Relevant bibliographies by topics / Bone anabolism

Academic literature on the topic 'Bone anabolism'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Bone anabolism"

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Ruan, Feng, Qiang Zheng, and Jinfu Wang. "Mechanisms of bone anabolism regulated by statins." Bioscience Reports 32, no. 6 (September 14, 2012): 511–19. http://dx.doi.org/10.1042/bsr20110118.

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Osteoporosis is a common disease in the elderly population. The progress of this disease results in the reduction of bone mass and can increase the incidence of fractures. Drugs presently used clinically can block the aggravation of this disease. However, these drugs cannot increase the bone mass and may result in certain side effects. Statins, also known as HMG-CoA (3-hydroxy-3-methylglutaryl-CoA) reductase inhibitors, have been widely prescribed for CVD (cardiovascular disease) for decades. Nonetheless, several studies have demonstrated that statins exert bone anabolic effect and may be helpful for the treatment of osteoporosis. Several experiments have analysed the mechanisms of bone anabolism regulated by statins. In the present paper, we review the mechanisms of promoting osteogenesis, suppressing osteoblast apoptosis and inhibiting osteoclastogenesis.
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Martin, T. "Uncoupling anabolism from bone resorption." Bone 44 (June 2009): S203. http://dx.doi.org/10.1016/j.bone.2009.03.016.

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Hariri, Hadla, Martin Pellicelli, and René St-Arnaud. "New PTH Signals Mediating Bone Anabolism." Current Molecular Biology Reports 3, no. 2 (April 22, 2017): 133–41. http://dx.doi.org/10.1007/s40610-017-0060-z.

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Klein, Gordon L. "The Role of Bone in Muscle Wasting." International Journal of Molecular Sciences 22, no. 1 (December 31, 2020): 392. http://dx.doi.org/10.3390/ijms22010392.

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This review describes the role of bone resorption in muscle atrophy as well as in muscle protein anabolism. Both catabolic and anabolic pathways involve components of the proinflammatory cytokine families and release of factors stored in bone during resorption. The juxtaposition of the catabolic and anabolic resorption-dependent pathways raises new questions about control of release of factors from bone, quantity of release in a variety of conditions, and relation of factors released from bone. The catabolic responses involve release of calcium from bone into the circulation resulting in increased inflammatory response in intensity and/or duration. The release of transforming growth factor beta (TGF-β) from bone suppresses phosphorylation of the AKT/mTOR pathway and stimulates ubiquitin-mediated breakdown of muscle protein. In contrast, muscle IL-6 production is stimulated by undercarboxylated osteocalcin, which signals osteoblasts to produce more RANK ligand, stimulating resorptive release of undercarboxylated osteocalcin, which in turn stimulates muscle fiber nutrient uptake and an increase in muscle mass.
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Tu, Xiaolin, Jesus Delgado-Calle, Keith W. Condon, Marta Maycas, Huajia Zhang, Nadia Carlesso, Makoto M. Taketo, David B. Burr, Lilian I. Plotkin, and Teresita Bellido. "Osteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone." Proceedings of the National Academy of Sciences 112, no. 5 (January 20, 2015): E478—E486. http://dx.doi.org/10.1073/pnas.1409857112.

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Osteocytes, >90% of the cells in bone, lie embedded within the mineralized matrix and coordinate osteoclast and osteoblast activity on bone surfaces by mechanisms still unclear. Bone anabolic stimuli activate Wnt signaling, and human mutations of components along this pathway underscore its crucial role in bone accrual and maintenance. However, the cell responsible for orchestrating Wnt anabolic actions has remained elusive. We show herein that activation of canonical Wnt signaling exclusively in osteocytes [dominant active (da)βcatOt mice] induces bone anabolism and triggers Notch signaling without affecting survival. These features contrast with those of mice expressing the same daß-catenin in osteoblasts, which exhibit decreased resorption and perinatal death from leukemia. daßcatOt mice exhibit increased bone mineral density in the axial and appendicular skeleton, and marked increase in bone volume in cancellous/trabecular and cortical compartments compared with littermate controls. daßcatOt mice display increased resorption and formation markers, high number of osteoclasts and osteoblasts in cancellous and cortical bone, increased bone matrix production, and markedly elevated periosteal bone formation rate. Wnt and Notch signaling target genes, osteoblast and osteocyte markers, and proosteoclastogenic and antiosteoclastogenic cytokines are elevated in bones of daßcatOt mice. Further, the increase in RANKL depends on Sost/sclerostin. Thus, activation of osteocytic β-catenin signaling increases both osteoclasts and osteoblasts, leading to bone gain, and is sufficient to activate the Notch pathway. These findings demonstrate disparate outcomes of β-catenin activation in osteocytes versus osteoblasts and identify osteocytes as central target cells of the anabolic actions of canonical Wnt/β-catenin signaling in bone.
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Horcajada, Marie-Noelle, and Elizabeth Offord. "Naturally Plant-Derived Compounds: Role in Bone Anabolism." Current Molecular Pharmacology 5, no. 2 (May 1, 2012): 205–18. http://dx.doi.org/10.2174/1874467211205020205.

