Journal articles: 'Age-related bone loss'

1

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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2

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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3

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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4

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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5

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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6

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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7

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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9

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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10

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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11

Fagundes Belchior, Gabriela, Ben Kirk, Evela Aparecida Pereira da Silva, and Gustavo Duque. "Osteosarcopenia: beyond age-related muscle and bone loss." European Geriatric Medicine 11, no. 5 (July 16, 2020): 715–24. http://dx.doi.org/10.1007/s41999-020-00355-6.

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12

Melov, S., D. Evans, J. Andersen, P. Kapahi, and G. J. Lithgow. "PHARMACOLOGICALLY TARGETING AGING SLOWS AGE-RELATED BONE LOSS." Innovation in Aging 1, suppl_1 (June 30, 2017): 1235–36. http://dx.doi.org/10.1093/geroni/igx004.4485.

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13

Jaovisidha, Suphaneewan, Jong K. Kim, David J. Sartoris, Enrique Bosch, Sharon Edelstein, Elizabeth Barrett-Connor, and Parichart Rojanaplakorn. "Scoliosis in Elderly and Age-Related Bone Loss." Journal of Clinical Densitometry 1, no. 3 (September 1998): 227–33. http://dx.doi.org/10.1385/jcd:1:3:227.

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14

Jardí, Ferran, Michaël R. Laurent, Frank Claessens, and Dirk Vanderschueren. "Estradiol and Age-Related Bone Loss in Men." Physiological Reviews 98, no. 1 (January 1, 2018): 1. http://dx.doi.org/10.1152/physrev.00051.2017.

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15

Maggio, D., R. Pacifici, A. Cherubini, G. Simonelli, M. Luchetti, M. C. Aisa, D. Cucinotta, S. Adami, and U. Senin. "Age-Related cortical bone loss at the metacarpal." Calcified Tissue International 60, no. 1 (January 1997): 94–97. http://dx.doi.org/10.1007/s002239900193.

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16

Thomsen, Karsten, Anders Gotfredsen, and Claus Christiansen. "Is postmenopausal bone loss an age-related phenomenon?" Calcified Tissue International 39, no. 3 (May 1986): 123–27. http://dx.doi.org/10.1007/bf02555106.

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17

Frost, H. M. "On age-related mammalian bone loss: Insights of the Utah paradigm." Veterinary and Comparative Orthopaedics and Traumatology 15, no. 03 (2002): 127–36. http://dx.doi.org/10.1055/s-0038-1632727.

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SummaryAn elegant design stratagem would make its loads control the strength of an organ intended to carry loads without breaking. Healthy load-bearing mammalian bones do exactly that. Physiologists begin to understand how they do it, and this article reviews some of the biological “machinery” responsible for it. Why? Because that machinery’s features show what can cause age-related bone loss, how it occurs, how a long-overlooked mechanism in bone marrow would contribute to it, why loss of whole-bone strength seems more important than loss of bone ‘mass’, and why some absorptiometric indicators of whole-bone strength are unreliable. The machinery’s features also show why strong muscles normally make strong bones, why persistently weak muscles normally make weak bones, and why loss of muscle strength usually causes a disuse-pattern osteopaenia. Those things could question long-accepted ‘wisdom’, but four observations concern that; (1) the questions concern what facts mean far more than the accuracy of the facts, and the basic facts now seem pretty clear;(2) this article must leave resolution of such questions, and of the devils that can hide in the details, to other times, places and people;(3) the plate tectonics story showed that better facts and ideas can change accepted wisdom dramatically;(4) and poor interdisciplinary communication delayed and still delays diffusion of better facts and ideas to many skeletal science and clinical disciplines that needed and need them.

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18

Millard, Susan M., Liping Wang, Lalita Wattanachanya, Dylan O’Carroll, Aaron J. Fields, Joyce Pang, Galateia Kazakia, Jeffrey C. Lotz, and Robert A. Nissenson. "Role of Osteoblast Gi Signaling in Age-Related Bone Loss in Female Mice." Endocrinology 158, no. 6 (April 12, 2017): 1715–26. http://dx.doi.org/10.1210/en.2016-1365.

