|
1. |
Perspectives: Caffeine and bone: Directions for research |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1149-1152
Linda K. Massey,
Preview
|
PDF (259KB)
|
|
ISSN:0884-0431
DOI:10.1002/jbmr.5650061102
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
2. |
Salmon stanniocalcin and bovine parathyroid hormone have dissimilar actions on mammalian bone |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1153-1159
Paula H. Stern,
Geetha Shankar,
Robert C. Fargher,
D. Harold Copp,
Christine E. Milliken,
Kanji J. Sato,
David Goltzman,
M.P.M. Herrmann‐Erlee,
Preview
|
PDF (479KB)
|
|
摘要:
AbstractStanniocalcin (STC), a calcium‐regulating glycoprotein hormone isolated from the corpuscles of Stannius of salmon, was tested for effects on bone and calcium metabolism in mammalian species (rats and mice). STC generally failed to alter serum calcium of parathyroidectomized rats at concentrations equimolar with effective concentrations of parathyroid hormone (PTH). STC did not increase cAMP in ROS 17/2.8 or UMR‐108 osteosarcoma cells, OK kidney cells, fetal rat limb bones, or neonatal mouse calvariae, and similarly failed to increase urinary cAMP in rats. STC did not consistently stimulate resorption in any of the rodent bone culture systems, although variable resorptive responses were elicited in fetal mouse calvariae. The results indicate that this fish hormone has limited, if any, PTH‐like activity on calcium metabolism in mammalian sy
ISSN:0884-0431
DOI:10.1002/jbmr.5650061103
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
3. |
Voltage‐dependent phosphate transport in osteoblast‐like cells |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1161-1166
KHANH V.Q. Luong,
Jacob Green,
Charles R. Kleeman,
Dean T. Yamaguchi,
Preview
|
PDF (425KB)
|
|
摘要:
AbstractPhosphate ion (Pi) in sufficient concentrations is crucial for bone mineralization. The osteoblast (OB) may be responsible for the transport of Pi into the bone interstitium, where mineralization occurs. We previously characterized a Na+‐dependent Pi transporter (NaPi) in the osteoblastic UMR‐106–01 cell line. In the present study, the alteration of Na+‐dependent Pi transport by changes in membrane potential was investigated. Depolarizing the cells with increasing concentrations of ambient K+and valinomycin resulted in a progressive decline in Na+‐dependent Pi uptake to a maximum of 28% at a membrane potential of −18 mV compared to control Na+‐dependent Pi uptake at a membrane potential of approximately −60 mV. Hyperpolarizing the cells with SCN−increased Na+‐dependent Pi uptake over control by 50% at an SCN−concentration of 70 mM. Determination of membrane potential by using the fluorescent probe, DiSC3(5), showed that the addition of Pi to cells in Na+‐containing medium resulted in a small depolarization. These data show that NaPi activity can be altered by membrane potential changes and that the initiation of Na+‐dependent Pi uptake is associated with depolarization of the plasma membrane of UMR‐106–01 cells. Taken together, the cotransport of Na+and Pi results in the movement of a net
ISSN:0884-0431
DOI:10.1002/jbmr.5650061104
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
4. |
Structural and composition studies on the mineral of newly formed dental enamel: A chemical, X‐ray diffraction, and31p and proton nuclear magnetic resonance study |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1167-1176
Laurence C. Bonar,
Masaharu Shimizu,
James E. Roberts,
Robert G. Griffin,
Melvin J. Glimcher,
Preview
|
PDF (786KB)
|
|
摘要:
AbstractThe present report describes a study of the development and maturation of the mineral component of dental enamel. We prepared porcine enamel of different stages of maturation, from the very immature enamel of unerupted teeth, with a mineral content of 45%, to fully mature enamel, with a mineral content of ∼99%. We fractionated the less mature enamel by density centrifugation and examined the enamel density fractions and unfractionated enamel by a variety of chemical and physical techniques, including conventional and radial distribution function x‐ray diffraction analysis, conventional and Fourier transform infrared spectroscopy,31P and1H nuclear magnetic resonance spectroscopy, and chemical analysis. The three most immature preparations, from unerupted teeth, had mineral contents of 45, 67, and 91 and Ca/P molar ratios of 1.41, 1.44, and 1.47. Density distribution histograms of