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Kramer, Ina, Hansjoerg Keller, Olivier Leupin, and Michaela Kneissel. "Does osteocytic SOST suppression mediate PTH bone anabolism?" Trends in Endocrinology & Metabolism 21, no. 4 (April 2010): 237–44. http://dx.doi.org/10.1016/j.tem.2009.12.002.

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Torre, Elisa. "Molecular signaling mechanisms behind polyphenol-induced bone anabolism." Phytochemistry Reviews 16, no. 6 (August 31, 2017): 1183–226. http://dx.doi.org/10.1007/s11101-017-9529-x.

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Cheng, Su-Li, Jian-Su Shao, Jun Cai, Oscar L. Sierra, and Dwight A. Towler. "Msx2 Exerts Bone Anabolism via Canonical Wnt Signaling." Journal of Biological Chemistry 283, no. 29 (May 15, 2008): 20505–22. http://dx.doi.org/10.1074/jbc.m800851200.

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Towler, Dwight A. "Skeletal anabolism, PTH, and the bone-vascular axis." Journal of Bone and Mineral Research 26, no. 11 (October 21, 2011): 2579–82. http://dx.doi.org/10.1002/jbmr.523.

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Dissertations / Theses on the topic "Bone anabolism"

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Fu, Xuekun. "The role of osteocyte Kindlin-2 in the anabolic actions of PTH in bone." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/741.

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In vertebrates, PTH receptor 1 (PTH1R) plays a pivotal role in control of bone development and homeostasis; however, how it is regulated is poorly defined. Here we report that Kindlin-2 binds to and modulates PTH1R to regulate bone mass and PTH actions. Deleting Kindlin-2 expression using the 10-kb mouse Dmp1-Cre severely impairs the anabolic effects of intermittent PTH on bone in adult mice with or without ovariectomy. Of particular interest, Kindlin-2 and Pth1r double heterozygous mice (Dmp1- Cre; Kindlin-2 f/+ ; Pth1r f/+ ), but not either singly heterozygous mice (Dmp1- Cre; Kindlin-2 f/+ or Dmp1-Cre; Pth1r f/+ ), display severe osteopenia and fail to increase bone mass in response to administration of intermittent PTH. Mechanistically, Kindlin-2 interacts with the C-terminal cytoplasmic region of PTH1R. When overexpressed, this region efficiently inhibits the endogenous PTH/PTH1R signaling in osteoblasts, which is reversed by introduction of a point mutation that abolishes the Kindlin-2 interaction. Furthermore, Kindlin-2 loss inhibits PTH-induced CREB phosphorylation and cAMP production in vitro and in bone. PTH upregulates, while estrogen deficiency downregulates, expression of Kindlin-2 in vitro and in bone. Collectively, we demonstrate that interplay between Kindlin-2 and PTH1R regulates bone mass by modulating PTH1R and provide a potential therapeutic target for metabolic bone diseases
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Soon, Grace Ing. "The bone anabolic potential of dietary lysine and phytochemicals." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613967.

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李振華. "Bone anabolic effect of flavonoids from Herba Epimedii in zebrafish and medaka." Thesis, University of Macau, 2010. http://umaclib3.umac.mo/record=b2454948.

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Miao, Dengshun. "Studies on the actions of bone anabolic drugs in vivo and in vitro." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300362.

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Matthies, Levi [Verfasser], and Eric [Akademischer Betreuer] Hesse. "The Role of Tgif1 in Bone Anabolic Signal Transduction / Levi Matthies ; Betreuer: Eric Hesse." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2018. http://d-nb.info/116227526X/34.

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Liang, Chao. "Aptamer-functionalized lipid nanoparticles targeting osteoblasts as a novel RNA Interference-based bone anabolic strategy." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/325.

