Relevant bibliographies by topics / Age-related bone loss

Academic literature on the topic 'Age-related bone loss'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Age-related bone loss"

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Googe, Mary Catherine. "Age-related bone loss in women." Orthopaedic Nursing 4, no. 1 (January 1985): 60. http://dx.doi.org/10.1097/00006416-198501000-00015.

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Horsman, A., D. H. Marshall, and M. Peacock. "Age-related bone loss and fractures." Bone 6, no. 1 (1985): 53. http://dx.doi.org/10.1016/8756-3282(85)90409-0.

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Kanis, J. A., J. E. Aaron, D. Evans, M. Thavarajah, and M. Beneton. "Bone loss and age-related fractures." Experimental Gerontology 25, no. 3-4 (January 1990): 289–96. http://dx.doi.org/10.1016/0531-5565(90)90064-9.

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Chan, George K., and Gustavo Duque. "Age-Related Bone Loss: Old Bone, New Facts." Gerontology 48, no. 2 (2002): 62–71. http://dx.doi.org/10.1159/000048929.

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Burr, David B. "Muscle Strength, Bone Mass, and Age-Related Bone Loss." Journal of Bone and Mineral Research 12, no. 10 (October 1, 1997): 1547–51. http://dx.doi.org/10.1359/jbmr.1997.12.10.1547.

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Kamei, Tsutomu, Kiyoshi Aoyagi, Tadashi Matsumoto, Yutaka Ishida, Kentaro Iwata, Hiroaki Kumano, Yoshio Murakami, and Yuzuru Kato. "Age-Related Bone Loss: Relationship between Age and Regional Bone Mineral Density." Tohoku Journal of Experimental Medicine 187, no. 2 (1999): 141–47. http://dx.doi.org/10.1620/tjem.187.141.

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Zang, Y., J. H. Song, S. H. Oh, J. W. Kim, M. N. Lee, X. Piao, J. W. Yang, et al. "Targeting NLRP3 Inflammasome Reduces Age-Related Experimental Alveolar Bone Loss." Journal of Dental Research 99, no. 11 (June 12, 2020): 1287–95. http://dx.doi.org/10.1177/0022034520933533.

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The cause of chronic inflammatory periodontitis, which leads to the destruction of periodontal ligament and alveolar bone, is multifactorial. An increasing number of studies have shown the clinical significance of NLRP3-mediated low-grade inflammation in degenerative disorders, but its causal linkage to age-related periodontitis has not yet been elucidated. In this study, we investigated the involvement of the NLRP3 inflammasome and the therapeutic potential of NLRP3 inhibition in age-related alveolar bone loss by using in vivo and in vitro models. The poor quality of alveolar bones in aged mice was correlated with caspase-1 activation by macrophages and elevated levels of IL-1β, which are mainly regulated by the NLRP3 inflammasome, in periodontal ligament and serum, respectively. Aged mice lacking Nlrp3 showed better bone mass than age-matched wild-type mice via a way that affects bone resorption rather than bone formation. In line with this finding, treatment with MCC950, a potent inhibitor of the NLRP3 inflammasome, significantly suppressed alveolar bone loss with reduced caspase-1 activation in aged mice but not in young mice. In addition, our in vitro studies showed that the addition of IL-1β encourages RANKL-induced osteoclastogenesis from bone marrow–derived macrophages and that treatment with MCC950 significantly suppresses osteoclastic differentiation directly, irrelevant to the inhibition of IL-1β production. Our results suggest that the NLRP3 inflammasome is a critical mediator in age-related alveolar bone loss and that targeting the NLRP3 inflammasome could be a novel option for controlling periodontal degenerative changes with age.
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Khosla, S. "Pathogenesis of Age-Related Bone Loss in Humans." Journals of Gerontology Series A: Biological Sciences and Medical Sciences 68, no. 10 (August 24, 2012): 1226–35. http://dx.doi.org/10.1093/gerona/gls163.

