scholarly journals Glucocorticoid-induced osteoporosis

2006 ◽  
Vol 50 (4) ◽  
pp. 793-801 ◽  
Author(s):  
Luiz Henrique de Gregório ◽  
Paulo G. Sampaio Lacativa ◽  
Ana Cláudia C. Melazzi ◽  
Luis Augusto Tavares Russo
Keyword(s):  
Vitamin D ◽  
Bone Loss ◽  
Bone Formation ◽  
Preventive Measures ◽  
Prevent Bone Loss ◽  
Antiresorptive Agents ◽  
Increased Risk ◽  
Prevention And Treatment ◽  
Small Doses ◽  
Risk Patients

Glucocorticoid-induced osteoporosis is the most frequent cause of secondary osteoporosis. Glucocorticoids cause a rapid bone loss in the first few months of use, but the most important effect of the drug is suppression of bone formation. The administration of oral glucocorticoid is associated with an increased risk of fractures at the spine and hip. The risk is related to the dose, but even small doses can increase the risk. Patients on glucocorticoid therapy lose more trabecular than cortical bone and the fractures are more frequent at the spine than at the hip. Calcium, vitamin D and activated forms of vitamin D can prevent bone loss and antiresorptive agents are effective for prevention and treatment of bone loss and to decrease fracture risk. Despite the known effects of glucocorticoids on bone, only a few patients are advised to take preventive measures and treat glucocorticoid-induced osteoporosis.

scholarly journals Importance of calcium, vitamin D and vitamin K for osteoporosis prevention and treatment

2008 ◽  
Vol 67 (2) ◽  
pp. 163-176 ◽  
Author(s):  
Susan A. Lanham-New
Keyword(s):  
Vitamin D ◽  
Bone Loss ◽  
Vitamin K ◽  
Hypovitaminosis D ◽  
Osteoporosis Prevention ◽  
Mineral Density ◽  
Increased Risk ◽  
Post Menopause ◽  
Exogenous Factors ◽  
The Uk

Throughout the life cycle the skeleton requires optimum development and maintenance of its integrity to prevent fracture. Bones break because the loads placed on them exceed the ability of the bone to absorb the energy involved. It is now estimated that one in three women and one in twelve men aged >55 years will suffer from osteoporosis in their lifetime and at a cost in the UK of >£1·7×109 per year. The pathogenesis of osteoporosis is multifactorial. Both the development of peak bone mass and the rate of bone loss are determined by key endogenous and exogenous factors. Ca supplements appear to be effective in reducing bone loss in women late post menopause (>5 years post menopause), particularly in those with low habitual Ca intake (<400 mg/d). In women early post menopause (<5 years post menopause) who are not vitamin D deficient, Ca supplementation has little effect on bone mineral density. However, supplementation with vitamin D and Ca has been shown to reduce fracture rates in the institutionalised elderly, but there remains controversy as to whether supplementation is effective in reducing fracture in free-living populations. Re-defining vitamin D requirements in the UK is needed since there is evidence of extensive hypovitaminosis D in the UK. Low vitamin D status is associated with an increased risk of falling and a variety of other health outcomes and is an area that requires urgent attention. The role of other micronutrients on bone remains to be fully defined, although there are promising data in the literature for a clear link between vitamin K nutrition and skeletal integrity, including fracture reduction.

scholarly journals Vitamin D Supplementation in Elderly Black Women Does Not Prevent Bone Loss: A Randomized Controlled Trial

2018 ◽  
Vol 33 (11) ◽  
pp. 1916-1922 ◽  
Author(s):  
John Aloia ◽  
Melissa Fazzari ◽  
Shahidul Islam ◽  
Mageda Mikhail ◽  
Albert Shieh ◽  
...  
Keyword(s):  
Vitamin D ◽  
Randomized Controlled Trial ◽  
Black Women ◽  
Bone Loss ◽  
Controlled Trial ◽  
Vitamin D Supplementation ◽  
Prevent Bone Loss ◽  
Randomized Controlled

scholarly journals 3579 The role of CypD/mPTP during osteogenic differentiation - a potential target to prevent bone loss

2019 ◽  
Vol 3 (s1) ◽  
pp. 24-24
Author(s):  
Rubens Sautchuk ◽  
Brianna H. Shares ◽  
Roman A. Eliseev
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Mitochondrial Function ◽  
Ectopic Bone Formation ◽  
Regulatory Mechanisms ◽  
Mrna Levels ◽  
Prevent Bone Loss ◽  
Ectopic Bone