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Osteoporosis remain major clinical challenges. RNA interference (RNAi) provides a promising approach for promoting osteoblastic bone formation to settle the challenges. However, the major bottleneck for translating RNAi with efficacy and safety to clinical bone anabolic strategy is lack of osteoblast-specific delivery systems for osteogenic siRNAs. Previously, we developed a targeting system involving DOTAP-based cationic liposomes attached to oligopeptides (AspSerSer)6, (also known as (DSS)6), which had good affinity for bone formation surface. Using this system, osteogenic Pleckstrin Homology Domain Containing, Family O Member 1 (Plekho1) siRNA could be specifically delivered to bone formation surface at tissue level and promoted bone formation in osteopenic rodents. However, concerns still exist regarding indirect osteoblast-specific delivery, detrimental retention in hepatocytes, mononuclear phagocyte system (MPS)-induced dose reduction and inefficient nanoparticle extravasation. Aptamers, selected by cell-based Systematic evolution of ligands by exponential enrichment (cell-SELEX), are single-stranded DNA (ssDNA) or RNA which binds to target cells specifically by distinct tertiary structures. By performing positive selection with osteoblasts and negative selection with hepatocytes and peripheral blood mononuclear cells (PBMCs), we aimed to screen an aptamer that could achieve direct osteoblast-specific delivery and minimal hepatocyte and PBMCs accumulation of Plekho1 siRNAs. In addition, lipid nanoparticles (LNPs) have been widely used as nanomaterials encapsulating siRNA due to their small particle size below 90 nm. Polyethylene glycol¡(PEG) as the mostly used hydrophilic polymer, could efficiently prevent LNPs from MPS uptake. So, LNPs with PEG shielding could serve as siRNA carriers to realize efficient extravasation from fenestrated capillaries to osteoblasts and help reduce MPS uptake of the siRNAs. Recently, we screened an aptamer (CH6) by cell-SELEX specifically targeting both rat and human osteoblasts and developed the aptamer-functionalized LNPs encapsulating osteogenic Plekho1 siRNA, i.e., CH6-LNPs-siRNA. Our results demonstrated that CH6-LNPs-siRNA had an average particle size below 90 nm and no significant cytotoxicity in vitro. CH6 aptamer facilitated osteoblast-selective uptake of Plekho1 siRNA and gene silencing in vitro. In this study, we further found that CH6 aptamer facilitated the bone-specific distribution of siRNA by biophotonic imaging and quantitative analysis. Immunohistochemistry results showed that CH6 achieved in vivo osteoblast-specific delivery of Plekho1 siRNA. Dose-response experiment indicated that CH6-LNPs-siRNA achieved almost 80% gene knockdown at the siRNA dose of 1.0 mg/kg and maintained 12 days for over 50% gene silencing. microCT, bone histomorphometry and mechanical testing confirmed that CH6 facilitated bone formation, leading to improved bone micro-architecture, increased bone mass and enhanced mechanical properties in osteoporotic rodents. Furthermore, CH6-LNPs-siRNA achieved better bone anabolic action when compared to the previously developed (AspSerSer)6-liposome-siRNA. There was no obvious toxicity in rats injected with CH6-LNPs-siRNA. All these results indicated that osteoblast-specific aptamer-functionalized LNPs could act as a novel RNAi-based bone anabolic strategy and advance selectivity of targeted delivery for osteogenic siRNAs from tissue level toward cellular level. In addition, the generation of ssDNA from double-stranded PCR products is an essential step in selection of aptamers in SELEX. We found that the size separation derived from unequal primers with chemical modification could be a satisfactory alternative to the classic magnetic separation.
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Marcu, Jahan Phillip. "Novel Insights into CB1 Receptor Signaling and the Anabolic Role of Cannabinoid Receptors in Bone." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/233543.

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Cell Biology
Ph.D.
Activation of the CB1 receptor is modulated by aspartate residue D2.63176 in transmembrane helix (TMH) II. Interestingly, D2.63 does not affect the affinity for ligand binding at the CB1 receptor. Studies in class A GPCRs have suggested an ionic interaction between residues of TMHII and VII. In this report, modeling studies identified residue K373, in the extracellular (EC)-3 loop, in charged interactions with D2.63. We investigated this possibility by performing reciprocal mutations and biochemical studies. D2.63176A, K373A, D2.63176A-K373A, and the reciprocal mutant with the interacting residues juxtaposed, D2.63176K-K373D were characterized using radioligand binding and guanosine 5'-3-O-(thio)triphosphate functional assays. None of the mutations resulted in a significant change in the binding affinity of CP55,940 or SR141716A. Computational results indicate that the D2.63176-K373 ionic interaction strongly influences the conformation(s) of the EC-3 loop, providing a structure-based rationale for the importance of the EC-3 loop to signal transduction in CB1. Specifically, the putative ionic interaction results in the EC-3 loop pulling over the top (extracellular side) of the receptor; this EC-3 loop conformation may serve protective and mechanistic roles. These results suggest that the ionic interaction between D2.63176 and K373 is crucial for CB1 signal transduction. This work may help to aide drug design efforts for the effective treatment of different diseases. The cannabinoid receptors of osteoblasts may represent a target for the treatment of bone disorders such as osteoporosis. Our research demonstrates that cannabinoids can affect important signaling molecules in osteoblasts. In MC3T3-E1 osteoblastic cells, the CB1 antagonist, AM251, has been reported to induce increases in Runx2 mRNA, mineralized bone nodule formation, and activation of signaling molecules such as ERK and AKT (Wu et al., 2011). Studies from our lab characterizing mice in which both CB1 and CB2 receptors were inactivated by homologous recombination have demonstrated increased bone mass coupled with enhanced osteoblast differentiation of bone marrow stromal cells in culture (manuscript in preparation). We explored the effect of antagonizing CB1 and CB2 cannabinoid receptors in osteoblastic cells to gain insights into molecular pathways that may help to explain the effects of the endocannabinoid system (ECS) in bone development. Our data was generated by running time course experiments with MC3T3-E1 cells under the influence of SR141716A, SR144528 or both in combination. The cells were harvested with a lysis buffer at specific time points and analyzed by western blot analysis. Quantification of protein activation was calculated using LiCor imaging equipment and software. Within 15 minutes, treatment with the CB1 receptor antagonist SR141716A resulted in several fold increases in pERK, pSMAD158, and pAKT. SR144528, a CB2 receptor antagonist, caused increases in pERK and pSMAD158, but not pAKT. When both antagonists were applied together, pERK and pSMAD158 levels increased, while pAKT signaling was diminished compared to SR141716A alone. The finding that cannabinoid receptor antagonists alter the activity of the SMAD158 complex is a novel finding, which suggests that cannabinoids can influence bone morphogenic signaling pathways, and therefore play a significant role in osteoblast differentiation and function.
Temple University--Theses
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Jay, Freya [Verfasser], and Marlon [Akademischer Betreuer] Schneider. "Role of amphiregulin in mediating the bone anabolic actions of parathyroid hormone / Freya Jay ; Betreuer: Marlon Schneider." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1117473953/34.

