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  • 1
    Electronic Resource
    Electronic Resource
    Effects of long-term daily administration of prostaglandin-E2 on maintaining elevated proximal tibial metaphyseal cancellous bone mass in male rats (1992)
    Springer
    Calcified tissue international 50 (1992), S. 245-252 
    Details
    ISSN: 1432-0827
    Keywords: Prostaglandin E2 ; Long-term treatment ; Cancellous bone ; Bone formation ; Bone resorption ; Bone turnover ; Remodeling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effects of long-term prostaglandin E2 (PGE2) on cancellous bone in proximal tibial metaphysis were studied in 7-month-old male Sprague-Dawley rats given daily subcutaneous injections of 0, 1, 3, and 6 mg PGE2/kg/day and sacrificed after 60, 120, and 180 days. Histomorphometric analyses were performed on double fluorescent-labeled undecalcified bone specimens. After 60 days of treatment, PGE2 produced diffusely labeled trabecular bone area, increased trabecular bone area, eroded and labeled trabecular perimeter, mineral apposition rate, and bone formation rate at all dose levels when compared with age-matched controls. In rats given PGE2 for longer time periods (120 and 180 days), trabecular bone area, diffusely labeled trabecular bone area, labeled perimeter, mineral apposition, and bone formation rates were sustained at the elevated levels achieved earlier at 60-day treatment. The eroded perimeter continued to increase until 120 days, then plateau. The observation that continuous systemic PGE2 administration to adult male rats elevated metaphyseal cancellous bone mass to 3.5-fold of the control level within 60 days and maintained it for another 120 days indicates that the powerful skeletal anabolic effects of PGE2 can be sustained with continuous administration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296289
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  • 2
    Electronic Resource
    Electronic Resource
    Dkk2 has a role in terminal osteoblast differentiation and mineralized matrix formation (2005)
    [s.l.] : Nature Publishing Group
    Nature genetics 37 (2005), S. 945-952 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Human and mouse genetic and in vitro evidence has shown that canonical Wnt signaling promotes bone formation, but we found that mice lacking the canonical Wnt antagonist Dickkopf2 (Dkk2) were osteopenic. We reaffirmed the finding that canonical Wnt signaling stimulates osteogenesis, including the ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng1614
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  • 3
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    Dkk2 has a role in terminal osteoblast differentiation and mineralized matrix formation (2005)
    Springer Nature
    Details
    Publication Date: 2005-07-31
    Print ISSN: 1061-4036
    Electronic ISSN: 1546-1718
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 4
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    A bispecific antibody targeting sclerostin and DKK-1 promotes bone mass accrual and fracture repair (2016)
    Springer Nature
    Details
    Publication Date: 2016-05-27
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 5
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    Estrogen receptor β selective ligands: Discovery and SAR of novel heterocyclic ligands (2005)
    Elsevier
    Details
    Publication Date: 2005-12-01
    Print ISSN: 0960-894X
    Electronic ISSN: 1464-3405
    Topics: Chemistry and Pharmacology , Medicine
    Published by Elsevier
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  • 6
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    Restoring and Maintaining Bone in Osteopenic Female Rat Skeleton (1992)
    In:  CASI
    Details
    Publication Date: 2019-06-28
    Description: This experiment contains the crucial data for the lose, restore, and maintain (LRM) concept, a practical approach for reversing existing osteoporosis. The LRM concept uses anabolic agents to restore bone mass and architecture (+ phase) and then switches to an agent with the established ability to maintain bone mass, to keep the new bone (+/- phase). The purpose of this study was to learn whether switching to an agent known chiefly for its ability to maintain existing bone mass preserves new bone induced by PGE2, in osteopenic,estrogen-depleted rats. The current study had three phases, the bone loss (-), restore (+), and maintain (+/-) phases. We ovariectomized (OX) or sham ovariectomized (sham-OX) 5.5 month-old female rats (- phase). The OX rats were treated 5 months postovariectomy with 1-6 mg PGE2, per kg/day for 75 days to restore lost cancellous bone mass (+ phase), and then PGE2, treatment was stopped and treatment began with 1 or 5 micro-g/kg of risedronate, a bisphosphonate, twice a week for 60 days (+/- phase). During the loss (-) phase, the cancellous bone volume of the proximal tibial metaphysis in the OX rat fell to 19% of initial and 30% of age-matched control levels. During the restore (+) phase, the cancellous bone volume in OX rats doubled. When PGE2 treatment was stopped, however, and no special maintenance efforts were made during the maintain (+/-) phase, the PGE2-induced cancellous bone disappeared. In contrast, the PGE2-induced cancellous bone persisted when the PGE2 treatment was followed by either a 1 or 5 micro-g treatment of risedronate per kg given twice a week for 60 days during the maintain (+/-) phase. The tibial shaft demonstrated very little cortical bone loss during the loss (-) phase in OX rats. The tibial shaft cortical bone fell some 8%. During the restore (+) phase, new cortical bone in OX rats increased by 22%. When PGE2 treatment was stopped and nothing was given during the maintain (+/-) phase, however, all but the PGE2-induced subperiosteal bone disappeared. In contrast, when PGE2 treatment was stopped and 1 micro-g risedronate per kg twice a week for 60 days was administered during the maintenance (+/-) phase, the PGE2-induced subperiosteal bone and some of the subendocortical bone and marrow trabeculae persisted. When 5 micro-g risedronate per kg was given twice a week, all the PGE2-induced bone persisted. The study shows that most of the new cancellous and cortical bone induced by PGE2, can be maintained for at least 60 days after discontinuing PGE2 by administering enough of the resorption inhibitor, risedronate. The lower dose of risedronate was not adequate to save most of the PGE2-induced endocortical bone.
