ISSN:0884-0431    

DOI:10.1002/jbmr.5650010502

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractTwenty‐seven asymptomatic patients treated with hemodialysis longer than 8 years (mean 12.9 ± 3.1 years) underwent bone biopsy to determine the prevalence of aluminum‐associated bone disease. None had excess aluminum exposure from the dialysate. Ten patients (37%) had aluminum‐associated bone disease as defined by a bone formation rate (BFR) below normal in the presence of stainable bone aluminum that covered more than 25% of the trabecular surface. The predominant type of bone histology in this group was the aplastic lesion characterized by low bone turnover, a decreased number of osteoblasts, and lack of excess unmineralized osteoid. Osteoblastic osteoid was highly correlated with stainable surface bone aluminum (r= ‐ .82,p<.001). Among the dynamic bone parameters, the double‐tetracycline labeled surface was a more sensitive indicator of impaired bone function than was the bone apposition rate (BAR), since half of the patients with aluminum‐associated bone disease had a normal BAR. In all of the biopsies the extent of double‐labeled surfaces was inversely proportional to the amount of stainable aluminum on the bone surface (r= ‐ .71,p<.001), whereas stainable bone aluminum did not correlate with BAR. In seven of the patients with aluminum‐associated bone disease, amino‐terminal PTH levels were in the normal range while only one patient had a normal plasma mid‐region PTH. PTH correlated directly with osteoblastic osteoid, BFR, and double‐labeled surfaces. These results indicate that long‐term oral aluminum intake in hemodialysis patients results in a high prevalence of aluminum‐associated bone disease. The decrease in osteoblast number appears to be the major mechanism for the low bone formation. Whether aluminum adversely affects the osteoblast population directly or decreases osteoblast number indirectly via suppression of PTH

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010503

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractTo determine whether immobilization acts directly on bone by alteration of mechanical loading or systemically, studies of the effects of immobilization were carried out on histomorphometry of diaphyses of tibiae and on subcutaneous implants of demineralized allogenic bone matrix of rats. The right hind leg of growing rats was denervated by severing the tibial nerve. A sham operation on the right hind leg was performed in control animals. Bone formation at the endosteal and periosteal surfaces was significantly lower in tibiae from limbs with severed nerves as compared to tibiae from the intact limbs of nerve‐sectioned rats and from both limbs of sham‐operated control rats. Bone formation was decreased at both 3 and 7 weeks after immobilization. The decreased formation resulted in significant reductions in cross‐sectional area. At 3 weeks post denervation, the periosteal bone formation rate was lower in tibiae of intact limbs from denervated rats as compared to tibiae from intact limbs of sham‐operated animals. This finding was attributed to reduced physical activity of the denervated rats. In the implants, nerve section did not alter the amount of implant matrix resorbed, the amount of bone matrix synthesized, or the amount of calcium in the implant. These findings support the hypothesis that inhibition of bone formation at the tibial diaphysis in response to immobilization resulted from altered mechanical loading and not from the production of substances acting systemically. Whereas the mean medullary area of tibiae was not altered by nerve section, it was decreased in tibiae of all groups compared to the values of basal controls, indicating that bone formation was greater than bone resorption. The findings are interpreted to mean that, in the rat, reducing the mechanical loading of an extremity inhibits bone formation at the tibial diaphysis of the affected limb and does not influence bone resorption at th

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010504

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractProteolipids and complexed acidic phospholipids that causein vitrohydroxyapatite formation, similarly cause hydroxyapatite deposition in 10‐μ pore Millipore chambers when implanted in rabbit muscle pouches. The amount of mineral deposited during a 3‐week period, based on the calcium and phosphate contents of the chambers, was directly related to the dry weight of the lipid implanted in the chamber. Chambers containing total lipid extract from rabbit bone from which the complexed acidic phospholipids had been removed, acidic phospholipids from which the the proteolipids had been removed, and empty chambers did not accumulate any detectable mineral during the course of the study. Chambers implanted with synthetic hydroxyapatite served as controls for chemical analyses. The presence of hydroxyapatite in the chambers was established 3 weeks after implantation based on electron microscopic, compositional, and wide‐angle X‐ray diffraction analyses of the deposits. In the cell‐free chambers, lipid‐induced hydroxyapatite deposition, but not bone matrix formation occurred. This study demonstrates that proteolipids and complexed acidic phospholipids can cause hydroxyapatite mineral deposition in a physiologic environment. To date, these lipids are the only materials isolated from mineralizing tissues, other than reconstituted collagen, that have been shown capable of causingin vivomineralization in the abse