OBJECTIVES/SPECIFIC AIMS: The study aims to further investigate how cyclophilin D (CypD), the key mPTP opening regulator, affects BMSCs fate and to determine potential regulatory mechanisms involved in CypD regulation during osteogenesis. METHODS/STUDY POPULATION: We evaluated CypD mRNA expression in mouse BMSCs and in osteogenic-like (OL) cells during the course of OB differentiation. CypD protein level was also probed. Moreover, BMSCs had their mPTP activity recorded during osteoinduction. We further analyzed the effect of CypD genetic deletion on osteogenesis in vitro and in vivo. For our in vivo model, we performed the ectopic bone formation assay to asses differences in ossicle formation when CypD KO BMSCs were transplanted compared to wild type littermate BMSCs. In our in vitro model, we transfected OL cells with either CypD gain of function or CypD loss of function vector and measured their osteogenic differentiation potential. Additionally, we treated BMSCs with CypD inhibitor and compare to non-treated BMSCs for mineralization level. To determine potential regulatory mechanisms involved in CypD regulation, we analyzed the CypD gene (Ppif) promoter for potential transcription factor (TF) binding sites and found multiple Smad-binding elements within this promoter. Smads (Smad1, 5, 8) are TFs downstream from Bone Morphogenic Protein (BMP) signaling pathway that transmit cell differentiation signaling, and exert either activating or inhibitory effects on a variety of genes. We also transfect OL cells with Smad1 vector and analyzed for CypD mRNA levels. RESULTS/ANTICIPATED RESULTS: - Our data showed that CypD mRNA levels decreased in both primary cells and OL cells at day 7 and day 14 in osteogenic media. - Osteogenic induction also decreased mPTP activity. - In vivo ectopic bone formation assay showed increased ossicle fo DISCUSSION/SIGNIFICANCE OF IMPACT: Our data suggest that downregulation of CypD increases OB differentiation due to improved OxPhos activity led by mPTP closure. Our results corroborate reports of CypD downregulation and mPTP closure during neuronal differentiation in developing rat brains as well as in cardiomyocyte differentiation in developing mouse hearts. Our studies also suggest a yet unknown mechanism linking differentiation signaling with mitochondrial function – BMP/Smad mediated downregulation of CypD transcription. As initially mentioned, in a previous study, our lab showed that CypD KO mice present higher mitochondrial function and osteogenicity in aged BMSCs and less osteoporosis burden. Taken together, these results suggest that CypD can be a potential target to prevent bone loss in aging.

scholarly journals New Bone Formation with Teriparatide [Human Parathyroid Hormone-(1–34)] Is Not Retarded by Long-Term Pretreatment with Alendronate, Estrogen, or Raloxifene in Ovariectomized Rats

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2008-2015 ◽  
Author(s):  
Yanfei L. Ma ◽  
Henry U. Bryant ◽  
Qingqiang Zeng ◽  
Allen Schmidt ◽  
Jennifer Hoover ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Formation Rate ◽  
Prior Exposure ◽  
Ovariectomized Rats ◽  
Mineral Density ◽  
Bone Formation Rate ◽  
Teriparatide Treatment ◽  
Antiresorptive Agents ◽  
Ovx Rats

With the ready availability of several osteoporosis therapies, teriparatide [human PTH-(1–34)] is likely to be prescribed to postmenopausal women with prior exposure to agents that prevent bone loss, such as bisphosphonates, estrogen, or selective estrogen receptor modulators. Therefore, we evaluated the ability of once daily teriparatide to induce bone formation in ovariectomized (Ovx) rats with extended prior exposure to various antiresorptive agents, such as alendronate (ABP), 17α-ethinyl estradiol (EE), or raloxifene (Ral). Sprague Dawley rats were Ovx and treated with ABP (28 μg/kg, twice weekly), EE (0.1 mg/kg·d), or Ral (1 mg/kg·d) for 10 months before switching to teriparatide 30 μg/kg·d for another 2 months. Analysis of the proximal tibial metaphysis showed that all three antiresorptive agents prevented ovariectomy-induced bone loss after 10 months, but were mechanistically distinct, as shown by histomorphometry. Before teriparatide treatment, ABP strongly suppressed activation frequency and bone formation rate to below levels in other treatment groups, whereas these parameters were not different from sham values for EE or Ral. Trabecular area for ABP, EE, and Ral were greater than that in Ovx controls. However, the trabecular bone effects of ABP were attributed not only to effects on the secondary spongiosa, but also to the preservation of primary spongiosa, which was prevented from remodeling. After 2 months of teriparatide treatment, lumbar vertebra showed relative bone mineral density increases of 18%, 7%, 11%, and 10% for vehicle/teriparatide, ABP/teriparatide, EE/teriparatide, and Ral/teriparatide, respectively, compared with 10 month levels. Histomorphometry showed that trabecular area was increased by 105%, 113%, 36%, and 48% for vehicle/teriparatide, ABP/teriparatide, EE/teriparatide, and Ral/teriparatide, respectively, compared with 10 month levels. Teriparatide enhanced mineralizing surface, mineral apposition rate, and bone formation rate in all groups. Compression testing of vertebra showed that teriparatide improved strength (peak load) and toughness in all groups to a proportionately similar extent compared with 10 month levels. These data showed a surprising ability of the rat skeleton to respond to teriparatide despite extensive pretreatment with ABP, EE, or Ral. Therefore, the mature skeleton of Ovx rats remains highly responsive to the appositional effects of teriparatide regardless of pretreatment status in terms of cancellous bone area or rate of bone turnover.

