrate that unloading reduces bone formation and increases bone resorption, and subsequent reloading restores reduced bone formation and suppresses increased bone resorption, closely associated with the changes in adherent stromal cell number, mineralized nodule formation, and the number of TRAP-positive multinucleated cells.
Low Body Mass Index Is an Important Risk Factor for Low Bone Mass and Increased Bone Loss in Early Postmenopausal Women
Authors: Ravn P. , Cizza G. , Bjarnason N. H. , Thompson D. , Daley M. , Wasnich R. D. , Mcclung M. , Hosking D. , Yates A. J. , Christiansen C. 
Published: April 2006

Abstract
Thinness (low percentage of body fat, low body mass index [BMI], or low body weight) was evaluated as a risk factor for low bone mineral density (BMD) or increased bone loss in a randomized trial of alendronate for prevention of osteoporosis in recently postmenopausal women with normal bone mass (n = 1609). The 2-year data from the placebo group were used (n = 417). Percentage of body fat, BMI, and body weight were correlated with baseline BMD (r = −0.13 to −0.43, p &lt; 0.01) and 2-year bone loss (r = −0.14 to −0.19, p &lt; 0.01). Women in the lowest tertiles of percentage of body fat or BMI had up to 12% lower BMD at baseline and a more than 2-fold higher 2-year bone loss as compared with women in the highest tertiles (p ≤ 0.004). Women with a lower percentage of body fat or BMI had higher baseline levels of urine N-telopeptide cross-links (r = −0.24 to −0.31, p &lt; 0.0001) and serum osteocalcin (r = −0.12 to −0.15, p &lt; 0.01). To determine if the magnitude of treatment effect of alendronate was dependent on these risk factors, the group treated with 5 mg of alendronate was included (n = 403). There were no associations between fat mass parameters and response to alendronate treatment, which indicated that risk of low bone mass and increased bone loss caused by thinness could be compensated by alendronate treatment. In conclusion, thinness is an important risk factor for low bone mass and increased bone loss in postmenopausal women. Because the response to alendronate treatment is independent of fat mass parameters, prevention of postmenopausal osteoporosis can be equally achieved in thinner and heavier women.
The Effect of Pregnancy on Bone Density and Bone Turnover
Authors: Naylor K. E. , Iqbal P. , Fledelius C. , Fraser R. B. , Eastell R. 
Published: April 2006

Abstract
During pregnancy, the mother adapts to meet the calcium demands of the fetus. The effect of this adaptation on the maternal skeleton is not fully understood. Our objectives were to evaluate changes in bone mineral density (BMD) and bone turnover during pregnancy. We studied 16 women longitudinally, with baseline measurements before pregnancy; then at 16, 26, and 36 weeks of pregnancy; and postpartum. We measured total-body BMD and biochemical markers of bone resorption (urinary pyridinium crosslinks and telopeptides of type I collagen) and bone formation (serum bone alkaline phosphatase, propeptides of type I procollagen [PINP] and osteocalcin). We also measured parathyroid hormone (PTH), insulin-like growth factor I (IGF-I), and human placental lactogen. Postpartum, BMD increased in the arms (2.8%, P&lt; 0.01) and legs (1.9%, P&lt; 0.01) but decreased in the pelvis (−3.2%, P&lt;0.05) and spine (−4.6%, P&lt; 0.01) compared with prepregnancy values. All biochemical markers, with the exception of osteocalcin concentration, increased during pregnancy. The change in IGF-I at 36 weeks was related to the change in biochemical markers (e.g., PINP, r = 0.72, P= 0.002). Pregnancy is a high-bone-turnover state. IGF-I levels may be an important determinant of bone turnover during pregnancy. Elevated bone turnover may explain trabecular bone loss during pregnancy.
1,25-Dihydroxyvitamin D3 as Well as Its Analogue OCT Lower Blood Calcium Through Inhibition of Bone Resorption in Hypercalcemic Rats with Continuous Parathyroid Hormone–Related Peptide Infusion
Authors: Endo Ko-Ichi , Katsumata Kyoko , Hirata Michinori , Masaki Toshimi , Kubodera Noboru , Nakamura Toshitaka , Ikeda Kyoji , Ogata Etsuro 
Published: April 2006

