0
selected
-
1.
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.
-
2.
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.
-
3.
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.
-
4.
Transcriptional Mechanisms of Secondary Fracture Healing.
Roberts, JL, Paglia, DN, Drissi, H
Current osteoporosis reports. 2018;(2):146-154
-
-
Free full text
-
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.
-
5.
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.
-
6.
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).
-
7.
Diacerein: Benefits, Risks and Place in the Management of Osteoarthritis. An Opinion-Based Report from the ESCEO.
Pavelka, K, Bruyère, O, Cooper, C, Kanis, JA, Leeb, BF, Maheu, E, Martel-Pelletier, J, Monfort, J, Pelletier, JP, Rizzoli, R, et al
Drugs & aging. 2016;(2):75-85
-
-
Free full text
-
Abstract
Diacerein is a symptomatic slow-acting drug in osteoarthritis (SYSADOA) with anti-inflammatory, anti-catabolic and pro-anabolic properties on cartilage and synovial membrane. It has also recently been shown to have protective effects against subchondral bone remodelling. Following the end of the revision procedure by the Pharmacovigilance Risk Assessment Committee of the European Medicines Agency, the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) constituted a panel of 11 experts to better define the real place of diacerein in the armamentarium for treating OA. Based on a literature review of clinical trials and meta-analyses, the ESCEO confirms that the efficacy of diacerein is similar to that of non-steroidal anti-inflammatory drugs (NSAIDs) after the first month of treatment, and superior to that of paracetamol. Additionally, diacerein has shown a prolonged effect on symptoms of several months once treatment was stopped. The use of diacerein is associated with common gastrointestinal disorders such as soft stools and diarrhoea, common mild skin reactions, and, uncommonly, hepatobiliary disorders. However, NSAIDs and paracetamol are known to cause potentially severe hepatic, gastrointestinal, renal, cutaneous and cardiovascular reactions. Therefore, the ESCEO concludes that the benefit-risk balance of diacerein remains positive in the symptomatic treatment of hip and knee osteoarthritis. Furthermore, similarly to other SYSADOAs, the ESCEO positions diacerein as a first-line pharmacological background treatment of osteoarthritis, particularly for patients in whom NSAIDs or paracetamol are contraindicated.
-
8.
The role of homocysteine in bone remodeling.
Vacek, TP, Kalani, A, Voor, MJ, Tyagi, SC, Tyagi, N
Clinical chemistry and laboratory medicine. 2013;(3):579-90
-
-
Free full text
-
Abstract
Bone remodeling is a very complex process. Homocysteine (Hcy) is known to modulate this process via several known mechanisms such as increase in osteoclast activity, decrease in osteoblast activity and direct action of Hcy on bone matrix. Evidence from previous studies further support a detrimental effect on bone via decrease in bone blood flow and an increase in matrix metalloproteinases (MMPs) that degrade extracellular bone matrix. Hcy binds directly to extracellular matrix and reduces bone strength. There are several bone markers that can be used as parameters to determine how high levels of plasma Hcy (hyperhomocysteinemia, HHcy) affect bone such as: hydroxyproline, N-terminal collagen 1 telopeptides. Mitochondrion serves an important role in generating reactive oxygen species (ROS). Mitochondrial abnormalities have been identified during HHcy. The mechanism of Hcy-induced bone remodeling via the mitochondrial pathway is largely unknown. Therefore, we propose a mitochondrial mechanism by which Hcy can contribute to alter bone properties. This may occur both through generations of ROS that activate MMPs and could be extruded into matrix to degrade bone matrix. However, there are contrasting reports on whether Hcy affects bone density, with some reports in favour and others not. Earlier studies also found an alteration in bone biomechanical properties with deficiencies of vitamin B12, folate and HHcy conditions. Moreover, existing data opens speculation that folate and vitamin therapy act not only via Hcy-dependent pathways but also via Hcy-independent pathways. However, more studies are needed to clarify the mechanistic role of Hcy during bone diseases.
-
9.
Bone turnover markers in primary hyperparathyroidism.
Costa, AG, Bilezikian, JP
Journal of clinical densitometry : the official journal of the International Society for Clinical Densitometry. 2013;(1):22-7
-
-
Free full text
-
Abstract
Primary hyperparathyroidism is an endocrine disorder characterized by elevated or inappropriate normal levels of parathyroid hormone in a setting of hypercalcemia. The inclusion of calcium on the basic metabolic bone panel has allowed this disorder to be diagnosed even in the absence of symptoms. Nevertheless, the skeleton can be a target of excess parathyroid hormone activity even during its asymptomatic presentation. Bone turnover markers a surrogate index of the process of the remodeling process at the level of bone, and thus can be useful to monitor skeleton involvement in primary hyperparathyroidism.
-
10.
Bone turnover markers.
Coates, P
Australian family physician. 2013;(5):285-7
Abstract
Bones are constantly remodelled to cope with the body's calcium requirements and to repair microscopic damage. The entire skeleton is replaced every 10 years in adults, and around 10% of the skeleton is involved in bone remodelling at any one time.