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Abstract Age-related bone loss is an important risk factor for fractures in the elderly; it results from an imbalance in bone remodeling mainly due to decreased bone formation. We have previously demonstrated that endogenous G protein–coupled receptor (GPCR)-driven Gi signaling in osteoblasts (Obs) restrains bone formation in mice during growth. Here, we launched a longitudinal study to test the hypothesis that Gi signaling in Obs restrains bone formation in aging mice, thereby promoting bone loss. Our approach was to block Gi signaling in maturing Obs by the induced expression of the catalytic subunit of pertussis toxin (PTX) after the achievement of peak bone mass. In contrast to the progressive cancellous bone loss seen in aging sex-matched littermate control mice, aging female Col1(2.3)+/PTX+ mice showed an age-related increase in bone volume. Increased bone volume was associated with increased bone formation at both trabecular and endocortical surfaces as well as increased bending strength of the femoral middiaphyses. In contrast, male Col1(2.3)+/PTX+ mice were not protected from age-related bone loss. Our results indicate that Gi signaling markedly restrains bone formation at cancellous and endosteal bone surfaces in female mice during aging. Blockade of the relevant Gi-coupled GPCRs represents an approach for the development of osteoporosis therapies—at least in the long bones of aging women.

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19

Zhang, Yu-Bin, Zhao-Ming Zhong, Gang Hou, Hui Jiang, and Jian-Ting Chen. "Involvement of Oxidative Stress in Age-Related Bone Loss." Journal of Surgical Research 169, no. 1 (July 2011): e37-e42. http://dx.doi.org/10.1016/j.jss.2011.02.033.

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20

Jilka, Robert L., and Charles A. O’Brien. "The Role of Osteocytes in Age-Related Bone Loss." Current Osteoporosis Reports 14, no. 1 (February 2016): 16–25. http://dx.doi.org/10.1007/s11914-016-0297-0.

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21

Birkenhäger-Frenkel, D. H., Ph Courpron, E. Clermonts, E. Hüpscher, M. F. Coutinho, and P. J. Meunier. "Trabecular thickness, intertrabecular distance and age-related bone loss." Bone 6, no. 5 (1985): 402. http://dx.doi.org/10.1016/8756-3282(85)90344-8.

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22

Goldspink, Geoffrey. "Age-Related Loss of Muscle Mass and Strength." Journal of Aging Research 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/158279.

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Age-related muscle wasting and increased frailty are major socioeconomic as well as medical problems. In the quest to extend quality of life it is important to increase the strength of elderly people sufficiently so they can carry out everyday tasks and to prevent them falling and breaking bones that are brittle due to osteoporosis. Muscles generate the mechanical strain that contributes to the maintenance of other musculoskeletal tissues, and a vicious circle is established as muscle loss results in bone loss and weakening of tendons. Molecular and proteomic approaches now provide strategies for preventing age-related muscle wasting. Here, attention is paid to the role of the GH/IGF-1 axis and the special role of the IGFI-Ec (mechano growth factor/MGF) which is derived from the IGF-I gene by alternative splicing. During aging MGF levels decline but when administered MGF activates the muscle satellite (stem) cells that “kick start” local muscle repair and induces hypertrophy.

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23

Lai, Pinling, Qiancheng Song, Cheng Yang, Zhen Li, Sichi Liu, Bin Liu, Mangmang Li, et al. "Loss of Rictor with aging in osteoblasts promotes age-related bone loss." Cell Death & Disease 7, no. 10 (October 2016): e2408-e2408. http://dx.doi.org/10.1038/cddis.2016.249.

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24

Raisz, Lawrence G., and Ego Seeman. "Causes of Age-Related Bone Loss and Bone Fragility: An Alternative View." Journal of Bone and Mineral Research 16, no. 11 (November 1, 2001): 1948–52. http://dx.doi.org/10.1359/jbmr.2001.16.11.1948.

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25

Ferguson, Virginia L., Reed A. Ayers, Ted A. Bateman, and Steven J. Simske. "Bone development and age-related bone loss in male C57BL/6J mice." Bone 33, no. 3 (September 2003): 387–98. http://dx.doi.org/10.1016/s8756-3282(03)00199-6.

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26

Fan, Ruoxun, He Gong, Xianbin Zhang, Jun Liu, Zhengbin Jia, and Dong Zhu. "Modeling the Mechanical Consequences of Age-Related Trabecular Bone Loss by XFEM Simulation." Computational and Mathematical Methods in Medicine 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/3495152.