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Laurent, Michaël R., Lenore Dedeyne, Jolan Dupont, Bea Mellaerts, Marian Dejaeger, and Evelien Gielen. "Age-related bone loss and sarcopenia in men." Maturitas 122 (April 2019): 51–56. http://dx.doi.org/10.1016/j.maturitas.2019.01.006.

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Khosla, Sundeep, and B. Lawrence Riggs. "Pathophysiology of Age-Related Bone Loss and Osteoporosis." Endocrinology and Metabolism Clinics of North America 34, no. 4 (December 2005): 1015–30. http://dx.doi.org/10.1016/j.ecl.2005.07.009.

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Dissertations / Theses on the topic "Age-related bone loss"

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Elbaz, Alexandre. "Implications and regulation of increasing bone marrow fat in age-related bone loss." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40765.

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The accumulation of fat in the marrow cavity is a consequence of the predominant mesenchymal stem cell differentiation into the adipocyte fate at the expense of the osteoblasts. Considering that these changes in stromal differentiation have an effect on bone health, we attempted to study bone marrow fat depots from a metabolic, lipotoxic and regulatory approach. In a fist attempt to study the potential metabolic role of bone marrow fat we observed the effect of calorie restriction (CR) on bone quality and marrow fat of aging rats subjected to a casein and soy protein diet. Bone quality and adipocyte quantification was obtained from rat tibia. Bone as well as adipogenic markers were quantified. CR was found to induce a significant decrease in bone quality. In contrast to CR rats, the ad libitum soy fed rats showed an overall better bone quality. Moreover, the results obtained showed that adipocytes were not mobilized during CR as no changes in leptin levels or adipocyte number were found. Finally we noticed that soy protein and not CR inhibited PPARgamma expression, a transcription factor required for adipogenesis. In summary, results from this first approach showed that bone marrow fat does not participate in lipid metabolism during moderate stages of starvation and that the detrimental effect of CR on bone mass could be prevented using a soy protein regime. A second approach to this subject involved looking at the mechanism through bone and fat interact within the bone marrow. We hypothesized that bone marrow adipocytes’ secretion of fatty acids (FA) induces changes in osteoblast differentiation, function and survival compatible with lipotoxicity. Using a co culture system of human pre-adipocytes and osteoblasts we showed that FAs negatively affect osteoblast differentiation and mineralization. Furthermore the effect could be prevented through the use of a FA syntase inhibitor, cerulenin. Gas chromatography/ mass spectrometry (GC\MS) analysis of co-culture su
L’ostéoporose sénile est souvent associée à une augmentation de gras dans la moelle osseuse. Cette accumulation de gras est une conséquence d’une différentiation prédominante de cellules souches en adipocytes en lieu d’ostéoblastes. Prenant en considération ce changement de différentiation, nous avons décidé d’étudier le gras de la moelle osseuse de trois différentes approches : métabolique, lipo-toxique et régulatrice. Nous avons premièrement observé les effets d’une restriction calorique (RC) sur la qualité osseuse ainsi que sur le gras de la moelle osseuse de rats nourris de caséine ou de soja. Les marqueurs osseux et adipogéniques ont aussi été quantifiés. La RC fut identifiée comme une cause de réduction de qualité osseuse. Contrairement aux rats subjugués à une RC, les rats qui furent subjugués à une diète « ad libitum » de soja ont démontré une qualité osseuse supérieure. Aucuns changements n’ont été identifiés quant aux niveaux d’expression de leptin ou de cellules grasses. Ces derniers résultats indiquent que les cellules grasses de la moelle osseuse ne sont pas mobilisées pendant les périodes de RC. La diète de soja est responsable pour l’attenuation de l’expression de PPARgamma .Les résultats de l’étude ont démontré en premier lieu que le gras de la moelle osseuse ne participe pas au métabolisme de lipides pendant les périodes de famines modérées ; puis en deuxième lieu que les effets de la RC sur les os peuvent être diminués par une diète de soja. En deuxième lieu, nous avons observé le mécanisme par lequel le gras de la moelle participe à la perte osseuse associé au vieillissement. Un modèle de co-cultures cellulaires de pré-adipocytes humains ainsi que d’ostéoblastes nous a permis de démontrer que les acides gras (AG) sécrétés par les adipocytes ont un effet inhibant sur la différentiation ainsi que sur la minéralisation des ostéoblastes. Aussi, nous av
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Marques, Elisa Amélia Alves Fernandes. "Exercise training, Bone and Aging. Evidence from different impact loading exercise interventions on age-related bone loss." Doctoral thesis, Faculdade de Desporto da Universidade do Porto, 2011. http://hdl.handle.net/10216/57106.