    Keywords: Life Sciences (General)
    Type: NASA-CR-202472 , NAS 1.26:202472 , Journal of Bone and Mineral Research; 7; 9; 1093 - 1104
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  • 7
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    Loss of Prostaglandin E2-induced Extra Cortical Bone after its Withdrawal in Rats (1992)
    In:  CASI
    Details
    Publication Date: 2019-07-13
    Description: The object of this study was to determine the fate of PGE2-induced new cortical bone mass after withdrawal of PGE2 administration. Seven-month-old male Sprague-Dawley rats were given subcutaneous injections of 1, 3 and 6 mg PGE2/kg/day for 60 days and then withdrawn for 60 and 120 days (on/off treatment). Histomorphometric analyses were performed on double-fluorescent-labeled undecalcified tibial shaft sections (proximal to the tibiofibular junction). In a previous report we showed that after 60, 120 and 180 days of daily PGE2 (on)treatment, a new steady state was achieved marked by increased total bone area (+ 16%, +25% and + 34% with 1, 3 and 6 mg PGE2/kg/day) when compared to age-matched controls. The continuous PGE2 treatment stimulated periosteal and endocortical lamellar bone formation, activated endocortical woven trabecular bone formation and intracortical bone resorption. These responses increased cortical bone mass since the bone formation exceeded bone resorption. The current study showed that after withdrawal of PGE2 for 60 and 120 days, the extra endocortical bone, which was induced by the first 60-days treatment, was resorbed, but the new subperiosteal bone persisted resulting in a tibial shaft with larger cross sectional and marrow areas. Despite that, there was still the same amount of bone mass in these shafts as in age-related controls. A new steady state was achieved after 60 days of withdrawal, in which the bone mass and bone formation activity approximated that of age-related controls. It was concluded that maintaining the extra PGE2-induced cortical bone mass depends on continuous daily administration of PGE2.
    Keywords: Life Sciences (General)
    Type: NASA-CR-204207 , NAS 1.26:204207 , BAM-00432 , Bone and Mineral (ISSN 0169-6009); 17; 31-47
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  • 8
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    Effects of Long-Term Daily Administration of Prostaglandin-E2 on Maintaining Elevated Proximal Tibial Metaphyseal Cancellous Bone Mass in Male Rats (1992)
    In:  CASI
    Details
    Publication Date: 2019-07-13
    Description: The effects of long-term prostaglandin E(sub 2) (PGE(sub 2)) on cancellous bone in proximal tibial metaphysis were studied in 7 month old male Sprague-Dawley rats given daily subcutaneous injections of 0, 1, 3, and 6 mg PGE(sub 2)/kg/day and sacrificed after 60, 120, and 180 days. Histomorphometric analyses were performed on double fluorescent-labeled undecalcified bone specimens. After 60 days of treatment, PGE(sub 2) produced diffusely labeled trabecular bone area, increased trabecular bone area, eroded and labeled trabecular perimeter, mineral apposition rate, and bone formation rate at all dose levels when compared with age-matched controls. In rats given PGE(sub 2) for longer time periods (120 and 180 days), trabecular bone area, diffusely labeled trabecular bone area, labeled perimeter, mineral apposition, and bone formation rates were sustained at the elevated levels achieved earlier at 60-day treatment. The eroded perimeter continued to increase until 120 days, then plateau. The observation that continuous systemic PGE(sub 2) administration to adult male rats elevated metaphyseal cancellous bone mass to 3.5-fold of the control level within 60 days and maintained it for another 120 days indicates that the powerful skeletal anabolic effects of PGE2 can be sustained with continuous administration .
