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RANKL/RANK/OPG Pathway: A Mechanism Involved in Exercise-Induced Bone Remodeling.
Tobeiha, M, Moghadasian, MH, Amin, N, Jafarnejad, S
BioMed research international. 2020;:6910312
Abstract
Bones as an alive organ consist of about 70% mineral and 30% organic component. About 200 million people are suffering from osteopenia and osteoporosis around the world. There are multiple ways of protecting bone from endogenous and exogenous risk factors. Planned physical activity is another useful way for protecting bone health. It has been investigated that arranged exercise would effectively regulate bone metabolism. Until now, a number of systems have discovered how exercise could help bone health. Previous studies reported different mechanisms of the effect of exercise on bone health by modulation of bone remodeling. However, the regulation of RANKL/RANK/OPG pathway in exercise and physical performance as one of the most important remodeling systems is not considered comprehensive in previous evidence. Therefore, the aim of this review is to clarify exercise influence on bone modeling and remodeling, with a concentration on its role in regulating RANKL/RANK/OPG pathway.
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The Bone Metabolic Response to Exercise and Nutrition.
Dolan, E, Varley, I, Ackerman, KE, Pereira, RMR, Elliott-Sale, KJ, Sale, C
Exercise and sport sciences reviews. 2020;(2):49-58
Abstract
Bone (re)modeling markers can help determine how the bone responds to different types, intensities, and durations of exercise. They also might help predict those at risk of bone injury. We synthesized evidence on the acute and chronic bone metabolic responses to exercise, along with how nutritional factors can moderate this response. Recommendations to optimize future research efforts are made.
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Human skeletal physiology and factors affecting its modeling and remodeling.
Nandiraju, D, Ahmed, I
Fertility and sterility. 2019;(5):775-781
Abstract
Human skeleton is a living tissue that performs structural and metabolic functions. It is not only the largest storehouse for calcium and other essential ions but also a depot for toxic chemicals faced by human body throughout life. Skeletal modeling starts at conception and then throughout life undergoes constant remodeling to adopt its shape and strength according to human needs. With the passage of time, like other tissues in the body, bones also bear the brunt of life and in this life long process loses its strength and vitality. Multiple genetic and environmental factors play an integral part in its formation, strength, and decline.
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Influence of antiretroviral therapy on bone metabolism of patients with chronic hepatitis B: a review.
Dessordi, R, Santana, RC, Navarro, AM
Revista da Sociedade Brasileira de Medicina Tropical. 2019;:e20180441
Abstract
Hepatitis B is a major public health problem worldwide and associated with significant mortality. To prevent or delay the deleterious effects of chronic infection by the hepatitis B virus, patients should be carefully followed, and antiviral therapy indicated according to specific recommendations. Currently, available drugs inhibit viral replication and slow or stop the progression of inflammation and fibrosis of the liver. However, the drugs for oral use in the treatment of hepatitis B, jointly referred to as nucleoside/nucleotide analogs, are indicated for prolonged use and have potential side effects. The reduction in bone mineral density was associated with the use of tenofovir, already evaluated in patients infected with HIV because the drug is also part of the therapeutic arsenal for this viral infection. There are few studies on the effects of tenofovir in patients with mono hepatitis B. Therefore, this literature review proposes to examine how hepatitis B acts in the body and the mechanisms by which antiretroviral drugs (especially tenofovir) can affect bone metabolism.
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Transcriptional Mechanisms of Secondary Fracture Healing.
Roberts, JL, Paglia, DN, Drissi, H
Current osteoporosis reports. 2018;(2):146-154
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Abstract
PURPOSE OF REVIEW Growing evidence supports the critical role of transcriptional mechanisms in promoting the spatial and temporal progression of bone healing. In this review, we evaluate and discuss new transcriptional and post-transcriptional regulatory mechanisms of secondary bone repair, along with emerging evidence for epigenetic regulation of fracture healing. RECENT FINDINGS Using the candidate gene approach has identified new roles for several transcription factors in mediating the reactive, reparative, and remodeling phases of fracture repair. Further characterization of the different epigenetic controls of fracture healing and fracture-driven transcriptome changes between young and aged fracture has identified key biological pathways that may yield therapeutic targets. Furthermore, exogenously delivered microRNA to post-transcriptionally control gene expression is quickly becoming an area with great therapeutic potential. Activation of specific transcriptional networks can promote the proper progression of secondary bone healing. Targeting these key factors using small molecules or through microRNA may yield effective therapies to enhance and possibly accelerate fracture healing.
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Is there a role for newer biomarkers in chronic kidney disease-mineral and bone disorder management?
Tan, SJ, Cai, MM
Nephrology (Carlton, Vic.). 2017;:14-18
Abstract
The current management of Chronic Kidney Disease-Mineral Bone Disorder (CKD-MBD) relies largely on clinical judgement and assessment of biochemical parameters including serum calcium, phosphate and intact parathyroid hormone concentrations. In the past two decades, there has been a leap in the understanding of the pathophysiology of CKD-MBD, leading to the discovery of novel biomarkers. The potential utility of these markers in this clinical setting is an area of intense investigation. In the absence of any guidelines aiding the clinician's understanding and application of these markers, we summarise the current available literature surrounding fibroblast growth factor-23, α-Klotho, sclerostin and serum calcification propensity testing and their respective assays in the context of CKD-MBD management.
