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Abstract Methoxsalen (MTS) is a natural bioactive compound found in a variety of plants that has many known biofunctions; however, its effects on osteoporosis and related mechanisms are not clear. This study examined whether MTS e...
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Abstract Methoxsalen (MTS) is a natural bioactive compound found in a variety of plants that has many known biofunctions; however, its effects on osteoporosis and related mechanisms are not clear. This study examined whether MTS exhibited preventive effects against postmenopausal osteoporosis. Female C3H/HeN mice were divided into four groups: Sham, ovariectomy (OVX), OVX with MTS (0.02% in diet), and OVX with estradiol (0.03?μg/day, s.c). After 6 weeks, MTS supplementation significantly increased femur bone mineral density and bone surface along with bone surface/total volume. MTS significantly elevated the levels of serum formation markers (estradiol, osteocalcin and bone-alkaline phosphatase) such as estradiol in OVX mice. Tartrate resistant acid phosphatase staining revealed that MTS suppressed osteoclast numbers and formation in femur tissues compared with the OVX group. Supplementation of MTS slightly up-regulated osteoblastogenesis-related genes ( Runx-2 , osterix , osteocalcin , and Alp ) expression, whereas it significantly down-regulated inflammatory genes ( Nfκb and Il6 ) expression in femur tissue compared with the OVX group. These results indicate that MTS supplementation effectively prevented OVX-induced osteoporosis via enhancement of bone formation and suppression of inflammatory response in OVX mice. Our study provides valid scientific information regarding the development and application of MTS as a food ingredient, a food supplement or an alternative agent for preventing postmenopausal osteoporosis. Graphical abstract Display Omitted Highlights ? Methoxsalen improves bone mineral density in ovariectomized mice. ? Methoxsalen increased serum bone-ALP, osteocalcin and estradiol levels. ? Methoxsalen down-regulated Il6 and Nfκb gene expression in femur.
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Introduction: Glucocorticoid-induced osteoporosis (GIOP) is the most common type of secondary osteoporosis. Patient selection and the treatment choice remain to be controversial. None of the proposed management guidelines are wide...
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Introduction: Glucocorticoid-induced osteoporosis (GIOP) is the most common type of secondary osteoporosis. Patient selection and the treatment choice remain to be controversial. None of the proposed management guidelines are widely accepted. We evaluate the available clinical data, the efficacy of current medication and we propose an overall algorithm for managing GIOP.
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Glucocorticoid therapy is the number one cause of secondary osteoporosis particularly effecting young individuals. Possessing an increased risk for fractures, glucocorticoid-induced osteoporosis might interfere with patients' well...
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Glucocorticoid therapy is the number one cause of secondary osteoporosis particularly effecting young individuals. Possessing an increased risk for fractures, glucocorticoid-induced osteoporosis might interfere with patients' well-being and quality of life. Therefore, proper treatment of bone loss and prevention from fractures are of great importance. There are a limited number of therapeutic and preventative options for glucocorticoid-induced osteoporosis. Denosumab, with its high anti-resorptive potential, has been studied several times among patients on glucocorticoid therapy. However, a comprehensive look analysing the current data is lacking. Thus, the objective of the current article is to evaluate the current evidence on the efficacy, as well as the safety profile of denosumab in glucocorticoid-induced osteoporosis. Pubmed/MEDLINE, Scopus and Web of Science databases were searched for the terms denosumab, glucocorticoid-induced osteoporosis, steroid-induced osteoporosis, glucocorticoids and osteoporosis. Relevant data regarding the efficacy and safety of denosumab among patients with glucocorticoid-induced osteoporosis was analysed. Denosumab contributes to increased bone mineral density and decreased bone-turnover marker levels among glucocorticoid users. It is an effective therapeutic option with a favourable safety profile in glucocorticoid-induced osteoporosis.
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Objective: To review the literature on the concomitant use of bisphosphonates and medications that can influence bone metabolism and potentially attenuate bisphosphonate antifracture efficacy. Data Sources: MEDLINE and CINAHL were...
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Objective: To review the literature on the concomitant use of bisphosphonates and medications that can influence bone metabolism and potentially attenuate bisphosphonate antifracture efficacy. Data Sources: MEDLINE and CINAHL were searched for articles published in English through December 2014 using the following terms: bisphosphonates, bone density conservation agents, acid-suppressive therapy, levothyroxine, thiazolidinediones (TZDs), selective serotonin reuptake inhibitors (SSRIs), bone fractures. Study Selection and Data Extraction: Studies were included if they reported results of concomitant use of any listed medications with bisphosphonates and risk of fractures and focused on women. Articles that focused generally on the use of one of the listed medications and fractures without explicitly examining the potential antifracture efficacy or attenuation of bisphosphonates were excluded. Data Synthesis: A total of 6 relevant studies were identified. Four epidemiological studies reported a statistically significant dose-dependent increase in the risk of fractures when bisphosphonates and acid-suppressive drugs were used together. One post hoc analysis of clinical trial data suggested no attenuation of the antifracture effects of bisphosphonates when used concomitantly with acid-suppressive therapy. One study involving bisphosphonates and SSRIs noted a statistically significant association between fracture risk and SSRI use. No study examining TZDs or levothyroxine with bisphosphonates was identified. Conclusions: Existing research suggests potential attenuation of bisphosphonate antifracture efficacy among patients taking acid-suppressive medications. Based on their pharmacological actions, TZDs, SSRIs, and levothyroxine have similar implications. The paucity of evidence in the literature associating the attenuation of bisphosphonate antifracture efficacy when combined with other medications suggests that further investigation is needed.