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The elderly are more likely to suffer from fracture because of age-related trabecular bone loss. Different bone loss locations and patterns have different effects on bone mechanical properties. Extended finite element method (XFEM) can simulate fracture process and was suited to investigate the effects of bone loss on trabecular bone. Age-related bone loss is indicated by trabecular thinning and loss and may occur at low-strain locations or other random sites. Accordingly, several ideal normal and aged trabecular bone models were created based on different bone loss locations and patterns; then, fracture processes from crack initiation to complete failure of these models were observed by XFEM; finally, the effects of different locations and patterns on trabecular bone were compared. Results indicated that bone loss occurring at low-strain locations was more detrimental to trabecular bone than that occurring at other random sites; meanwhile, the decrease in bone strength caused by trabecular loss was higher than that caused by trabecular thinning, and the effects of vertical trabecular loss on mechanical properties were more severe than horizontal trabecular loss. This study provided a numerical method to simulate trabecular bone fracture and distinguished different effects of the possible occurrence of bone loss locations and patterns on trabecular bone.

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27

Isales, Carlos, Ke-Hong Ding, Wendy Bollag, Meghan McGee-Lawrence, William Hill, Xing-ming Shi, Sadanand Fulzele, and Mark Hamrick. "3-Hydroxyanthranilic acid Administration Did Not Prevent Age Related Bone Loss." Innovation in Aging 5, Supplement_1 (December 1, 2021): 676–77. http://dx.doi.org/10.1093/geroni/igab046.2547.

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Abstract Aging is associated with accumulation of various tryptophan degradation products that may having either bone anabolic or catabolic effects. In epidemiologic studies, elevated levels of 3-hydroxyanthranilic acid (3-HAA) are associated with a higher bone mineral density (BMD). We have previously shown that the C57BL/6 mouse loses bone mass with age. Thus, we hypothesized that administering 3-HAA via a daily intraperitoneal (IP) injection would result in preserved or increased BMD. In an IACUC-approved protocol, we injected 26-month-old C57BL/6 mice with either a low dose (0.5 mg) or high dose (5 mg) of 3-HAA IP five days a week for eight weeks. At the end of this time mice were sacrificed and body composition and bone mineral density measured by DigiMus. BMD was significantly lower in the high dose 3-HAA group: 0.0570 + 0.004 vs 0.0473 + 0.006 vs 0.0432 + 0.0075 gm/cm2, (means+SD, Control vs 0.5 mg 3HAA vs 5 mg 3HAA, p=0.004, 0 vs 5.0 mg, n=6-9/group). 3-HAA had no significant impact on body composition (lean body mass: 86.7 + 1.7% vs 86.2 + 2.7% vs 86.1 + 2.0%, Control vs 0.5 mg vs 5.0 mg 3-HAA, p=ns; and fat mass 12.6 + 2.0% vs 13.8 + 2.7% vs 13.9 + 2.0% vs 0.2%, Control vs 0.5 vs 5 mg 3-HAA, p=ns). Thus, 3-HAA did not prevent bone loss in older mice but instead significantly worsened bone loss. 3-HAA is known to have both pro- and anti- oxidant effects depending on the environment. These data would suggest that at the higher concentrations 3-HAA is acting predominantly as a pro-oxidant molecule accelerating age-related bone loss.

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28

Lee, Sun Young, Ka Hyon Park, Gyuseok Lee, Su-Jin Kim, Won-Hyun Song, Seung-Hee Kwon, Jeong-Tae Koh, Yun Hyun Huh, and Je-Hwang Ryu. "Hypoxia-inducible factor-2α mediates senescence-associated intrinsic mechanisms of age-related bone loss." Experimental & Molecular Medicine 53, no. 4 (April 2021): 591–604. http://dx.doi.org/10.1038/s12276-021-00594-y.

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AbstractAging is associated with cellular senescence followed by bone loss leading to bone fragility in humans. However, the regulators associated with cellular senescence in aged bones need to be identified. Hypoxia-inducible factor (HIF)−2α regulates bone remodeling via the differentiation of osteoblasts and osteoclasts. Here, we report that HIF-2α expression was highly upregulated in aged bones. HIF-2α depletion in male mice reversed age-induced bone loss, as evidenced by an increase in the number of osteoblasts and a decrease in the number of osteoclasts. In an in vitro model of doxorubicin-mediated senescence, the expression of Hif-2α and p21, a senescence marker gene, was enhanced, and osteoblastic differentiation of primary mouse calvarial preosteoblast cells was inhibited. Inhibition of senescence-induced upregulation of HIF-2α expression during matrix maturation, but not during the proliferation stage of osteoblast differentiation, reversed the age-related decrease in Runx2 and Ocn expression. However, HIF-2α knockdown did not affect p21 expression or senescence progression, indicating that HIF-2α expression upregulation in senescent osteoblasts may be a result of aging rather than a cause of cellular senescence. Osteoclasts are known to induce a senescent phenotype during in vitro osteoclastogenesis. Consistent with increased HIF-2α expression, the expression of p16 and p21 was upregulated during osteoclastogenesis of bone marrow macrophages. ChIP following overexpression or knockdown of HIF-2α using adenovirus revealed that p16 and p21 are direct targets of HIF-2α in osteoclasts. Osteoblast-specific (Hif-2αfl/fl;Col1a1-Cre) or osteoclast-specific (Hif-2αfl/fl;Ctsk-Cre) conditional knockout of HIF-2α in male mice reversed age-related bone loss. Collectively, our results suggest that HIF-2α acts as a senescence-related intrinsic factor in age-related dysfunction of bone homeostasis.