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Marques, Elisa Amélia Alves Fernandes. "Exercise training, Bone and Aging. Evidence from different impact loading exercise interventions on age-related bone loss." Tese, Faculdade de Desporto da Universidade do Porto, 2011. http://hdl.handle.net/10216/57106.

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Akter, Rahima. "Role of lamin A/C in the cellular features of age-related bone loss." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32525.

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Lamin A/C, an important component of the nuclear envelope, has been associated with cell differentiation and tissue development. In bone, recent studies have described that altered function of lamin A/C, due to mutations or incorrect processing, is associated with accelerated and severe bone loss. This could be due to alterations in the differentiation of mesenchymal stem cells (MSC) induced by lack of lamin A/C activity. Therefore, considering that decreased osteoblastogenesis and increased adipogenesis are the characteristic changes observed within bone marrow microenvironment that leads to age-related bone loss, we have studied the effect of inhibition of lamin A/C on MSC into either osteoblasts or adipocytes both in vitro and in vivo. For in vitro studies, we identified the effect of pharmacological inhibition of lamin A/C on adipogenesis. Subsequently, we inhibited lamin A/C by using different doses of lamin A/C siRNA in osteogenic and adipogenic differentiating MSCs as well as normal human osteoblasts. To further verify our results, we have used Zmpste24-/- null progeroid mice that lacks mature lamin A/C and studied the bone changes in absence of mature lamin A/C in in vivo. We have found that partial inhibition of lamin A/C decreased osteoblast differention and function without affecting their survival. Furthermore, our animal studies showed that absence of mature lamin A/C induced a reduction in bone mass and bone quality associated with low bone turnover. In contrast, accumulation of prelamin A induced significant levels of adipogenesis within the bone marrow cavity. In summary, our results provide evidence in support of a pivotal role of lamin A/C in the comm
Lamin A/C, un important composant de l'enveloppe nucléaire, a été associé avec la différentiation cellulaire et le développement tissulaire. Dans l'os, des études récentes ont demontrée que l'alteration de lamin A/C, due a des mutations du gène LMNA, est associée avec une perte accélérée et sevère de l'os. Ceci pourrait être dû à une altération de la différentiation des cellules souches mésenchymateuses (CSM) induit par une perte de l'activité de lamin A/C. Par conséquent, en considerant que la diminution de l'ostéoblastogènese et l'augmentation de l'adipogènese sont les changements caractéristiques observés à l'intérieur du micro-environnement de la moelle osseuse qui mènent à une perte osseuse relié à l'âge, nous avons étudié l'effet de l'inhibition de lamin A/C sur la différentiation des cellules souches soit en adipocyte ou en ostéoblast in vitro et in vivo. Pour les études in vitro, nous avons identifiés l'effet de l'inhibition pharmacologique de lamin A/C sur l'adipogènese. Par la suite, nous avons inhibé lamin A/C en utilisant différentes doses de lamin A/C siRNA sur les cellules souches en différentiatiation en ostéoblast et en adipocytes et aussi sur des ostéoblast humaine. Pour confirmer nos résultats précedents, nous avons utilisés un modèle progerique murin Zmste24-/-. Ces souris ne possedent pas la forme mature de lamin A/C. Nous avons etudiés les changements osseux en absence de la forme mature de lamin A/C in vivo. Nous avons trouvé qu'une inhibition partielle de lamin A/C diminue la différentiation et la fonction des ostéoblastes sans affecter leur survie. En outre, nos études sur les souris ont d
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Brickley, Megan Bronwyn. "Age-related bone loss and osteoporosis in archaeological bone : a study of two London collections, Redcross Way and Farringdon Street." Thesis, University College London (University of London), 1997. http://discovery.ucl.ac.uk/1317654/.