scholarly journals Magnesium Picolinate Improves Bone Formation by Regulation of RANK/RANKL/OPG and BMP-2/Runx2 Signaling Pathways in High-Fat Fed Rats

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3353
Author(s):  
Emre Sahin ◽  
Cemal Orhan ◽  
Tansel Ansal Balci ◽  
Fusun Erten ◽  
Kazim Sahin
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
Mineral Density ◽  
Protein Levels ◽  
Prevent Bone Loss ◽  
Osteogenic Protein ◽  
Affect Bone Metabolism

Magnesium (Mg) deficiency may affect bone metabolism by increasing osteoclasts, decreasing osteoblasts, promoting inflammation/oxidative stress, and result in subsequent bone loss. The objective of the present study was to identify the molecular mechanism underlying the bone protective effect of different forms of Mg (inorganic magnesium oxide (MgO) versus organic magnesium picolinate (MgPic) compound) in rats fed with a high-fat diet (HFD). Forty-two Wistar albino male rats were divided into six group (n = 7): (i) control, (ii) MgO, (iii) MgPic, (iv) HFD, (v) HFD + MgO, and (vi) HFD + MgPic. Bone mineral density (BMD) increased in the Mg supplemented groups, especially MgPic, as compared with the HFD group (p < 0.001). As compared with the HFD + MgO group, the HFD + MgPic group had higher bone P (p < 0.05) and Mg levels (p < 0.001). In addition, as compared to MgO, MgPic improved bone formation by increasing the levels of osteogenetic proteins (COL1A1 (p < 0.001), BMP2 (p < 0.001), Runx2 (p < 0.001), OPG (p < 0.05), and OCN (p < 0.001), IGF-1 (p < 0.001)), while prevented bone resorption by reducing the levels of RANK and RANKL (p < 0.001). In conclusion, the present data showed that the MgPic could increase osteogenic protein levels in bone more effectively than MgO, prevent bone loss, and contribute to bone formation in HFD rats.

FACTS AND SPECULATIONS ON VITAMIN D IN PREVENTION AND TREATMENT OF ATOPIC DERMATITIS

2019 ◽  
Vol 72 (8) ◽  
pp. 1527-1531
Author(s):  
Anna Lis-Święty ◽  
Dorota Milewska-Wróbel
Keyword(s):  
Vitamin D ◽  
Atopic Dermatitis ◽  
General Population ◽  
Cellular Proliferation ◽  
Immune Functions ◽  
Atopic Dermatitis Severity ◽  
Physiological Processes ◽  
Increased Risk ◽  
Prevention And Treatment ◽  
Meta Analyses

Recently, age- and weight-specific recommendations for prevention, supplementation and treatment of vitamin D (VD) deficiency in the general population and in groups at increased risk of the deficiency (i.a. atopic dermatitis) has been presented by the Polish Experts group. VD regulates many physiological processes in the skin ranging from cellular proliferation, differentiation, and apoptosis to barrier maintenance and immune functions. VD deficiency has been associated with increased incidence and severity of atopic dermatitis. In addition, VD supplementation was shown to decrease atopic dermatitis severity in several studies, but the findings obtained in systematic reviews and meta-analyses are controversial.

scholarly journals Olive Oil and Vitamin D Synergistically Prevent Bone Loss in Mice

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e115817 ◽  
Author(s):  
Camille Tagliaferri ◽  
Marie-Jeanne Davicco ◽  
Patrice Lebecque ◽  
Stéphane Georgé ◽  
Marie-Jo Amiot ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Loss ◽  
Olive Oil ◽  
Prevent Bone Loss

scholarly journals Osteoblasts in osteoporosis: past, emerging, and future anabolic targets