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Effects of omega-3 fatty acids on bone turnover markers in postmenopausal women: systematic review and meta-analysis.
Shen, D, Zhang, X, Li, Z, Bai, H, Chen, L
Climacteric : the journal of the International Menopause Society. 2017;(6):522-527
Abstract
AIM: There is conflicting evidence regarding the effects of omega-3 fatty acids on bone turnover markers in postmenopausal women. Thus, we systematically reviewed the efficacy of omega-3 fatty acids by conducting a meta-analysis of available randomized controlled trials. METHODS PubMed, Embase, Cochrane Library and Scopus were searched in December 2016. The standardized mean difference (SMD) or weighted mean difference (WMD) and the corresponding 95% confidence intervals (CIs) were calculated using a fixed-effects model. RESULTS Eight trials were included in the present meta-analysis. The pooled findings did not identify significant decreases in bone-specific alkaline phosphatase (SMD -0.08, 95% CI -0.29 to 0.12, p = 0.429) and collagen type I cross-linked C-telopeptide (WMD 0 ng/ml, 95% CI -0.04 to 0.04, p = 0.899). There was a significant decrease in osteocalcin (WMD -0.86 ng/ml, 95% CI -1.68 to -0.04, p = 0.040) as compared with control. CONCLUSION Omega-3 fatty acids reduced postmenopausal women's serum osteocalcin. Further well-designed studies are needed to verify the effects of omega-3 fatty acids on bone mass density and other bone turnover markers in postmenopausal women. CLINICAL TRIAL REGISTRATION NUMBER CRD42016053219 ( https://www.crd.york.ac.uk/PROSPERO/ ).
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Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters.
Ketteler, M, Block, GA, Evenepoel, P, Fukagawa, M, Herzog, CA, McCann, L, Moe, SM, Shroff, R, Tonelli, MA, Toussaint, ND, et al
Kidney international. 2017;(1):26-36
Abstract
The KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of CKD-MBD represents a selective update of the prior CKD-MBD Guideline published in 2009. This update, along with the 2009 publication, is intended to assist the practitioner caring for adults and children with chronic kidney disease (CKD), those on chronic dialysis therapy, or individuals with a kidney transplant. This review highlights key aspects of the 2017 CKD-MBD Guideline Update, with an emphasis on the rationale for the changes made to the original guideline document. Topic areas encompassing updated recommendations include diagnosis of bone abnormalities in CKD-mineral and bone disorder (MBD), treatment of CKD-MBD by targeting phosphate lowering and calcium maintenance, treatment of abnormalities in parathyroid hormone in CKD-MBD, treatment of bone abnormalities by antiresorptives and other osteoporosis therapies, and evaluation and treatment of kidney transplant bone disease.
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Effects of obesity treatments on bone mineral density, bone turnover and fracture risk in adults with overweight or obesity.
Harper, C, Pattinson, AL, Fernando, HA, Zibellini, J, Seimon, RV, Sainsbury, A
Hormone molecular biology and clinical investigation. 2016;(3):133-149
Abstract
BACKGROUND New evidence suggests that obesity is deleterious for bone health, and obesity treatments could potentially exacerbate this. MATERIALS AND METHODS This narrative review, largely based on recent systematic reviews and meta-analyses, synthesizes the effects on bone of bariatric surgery, weight loss pharmaceuticals and dietary restriction. RESULTS AND CONCLUSIONS All three obesity treatments result in statistically significant reductions in hip bone mineral density (BMD) and increases in bone turnover relative to pre-treatment values, with the reductions in hip BMD being strongest for bariatric surgery, notably Roux-en Y gastric bypass (RYGB, 8%-11% of pre-surgical values) and weakest for dietary restriction (1%-1.5% of pre-treatment values). Weight loss pharmaceuticals (orlistat or the glucagon-like peptide-1 receptor agonist, liraglutide) induced no greater changes from pre-treatment values than control, despite greater weight loss. There is suggestive evidence that liraglutide may increase bone mineral content (BMC) - but not BMD - and reduce fracture risk, but more research is required to clarify this. All three obesity treatments have variable effects on spine BMD, probably due to greater measurement error at this site in obesity, suggesting that future research in this field could focus on hip rather than spine BMD. Various mechanisms have been proposed for BMD loss with obesity treatments, notably reduced nutritional intake/absorption and insufficient exercise, and these are potential avenues for protection against bone loss. However, a pressing outstanding question is whether this BMD reduction contributes to increased fracture risk, as has been observed after RYGB, and whether any such increase in fracture risk outweighs the risks of staying obese (unlikely).
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[Bone histomorphometry;A role of evaluation for bone quality and mechanical strength].
Yamamoto, N, Takahashi, H, Shimakura, T
Clinical calcium. 2016;(1):9-15
Abstract
Bone histomorphometry is defined as a quantitative evaluation of bone remodeling and bone turnover. Bone remodeling is the important mechanism for calcium metabolism and mechanical usage. The changes of bone remodeling in special condition with metabolic bone disease or osteoporosis agents have the effectiveness on bone mechanical strength.