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This thesis examines the ways in which age- and sex-related bone loss in archaeological bone can be assessed, with a view to providing criteria by which osteoporosis should be diagnosed. Sample material for this investigation came from two London collections of skeletal material dated 1700-1850 (Redcross Way and Farringdon Street). A comparative study using a wide range of techniques for the detection of bone loss was carried out on the samples from Redcross Way. Sample numbers were then increased through the inclusion of the material from Farringdon Street in order to provide sufficient data to examine changes seen in relation to age and sex. Current research into bone biology and knowledge of osteoporosis in the present day population was reviewed in the context of possible observations that can be made on archaeological bone. There is a large body of historical literature available relating to the period covered by this study (AD 1700-1850). A review was made of material relating to population demographics and medical literature relating to fractures. This work showed that it is valid to study osteoporosis in populations of this period, as a significant number of individuals reached an age at which today they could be considered at risk of sustaining an osteoporotic fracture. Literature relating to fractures contained significant numbers of reports of cases of fracture which, from knowledge of such fracture in the present population, fit the criteria of osteoporotic fractures. Archaeological bone was examined using non-invasive investigative techniques many of which are in current clinical use for the determination of osteoporosis. These were: dual energy x-ray absorptiometry; low angle x-ray scattering; and optical densitometry. Optical densitometry was also applied to bone slices. Cortical bone was assessed through calculation of its area, and thickness. The cortical index were calculated from radiographs. Trabecular bone loss was assessed from femoral radiographs using the Singh index, and stereometric measurements made using close range photogrammetry. The possibility of the archaeological bone material having undergone post-mortem (diagenetic) changes, which can adversely affect results obtained from non-invasive investigations, was briefly addressed. Mineral deposition was found to have occurred in some of the sample material examined. It was found that the direct examination and measurement of the three dimensional trabecular architecture through stereometric analysis provided the best indication of bone loss and, possibly osteoporosis. Where sample material cannot be sectioned and non-invasive investigative techniques have to be applied, low angle x-ray scattering, which produces quantitative and qualitative measurements of trabecular bone, produced the most reliable results. Both these techniques overcame the problems associated with diagenetic change in archaeological material. The results from the investigation of the Redcross way and Farrmgdon Street skeletal material showed that age- and sex-related bone loss was taking place, with loss occurring at an earlier age and being more severe in females than males. The conclusion is made that patterns of loss observed in the archaeological bone broadly mirror those seen in the present day population.
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Books on the topic "Age-related bone loss"

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Brickley, Megan Bronwyn. Age-related bone loss and osteoporosis in archaeological bone: A study of two London collections, Redcross Way and Farringdon Street. London: Institute of Archaeology, University of London, 1997.

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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Effects of maternal age on pregnancy outcomes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0034.

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Maternal age on both ends of the reproductive spectrum (teenage and 35+) is associated with increased risk of adverse pregnancy outcomes, as compared with the age range from 20–34 years old. Some of the increase in pregnancy complications in older mothers is caused by underlying age-related health issues such as hypertension and diabetes, the prevalence of which increases linearly with age. The risks associated with young maternal age are more related to nutritional deficits and the fact that pregnant adolescents may still be growing themselves. Poor fetal growth often seen in adolescent pregnancies possibly results from competition for nutrients. Maternal bone loss is also a concern, as adolescent diets are commonly low in calcium and vitamin D. Pregnant adolescents may benefit from calcium supplementation to compensate for the increased need for their own bone growth and should at minimum receive vitamin D supplements, as recommended for all pregnant women.
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Book chapters on the topic "Age-related bone loss"

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Frost, Harold M. "On Changing Views about Age-Related Bone Loss." In Bone Loss and Osteoporosis, 19–31. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-8891-1_2.