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Aschenberg, Sophie [Verfasser], and Georg [Akademischer Betreuer] Schett. "Catabolic and anabolic periarticular bone changes in patients with rheumatoid arthritis: a computed tomography study on the role of age, disease duration and bone markers / Sophie Aschenberg. Gutachter: Georg Schett." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2014. http://d-nb.info/1075741653/34.

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Guimarães, Ana Paula Franttini Garcia Moreno. "Decanoato de nandrolona, qualidade óssea e calo ósseo em fratura do fêmur de rato." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17142/tde-29032018-100618/.

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Tem havido grande interesse na investigação de substâncias de ação sistêmica que atuam sobre o sistema musculoesquelético, no sentido de melhorar a qualidade óssea e muscular, e assim, evitar fraturas patológicas decorrentes de osteoporose. Os esteroides anabólicos androgênicos têm importante atuação no metabolismo sistêmico geral, sendo que no osso aumenta sua resistência, massa e, no músculo, combate a sarcopenia. Entretanto, não há investigações consistentes sobre a possível atuação dessas substâncias na consolidação óssea. Este estudo teve como objetivo avaliar o efeito do decanoato de nandrolona na consolidação óssea e na qualidade óssea de fêmures de ratos machos adultos jovens da linhagem Wistar. Foram utilizados 112 animais, divididos em 04 grupos com 02 subgrupos (14 e 28 dias). Um grupo controle (n=17) foi formado por animais sem intervenção, mas apenas com a injeção de veículo inerte. Em outro grupo foi provocada fratura da diáfise do fêmur (n=26). No terceiro grupo os animais receberam apenas decanoato de nandronola (n=23). No quarto grupo foi provocada fratura na diáfise do fêmur associada à administração da mesma dosagem de decanoato de nandrolona (n=26). A fratura provocada no fêmur foi pelo método fechado e obtida com auxílio de uma guilhotina com lâmina romba. Em seguida, a fratura foi fixada por um fio de Kirschner de 1,0 mm de espessura, inserido no canal medular, e o membro pélvico foi radiografado em perfil. O decanoato de nandrolona foi aplicado na dose de 10 mg/kg de massa corporal, por via intramuscular, 02 vezes por semana, durante 14 ou 28 dias, conforme o subgrupo. Após a eutanásia os fêmures direitos foram dissecados e tiveram o comprimento medido. A densidade mineral óssea e o conteúdo mineral ósseo foram determinados pelo método da absorciometria de raios X de dupla energia (DXA). A resistência óssea foi determinada pelo ensaio mecânico de flexão em dois pontos, com o cálculo com a da força máxima e rigidez. O calo ósseo foi avaliado microscopicamente em cortes histológicos corados pela hematoxilina e eosina e examinados em luz comum para a obtenção do seu volume por técnica morfométrica. As outras secções foram coradas em picrosirius red e examinadas em luz polarizada para a quantificação do colágeno tipo I. A significância estatística foi estabelecida em 5%. Não houve diferença significante entre os animais tratados e não tratados pelo decanoato de nandrolona quanto à densidade mineral óssea, conteúdo mineral ósseo, resistência mecânica, tanto para o osso sem fratura, quanto para o calo ósseo. A quantidade de colágeno tipo I também não foi diferente, entretanto, o volume de osso neoformado nos grupos que receberam o esteroide anabolizante foi significantemente maior. A massa corporal foi maior nos grupos que receberam decanoato de nandrolona, embora sem significância estatística. O comprimento ósseo foi maior aos 28 dias no grupo tratado com decanoato de nandrolona. A massa do calo também teve valor significativamente maior aos 28 dias nos animais que receberam o decanoato de nandrolona. Com base nos resultados encontrados, sob as condições experimentais e métodos de avaliação empregados, o decanoato de nandrolona não causou efeitos significativos benéficos ou maléficos, tanto na qualidade do calo ósseo, como na qualidade do osso normal íntegro do rato adulto jovem.
There has been a great interest in investigating systemic substances that can positively act on the musculoskeletal system to improve the bone quality thus avoiding osteoporotic fractures. The anabolic androgenic steroids have an important influence on general metabolism and can increase the bone resistance and bone mass. On muscle, it improves sarcopenic conditions. However, there is no consistent investigation of a possible action of these substances on bone callus. Thus, the aim of this study was to evaluate the effect of decanoate of nandrolone on fracture healing and bone quality of young adult male Wistar rats. One hundred animals were divided into 04 groups and 02 subgroups (14 and 28 days). A control group consisted of animals without any intervention (n=17). In the second group, a femoral shaft fracture was performed (n=26). In the third group, the animals received only decanoate of nandronole (n=23). In the fourth group, a fracture in the femoral shaft was performed and associated with administration of the same dose of decanoate of nandrolone (n=26). The fracture created in the femur was obtained by closed method and achieved with the aid of a blunt blade guillotine. After that, the fracture was fixed with a 1.0 mm thick Kirschner wire that was inserted into the medullary canal, and the limb was X-rayed in profile. Ten mg/kg of body mass of decanoate of nandrolone was administered intramuscularly, 02 times a week for 14 or 28 days, depending on the subgroup. After euthanasia, the right femurs were dissected and had the length measured. Bone mineral density and bone mineral content were determined by the dual-energy x-ray absorptiometry method (DXA). The mechanical properties maximum force and stiffness were determined by the twopoint bending test. The bone callus was evaluated microscopically in sections stained with hematoxylin and eosin and examined under ordinary light microscope to calculate the volume of bone callus by the morphometric technique. Other sections were stained in picrosirius red and examined under polarized light for quantification of type I collagen. The statistical significance was set at 5%. There was no significant difference between the animals treated and not treated with nandrolone decanoate for bone mass density, bone mineral content, mechanical resistance and type I collagen, both for the intact bone and for the bone callus. However, the body mass was higher in the groups that received nandrolone decanoate, although without statistical significance. The femur length was greater in the 28th day in the group treated with nandrolone decanoate. Callus mass also had significant increase at 28 days for animals that received nandrolone decanoate. Based on the results and under the experimental conditions and methods of evaluation, the decanoate of nandrolone did not cause significant benefit or harmfull effects both on callus and on bone qualities.
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Books on the topic "Bone anabolism"