the three fractions show that the early maturation of dental enamel mineral is accompanied by an increase in tissue density, reflecting the increase in mineral content. The density distribution in each sample is relatively narrow, indicating that the maturation process occurs at a fairly homogeneous rate, with all enamel in an anatomically defined zone mineralizing to about the same extent. X‐ray diffraction studies indicate that even the least mature, least mineralized of these immature samples is considerably more crystalline than the most mature bone mineral studied and that crystalline perfection of the enamel crystals increases further with maturation. Both theaandcaxes of the mineral unit cell expand significantly during early stages of maturation. Solid‐state31P nuclear magnetic resonance spectroscopy studies indicate that dental enamel contains a DCPD‐like HPO4component in an apatitic lattice, similar to the component previously observed in bone and some synthetic calcium phosphates. The proportion of this DCPD‐like component decreases with maturation but is readily detectable even in fully mature enamel. The infrared spectroscopic studies indicate that the 3570 cm−1band ascribed to the OH−group of the hydroxyapatite crystals is absent in the least mature enamel but can be detected and becomes progressively stronger as the enamel becomes more mature. The increase in the content of the OH−groups of the apatite crystals is concomitant with the observed increase in unit cell parameters. Similar studies on very young and very old mature bone of four different species failed to detect the pres
ISSN:0884-0431
DOI:10.1002/jbmr.5650061105
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
5. |
Preventive effects of clomiphene citrate on estrogen‐deficiency osteopenia elicited by LHRH agonist administration in the rat |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1177-1182
Ailsa Goulding,
Lorryn Fisher,
Preview
|
PDF (447KB)
|
|
摘要:
AbstractThe estrogen agonist and antagonist clomiphene citrate has been shown to prevent bone loss induced by ovariectomy in the rat. In young women estrogen‐deficiency bone loss is a clinical problem associated with the use of luteinizing hormone releasing hormone (LHRH) agonists, such as buserelin, to treat endometriosis. The aim of this study was to determine whether clomiphene citrate (10 mg/kg body weight per week orally) would prevent the osteopenic effect of buserelin (25 μg/kg body weight per day SC) in the rat. Four groups of animals with45Ca‐labeled skeletons were studied for 4 weeks: group A, placebo controls; group B, buserelin; group C, clomiphene; and group D, buserelin + clomiphene. Bone resorption was monitored by measuring the urinary excretion of45Ca and hydroxyproline. Clomiphene slowed bone breakdown and inhibited the osteopenic effect of buserelin. Total‐body calcium values (mean ± SD) were (mg) 2635 ± 181, 2267 ± 85, 2566 ± 126, and 2624 ± 77 in groups A to D, respectively. Osteopenia was present only in group B (P<0.001). Interestingly buserelin lowered blood 17β‐estradiol and uterine weights to a similar extent in the presence and absence of clomiphene. Because clomiphene inhibited estrogen‐deficiency bone loss in buserelin‐treated rats without depressing the hypoestrogenic action of this LHRH agonist, it is suggested that the use of clomiphene to protect the skeleton during LHRH agonist therapy of endometriosis warr
ISSN:0884-0431
DOI:10.1002/jbmr.5650061106
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
6. |
X‐ray microanalysis of fluoride distribution in microfracture calluses in cancellous iliac bone from osteoporotic patients treated with fluoride and untreated |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1183-1190
Georges Boivin,
Brigitte Grousson,
Pierre J. Meunier,
Preview
|
PDF (1978KB)
|
|
摘要:
AbstractFluoride is able to augment cancellous bone mass in vertebral osteoporosis but is responsible for osteoarticular side effects in which microfractures are thought to be involved. During healing of these microfractures, a callus is formed all around the cancellous fracture line. Our hypothesis is that in fluoride‐treated osteoporotic patients, calluses are bone sites where fluoride is focally deposited at a high concentration, and this could induce a local defect of calcification with a poor healing of microfractures. Our aim was to validate this hypothesis on several calluses following microfractures in undecalcified iliac cancellous bone from six women with osteoporosis (four fluoride treated and two untreated). Histologically normal iliac cancellous bone tissue, taken from a subject having neither fluoride treatment nor microfracture, was also examined. Selected areas, including new woven bone (calluses) and old lamellar bone, were carbon‐coated and analyzed using an electron microprobe. FluorideKαand calciumKαradiations were detected with wavelength and energy‐dispersive spectrometers, respectively. In old lamellar bone at a distance from microfractures, the fluoride level was similar in normal and untreated osteoporotic patients but was slightly increased in treated osteoporotic patients. In untreated osteoporotic patients, the fluoride level was slightly higher (about 1.2 times) at the site of microfractures (lamellar and woven bone) than in lamellar bone far from such fractures, but fluoride was homogeneously distributed in lamellar and woven bone. In contrast, in treated osteoporotic patients, fluoride content was much higher (about 1.7 times) at the site of microfractures (lamellar and woven bone) than in lamellar bone far from fractures, but fluoride was heterogeneously distributed within the calluses, with the highest level in woven bone and the smallest in adjacent lamellar bone. The present data demonstrate that fluoride is preferentially concentrated in calluses of cancellous microfractures in fluoride‐treated osteoporotic patients. It is likely but remains to be proven that this focal increase in fluoride uptake compromises the healing of micro
ISSN:0884-0431
DOI:10.1002/jbmr.5650061107
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
7. |
Effects of 17β‐estradiol on calcitonin secretion and content in a human medullary thyroid carcinoma cell line |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1191-1196
Marise Lazaretti‐Castro,
Andreas Grauer,
Yalem Mekonnen,
Friedhelm Raue,
Reinhard Ziegler,
Preview
|
PDF (442KB)
|
|
摘要:
AbstractThe presence of a direct estrogen effect on calcitonin secretion is controversial. Because most of the data available were obtained from complex in vivo systems, we chose an in vitro approach to assess the problem. Using a human C cell carcinoma cell line (TT cells) with well‐documented estrogen receptors, we investigated the effect of 17β‐estradiol (E2) on basal and stimulated calcitonin secretion, on calcitonin content, and on total cellular protein. After short (30 and 180 minutes) and long‐term (24 h to 6 days) incubation of the cells with different concentrations of E2(from 0.01 to 100 nM) we observed no stimulatory but a transient dose‐dependent inhibitory effect on CT secretion and content. The nadir of the effect on CT secretion appeared at 24 h, demonstrating a reduction to 80.5 ± 7.8% of control at 1 nM and to 59.1 ± 15% of control at 100 nM E2. After 72 h, the CT levels of the E2‐exposed groups returned to control levels. The acute stimulation of the cells with TPA plus forskolin after preincubation with E2up to 6 days showed no difference in the increment of CT release compared to the control groups. Additionally, E2had a dose‐dependent stimulatory effect on cell protein content. The data demonstrate the absence of a direct stimulatory effect of E2on CT secretion, revealing a dose‐dependent inhibitory effect on CT secre
ISSN:0884-0431
DOI:10.1002/jbmr.5650061108
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
8. |
Lack of effects of neutralization of parathyroid hormone‐related protein on calcium homeostasis in neonatal mice |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1197-1202
Subhash C. Kukreja,
James J. D'Anza,
Mary E. Melton,
Sarah A. Wimbiscus,
Vivian Grill,
John T. Martin,
Preview
|
PDF (358KB)
|
|
摘要:
AbstractLarge quantities of parathyroid hormone‐related protein (PTHrP) are present in the milk of various species. It has been suggested that PTHrP may play a role in neonatal calcium homeostasis. In the present study we evaluated the effect of neutralization of amino‐terminal PTHrP activity by passive immunization in 1‐day‐old mouse pups. Neutralization of amino‐terminal PTHrP activity had no significant effect on serum calcium or whole‐body calcium content in the neonatal mice. In additional studies, we demonstrated that subcutaneous administration of PTHrP‐(1–34) increased serum calcium, whereas oral administration had no significant effect in 3‐day‐old pups. The studies therefore demonstrate that the amino terminus of PTHrP may not play a significant role in neonatal calcium homeostasis. Local effects of PTHrP cannot be excluded by the results o