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Mosekilde, Lis. "Mechanisms of Age-Related Bone Loss." In Ageing Vulnerability: Causes and Interventions, 150–71. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868694.ch14.

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Welch, Ailsa A. "Dietary Fat Composition and Age-Related Muscle Loss." In Nutritional Influences on Bone Health, 71–81. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-2769-7_6.

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Brickley, Megan B., and Sabrina C. Agarwal. "Techniques for the Investigation of Age-Related Bone Loss and Osteoporosis in Archaeological Bone." In Bone Loss and Osteoporosis, 157–72. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-8891-1_10.

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Shea, M. Kyla, and Sarah L. Booth. "Vitamin K’s Role in Age-Related Bone Loss: A Critical Review." In Nutrition and Bone Health, 471–86. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2001-3_29.

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Christiansen, C. "Prophylactic treatment for age-related bone loss in women." In The Climacteric in Perspective, 105–17. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4145-8_11.

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Riggs, B. Lawrence. "Endocrine Causes of Age-Related Bone Loss and Osteoporosis." In Endocrine Facets of Ageing, 247–64. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470846542.ch15.

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Verschueren, Sabine, An Bogaerts, and Ekaterina Tankisheva. "Vibration Training as Means to Counteract Age-Related Muscle and Bone Loss." In Non-Pharmacological Management of Osteoporosis, 127–43. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54016-0_10.

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Mosekilde, L. "Age-Related Loss of Vertebral Trabecular Bone Mass and Structure — Biomechanical Consequences." In Biomechanics of Diarthrodial Joints, 83–96. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3450-0_4.

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Seeman, Ego. "The material and structural basis of the growth-related gain and age-related loss of bone strength." In Osteoporosis: a lifecourse epidemiology approach to skeletal health, 105–22. Boca Raton, FL : CRC Press/Taylor & Francis Group, [2018]: CRC Press, 2018. http://dx.doi.org/10.1201/9781351234627-9.

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Conference papers on the topic "Age-related bone loss"

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Ni, Qingwen, Juffry S. Nyman, Xiaodu Wang, and Daniel P. Nicolella. "The Characterization of Age-Related Human Cortical Bone Porosity, Water Distribution Changes by Nuclear Magnetic Resonance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176213.

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Previous studies have shown that bone fracture toughness is also significantly correlated to changes in porosity, microarchitecture, osteonal morphology, collagen integrity, microdamage, and the interactions of water with collagen and mineral phases, all of which are measures of bone quality. Currently, the influence of water removal on the strength and toughness of cortical bone has studied by Nyman et al [1]. The results have shown that loss of water in the collagen phase decreases the toughness of bone, whereas loss of water associated with the mineral phase decreases both bone strength and toughness. However, in that paper the loss of water was used the dehydration method for such mechanism studies. Here, we hypothesize that the NMR relaxation technique can non-destructively and non-invasively assess the porosity, bound water (water bound to collage and mineral phases) and mobile water (water within the pores).
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Ortega, A. M., T. A. Bateman, E. W. Livingston, R. C. Paietta, S. M. Gonzalez, L. S. Stodieck, and V. L. Ferguson. "Spaceflight Related Changes in Structure and Strength of Mouse Trabecular and Cortical Bone From the STS-118 Space Shuttle Mission." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14785.