Abstract
The effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and its analogue 22-oxa-1,25(OH)2D3 (22-oxacalcitriol) (OCT) on calcium and bone metabolism were examined in an animal model of hypercalcemia with continuous infusion of parathyroid hormone–related peptide (PTHrP), to determine whether active vitamin D could counteract the skeletal action of PTHrP in addition to its reported effect in suppressing the production of PTHrP in cancer cells. Parathyroid glands were removed from 8-week-old Sprague–Dawley rats to eliminate the confounding effects of endogenous PTH. Animals were then continuously infused with human PTHrP(1–34) at a constant rate via osmotic minipumps for 2 weeks, and at the same time treated orally or intravenously with OCT or 1,25(OH)2D3 four to nine times during the 2-week period. Under these conditions, OCT and, surprisingly, 1,25(OH)2D3 alleviated hypercalcemia in a dose-dependent manner. 1,25(OH)2D3 and OCT suppressed the urinary excretion of deoxypyridinoline, although they did not affect renal calcium handling, suggesting that the antihypercalcemic effect is attributable to the inhibition of bone resorption. These active vitamin D compounds also counteracted the effects of PTHrP at the proximal renal tubules, as reflected by a decrease in phosphate excretion. Histomorphometric analysis of bone revealed a dose-related decrease in parameters of bone resorption. These results suggest that 1,25(OH)2D3 as well as OCT has the potential to alleviate hypercalcemia, at least in part, through the inhibition of bone resorption in hypercalcemic rats with constant PTHrP levels. We propose that the main function of active vitamin D in high bone-turnover states is to inhibit bone resorption, and this may have important implications for the understanding of the role of active vitamin D in the treatment of metabolic bone diseases, such as osteoporosis.
Cementum-Forming Cells Are Phenotypically Distinct from Bone-Forming Cells
Authors: Grzesik Wojciech J. , Cheng Hui , Oh Julia S. , Kuznetsov Sergei A. , Mankani Mahesh H. , Uzawa Katsuhiro , Robey Pamela Gehron , Yamauchi Mitsuo 
Published: April 2006

Abstract
Normal human cementum-derived cells (HCDCs), expanded in vitro, formed mineralized matrix when attached to a ceramic carrier and transplanted subcutaneously into immunodeficient mice. The mineralized matrix elaborated by transplanted HCDC exhibited several features identical to cementum in situ and was significantly different from bone deposited by similarly transplanted human bone marrow stromal cells (BMSCs). No bone marrow formation and very few or no tartrate-resistant acid phosphatase (TRAP)-positive cells (osteoclasts and osteoclastic precursors) were found in HCDC transplants. In contrast, in BMSC transplants both hematopoiesis and TRAP-positive cells were routinely observed. Furthermore, compared with BMSC-derived matrix, HCDC-derived matrix was less cellular, numerous empty lacunae were present, and fewer cells were found on the cementum matrix/ceramic carrier interface. The organization of collagen fibers in HCDC-derived matrix, as visualized by using the Picrosirus red staining method, was similar to cementum, with typical unorganized bundles of collagen fibers. In contrast, bone matrix elaborated by transplanted BMSC had lamellar structure, identical to mature bone in situ. Finally, cementocytes embedded in the cementum-like matrix were immunopositive for fibromodulin and lumican, whereas osteocytes within the bonelike matrix were negative. This pattern is consistent with the cementum and bone in situ, respectively. These results indicate that human cementum cells are phenotypically distinct from bone cells and provide further validation of the combined in vitro/in vivo model of human cementogenesis recently developed in our laboratory.
Stimulation of Sodium-Dependent Phosphate Transport and Signaling Mechanisms Induced by Basic Fibroblast Growth Factor in MC3T3-E1 Osteoblast-like Cells
Authors: Suzuki Atsushi , Palmer Gaby , Bonjour Jean-Philippe , Caverzasio Joseph 
Published: April 2006

Abstract
Physiological and pathological observations indicate that basic fibroblast growth factor (bFGF) is an important regulator of osteoblastic cell differentiation and in particular of cranial ossification. Experimental evidence suggests that inorganic phosphate (Pi) transport could be an important function of bone matrix calcification. In the present study, we address the influence of bFGF on Pi transport activity in MC3T3-E1 osteoblast-like cells derived from mouse calvaria. The results indicate that bFGF is a potent and selective stimulator of sodium-dependent Pi transport in these cells. The change in Pi transport activity induced by bFGF depends on transcription and translation and corresponds to a change in the maximum velocity of the Pi transport system (Vmax). These observations suggest that enhanced Pi transport activity in response to bFGF may result from insertion of newly synthesized Pi transporters into the plasma membrane. A selective inhibitor of fibroblast growth factor receptor (FGFR) tyrosine kinase, SU5402, blunted the stimulation of Pi transport induced by bFGF. It also prevented the increase in protein tyrosine phosphorylation induced by bFGF, including phosphorylation of FGFR-1, FGFR-2, phospholipase C-γ (PLC-γ), and Shc as well as the recruitment of the Grb2/Sos signaling complex. In addition, bFGF- induced the activation of the mitogen-activated protein (MAP) kinases extracellular signal–regulated kinase (ERK) and p38, effects that were prevented by SU5402. Both the protein kinase C (PKC) inhibitor calphostin C and PKC down-regulation suppressed the stimulatory effect of bFGF on Pi transport. Selective inhibitors of ERK and p38 MAP kinases slightly reduced this cellular response with a significant effect observed with the highest concentration of the p38 MAP kinase inhibitor. In conclusion, the results of this study indicate that bFGF selectively stimulates Pi transport in calvaria-derived osteoblastic cells. The main signaling mechanism responsible for this effect involves tyrosine phosphorylation of PLC-γ and activation of PKC, with a possible contribution of the p38 MAP kinase pathway.