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Whitfield, James F. Growing bone. 2nd ed. Austin, Tex: Landes Bioscience, 2007.

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Whitfield, James F. Growing bone. 2nd ed. Austin, Tex: Landes Bioscience, 2007.

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Whitfield, James F. Growing bone. 2nd ed. Austin, Tex: Landes Bioscience, 2007.

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C, Farach-Carson Mary, and United States. National Aeronautics and Space Administration., eds. Round 1 progress report: Anabolic vitamin D analogs as countermeasures to bone loss. [Washington, DC: National Aeronautics and Space Administration, 1997.

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Principles Of Bone Regeneration. Springer, 2012.

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Whitfield, James F. Growing Bone. Landes Bioscience, 2005.

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Whitfield, James F. Growing Bone. Taylor & Francis Group, 2007.

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Whitfield, James F. Growing Bone. Taylor & Francis Group, 2007.

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Boonstra, Johannes. Gi Phase Progression. Eurekah.Com Inc, 2004.

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Book chapters on the topic "Bone anabolism"

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Rosen, Clifford J. "Bone Anabolic Agents." In Atlas of Osteoporosis, 195–207. London: Current Medicine Group, 2003. http://dx.doi.org/10.1007/978-1-4757-4561-0_17.

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Bab, Itai A. "Anabolic Agents in Bone Repair." In Principles of Bone Regeneration, 51–58. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2059-0_4.

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Geusens, P., D. Vanderschueren, and S. Boonen. "Androgens and Anabolic Steroids." In Management of Fractures in Severely Osteoporotic Bone, 462–73. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-3825-9_33.

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Chambers, Tim J., Jade Wei Mun Chow, Jennifer M. Lean, and Jonathan H. Tobias. "The Anabolic Action of Estrogen on Rat Bone." In Sex Steroids and Bone, 19–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03043-1_2.

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Olgun, Z. Deniz, Arianna Gianakos, Jonathan E. Jo, and Joseph M. Lane. "Bisphosphonates, Denosumab, and Anabolic Agents in the Treatment of Metastatic Bone Disease." In Metastatic Bone Disease, 121–29. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-5662-9_12.

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Ramchand, Sabashini K., and Ego Seeman. "Reduced Bone Modeling and Unbalanced Bone Remodeling: Targets for Antiresorptive and Anabolic Therapy." In Bone Regulators and Osteoporosis Therapy, 423–50. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/164_2020_354.