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Rapid bone loss during spaceflight is a well-established and continuing medical issue for astronauts. It has been reported that astronauts have displayed bone loss at rates of up to 2.7%/month in weight-bearing bones, or about 6 times that of post-menopausal women [1]. Rodent models have provided a means to further our understanding of the effects of microgravity on bone quality, both from studies in which rodents have flown aboard space missions and those in which weightlessness is simulated on earth through musculoskeletal unloading [2]. Such studies have the potential to not only further our understanding of the cause of decreased bone integrity in space, but also provide an accelerated model for the study of osteo-degenerative diseases affecting the general public, leading to improved treatment methods for both spaceflight and age or illness related osteoporosis.
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Dong, X. Neil, Daniel M. Sparkman, Huijie Leng, Harry R. Millwater, and Xiaodu Wang. "Probabilistic Prediction of Microdamage Progression in Bone." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192653.

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Age-related bone fractures are a major health concern to the elderly population. In addition to the loss of bone mass, the deterioration of bone quality is another major reason for such fractures. The decline of bone quality is manifested with the accumulation of microdamage in bone with age [1]. Two major types of microdamage have been observed in bone tissue: linear microcracks and diffuse damage [2]. Linear microcracks are individual cracks at a size of microns or larger and are usually visible under an optical microscope. On the other hand, diffuse damage is detectable only by staining and consists of an extensive network of fine, ultrastructural-level defects. The mechanisms for the formation of these two distinct types of microdamage in bone are still unclear. In this study, probabilistic finite element models of mineral-collagen composites were used to study the progression of microdamage in bone, thereby exploring the conditions under which linear microcracks and diffuse damage are produced in bone.
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Kim, Chi Hyun, Erica Takai, Nicole Culella, and X. Edward Guo. "Measurements of In Vivo Strains in the Rat Tail Vertebra." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32597.

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The study of bone adaptation is important in understanding the etiology of age-related bone fractures, developing optimal designs for total joint replacements, and preventing bone loss during prolonged space flight. Numerous studies have attempted to quantify the relationship between mechanical loading and bone adaptation [1,2,3,4]. An in vivo rat tail vertebra model has been developed for trabecular bone adaptation studies where a controlled mechanical load can be applied to a whole vertebra [3]. The load levels applied in vivo were selected using in vitro strain gage measurements on cadaveric rat tails, resulting strains in the cortical shell of tail vertebrae within the physiological range. However, it is not clear what the physiological strain level in the rat tail vertebrae in vivo during normal cage activities is. In addition, the in vivo strain in the rat tail vertebra subjected to mechanical loads has not been quantified.
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Wang, Xiaodu, Jeffry Nyman, and Michael Reyes. "Mode Changes in the Post-Yield Behavior of Bone." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175438.

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A number of factors across multiple length scales (Table 1) may contribute to the mechanical competence of bone (i.e., the resistance to fracture). This structural complexity hinders a complete mechanistic explanation (model) for elderly bone fragility. Although age-related loss of bone mass has been viewed as the reason for the rising incidence of bone fractures in the elderly,(2) bone quality is more meaningful to provide insights into why individuals with ‘normal’ bone mineral density (BMD) suffer fractures. Bone is a hierarchical and hydrated composite of mineral and collagen phases,(3, 4) showing a rather complex response to the mechanical loading.(5, 6) While previous research has investigated the resistance of bone to crack propagation,(7, 8) fatigue behavior,(9–11) and mechanical changes to load-induced damage,(12–14) little is known about the mechanical behavior of bone as a function of progressive deformation (strain). In this study, by employing a previously developed progressive loading scheme,(15) we intend to investigate the progressive stress-strain behavior of bone with increasing strain levels, so as to gain more information on the underlying mechanisms for post-yield behavior of bone. It is hypothesized that the post-yield behavior of bone varies with the increasing strain, which plays a significant role in sustaining the toughness or quality of bone.
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Guo, X. Edward, Erica Takai, Kai Liu, and Xiaodong Wang. "An Exploration of Cell Stress and Deformation Under Shear Flow." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23160.