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29

Farr, Joshua N., Ming Xu, Megan M. Weivoda, David G. Monroe, Daniel G. Fraser, Jennifer L. Onken, Brittany A. Negley, et al. "Targeting cellular senescence prevents age-related bone loss in mice." Nature Medicine 23, no. 9 (August 21, 2017): 1072–79. http://dx.doi.org/10.1038/nm.4385.

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30

HORSMAN, A., D. H. MARSHALL, and M. PEACOCK. "A Stochastic Model of Age-related Bone Loss and Fractures." Clinical Orthopaedics and Related Research &NA;, no. 195 (May 1985): 207???215. http://dx.doi.org/10.1097/00003086-198505000-00024.

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31

Tresguerres, Isabel F., Faleh Tamimi, Hazem Eimar, Jake Barralet, Jesús Torres, Luis Blanco, and Jesús A. F. Tresguerres. "Resveratrol As Anti-Aging Therapy for Age-Related Bone Loss." Rejuvenation Research 17, no. 5 (October 2014): 439–45. http://dx.doi.org/10.1089/rej.2014.1551.

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32

Melton, L. Joseph, B. Lawrence Riggs, Sara J. Achenbach, Shreyasee Amin, Jon J. Camp, Peggy A. Rouleau, Richard A. Robb, Ann L. Oberg, and Sundeep Khosla. "Does Reduced Skeletal Loading Account for Age-Related Bone Loss?" Journal of Bone and Mineral Research 21, no. 12 (December 1, 2006): 1847–55. http://dx.doi.org/10.1359/jbmr.060908.

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33

Malkin, I., D. Karasik, G. Livshits, and E. Kobyliansky. "Modelling of age-related bone loss using cross-sectional data." Annals of Human Biology 29, no. 3 (January 2002): 256–70. http://dx.doi.org/10.1080/03014460110075729.

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34

Wang, L., J. Banu, C. A. Mcmahan, and D. N. Kalu. "Male rodent model of age-related bone loss in men." Bone 29, no. 2 (August 2001): 141–48. http://dx.doi.org/10.1016/s8756-3282(01)00483-5.

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35

Horsman, A., and D. H. Marshall. "Age-related bone loss and fracture risk: A stochastic model." Mathematical Modelling 7, no. 5-8 (1986): 991–1001. http://dx.doi.org/10.1016/0270-0255(86)90145-4.

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36

Clarke, B. L. "Does Reduced Skeletal Loading Account for Age-Related Bone Loss?" Yearbook of Endocrinology 2008 (January 2008): 200–201. http://dx.doi.org/10.1016/s0084-3741(08)79092-9.

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37

Zebaze, R., A. Ghasem-Zadeh, A. Bohte, S. Iuliano-Burns, E. Mackie, and E. Seeman. "Age-related bone loss: The effect of neglecting intracortical porosity." Bone 44 (May 2009): S117—S118. http://dx.doi.org/10.1016/j.bone.2009.01.261.

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38

Fujiyama, Kaoru, Takeshi Kiriyama, Masako Ito, Hironori Kimura, Masako Tsuruta, Kiyoto Ashizawa, Yuji Nagayama, et al. "Subnormal secretion of parathyroid hormone prevents age-related bone loss." Journal of Bone and Mineral Metabolism 12, S1 (February 1994): S69—S70. http://dx.doi.org/10.1007/bf02375678.

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39

Aguirre, J. I., M. P. Akhter, K. G. Neuville, C. R. Trcalek, A. M. Leeper, A. A. Williams, M. Rivera, et al. "Age-related periodontitis and alveolar bone loss in rice rats." Archives of Oral Biology 73 (January 2017): 193–205. http://dx.doi.org/10.1016/j.archoralbio.2016.10.018.

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40

Sumner, Dale R., M. E. Morbeck, and J. J. Lobick. "Apparent age-related bone loss among adult female Gombe chimpanzees." American Journal of Physical Anthropology 79, no. 2 (June 1989): 225–34. http://dx.doi.org/10.1002/ajpa.1330790210.

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41

Sophocleous⁎, A., E. Landao-Bassonga, R. van 't Hof, S. H. Ralston, and A. I. Idris. "The type 2 cannabinoid receptor protects against age-related bone loss and ovariectomy induced bone loss by stimulating bone formation." Bone 47 (June 2010): S42—S43. http://dx.doi.org/10.1016/j.bone.2010.04.075.

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42

Wang, Tiantian, Hongchen He, Shaxin Liu, Chengsen Jia, Ziyan Fan, Can Zhong, Jiadan Yu, Honghong Liu, and Chengqi He. "Autophagy: A Promising Target for Age-related Osteoporosis." Current Drug Targets 20, no. 3 (January 25, 2019): 354–65. http://dx.doi.org/10.2174/1389450119666180626120852.

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Autophagy is a process the primary role of which is to clear up damaged cellular components such as long-lived proteins and organelles, thus participating in the conservation of different cells. Osteoporosis associated with aging is characterized by consistent changes in bone metabolism with suppression of bone formation as well as increased bone resorption. In advanced age, not only bone mass but also bone strength decrease in both sexes, resulting in an increased incidence of fractures. Clinical and animal experiments reveal that age-related bone loss is associated with many factors such as accumulation of autophagy, increased levels of reactive oxygen species, sex hormone deficiency, and high levels of endogenous glucocorticoids. Available basic and clinical studies indicate that age-associated factors can regulate autophagy. Those factors play important roles in bone remodeling and contribute to decreased bone mass and bone strength with aging. In this review, we summarize the mechanisms involved in bone metabolism related to aging and autophagy, supplying a theory for therapeutic targets to rescue bone mass and bone strength in older people.

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43

Todd, Henry, Gabriel L. Galea, Lee B. Meakin, Peter J. Delisser, Lance E. Lanyon, Sara H. Windahl, and Joanna S. Price. "Wnt16 Is Associated with Age-Related Bone Loss and Estrogen Withdrawal in Murine Bone." PLOS ONE 10, no. 10 (October 9, 2015): e0140260. http://dx.doi.org/10.1371/journal.pone.0140260.

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44

von Wowern, Nina. "Bone mineral content of mandibles: Normal reference values—Rate of age-related bone loss." Calcified Tissue International 43, no. 4 (October 1988): 193–98. http://dx.doi.org/10.1007/bf02555134.

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45

Karesvuo, Petteri, Ulvi K. Gursoy, Pirkko J. Pussinen, Anna L. Suominen, Sisko Huumonen, Eija Vesti, and Eija Könönen. "Alveolar Bone Loss Associated With Age-Related Macular Degeneration in Males." Journal of Periodontology 84, no. 1 (January 2013): 58–67. http://dx.doi.org/10.1902/jop.2012.110643.

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46

Seeman, E. "Age- and Menopause-Related Bone Loss Compromise Cortical and Trabecular Microstructure." Journals of Gerontology Series A: Biological Sciences and Medical Sciences 68, no. 10 (July 5, 2013): 1218–25. http://dx.doi.org/10.1093/gerona/glt071.

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47

Frost, Harold M. "On Our Age-Related Bone Loss: Insights from a New Paradigm." Journal of Bone and Mineral Research 12, no. 10 (October 1, 1997): 1539–46. http://dx.doi.org/10.1359/jbmr.1997.12.10.1539.

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48

Jilka, Robert L., Robert J. Shmookler Reis, and Stavros C. Manolagas. "Age-related bone loss: lessons from the osteoporotic SAMP6 mouse model." International Congress Series 1260 (February 2004): 55–60. http://dx.doi.org/10.1016/s0531-5131(03)01566-8.

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49

Pignolo, Robert J., Rebekah M. Samsonraj, Susan F. Law, Haitao Wang, and Abhishek Chandra. "Targeting Cell Senescence for the Treatment of Age-Related Bone Loss." Current Osteoporosis Reports 17, no. 2 (February 26, 2019): 70–85. http://dx.doi.org/10.1007/s11914-019-00504-2.

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50

Khosla⁎, S. "Mechanisms of age-related bone loss (ECTS Excellence in Research Lecture)." Bone 50 (May 2012): S27. http://dx.doi.org/10.1016/j.bone.2012.02.067.

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

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