ISSN:0884-0431
DOI:10.1002/jbmr.5650061109
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
9. |
Modulation of PTH‐stimulated osteoclastic resorption by bisphosphonates in fetal mouse bone explants |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1203-1210
Gabri van der Pluijm,
Clemens W.G.M. Löwik,
Henny de Groot,
Marcel J. Alblas,
Lianne J. A. van der Wee‐Pals,
OLAV L. M. Bijvoet,
Socrates E. Papapoulos,
Preview
|
PDF (1880KB)
|
|
摘要:
AbstractWe examined the effects of the bisphosphonates Cl2MDP, APD, and Me2APD on osteoclastic resorption in the absence and presence of PTH using fetal mouse osteoclast‐free bone explants cocultured with fetal liver as a source of osteoclast precursors. Results revealed qualitative and quantitative differencs among the bisphosphonates tested. With Cl2MDP and APD fractional inhibition of resorption (measured as45Ca release) in the presence of PTH was proportional to that obtained in its absence. In contrast, Me2APD, which is the most potent inhibitor of the three, was found at low concentrations (≤5 × 10−7M) to enhance the PTH‐stimulated osteoclastic resorption. APD as well, at concentrations that could not inhibit resorption, had a similar effect, but Cl2MDP did not. These studies describe a new phenomenon, that low doses of nitrogen‐containing bisphosphonates can act synergistically with PTH and enhance osteoclastic resorption. These findings may have clinical implications in the management of patients with increased osteoclastic resorption due to parathyroid ov
ISSN:0884-0431
DOI:10.1002/jbmr.5650061110
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
10. |
Impairment of gamma carboxylation of circulating osteocalcin (bone gla protein) in elderly women |
|
Journal of Bone and Mineral Research,
Volume 6,
Issue 11,
1991,
Page 1211-1216
Louisa Plantalech,
Marc Guillaumont,
Philippe Vergnaud,
Michel Leclercq,
Pierre D. Delmas,
Preview
|
PDF (501KB)
|
|
摘要:
AbstractOsteocalcin, also called bone gla protein, is a unique noncollagenous protein of the extracellular matrix of bone that circulates in blood. Oseteocalcin contains three residues of the vitamin K‐dependent γ‐carboxyglutamic acid (gla) responsible for the affinity of osteocalcin for bone mineral. In animals treated with the vitamin K antagonist warfarin, the osteocalcin content of bone is markedly reduced and the fraction of osteocalcin released into the circulation is increased. Most studies have shown that osteocalcin increases with aging in women, reflecting an increase in bone turnover, especially after the menopause. To determine if this increase in osteocalcin could be associated with impaired carboxylation, we measured total and noncarboxylated osteocalcin in the serum of 72 women of various ages: 22 premenopausal (31 ± 7 years old), 20 early postmenopausal (54 ± 3 years), and 30 elderly women (85 ± 8 years). As previously reported, total serum osteocalcin was significantly increased in early postmenopausal and elderly women. Noncarboxylated serum osteocalcin was slightly increased in early postmenopausal women (0.95 ± 0.4 versus 0.65 ± 0.5 ng/ml in premenopausal women), markedly elevated in elderly women (1.59 ± 1.1 ng/ml,p<0.001), and correlated with age (r= 0.47,p<0.001). Elderly women had values of the same magnitude as in 10 patients on chronic warfarin therapy (1.94 ± 1.1 ng/ml). As a consequence, the increase in carboxylated serum osteocalcin was significant in early postmenopausal women but not in elderly women. Serum levels of vitamin K1and of menaquinones 6, 7, and 8 were measured in some of the young and elderly women. No difference was found, which does not suggest a major vitamin K deficiency in elderly women. Conversely, our data may be related to an inadequate recycling of vitamin K or to an intrinsic defect of the carboxylation system within the osteoblasts of elderly people. In conclusion, we have shown that circulating osteocalcin is undercarboxylated in elderly women through an unknown mechanism, suggesting a decrease in the osteocalcin content of bone. Further studies should be conducted to determine the importance of these abnormalities in the pathogenesis of the bone loss occurring
ISSN:0884-0431
DOI:10.1002/jbmr.5650061111
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1991
数据来源: WILEY
|
|