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010505

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractA subclass of highly serum‐dependent bone cells has been identified among the cells released early from calvaria following digestion in collagenase. Partial purification for these cells has been carried out based on the observation that they require serum for attachment to polystyrene culture flasks. This subclass of bone cells differs from adherent cells and late released osteoblasts, in that they express almost no cAMP response to PTH, require high levels of serum (10%) for initial growth and proliferation, and do not increase DNA synthesis in response to PTH. In common with adherent cells and late released osteoblasts, their proliferation is decreased by 1,25(OH)2D3at doses above 0.2 ng/ml and they respond to PGE2with increased DNA synthesis. These similarities suggest an ontogenic relationship with osteoblasts. Based on their differences, however, provisional identification of these cells as relatively undifferentiated mesenchymal cells is suggeste

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010506

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractThe solid mineral phases of calcium‐phosphate (Ca‐P) in the long bones from embryonic chicks between the ages of 9 and 13 days have been examined by high voltage (1.0 MV) electron microscopy and electron micro‐diffraction. The study was undertaken to identify the chemical and crystallographic nature of the inorganic mineral phase(s) prepared under conditions which significantly reduce artifacts of specimen preparation and microscopic examination of the tissues.Electron microdiffraction patterns of solid mineral phase particles in the osteoid matrices of the subperiosteal region of tibiae were principally those of poorly crystalline hydroxyapatite. In rare instances (less than 1% of the estimated volume of the mineral phase present in the zone of early mineralization), relatively large single crystals were observed within clusters of hydroxyapatite. From calculations of both interplanar spacings and measurements of angular displacement of diffraction reflections from single crystal microdiffraction patterns, two distinct phases other than hydroxyapatite were identified: brushite and β‐tricalcium phosphate. A third phase, resembling an apatite, remains unidentified. The results suggest that very small amounts of nonapatitic phases of Ca‐P exist in chicken bone tissue. No temporal relationship could be established between the nonapatitic and apatitic phases. There is at present no evidence from this study to support the concept that nonapatitic phases are precursors of a final apatitic pha

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010507

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractThe objective of this investigation was to examine the redox status of chondrocytes in normal and rachitic growth cartilages and to relate energy metabolism to cell maturation and the initiation of mineralization. The redox status was evaluated by chemical analysis and by microfluorimetric scanning of rapidly frozen, freeze‐fractured tibial growth cartilages. In the normal epiphysis, the redox pattern of both avian and lagomorph cartilages were very similar. Thus, in the proliferative tissue zone the NAD/NADH ratio was high; in the hypertrophic zone, the cells appeared to be reduced. The sharp border between the two zones suggested that the redox shift may be associated with development of hypoxia. Induction of rickets resulted in a fivefold decrease in the total concentration of pyridine nucleotides in the proliferating and hypertrophic zones. Furthermore, the NAD/NADH ratio was profoundly disturbed. In the mineralizing zone, there was an accumulation of reduced pyridine nucleotide. Healing, initiated by administration of vitamin D to the rachitic birds, caused a rapid increase in NAD and NADH in all zones of the growth cartilage. It was concluded that vitamin D deficiency leads to changes in the energy metabolism of growth cartilage and that these changes were related to the defective mineralization of the rachitic tissu