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Fourier transform infrared spectroscopy is utilized to examine the effects of increased calcium, vitamin D, and combined calcium-vitamin D supplementation on osteoporotic rabbit bones with induced inflammation. The study includes ...
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Fourier transform infrared spectroscopy is utilized to examine the effects of increased calcium, vitamin D, and combined calcium-vitamin D supplementation on osteoporotic rabbit bones with induced inflammation. The study includes different bone sites (femur, tibia, humerus, vertebral rib) in an effort to explore possible differences among the sites. We evaluate the following parameters: mineral-to-matrix ratio, carbonate content, and non-apatitic species (labile acid phosphate and labile carbonate) contribution to bone mineral. Results show that a relatively high dose of calcium or calcium with vitamin D supplementation increases the bone mineralization index significantly. On the other hand, vitamin D alone is not as effective in promoting mineralization even with high intake. Mature B-type apatite was detected for the group with calcium supplementation similar to that of aged bone. High vitamin D intake led to increased labile species concentration revealing bone formation. This is directly associated with the suppression of pro-inflammatory cytokines linked to induced inflammation. The latter is known to adversely alter bone metabolism, contributing to the aetiopathogenesis of osteoporosis. Thus, a high intake of vitamin D under inflammation-induced osteoporosis does not promote mineralization but suppresses bone resorption and restores metabolic balance.
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Compound Luolong Jiangu Capsule (CLJC) is a classic traditional Chinese medicine prescription for patients with osteoporosis. This study explored the potential mechanisms of the protective effects of CLJC on glucocorticoid-induced...
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Compound Luolong Jiangu Capsule (CLJC) is a classic traditional Chinese medicine prescription for patients with osteoporosis. This study explored the potential mechanisms of the protective effects of CLJC on glucocorticoid-induced osteoporosis in rats. After oral administration of CLJC for 8 weeks, osteoporosis was induced in the rats by dexamethasone treatment for twice a week. The expression levels of HP, ALP, TRAP, IL-6, TNF-alpha and IL-1 beta in bone samples as well as the concentrations of MDA and SOD in serum samples were determined using ELISA reagent kits. Besides, Western blotting was used to assess the expression levels of proteins involved in NF-kappa B/Nrf-2/HO-1 pathway. Our results showed that oral CLJC noticeably reduced the pathological damage of glucocorticoid-induced osteoporosis, decreased oxidative stress and suppressed the expression of inflammatory cytokines in bone and serum samples. It was also observed that oral administration of CLJC significantly suppressed the protein expression of Nrf-2, HO-1, p65/p-p65 and IkBa/p-IkBa. In conclusion, CLJC can play a protective role in glucocorticoid-induced osteoporosis by enhancing the antioxidant system and reducing inflammatory responses.
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Osteoporosis and fragility fractures are a major public health issue.Secondary osteoporosis is characterised by the presence of an underlying disease, deficiency, or use of a drug.Conditions that increase speculation for secondary...
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Osteoporosis and fragility fractures are a major public health issue.Secondary osteoporosis is characterised by the presence of an underlying disease, deficiency, or use of a drug.Conditions that increase speculation for secondary osteoporosis include fragility fractures amongst the younger men or premenopausal women, markedly decreased Bone Mineral Density (BMD) values, and fractures despite conforming to anti-osteoporotic therapy.Since the emphasis is on the treatment of the primary disorder, a diagnosis of osteoporosis and thus the opportunity of preventive intervention can be missed.With this review, the authors objective is to emphasise the importance of secondary osteoporosis, discuss the causes and their mechanism and summarise treatment options.
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Objective:Osteoporosis and hypertension are age-related chronic diseases with increased morbidity rates among postmenopausal women. Clinical epidemiological investigations have demonstrated that hypertensive patients treated with ...
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Objective:Osteoporosis and hypertension are age-related chronic diseases with increased morbidity rates among postmenopausal women. Clinical epidemiological investigations have demonstrated that hypertensive patients treated with 1-selective -blockers have a higher bone mineral density (BMD) and lower fracture risk. Nevertheless, no fundamental studies have examined the relationships between 1-selective -blockers and these effects. The present study explored the effects and mechanisms of metoprolol in the in vitro treatment of osteoblasts and the in vivo treatment of ovariectomy-induced osteoporosis in rats.Methods:Primary osteoblasts were obtained by digestion of the cranial bones of 24-hour-old Sprague-Dawley rats. After metoprolol treatment, cell proliferation and differentiation capacities were assessed at the corresponding time points. In addition, 3-month-old female Sprague-Dawley rats (200-220g) were divided into a sham-operated group (n=8) and three ovariectomized (OVX) (bilateral removal of ovaries) groups as follows: vehicle (OVX; n=8), low-dose metoprolol (L-M, oral, 120mg/kg/d; n=8), and high-dose metoprolol (H-M, oral, 240mg/kg/d; n=8). After 12 weeks of metoprolol treatment, BMD, microarchitecture, and biomechanical properties were evaluated.Results:The results indicated that the treatments with 0.01 to 0.1M metoprolol increased osteoblast proliferation, alkaline phosphatase activity, and calcium mineralization, and promoted the expression of osteogenic genes. The in vivo study indicated that administration of metoprolol to OVX rats resulted in maintenance of the BMDs of the L4 vertebrae. Moreover, amelioration of trabecular microarchitecture deterioration and preservation of bone biomechanical properties were detected in the trabecular bones of the OVX rats.Conclusions:Our findings indicate that metoprolol prevents estrogen deficiency-induced bone loss by increasing the number and enhancing the biological functions of osteoblasts, implying its potential use as an alternative treatment for postmenopausal osteoporosis in hypertensive patients.
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