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Bilezikian, John P., and Natalie E. Cusano. "Combination Anabolic and Antiresorptive Therapy for Osteoporosis." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 444–47. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch53.

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Krstenansky, J. L., T. L. Ho, Z. Avnur, D. Leaffer, J. P. Caulfield, and B. H. Vickery. "RS-66271: Molecular design and in vivo bone anabolic activity." In Peptides 1994, 133–34. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_50.

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Remer, Thomas, and Lars Libuda. "Bone-Anabolic Impact of Dietary High Protein Intake Compared with the Effects of Low Potential Renal Acid Load, Endogenous Steroid Hormones, and Muscularity in Children." In Nutritional Influences on Bone Health, 187–96. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84882-978-7_27.

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Soper, David Lindsey, Yili Wang, Biswanath De, Mitchell Anthony deLong, Michelle Jeanine Dirr, Michele Elaine Soehner, Mark Walden Lundy, Glen Edward Mieling, and John August Wos. "The Design and Synthesis of Selective Prostaglandin Analogs As Bone Anabolic Agents for the Potential Treatment of Osteoporosis." In Advances in Experimental Medicine and Biology, 303–7. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0193-0_46.

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Conference papers on the topic "Bone anabolism"

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Askew, Michael J., Gary B. Schneider, Kristina J. Grecco, Jason Hsu, Emily Mugler, and Donald A. Noe. "Effect of Pharmaceutical Bone Growth Stimulation With Novel Anabolic Peptides: Biomechanical and Bone Density Measurements in a Rat Model." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43044.

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Pharmaceutical bone growth stimulation holds promise for prevention and treatment bone disorders, and the enhancement of fracture healing. Bone growth hormones have begun to have limited clinical use, but can illicit adverse side effects. Recent studies have shown that short peptides (less than 15 amino acids) derived from the protein sequence of Vitamin D Binding Protein (DBP), can enhance bone formation (osteogenesis). These peptides may have potential as controllable bone growth stimulators without the adverse side effects and cost of bone growth hormones. Rats, injected every other day for two weeks with DBP-based peptide fragments ranging from 3 to 13 amino acids in length, were euthanized and the tibias and femurs were scanned by peripheral quantitative computerized tomography (pQCT) to determine bone density and cross-sectional geometric properties. The bones were then tested in three-point bending to determine strength and bending modulus. Injection of DBP-based peptides over only a 2-week period resulted in significant (p<0.05) increases in bone density and material properties in the experimental rat bones in comparison to controls injected with saline. The short length of these effective peptides suggests their use not only in systemic injections but also as clinically convenient pills taken orally for pharmaceutically induced bone growth stimulation.
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Uddin, Sardar M. Zia, and Yi-Xian Qin. "Anabolic Effects of Ultrasound as Countermeasures of Simulated Microgravity in In-Vitro and In-Vivo Functional Disuse Models." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53796.

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Microgravity (MG) during space flight has been known to cause adverse effect on bone quality. Data collected from studies done on spaceflights show loss of 1–1.6% bone mineral density (BMD) per space-flight-month[1]. Most BMD has been recorded in load-bearing bones [2]. Some studies has considered using drugs and different growth factors to maintain bone mass in microgravity conditions but it can be too expensive to maintain over longer periods of time besides the systematic effects of such treatments [3]. Considering the effects of microgravity are partially attributed to lack of mechanical force on bone tissue, which alters gene expression, reduction in transcription factors and growth factors. Furthermore, lack of gravity effects cell growth, proliferation, differentiation, cytoskeleton polymerization and cellular morphology [4, 5]. Thus to reverse these adverse effects on bone physiology, it is important to provide cells with mechanical stimulus which can provide essential mechanical signal for cells to counter the effects of microgravity. Ultrasound acoustic vibrations can be readily applied in, in vivo and human studies and has shown anabolic effects on osteopenic bone tissue [6]. Furthermore, ultrasound is a non-invasive and more target specific treatment relative to cyclic strain and vibration. The objective of this study is to see effects of low intensity pulsed ultrasound (LIPUS) on disused bone model and osteogenic activity of osteoblast cells cultures in simulated microgravity. This will help us understand that effects of ultrasound on microgravity and mechanotransduction pathway responsible for anabolic effect on bone cells.
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Coughlin, Thomas R., Laoise M. McNamara, Peter E. McHugh, and Glen L. Niebur. "Shear Stress Within Trabecular Bone Marrow due to Low Magnitude High Frequency Vibration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53803.