2011 ◽  
Vol 165 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Pierre J Marie ◽  
Moustapha Kassem
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Matrix ◽  
Bone Fragility ◽  
Osteoblastic Cell ◽  
Medline Search ◽  
Cell Functions ◽  
Age Related ◽  
Increased Risk

ObjectiveAge-related bone loss is associated with significant changes in bone remodeling characterized by decreased trabecular and periosteal bone formation relative to bone resorption, resulting in bone fragility and increased risk of fractures. Prevention or reversal of age-related decrease in bone mass and increase in bone fragility has been based on inhibition of bone resorption using anticatabolic drugs. The current challenge is to promote osteoblastogenesis and bone formation to prevent age-related bone deterioration.MethodsA limited number of approved therapeutic molecules are available to activate bone formation. Therefore, there is a need for anabolic drugs that promote bone matrix apposition at the endosteal, endocortical, and periosteal envelopes by increasing the number of osteoblast precursor cells and/or the function of mature osteoblasts. In this study, we review current therapeutics promoting bone formation and anabolic molecules targeting signaling pathways involved in osteoblastogenesis, based on selected full-text articles searched on Medline search from 1990 to 2010.Results and discussionWe present current therapeutic approaches focused on intermittent parathyroid hormone and Wnt signaling agonists/antagonists. We also discuss novel approaches for prevention and treatment of defective bone formation and bone loss associated with aging and osteoporosis. These strategies targeting osteoblastic cell functions may prove to be useful in promoting bone formation and improving bone strength in the aging population.

scholarly journals Predictors of postoperative atrial fibrillation

2021 ◽  
Vol 25 (1) ◽  
pp. 94-116
Author(s):  
M. Kadyrova ◽  
Yu. A. Stepanova ◽  
M. S. Grinberg ◽  
V. Yu. Raguzina ◽  
E. S. Malyshenko ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Antiarrhythmic Drugs ◽  
Heart Surgery ◽  
Preventive Measures ◽  
Cardiovascular Complications ◽  
Postoperative Atrial Fibrillation ◽  
Global Literature ◽  
Factors Associated ◽  
Prevention And Treatment ◽  
Risk Patients

Review purpose: to study the occurrence predictors of postoperative atrial fibrillation (PAF), effective predicting and treating methods according to global literature.Currently, PAF is considered one of the most frequent events among all cardiovascular complications as it develops in 30–65% of cases in patients after heart surgery. In recent decades, the PAF incidence has steadily increased despite advances in surgery and anesthesiology. PAF is a significant complication that affects the course of the postoperative period and requires special attention, since it leads to a longer hospital stay, increased treatment costs and can also lead to lethal outcomes in patients in this category. Considering PAF consequences, many studies have been performed to identify factors associated with the atrial fibrillation pathophysiology, to develop preventive measures aimed at treating high risk patients and minimize the side effects of antiarrhythmic drugs. The review and analysis of the global literature on the PAF causes, prevention and treatment are presented. 

scholarly journals Morroniside promotes the osteogenesis by activating PI3K/Akt/mTOR signaling

2021 ◽  
Vol 85 (2) ◽  
pp. 332-339
Author(s):  
Hui Liu ◽  
Xi Li ◽  
Jingui Lin ◽  
Miaokuo Lin
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Osteoblast Differentiation ◽  
Mtor Signaling ◽  
Detailed Mechanism ◽  
Pharmacological Inhibition ◽  
Prevent Bone Loss ◽  
In Vivo Assays ◽  
Ovariectomized Mice

ABSTRACT Morroniside exerts a proosteogenic effect, which can prevent bone loss. However, the detailed mechanism underlying Morroniside-regulated bone formation is unclear. Morroniside can maintain cell homeostasis by promoting PI3K/Akt/mTOR signaling. The purpose of this study is to explore the significance of PI3K/Akt/mTOR signaling in Morroniside-regulated osteogenesis. The results showed that Morroniside promoted the activities of PI3K, Akt, and mTOR in osteoblast precursor MC3T3-E1. The differentiation of MC3T3-E1 to mature osteoblasts promoted by Morroniside can be reversed by the pharmacological inhibition of PI3K or mTOR. Importantly, in the presence of Morroniside, the osteoblast differentiation suppressed by PI3K inhibitor was reversed by mTOR overexpression. In vivo assays showed that in bone tissue of ovariectomized mice, Morroniside-enhanced osteoblast formation was reversed by the pharmacological inhibition of PI3K or mTOR. In conclusion, Morroniside can promote the osteogenesis through PI3K/Akt/mTOR signaling, which provides a novel clue for the strategy of Morroniside in treating osteoporosis.

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