The osteoblast-derived paracrine factor osteoprotegerin (OPG) is considered to play a key role in inhibition of osteoclast formation and activity. Recently, raloxifene, a nonsteroidal benzothiophene, was found to exert anti-resorptive effects via modulating OPG expression in osteoblasts. To explore whether raloxifene regulates bone metabolism via an OPG-dependant pathway in vivo, we investigated the effects of raloxifene on bone loss in Opg-deficient mice. The results show that bone mineral density and bone strength are increased in mice deficient for Opg after treatment with raloxifene for 30 days. Histomorphometric analysis shows that raloxifene can increase bone trabecular area and decrease the number of osteoclasts in Opg (-/-) mice. Moreover, raloxifene reduces Rankl transcription and serum level of Rankl, which is dramatically increased in Opg knockout mice. These results suggest that raloxifene-induced inhibition of bone resorption may be independent of Opg pathway in mice.
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Raloxifene, a selective estrogen receptor modulator, is estrogen-like in the skeleton and cardiovascular system and antiestrogenic in reproductive tissues. In contrast to estrogens, raloxifene is not indicated for the treatment of hot flashes. This study was designed to examine the characteristics of hot flashes among healthy postmenopausal women participating in osteoporosis prevention trials who were receiving raloxifene or placebo.
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Liposomes were prepared by thin film hydration method using 1:1 molar ratio of DSPC:Cholesterol and characterized for vesicle size, zeta potential, %entrapment efficiency, loading, drug release and transmission electron microscopy. Radiolabeling of RLH was performed with reduced technetium-99m ((99m)Tc). Binding affinity of (99m)Tc-labeled complexes was assessed by diethylene triamine penta acetic acid (DTPA) challenge test. Biodistribution study was done in New Zealand white female rabbits by administering the formulation intravaginally.
Limitations include the lack of a control group, the possibility of the changes being due to the natural disease course, and potential selection bias.
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Only bisphosphonates are cost-effective for fracture prevention in osteoporotic women aged 65 or older and this economic advantage is also maintained in subsets who have a lower relative risk of future fracture.
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Little information is available on the comparative effectiveness of osteoporosis pharmacotherapies.
Two types of mammary tumors were studied: tumors transplanted in BALB/c mice that are medroxyprogesterone acetate (MPA)-dependent for growth, and tumors induced in Sprague-Dawley rats by intraperitoneal injection of N-nitroso-N-methylurea (NMU). Tumors from mice treated with MPA, E(2), Tam or Ral and NMU-treated rats were analyzed and compared to that of control.
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The percentage of Ki-67-stained nuclei per 500 cells in the mammary epithelium was 42.33 ± 6.18 and 15.51 ± 3.71 [mean ± standard error of the mean (SEM)] in the control and experimental groups, respectively (p < 0.001).
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A review of all published reports was facilitated by the use of Medline computer searches.
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Tamoxifen had an oestrogen receptor dependent, direct, inhibitory effect on human osteoclast differentiation and bone resorption, whereas ospemifene and raloxifene required osteoblastic cells to achieve a similar inhibition. The effects of ospemifene and raloxifene were mediated by oestrogen receptors by a mechanism involving paracrine induction of osteoprotegerin in cultures with osteoblast derived osteosarcoma cells.
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A set of now-completed, randomised clinical trials form the basis of our clinical understanding of the effects of raloxifen on the bones and are discussed in the paper.
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This study examined patients' risk profiles and adherence to treatment in relation to the effect of risedronate and raloxifene on hip fracture incidence. Administrative billing data were used to follow two cohorts of women aged 65 and older after starting therapy with either risedronate (n = 86,735) or raloxifene (n = 37,726). The fracture risk profile was described using a 6-month history period before starting therapy. Effectiveness of each therapy was evaluated by comparing the incidence of hip fractures during the first 3 months with the subsequent 12 months among women adherent (medication possession ratio >80%) compared with those non-adherent to treatment. At the start of therapy, the raloxifene cohort was younger than the risedronate cohort (median age 73 vs. 76 years) and had fewer prior fractures (p < 0.01 for both). In the first 3 months of therapy, hip fracture incidence was lower in the raloxifene group (0.51 per 100 person-years) compared with the risedronate group (0.94 per 100 person-years). In the subsequent 12 months, the incidence of hip fractures decreased among patients adherent to the risedronate regimen [relative risk (RR) 0.70, 95% CI 0.59-0.84, p < 0.01] and did not change significantly among patients adherent to the raloxifene regimen (RR 1.02, 95% CI 0.73-1.44). In poorly adherent patients, neither drug decreased hip fracture risk. Risedronate treatment in adherent patients rapidly decreased the risk of hip fractures, whereas raloxifene treatment did not.
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Postmenopausal hormone therapy (HT) is associated with an increased risk for arterial and venous thrombosis.
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Raloxifene is a selective oestrogen receptor modulator with effects on bone and breast cancer and cardiovascular disease risk. The aim of this study was to examine the influence of raloxifene treatment on surrogate markers of atherosclerosis and the correlation of these markers with raloxifene serum concentrations.
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Most domains in the Osteoporosis Assessment Questionnaire 2.0 demonstrated robust psychometric properties; however, several domains not showing these criteria may need to be reassessed and removed for a potentially shorter and validated version of the Osteoporosis Assessment Questionnaire.
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The treatment that is proposed in this study can constitute a temporary alternative during the period of transition from HT to raloxifene.