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Low magnitude high frequency (LMHF) loading is anabolic to bone. LMHF loading for one year resulted in a 32% increase in the trabecular bone volume, decreased trabecular spacing and increased trabecular number in a sheep model (1). In contrast, no change was seen in cortical bone, suggesting the anabolic effect is limited to the trabecular compartment. Rats subjected to 90 Hz vibration developed greater trabecular bone volume and thicker trabeculae than rats subjected to vibration at 45 Hz (2). However, the strain induced in the bone during the 90 Hz vibration was significantly lower than during the 45 Hz vibration, indicating that the effect does not depend on matrix strain. As such, shear stress in the marrow may be the anabolic signal in this loading regimen.
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Altman, Allison R., Beom Kang Huh, Abhishek Chandra, Wei-Ju Tseng, Ling Qin, and X. Sherry Liu. "3D In Vivo Bone Dynamic Imaging of PTH’s Anabolic Action." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14671.

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Aging shifts bone remodeling toward a negative balance between bone formation and resorption, causing bone loss and increased fracture risk. Anti-resorptive agents are commonly used to inhibit bone resorption and stabilize bone mass. While they are effective to prevent further bone loss, there is also a great need for anabolic agents which can reverse bone deterioration and regain lost skeletal integrity. Intermittent parathyroid hormone (PTH) treatment is the only FDA-approved anabolic treatment for osteoporosis, which greatly stimulates bone formation. Combined therapy of anti-resorptive drugs, such as alendronate (ALN), and PTH have been proposed and are expected to further stimulate bone formation. However, studies show conflicting results regarding the effectiveness of combined treatments: some have reported the addition of ALN to impair PTH function [1, 2], while others suggest an improvement over PTH monotherapy [3, 4]. The first objective of this study is to document the immediate changes of individual trabecular structures due to PTH and combined therapy within 12 days using in vivo micro computed tomography (μCT). As PTH is typically prescribed for 1 to 3 years to osteoporotic patients, a treatment of 12 days for rats (approximately equivalent to one year of human life) may be more clinically relevant than long-term treatment studies on rats. The secondary purpose of this study was to gain insight into the mechanism of combined versus PTH treatments through a bone dynamic imaging strategy to track events over an individual remodeling site. We hypothesized that PTH and combined treatments would immediately enhance bone formation on the trabecular surface.
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Hart, Stephen A., and Marcelo J. Dapino. "Accelerated Bone Growth Remotely Induced by Magnetic Fields and Smart Materials." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175966.

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Bone structure is exquisitely matched to its physical loading environment. From the cartilaginous skeletal framework formed in the embryo to the aging skeleton, bone architecture is directly related to function. Bone is a dynamic system, constantly remodeling itself by absorbing old tissue and forming new tissue. This capability allows bone architecture to become optimized to the loading environment. Julius Wolff [1] first postulated that bone structure adapts to changing stress environments in 1892. Exact understanding of the process of mechanotransduction, however, has remained elusive. In addition to normal remodeling, bone growth has been shown to occur along the diaphysis, or shaft portion, of long bones such as the femur when placed in dynamic bending. Bone in this region is dense and is known as cortical bone. A bending moment placed on a long bone will cause the bone to curve creating a region of tension on one side and a region of compression on the opposing side. As the bending moment is cycled, fluid within the bone will flow from the region of compression to the region of tension creating fluid shear on cell walls within the bone which promotes the anabolic response of growth [2]. Growth from such stimuli is thought to be mediated by fluid flow around quiescent bone cells, osteocytes, and their canalicular process coursing through the bone structure [3]. Growth in this manner is directed in a latitudinal direction creating a thicker and stronger diaphysis.
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Vallapuri, Teja, Colin Crean, John Chirgwin, G. David Roodman, and Attaya Suvannasankha. "Abstract 693: Effects of a bone-anabolic agent on metastatic bone cancer growth." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-693.

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Yanoso, Laura, Justin Jacobson, Tulin Dadali, David Reynolds, and Hani Awad. "Evaluation of Polylactic Acid/Beta-Tricalcium Phosphate Scaffolds as Segmental Bone Graft Substitutes." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192978.

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The use of processed structural allografts for treatment of massive segmental defects in long bones can be complicated by poor incorporation and remodeling of the devitalized graft, foreign-body reaction and micro-damage accumulation which often leads to catastrophic graft failure [1]. It is therefore useful to develop a bioengineered, biodegradable scaffold that is able to stimulate healing of the defect region. The use of bioengineered scaffolds has been limited due to their poor mechanical strength that does not permit withstanding large in vivo loads and due to their poor osteoinductive properties. We therefore investigated the use of rigid polylactic acid/beta-tricalcium phosphate (PLA/βTCP) composites used in conjunction with osteoinductive factors such as growth hormones (parathyroid hormone (PTH)) and growth factors (bone morphogenic protein-2 (BMP-2) & vascular endothelial growth factor (VEGF)) to stimulate bone formation and vessel ingrowth in the segmental defect region. We examined the physical characteristics of the scaffolds, and evaluated their osteoinductive potential in a clinically-relevant mouse model of a femoral segmental defect with or without PTH treatment. Finally, we used an ectopic bone formation model to assess the efficacy of the scaffold in site-specific delivery of bone anabolic factors.
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Fields, Aaron J., Susan M. Millard, Jeannie F. Bailey, Dylan O’Carroll, Jeffrey C. Lotz, and Robert A. Nissenson. "Bone Biomechanical Behavior in Adult Mice is Regulated by Osteoblast Gi Signaling in a Sex- and Site-Specific Manner." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53773.