    Keywords: Life Sciences (General)
    Type: NASA-CR-202469 , NAS 1.26:202469 , Calcified Tissue International; 50; 245-252
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  • 9
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    Effects of Daily Administration of Prostaglandin E2 and Its Withdrawal on the Lumbar Vertebral Bodies in Male Rats (1992)
    In:  CASI
    Details
    Publication Date: 2019-07-13
    Description: The effects of daily prostaglandin E2 (PGE2) treatment (on) and PGE2 treatment followed by withdrawal (on-off) on cancellous bone in lumbar vertebral bodies were studied in 7 month-old male Sprague-Dawley rats. The first groups of rats were given daily subcutaneous injections of 0, 1, 3, and 6 mg PGE2/kg/d for 60,120, and 180 days, and the second group of rats were given PGE2 for 60 days followed by withdrawal for 60 and 120 days. Histomorphometric analyses were performed on double-fluorescent labeled undecalcified sections of fourth lumbar vertebral bodies. Systemic PGE2 treatment elevated cancerous bone mass of lumbar vertebral bodies 26-60%, above control levels within 60 days and continued treatment maintained it for another 120 days, but the excess bone was lost after the treatment was witndrawn. PGE2 treatment for 60 days increased trabecular bone area, trabecular width, and bone formation parameters, and shortened remodeling periods in a dose-response manner. These changes were sustained at the levels achieved by 60-day treatment in the rats treated for 120 and 180 days. The eroded perimeter increased at day 60 and further at day 120 and then plateaued. In the on-off treated rats, the cancenous bone area, bone formation, and resorption parameters returned to near age-related controls by 60 days after withdrawal and were maintained there after 120 days of withdrawal. Therefore, we conclude that the continuous treatment is needed in order to maintain the PGE2-induced bone gain. When these findings were compared to those previously reported for the proximal tibial metaphyses, we found that the proximal tibial spongiosa was much more responsive to PGE2 treatment than the fourth lumbar vertebral body.
    Keywords: Life Sciences (General)
    Type: NASA-CR-202470 , NAS 1.26:202470 , The Anatomical Record; 234; 172-182
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  • 10
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    Prostaglandin E2 Increased Rat Cortical Bone Mass When Administered Immediately Following Ovariectomy (1993)
    In:  CASI
    Details
    Publication Date: 2019-07-13
    Description: To investigate the effects of ovariectomy and the simultaneous administration of prostaglandin E2 (PGE2) on rat tibial shaft cortical bone histomorphometry, thirty-five 3 month-old female Sprague-Dawley rats were either ovariectomized (OVX), or sham ovariectomy (sham-OVX). The OVX rats were divided into three groups and treated with 0, 1 and 6 mg PGE2/kg/day for 90 days. The double fluorescent labeled undecalcified tibial shaft cross sections (proximal to the tibiofibular junction) of all the subjects were used for histomorphometry analysis. No differences in cross-sectional area and cortical bone area were found between sham-OVX and OVX controls, but OVX increased marrow area, intracortical porosity area and endocortical eroded perimeter. Periosteal and endocortical bone formation rates decreased with aging yet OVX prevented these changes. These OVX-induced increases in marrow area and endocortical eroded perimeter were prevented by 1 mg PGE2/kg/day treatment and added bone to periosteal and endocortical surfaces and to the marrow cavity. At the 6 mg/kg/day dose level, PGE2-treated OVX rats increased total tissue area, cortical bone area, marrow trabmular bone area, minimal cortical width and intracortical porosity area, and decreased marrow area compared to basal, sham-OVX and OVX controls. In addition, periosteal bone formation was elevated in the 6 mg PGE2/kg/day-treated OVX rats compared to OVX controls. Endocortical eroded perimeter increased from basal and sham-OVX control levels, but decreased from OVX control levels in the 6 mg PGE2/kg/day-treated OVX rats. Our study confirmed that ovariectomy does not cause osteopenia in tibial shaft cortical bone in rats, but it does stimulate endocortical bone resorption and enlarges marrow area. The new findings from the present study demonstrate that PGE2 prevents the OVX-induced increases in endocortical bone resorption and marrow area and adds additional bone to periosteal and endocortical surfaces and to marrow cavity to increase total bone mass in the tibial shaft of OVX rats when given immediately following ovafiectomy.
    Keywords: Life Sciences (General)
    Type: NASA-CR-202475 , NAS 1.26:202475 , Bone and Mineral (ISSN 0169-6009); 21; 189-201
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