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Abstract The biological response of bone cells (osteoblasts and/or osteocytes) to mechanical loading is an important basic science topic in the mechanism of mechano-signal transduction in bone adaptation to mechanical loading. The characterization of this mechanism of signal transduction is crucial in the understanding of the etiology of age-related bone loss, bone loss during space flight and the optimal design of implants for total joint replacements. It has been hypothesized that deformation-generated fluid shear stress is one of the major mechanical stimuli that bone cells respond to. Many in vitro experiments utilize a parallel-plate flow chamber by imposing fluid shear stress on cultured osteoblasts. For example, changes in intracellular Ca++ levels and mitogen-activated protein kinase (MAPK) phosphorylation has been quantified in response to applied shear flow [1,2]. In these studies, the flow shear stress at the wall of the flow chamber τ wall = 6 μ Q w h 2 , where Q is the volumetric flow rate, w and h are the width and height of the flow chamber, respectively, and μ is the media viscosity. However, this wall shear stress may not indicate the actual stress state which bone cells experience, which depends on the details of the flow-cell interaction, including the mechanical properties of the cell, the attachment condition of the cell to the wall as well as the cell density. In order to obtain a quantitative relationship between the biological response of bone cells to applied shear flow, it is necessary to quantify in detail the flow-cell interaction in a typical shear flow experiment. The objective of this study was to quantify the shear stress within the cell under applied shear flow, incorporating fully coupled flow and solid deformation analyses using the finite element technique. Specifically, we examined the influence of the elastic modulus of the cell and the spacing distance between cells on the shear stress within the cell.
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Kampshoff, Christoph, Jannis Schaeper, Carlos Duque Afonso, Dirk Beutner, Tim Salditt, Tobias Moser, and Alexander Meyer. "Investigating age-related hearing loss in the primate cochlea." In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1711200.

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Ni, Qingwen, and Naniel P. Nicolella. "Assessment of Bone Quality Associated With Loosely and Tightly Bound Water." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19300.

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Abstract:
Previous studies have shown that the age-related increase in bone porosity results a decrease in bone strength, and porosity is related to the volume of mobile water in the pores. In addition, since water is also bound to collagen and mineral, changes in the amount of bound water will potentially affect the bone strength. It is known that the removal of the loosely bound water (via hydrogen bonding) requires less energy than the water molecules trapped inside collagen molecules, which in turn requires similar or less energy than water molecules bound to the surface charges of mineral apatite (more ionic in nature). Also, water that is imbedded in the lattice of hydroxyapatite (more covalent in nature) requires the highest energy to dislodge. However, there is no traditional method that can determine mobile and bound water, further for loosely and tightly bound ware accurately, non-destructively and non-invasively. Here, we propose that by using NMR Car-Purcell-Meiboom-Gill (CPMG) spin-spin relaxation measurement to determine the mobile water, and the NMR inversion T2-FID spectrum derived from NMR free induction decay (FID) measurements for estimating the bound and free water distribution. Furthermore, after comparison of the total water lost (weighing method) within tissue by using drying (free dry) on the air to the total mobile water lost measured by NMR CPMG method, then, the total loosely bound water lost can be estimated. Following this, the mechanical test will be used to evaluate the bone quality related to the tightly and loosely bound water within bone. This information can be used to further assessment of bone quality.
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Reports on the topic "Age-related bone loss"

1

Christiansen, Blaine A. The Role of Peripheral Nerve Function in Age-Related Bone Loss and Changes in Bone Adaptation. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613982.

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2

Christiansen, Blaine A. The Role of Peripheral Nerve Function in Age-Related Bone Loss and Changes in Bone Adaptation. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598422.

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3

Donohue, Henry J., Christopher Niyibizi, and Alayna Loiselle. Induced Pluripotent Stem Cell Derived Mesenchymal Stem Cells for Attenuating Age-Related Bone Loss. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada606237.

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4

Donahue, Henry J. Induced Pluripotent Stem Cell Derived Mesenchymal Stem Cells for Attenuating Age-Related Bone Loss. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada581680.

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Journal articles
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