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Osteoporosis decreases bone strength owing to loss of bone mass and deterioration in bone microstructure. The maintenance of bone mass and microstructure depends, at least in part, on the signaling and function of osteoblasts. For example, Gi-coupled signaling by G-protein coupled receptors endogenous to osteoblasts has been shown to restrict cortical and trabecular bone formation in female mice [1,2]. This suggests that inhibiting Gi-coupled signaling in osteoblasts may be an effective strategy for the development of anabolic osteoporosis therapies. However, it remains unclear whether inhibiting Gi-coupled signaling improves bone biomechanical behavior. Thus, the objectives of this study were to: 1) quantify the effect of Gi-coupled signaling on bone strength and bone stiffness; and 2) determine the effects of this signaling mechanism on cortical and trabecular microstructure and on the relationship between mechanical behavior and microstructure.
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Qin, Yi-Xian, Tamara Kaplan, and Hoyan Lam. "Anabolic Fluid Flow as Dependent on It Dose and Frequency in Bone Formation and Inhibition of Bone Loss." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61388.

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Anabolic response of bone to interstitial fluid flow is strongly dependent on the dynamic components of the fluid pressure, implying that fluid flow is a critical regulatory component to bone mass and morphology. While the fluid stimulus can be potentially applied for therapeutic in promoting turnover, the hypothesis of fluid induced bone adaptation was evaluated in an avian ulna model using varied flow rates and magnitudes. Total of 12 one-year old male avian animals was used in this study. A sinusoidal fluid pressure was applied to the experimental ulna 10 min/day for 4 weeks. Three experimental groups of loading were performed at 1 and 30 Hz of fluid loading. The results reveal an increase of 22.7%±7.2 in trabecular volume for group of 30 Hz, 76mmHg loading, while it had only 0.5 % increase at 1Hz, 76 mmHg loading. Under physiologic fluid pressure, a higher flow rate of stimuli generates much higher remodeling response than a lower rate of loading. This implies that bone turnover may be sensitive to the dynamic components of fluid flow, thereby initiating the adaptive response.
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Qin, Yi-Xian, Hoyan Lam, and Murtaza Malbari. "The Effects of Loading Rate and Duration on Mitigation of Osteopenia by Dynamic Muscle Stimulation." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206685.

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Musculoskeletal adaptations to aging and disuse environment have significant physiological effects on skeletal health, i.e., osteopenia and bone loss. Osteoporosis often occurs together with muscle loss. Such musculoskeletal complications cause severe physiologic changes and have been proposed the synergistic effects of muscle function and bone adaptation. The role of mechanobiology in the skeletal tissue may be closely related to load-induced transductive signals, e.g., bone fluid flow, which is proposed to be a critical mediator of bone and muscle adaptation. The skeletal muscle may serve as a muscle pump that may mediate bone mechanotransduction via modulation of intramedullary pressure. Muscular stimulation (MS) is proposed to be used to simultaneously treat both muscle and bone loss. Indeed, our recent data have demonstrated that high frequency, short duration stimulation can inhibit bone loss and muscle atrophy. Although 10 min dynamic loading can effectively attenuate bone loss, it cannot totally recover disuse osteopenia. The optimal parameters required for such treatment are unclear. Studies have separately investigated the optimal signal parameters for bone or muscle. Insertion of recovery periods during high frequency stimulations to extend the loading cycles have shown potential to reduce muscle atrophy by minimizing fatigue and mimicking physiologic contractions, and demonstrated enhancement of bone remodeling. The overall hypothesis for this study is that dynamic MS can enhance anabolic activity in bone, and inhibit bone loss in a functional disuse condition. Combined high frequency and sufficient loading cycle may be able to completely mitigate bone loss induced by disuse osteopenia.
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Reports on the topic "Bone anabolism"

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Xiao, Guozhi. ATF4, A Novel Mediator of the Anabolic Actions of PTH on Bone. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada499647.

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Xiao, Guozhi. ATF4, A Novel Mediator of the Anabolic Actions of PTH on Bone. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada541206.

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Xiao, Guozhi. ATF4, A Novel Mediator of the Anabolic Actions of PTH on Bone. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada508520.

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Xiao, Guozhi. ATF4, A Novel Mediator of the Anabolic Actions of PTH on Bone. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada550617.

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Xiao, Guozhi. ATF4, A Novel Mediator of the Anabolic Actions of PTH on Bone. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada558869.

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Qin, Weiping. Anabolic Steroids as a Novel Therapeutic Strategy for the Prevention of Bone Loss after Spinal Cord Injury: Animal Model and Molecular Mechanism. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada591955.

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