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010508

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

Abstract1,25‐dihydroxy vitamin D3produces pronounced shape changes in fetal rat calvaria and osteosarcoma‐derived (ROS 17/2.8) osteoblastic cells, characterized by retracting processes and cell rounding followed by aggregation of cells. The 1,25(OH)2D3effect on ROS 17/2.8 morphology was determined morphometrically on scanning electron micrographs. The hormone effect was found to be dose dependent between 10−12and 10−9M. The shape changes appeared 12 h after hormone (10−10M) addition and were present in 80% of the ROS 17/2.8 cells and in 50% of the calvaria cells at 72 h. Cycloheximide at 1 μM, inhibited the hormone‐dependent change in morphology. The 1,25(OH)2D3effects were partially mimicked by 10−8M25(OH)D3but not by 10−10M25(OH)D3or 10−11‐10−8M24,25(OH)2D3. 1,25‐dihydroxy vitamin D3also increased cell proliferation twofold at 14 days in serum‐free medium.1,25(OH)2D3treatment produced changes in microfilament organization, visualized with rhodamine‐conjugated phalloidin. Microfilaments were localized at the terminal attachment points and in the perinuclear region, and few if any, were seen in the retracting processes themselves. Estimation of cytoskeletal actin and myosin by gel electrophoresis of Triton X‐100 nonextractable proteins showed a 30% reduction in these proteins in the hormone‐treated cells. Microtubules visualized by indirect immunofluorescence showed no major changes in organization. Both colchicine and cytochalasin D altered the hormone‐induced shape change, suggesting that both microfilaments and microtubules were required for this process.Thus, 1,25(OH)2D3had pronounced effects on cell shape in osteoblastic cells, probably viade novoprotein synthesis. These changes lead to rearrangement of the cytoskel

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010509

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractMammary glands are target tissues for 1,25‐dihydroxyvitamin D3(1,25(OH)2D3). We have examined a mouse mammary tumor cell line (GR) for receptors of 1,25(OH)2D3and have examined alterations in the growth and morphology of these cells in response to 1,25(OH)2D3. GR cells contain a high affinity (Kd ∼ 10−11), lowcapacity receptor with a high specificity for 1,25(OH)2D3. The 1,25(OH)2D3receptor in GR cells has a sedimentation coefficient of 3.5 and elutes from DEAE cellulose columns with ∼ 0.15MKCI. These properties of the receptor are similar to those reported for other 1,25(OH)2D3receptors. 1,25(OH)2D3is internalized by GR cellsin situand specifically bound 1,25(OH)2D3is found predominantly, if not entirely, in the nucleus as determined by cell fractionation and autoradiographic techniques. The incubation of GR cells in culture for 7 days with 1,25(OH)2D, markedly alters cell growth. Cell growth is retarded in a dose‐dependent manner; physiologic concentrations (10−10M) of l,25(OH)2D3retard cell growth by approximately 50%. In addition, GR cells incubated with 10−9to 10−8M1,25(OH)2D3undergo marked morphological changes. The incubation of GR cells with other vitamin D metabolites such as 25‐hydroxyvitamin D3(25(OH)D3) at a concentration of 10−9Mdoes not significantly alter cell growth or morphology. The presence of high affinity receptors for 1,25(OH)2D3, the specific internalization of 1,25(OH)2D3predominantly into the nuclei, and the significant effects of physiological concentrations of 1,25(OH)2D3on cell growth suggest a direct, specific, nuclear effect of 1,25(OH)2D3on GR cells. The mouse mammary tumor model might be useful in examining the effect of 1,25(OH)2D

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010510

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractIt is likely that immune cells in the bone marrow produce factors which are involved in the local control of bone remodeling. Immune cell products such as interleukin‐1 and the tumor necrosis factors are potent stimulators of bone resorptionin vitro. In this paper, we have studied the effects of recombinant murine interferonγ on bone resorption stimulated by these agents and the systemic calcium‐regulating hormones 1,25(OH)2vitamin D3and parathyroid hormone. We found that interferon‐7 completely abolished bone resorption stimulated by the cytokines interleukin‐1, tumor necrosis factor α and tumor necrosis factor ß. In contrast, parathyroid hormone‐ and 1,25(OH)2vitamin D3‐stimulated bone resorption were not significantly affected by the addition of interferon‐γ under the same conditions. Parathyroid hormone‐stimulated bone resorption was inhibited slightly when larger concentrations of interferon‐γ were used for more prolonged periods. The inhibitory effects on cytokine‐stimulated bone resorption occurred at interferon concentrations of 100 U/ml (half‐maximal) to 300 U/ml (complete inhibition). This relatively selective inhibition of cytokine‐stimulated bone resorption by an immune cell product may have physiological significance in the local control of trabecular bon

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010511

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY