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Journal articles on the topic 'Bone formation/resorption'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

Li, Binbin, and Shifeng Yu. "Genistein Prevents Bone Resorption Diseases by Inhibiting Bone Resorption and Stimulating Bone Formation." Biological & Pharmaceutical Bulletin 26, no. 6 (2003): 780–86. http://dx.doi.org/10.1248/bpb.26.780.

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2

Slootweg, M. C., W. W. Most, E. van Beek, L. P. C. Schot, S. E. Papapoulos, and C. W. G. M. Löwik. "Osteoclast formation together with interleukin-6 production in mouse long bones is increased by insulin-like growth factor-I." Journal of Endocrinology 132, no. 3 (March 1992): 433–38. http://dx.doi.org/10.1677/joe.0.1320433.

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ABSTRACT Insulin-like growth factor-I (IGF-I) is a potent stimulator of bone formation. Whether this growth factor also induces bone resorption has not been studied in detail. We used two organ culture systems to examine the direct effect of IGF-I on bone resorption. Fetal mouse radii/ulnae, containing mature osteoclasts, showed no response to IGF-I, indicating that osteoclastic activity is not influenced by IGF-I. Fetal mouse metacarpals/metatarsals, containing just osteoclast precursors and progenitors, showed an increase in resorption in response to IGF-I, indicating that IGF-I stimulates t
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3

Yavropoulou, Maria P., Helen P. Vafiadou, Olympia E. Anastasiou, Vasiliki Tsavdaridou, Georgia H. Kokaraki, and John G. Yovos. "Pioglitazone affects bone resorption but not bone formation." Bone 42 (March 2008): S91. http://dx.doi.org/10.1016/j.bone.2007.12.173.

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4

Kitaura, Hideki, Aseel Marahleh, Fumitoshi Ohori, Takahiro Noguchi, Wei-Ren Shen, Jiawei Qi, Yasuhiko Nara, Adya Pramusita, Ria Kinjo, and Itaru Mizoguchi. "Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption." International Journal of Molecular Sciences 21, no. 14 (July 21, 2020): 5169. http://dx.doi.org/10.3390/ijms21145169.

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The process of bone remodeling is the result of the regulated balance between bone cell populations, namely bone-forming osteoblasts, bone-resorbing osteoclasts, and the osteocyte, the mechanosensory cell type. Osteoclasts derived from the hematopoietic stem cell lineage are the principal cells involved in bone resorption. In osteolytic diseases such as rheumatoid arthritis, periodontitis, and osteoporosis, the balance is lost and changes in favor of bone resorption. Therefore, it is vital to elucidate the mechanisms of osteoclast formation and bone resorption. It has been reported that osteoc
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5

Franco, Leonardo, and Mario Alejandro Ortíz Salazar. "Biochemical markers of bone metabolism." Revista Estomatología 18, no. 1 (September 28, 2017): 30–34. http://dx.doi.org/10.25100/re.v18i1.5707.

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The quantity and quality of bone tissue renewal are dependent on the generation of new bone (deposition) mediated by osteoblasts and the loss (resorption) mediated by osteoclasts. For each of these processes there are important markers that can be measured in serum or urine.
 Resorption markers are products of metabolic degradation of bone matrix in particu-lar of the type I collagen (hydroxyproline, pyridinoline and deoxypyridinoline). In addition, the resorptive activity can also be evaluated through the tartrate resistant acid phosphatase (TRAP) and calcium-creatinine ratio in urine. B
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6

Erjavec, Igor, Jelena Brkljacic, Slobodan Vukicevic, Boris Jakopovic, and Ivan Jakopovich. "Mushroom Extracts Decrease Bone Resorption and Improve Bone Formation." International Journal of Medicinal Mushrooms 18, no. 7 (2016): 559–69. http://dx.doi.org/10.1615/intjmedmushrooms.v18.i7.10.

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7

Yamaguchi, Masayoshi. "Role of zinc in bone formation and bone resorption." Journal of Trace Elements in Experimental Medicine 11, no. 2-3 (1998): 119–35. http://dx.doi.org/10.1002/(sici)1520-670x(1998)11:2/3<119::aid-jtra5>3.0.co;2-3.

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8

Buckland, Jenny. "Dual role for Wnt4: bone formation and bone resorption." Nature Reviews Rheumatology 10, no. 10 (August 26, 2014): 575. http://dx.doi.org/10.1038/nrrheum.2014.146.

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9

Hirayama, T., A. Sabokbar, and NA Athanasou. "Effect of corticosteroids on human osteoclast formation and activity." Journal of Endocrinology 175, no. 1 (October 1, 2002): 155–63. http://dx.doi.org/10.1677/joe.0.1750155.

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Chronic corticosteroid treatment is known to induce bone loss and osteoporosis. Osteoclasts are specialised bone-resorbing cells that are formed from mononuclear phagocyte precursors that circulate in the monocyte fraction. In this study we have examined the effect of the synthetic glucocorticoid, dexamethasone, on human osteoclast formation and bone-resorbing activity. Human monocytes were cultured for up to 21 days on glass coverslips and dentine slices, with soluble receptor activator for nuclear factor kappaB ligand (RANKL; 30 ng/ml) and human macrophage-colony stimulating factor (M-CSF; 2
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10

Lean, J. M., J. W. M. Chow, and T. J. Chambers. "The rate of cancellous bone formation falls immediately after ovariectomy in the rat." Journal of Endocrinology 142, no. 1 (July 1994): 119–25. http://dx.doi.org/10.1677/joe.0.1420119.

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Abstract We have recently found that administration of oestradiol-17β (OE2) to rats stimulates trabecular bone formation. It is not known, however, whether oestrogen has a similar action on bone formation rate under physiological circumstances. Oestrogen is known to suppress bone resorption, and oestrogen-deficient states in the rat, as in humans, are associated with an increase in bone resorption that entrains an increase in bone formation. To see if the latter masks a relative reduction in bone formation, due to oestrogen deficiency, we measured bone formation very early after ovariectomy, b
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11

Suda, Tatsuo, and Naoyuki Takahashi. "Control mechanism of bone formation and resorption." Ensho 9, no. 5 (1989): 359–67. http://dx.doi.org/10.2492/jsir1981.9.359.

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12

Andersen, Thomas L., Mohamed E. Abdelgawad, Helene B. Kristensen, Ellen M. Hauge, Lars Rolighed, Jens Bollerslev, Per Kjærsgaard-Andersen, and Jean-Marie Delaisse. "Understanding Coupling between Bone Resorption and Formation." American Journal of Pathology 183, no. 1 (July 2013): 235–46. http://dx.doi.org/10.1016/j.ajpath.2013.03.006.

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13

Marcus, R. "Biochemical assessment of bone resorption and formation." Bone 18, no. 1 (January 1996): S15—S16. http://dx.doi.org/10.1016/8756-3282(95)00375-4.

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14

Piec, Grazyna, Jelena Mirkovitch, Silvia Palacio, Peter F. Mühlradt, and Rolf Felix. "Effect of MALP-2, a Lipopeptide fromMycoplasma fermentans, on Bone Resorption In Vitro." Infection and Immunity 67, no. 12 (December 1, 1999): 6281–85. http://dx.doi.org/10.1128/iai.67.12.6281-6285.1999.

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ABSTRACT Mycoplasmas may be associated with rheumatoid arthritis in various animal hosts. In humans, mycoplasma arthritis has been recorded in association with hypogammaglobulinemia. Mycoplasma fermentans is one mycoplasma species considered to be involved in causing arthritis. To clarify which mycoplasmal compounds contribute to the inflammatory, bone-destructive processes in arthritis, we used a well-defined lipopeptide, 2-kDa macrophage-activating lipopeptide (MALP-2) from M. fermentans, as an example of a class of macrophage-activating compounds ubiquitous in mycoplasmas, to study its effe
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15

Dacquin, Romain, Rachel A. Davey, Catherine Laplace, Régis Levasseur, Howard A. Morris, Steven R. Goldring, Samuel Gebre-Medhin, Deborah L. Galson, Jeffrey D. Zajac, and Gérard Karsenty. "Amylin inhibits bone resorption while the calcitonin receptor controls bone formation in vivo." Journal of Cell Biology 164, no. 4 (February 16, 2004): 509–14. http://dx.doi.org/10.1083/jcb.200312135.

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Amylin is a member of the calcitonin family of hormones cosecreted with insulin by pancreatic β cells. Cell culture assays suggest that amylin could affect bone formation and bone resorption, this latter function after its binding to the calcitonin receptor (CALCR). Here we show that Amylin inactivation leads to a low bone mass due to an increase in bone resorption, whereas bone formation is unaffected. In vitro, amylin inhibits fusion of mononucleated osteoclast precursors into multinucleated osteoclasts in an ERK1/2-dependent manner. Although Amylin +/− mice like Amylin-deficient mice displa
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16

Zhong, Qing, Takashi Itokawa, Supriya Sridhar, Ke-Hong Ding, Ding Xie, Baolin Kang, Wendy B. Bollag, et al. "Effects of glucose-dependent insulinotropic peptide on osteoclast function." American Journal of Physiology-Endocrinology and Metabolism 292, no. 2 (February 2007): E543—E548. http://dx.doi.org/10.1152/ajpendo.00364.2006.

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Acute nutrient ingestion leads to a rapid inhibition of bone resorption while effects on makers of bone formation are less marked or absent, suggesting that there is a transient shift toward skeletal accretion in the immediate postprandial period. The cellular bases for these effects are not clear. Glucose-dependent insulinotropic peptide (GIP), a known modulator of glucose-induced insulin secretion, is secreted from intestinal endocrine cells in response to nutrient ingestion. In addition to the effect of GIP on pancreatic β-cells, GIP receptors are expressed by osteoblastic cells in bone, su
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17

Kitaura, Hideki, Saika Ogawa, Fumitoshi Ohori, Takahiro Noguchi, Aseel Marahleh, Yasuhiko Nara, Adya Pramusita, et al. "Effects of Incretin-Related Diabetes Drugs on Bone Formation and Bone Resorption." International Journal of Molecular Sciences 22, no. 12 (June 19, 2021): 6578. http://dx.doi.org/10.3390/ijms22126578.

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Patients with type 2 diabetes have an increased risk of fracture compared to the general population. Glucose absorption is accelerated by incretin hormones, which induce insulin secretion from the pancreas. The level of the incretin hormone, glucagon-like peptide-1 (GLP-1), shows an immediate postprandial increase, and the circulating level of intact GLP-1 is reduced rapidly by dipeptidyl peptidase-4 (DPP-4)-mediated inactivation. Therefore, GLP-1 receptor agonists and DPP-4 inhibitors are effective in the treatment of type 2 diabetes. However, these incretin-related diabetic agents have been
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18

Gerber, Thomas, Cornelia Ganz, Werner Götz, Kai Helms, Christoph Harms, and Thomas Mittlmeier. "Nanostructured Bone Grafting Substitutes Versus Autologous Cancellous Bone – An Animal Experiment in Sheep." Key Engineering Materials 631 (November 2014): 202–6. http://dx.doi.org/10.4028/www.scientific.net/kem.631.202.

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In an In vivo study the full synthetic bone substitute NanoBone® S (NBS) was analyzed using a standardized bone defect (6 x 12 x 24mm) model in the ovine tibial metaphysis. The defect on the left side was filled with NBS granules and on the right side, autologous bone, harvested from the hip of the same animal, was inserted. After six, 12 and 26 weeks sheep were sacrificed and the tibiae analyzed. Quantitative histomorphological analysis after six weeks showed a resorption of biomaterial from over 60 to 24 percent. In contrast the bone formation after 6, and 12 weeks revealed an osteoneogenesi
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19

Marie, P. J., L. Cancela, N. Le Boulch, and L. Miravet. "Bone changes due to pregnancy and lactation: influence of vitamin D status." American Journal of Physiology-Endocrinology and Metabolism 251, no. 4 (October 1, 1986): E400—E406. http://dx.doi.org/10.1152/ajpendo.1986.251.4.e400.

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The effects of pregnancy and lactation on endosteal bone formation and resorption were evaluated in vitamin D-depleted (-D) and vitamin D-repleted (+D) rats. Pregnancy induced a marked stimulation of osteoclastic bone resorption and of static and dynamic parameters of bone formation and mineralization. Bone resorption increased independently of vitamin D status and did not correlate with plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D] levels, but it was associated with increased plasma immunoreactive parathyroid hormone (iPTH) concentrations. Stimulation of the endosteal bone formation rate was m
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20

BERRY, PATRICIA A., ROSE A. MACIEWICZ, FLAVIA M. CICUTTINI, MARK D. JONES, CAROLINE J. HELLAWELL, and ANITA E. WLUKA. "Markers of Bone Formation and Resorption Identify Subgroups of Patients with Clinical Knee Osteoarthritis Who Have Reduced Rates of Cartilage Loss." Journal of Rheumatology 37, no. 6 (April 15, 2010): 1252–59. http://dx.doi.org/10.3899/jrheum.091055.

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Objective.To determine whether serum markers of bone formation and resorption, used individually or in combination, can be used to identify subgroups who lose cartilage volume at different rates over 2 years within a knee osteoarthritis (OA) population.Methods.Changes in cartilage volume over 2 years were measured in 117 subjects with knee OA using magnetic resonance imaging. We examined relationships between change in cartilage volume and baseline serum markers of bone formation [intact N-terminal propeptide of type I procollagen (PINP) and osteocalcin] and resorption [N-telopeptide of type I
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21

Bacovsky, Jaroslav, Vlastimil Scudla, Marketa Vytrasova, Marie Budikova, and Miroslav Myslivecek. "Monitoring of bone resorption and bone formation in multiple myeloma." Biomedical Papers 146, no. 2 (December 1, 2002): 59–61. http://dx.doi.org/10.5507/bp.2002.012.

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22

Chen, Yu-Si, Qi Guo, Li-Juan Guo, Ting Liu, Xian-Ping Wu, Zhang-Yuan Lin, Hong-Bo He, and Tie-Jian Jiang. "GDF8 inhibits bone formation and promotes bone resorption in mice." Clinical and Experimental Pharmacology and Physiology 44, no. 4 (March 27, 2017): 500–508. http://dx.doi.org/10.1111/1440-1681.12728.

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23

Huang, Willis, and Edward M. Schwarz. "Mechanisms of bone resorption and new bone formation in spondyloarthropathies." Current Rheumatology Reports 4, no. 6 (December 2002): 513–17. http://dx.doi.org/10.1007/s11926-002-0059-0.

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24

Stechschulte, L. A., P. J. Czernik, Z. C. Rotter, F. N. Tausif, C. A. Corzo, D. P. Marciano, A. Asteian, et al. "PPARG Post-translational Modifications Regulate Bone Formation and Bone Resorption." EBioMedicine 10 (August 2016): 174–84. http://dx.doi.org/10.1016/j.ebiom.2016.06.040.

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25

Bernhardt, Anne, Jana Bacova, Uwe Gbureck, and Michael Gelinsky. "Influence of Cu2+ on Osteoclast Formation and Activity In Vitro." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2451. http://dx.doi.org/10.3390/ijms22052451.

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Background: Copper-containing biomaterials are increasingly applied for bone regeneration due to their pro-angiogenetic, pro-osteogenetic and antimicrobial properties. Therefore, the effect of Cu2+ on osteoclasts, which play a major role in bone remodeling was studied in detail. Methods: Human primary osteoclasts, differentiated from human monocytes were differentiated or cultivated in the presence of Cu2+. Osteoclast formation and activity were analyzed by measurement of osteoclast-specific enzyme activities, gene expression analysis and resorption assays. Furthermore, the glutathione levels
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26

Malaval, Luc, Ndéyé Marième Wade-Guéye, Maya Boudiffa, Jia Fei, Ralph Zirngibl, Frieda Chen, Norbert Laroche, et al. "Bone sialoprotein plays a functional role in bone formation and osteoclastogenesis." Journal of Experimental Medicine 205, no. 5 (May 5, 2008): 1145–53. http://dx.doi.org/10.1084/jem.20071294.

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Bone sialoprotein (BSP) and osteopontin (OPN) are both highly expressed in bone, but their functional specificities are unknown. OPN knockout (−/−) mice do not lose bone in a model of hindlimb disuse (tail suspension), showing the importance of OPN in bone remodeling. We report that BSP−/− mice are viable and breed normally, but their weight and size are lower than wild-type (WT) mice. Bone is undermineralized in fetuses and young adults, but not in older (≥12 mo) BSP−/− mice. At 4 mo, BSP−/− mice display thinner cortical bones than WT, but greater trabecular bone volume with very low bone for
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Florencio-Silva, Rinaldo, Gisela Rodrigues da Silva Sasso, Estela Sasso-Cerri, Manuel Jesus Simões, and Paulo Sérgio Cerri. "Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells." BioMed Research International 2015 (2015): 1–17. http://dx.doi.org/10.1155/2015/421746.

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Bone tissue is continuously remodeled through the concerted actions of bone cells, which include bone resorption by osteoclasts and bone formation by osteoblasts, whereas osteocytes act as mechanosensors and orchestrators of the bone remodeling process. This process is under the control of local (e.g., growth factors and cytokines) and systemic (e.g., calcitonin and estrogens) factors that all together contribute for bone homeostasis. An imbalance between bone resorption and formation can result in bone diseases including osteoporosis. Recently, it has been recognized that, during bone remodel
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28

Hardy, R., and M. S. Cooper. "Bone loss in inflammatory disorders." Journal of Endocrinology 201, no. 3 (February 24, 2009): 309–20. http://dx.doi.org/10.1677/joe-08-0568.

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Chronic inflammatory diseases of almost any cause are associated with bone loss. Bone loss is due to direct effects of inflammation, poor nutrition, reduced lean body mass, immobility and the effects of treatments, especially glucocorticoids. These mechanisms are complex and interrelated but are ultimately mediated through effects on the bone remodelling cycle. Inflammatory disease can increase bone resorption, decrease bone formation but most commonly impacts on both of these processes resulting in an uncoupling of bone formation from resorption in favour of excess resorption. This review wil
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29

Tani-Ishii, N., A. Tsunoda, T. Teranaka та T. Umemoto. "Autocrine Regulation of Osteoclast Formation and Bone Resorption by IL-1α and TNFα". Journal of Dental Research 78, № 10 (жовтень 1999): 1617–23. http://dx.doi.org/10.1177/00220345990780100601.

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Bone resorption is regulated by the cytokines within marrow cells that mediate osteoclast formation and activation. IL-1 and TNF induce bone resorption by stimulating the production of osteoclast-like multinucleated cells and by increasing the bone-resorbing activity of formed osteoclasts. This study was designed to detect IL-1 and TNF in osteoclasts in vitro and to determine whether these cytokines up-regulate osteoclast differentiation and bone resorption. The production of IL-1α, -β, and TNFa, β in osteoclasts was examined immunohistochemically and by in situ hybridization. In the co-cultur
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Na, WooJin, and Young-Hee Kang. "Aesculetin Inhibits Bone Resorption Through Down-Regulating Differentiation and Lysosomal Formation in Osteoclasts." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 442. http://dx.doi.org/10.1093/cdn/nzaa045_075.

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Abstract Objectives For the optimal resorption of mineralized bone extracellular matrix, osteoclasts require the generation of a resorption lacuna characterized by the presence of specific proteases and a low pH. Thus, bone resorption by osteoclasts highly rely on lysosomes, the organelles specialized in intra- and extracellular material degradation. Aesculetin, a derivative of coumarin, possesses anti-inflammatory and anti-bacterial effects. The purpose of this study was to identify that aesculetin inhibited osteoclast differentiation and bone resorption through down-regulating lysosomal form
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31

Fu, Chao, and Ruyi Shi. "Osteoclast biology in bone resorption: a review." STEMedicine 1, no. 4 (September 3, 2020): e57. http://dx.doi.org/10.37175/stemedicine.v1i4.57.

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What we know about bone resorption has changed a lot in the last few decades. The osteoclast is the only cell to nibble and break down the bone, and in the formation and resorption of bone tissue, osteoclasts play an important role. Once the balance of bone formation and bone loss is out of control, diseases like osteopetrosis and osteoporosis occur. Bone resorption is a unique function of osteoblasts, which are multinucleated cells formed by the fusion of mononuclear progenitor cells of the monocyte/macrophage family. In the formation of osteoclasts, there are two main factors affecting this
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Kenkre, JS, and JHD Bassett. "The bone remodelling cycle." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 55, no. 3 (March 4, 2018): 308–27. http://dx.doi.org/10.1177/0004563218759371.

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The bone remodelling cycle replaces old and damaged bone and is a highly regulated, lifelong process essential for preserving bone integrity and maintaining mineral homeostasis. During the bone remodelling cycle, osteoclastic resorption is tightly coupled to osteoblastic bone formation. The remodelling cycle occurs within the basic multicellular unit and comprises five co-ordinated steps; activation, resorption, reversal, formation and termination. These steps occur simultaneously but asynchronously at multiple different locations within the skeleton. Study of rare human bone disease and anima
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Mamedova, Elizaveta O., Tatiana A. Grebennikova, Zhanna E. Belaya, and Liudmila Y. Rozhinskaya. "Sclerostin antibodies as novel anabolic therapy for osteoporosis." Osteoporosis and Bone Diseases 21, no. 3 (April 8, 2019): 21–29. http://dx.doi.org/10.14341/osteo10127.

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Osteoporosis medications are divided into two groups: those inhibiting bone resorption and formation (bisphosphonates and denosumab), and those stimulating bone formation i.e. having an anabolic effect. The latter include teriparatide, parathyroid hormone 1-84 and abaloparatide, all of which stimulate bone resorption as well as bone formation, which limits their anabolic effect.&#x0D; The discovery of sclerostin – the key inhibitor of bone formation – has led to development of the concept that inhibition of this protein could stimulate bone formation. Romosozumab is a human monoclonal antibody
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34

Langdahl, Bente, Serge Ferrari, and David W. Dempster. "Bone modeling and remodeling: potential as therapeutic targets for the treatment of osteoporosis." Therapeutic Advances in Musculoskeletal Disease 8, no. 6 (October 6, 2016): 225–35. http://dx.doi.org/10.1177/1759720x16670154.

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The adult skeleton is renewed by remodeling throughout life. Bone remodeling is a process where osteoclasts and osteoblasts work sequentially in the same bone remodeling unit. After the attainment of peak bone mass, bone remodeling is balanced and bone mass is stable for one or two decades until age-related bone loss begins. Age-related bone loss is caused by increases in resorptive activity and reduced bone formation. The relative importance of cortical remodeling increases with age as cancellous bone is lost and remodeling activity in both compartments increases. Bone modeling describes the
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Vacher, Jean, Michael Bruccoleri, and Monica Pata. "Ostm1 from Mouse to Human: Insights into Osteoclast Maturation." International Journal of Molecular Sciences 21, no. 16 (August 5, 2020): 5600. http://dx.doi.org/10.3390/ijms21165600.

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The maintenance of bone mass is a dynamic process that requires a strict balance between bone formation and resorption. Bone formation is controlled by osteoblasts, while osteoclasts are responsible for resorption of the bone matrix. The opposite functions of these cell types have to be tightly regulated not only during normal bone development, but also during adult life, to maintain serum calcium homeostasis and sustain bone integrity to prevent bone fractures. Disruption of the control of bone synthesis or resorption can lead to an over accumulation of bone tissue in osteopetrosis or convers
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Fuller, K., J. M. Owens, C. J. Jagger, A. Wilson, R. Moss, and T. J. Chambers. "Macrophage colony-stimulating factor stimulates survival and chemotactic behavior in isolated osteoclasts." Journal of Experimental Medicine 178, no. 5 (November 1, 1993): 1733–44. http://dx.doi.org/10.1084/jem.178.5.1733.

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Macrophage colony-stimulating factor (M-CSF) is known to play an important role in osteoclast formation. However, its actions on mature cells have not been fully characterized. We now report that M-CSF dramatically stimulates osteoclastic motility and spreading; osteoclasts responded to a gradient of M-CSF with orientation, and random cell polarization occurred after isotropic exposure. M-CSF also supported the survival of osteoclasts by preventing apoptosis. Paradoxically, M-CSF inhibits bone resorption by isolated osteoclasts. We found that this was effected predominantly by reduction in the
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37

Suda, Tatsuo. "The Control Mechanism of Bone Formation and Resorption." Journal of the Kyushu Dental Society 45, no. 4 (1991): 549–51. http://dx.doi.org/10.2504/kds.45.549.

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38

Leah, Emma. "Nitroglycerin ointment boosts bone formation and reduces resorption." Nature Reviews Rheumatology 7, no. 4 (April 2011): 196. http://dx.doi.org/10.1038/nrrheum.2011.32.

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39

Kim, Beom-Jun, Young-Sun Lee, Sun-Young Lee, Wook-Young Baek, Young Jin Choi, Sung Ah Moon, Seung Hun Lee, et al. "Osteoclast-secreted SLIT3 coordinates bone resorption and formation." Journal of Clinical Investigation 128, no. 4 (March 5, 2018): 1429–41. http://dx.doi.org/10.1172/jci91086.

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40

Williams, S., A. Wakisaka, Q. Q. Zeng, J. Barnes, S. Seyedin, G. Martin, W. J. Wechter, and C. T. Liang. "Effect of Minocycline on Osteoporosis." Advances in Dental Research 12, no. 1 (November 1998): 71–75. http://dx.doi.org/10.1177/08959374980120012401.

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The effect of oral minocycline on osteopenia in ovariectomized (OVX) old rats was examined in this study. Rats were divided into 4 groups: sham-operated, OVX followed by treatment with vehicle, minocycline, or 17β-estradiol. The treatment was initiated one day after OVX and proceeded for 8 wks. OVX reduced bone mineral density (BMD) in the whole femur and in the femoral regions that are enriched in trabecular bone. Treatment with minocycline or estrogen prevented a decrease in BMD. Femoral trabecular bone area, trabecular number, and trabecular thickness were reduced, and trabecular separation
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Southmayd, Emily A., Nancy I. Williams, Rebecca J. Mallinson, and Mary Jane De Souza. "Energy Deficiency Suppresses Bone Turnover in Exercising Women With Menstrual Disturbances." Journal of Clinical Endocrinology & Metabolism 104, no. 8 (March 21, 2019): 3131–45. http://dx.doi.org/10.1210/jc.2019-00089.

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Abstract Context In exercising women, energy deficiency can disrupt the balance of bone formation and resorption, resulting in bone loss and an altered rate of bone turnover, which may influence future bone mineral density and fracture risk. Objective To assess the effects of energy status and estrogen status on bone turnover. Design Cross-sectional. Setting The Women’s Health and Exercise Laboratory at Pennsylvania State University. Participants Exercising women (n = 109) operationally defined as energy deficient or replete based on total triiodothyronine concentration and as estrogen deficie
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42

Jensen, Pia Rosgaard, Thomas Levin Andersen, Brenda L. Pennypacker, Le T. Duong, Lars H. Engelholm, and Jean-Marie Delaissé. "A supra-cellular model for coupling of bone resorption to formation during remodeling: lessons from two bone resorption inhibitors affecting bone formation differently." Biochemical and Biophysical Research Communications 443, no. 2 (January 2014): 694–99. http://dx.doi.org/10.1016/j.bbrc.2013.12.036.

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43

Szulc, Pawel. "Biochemical Bone Turnover Markers and Osteoporosis in Older Men: Where Are We?" Journal of Osteoporosis 2011 (2011): 1–5. http://dx.doi.org/10.4061/2011/704015.

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In men aged less than 60, the association of serum and urinary levels of biochemical bone turnover markers (BTMs) and bone mineral density (BMD) is weak or not significant. After this age, higher BTM levels are correlated weakly, but significantly, with lower BMD and faster bone loss. Limited data from the cohort studies suggest that BTM measurement does not improve the prediction of fragility fractures in older men in comparison with age, BMD, history of falls and fragility fractures. Testosterone replacement therapy (TRT) decreases bone resorption. During TRT, bone formation markers slightly
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Lee, Jin-Young, Da-Ae Kim, Eun-Young Kim, Eun-Ju Chang, So-Jeong Park, and Beom-Jun Kim. "Lumican Inhibits Osteoclastogenesis and Bone Resorption by Suppressing Akt Activity." International Journal of Molecular Sciences 22, no. 9 (April 29, 2021): 4717. http://dx.doi.org/10.3390/ijms22094717.

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Lumican, a ubiquitously expressed small leucine-rich proteoglycan, has been utilized in diverse biological functions. Recent experiments demonstrated that lumican stimulates preosteoblast viability and differentiation, leading to bone formation. To further understand the role of lumican in bone metabolism, we investigated its effects on osteoclast biology. Lumican inhibited both osteoclast differentiation and in vitro bone resorption in a dose-dependent manner. Consistent with this, lumican markedly decreased the expression of osteoclastogenesis markers. Moreover, the migration and fusion of p
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Ryu, Seung Min, Myun Whan Ahn, Chul Hyun Park, Gun Woo Lee, In Hwan Song, Hyo Sae Ahn, Jooseong Kim, and Sukyoung Kim. "Effect of water glass coating of tricalcium phosphate granules on in vivo bone formation." Journal of Biomaterials Applications 33, no. 5 (November 2018): 662–72. http://dx.doi.org/10.1177/0885328218808038.

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Background Recently, some authors introduced a water glass (WG, sodium-silicate glass; Na2O·SiO2·nH2O) coating over tricalcium phosphate (TCP) bioceramic to modulate its resorption rate and enhance the bone cell behaviors. In this study, four different types of granular samples were prepared to evaluate the ability of new bone formation in vivo using micro-computed tomography and histology. Methods Four types sample groups: group A (pure HA as a negative resorption control); group B (pure TCP as a positive resorption control); group C (WG-coated TCP as an early resorption model); and group D (
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46

Ueland, Thor. "GH/IGF-I and bone resorption in vivo and in vitro." European Journal of Endocrinology 152, no. 3 (March 2005): 327–32. http://dx.doi.org/10.1530/eje.1.01874.

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IGF-I may act as one of several coupling agents by activating bone formation and bone resorption. In vivo studies in normal subjects, postmenopausal women and patients with excess or diminished GH production (acromegaly and GHD) indicate that both GH and IGF-I activate osteoclasts, but that GH has a more pronounced effect, independently of IGF-I. In vitro, GH and IGF receptors have been demonstrated on osteoclasts and both GH and IGF-I may directly modify osteoclast function and activity. In addition to direct effects on osteoclasts, GH and IGF-I may affect bone resorption indirectly by stimul
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Elefteriou, Florent, Shu Takeda, Xiuyun Liu, Dawna Armstrong, and Gerard Karsenty. "Monosodium Glutamate-Sensitive Hypothalamic Neurons Contribute to the Control of Bone Mass." Endocrinology 144, no. 9 (September 1, 2003): 3842–47. http://dx.doi.org/10.1210/en.2003-0369.

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Abstract Using chemical lesioning we previously identified hypothalamic neurons that are required for leptin antiosteogenic function. In the course of these studies we observed that destruction of neurons sensitive to monosodium glutamate (MSG) in arcuate nuclei did not affect bone mass. However MSG treatment leads to hypogonadism, a condition inducing bone loss. Therefore the normal bone mass of MSG-treated mice suggested that MSG-sensitive neurons may be implicated in the control of bone mass. To test this hypothesis we assessed bone resorption and bone formation parameters in MSG-treated mi
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Faraz, Shahdabul, Roger N. Pearse, Sujitha Yadlapati, David Jayabalan, Adriana C. Rossi, Tomer M. Mark, Ruben Niesvizky, and Joseph Lane. "The Clinical Utility of Bone Resorption and Bone Formation Markers in Multiple Myeloma." Blood 126, no. 23 (December 3, 2015): 5373. http://dx.doi.org/10.1182/blood.v126.23.5373.5373.

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Abstract Introduction: While bone resorption markers such as urinary N-terminal telopeptide (NTx) have long been used in research, serum C-terminal telopeptide (CTx) has become the preferred marker of bone status in multiple myeloma (MM). A full understanding of the clinical utility of CTx, as well as the bone formation markers osteocalcin (OC) and bone-specific alkaline phosphatase (BSAP), in MM is still lacking. In this study, we evaluated levels of CTx, OC, and BSAP in a cohort of MM patients to better understand their roles. Methods: One set of CTx, OC, and BSAP data was obtained by random
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Tumber, A., S. Papaioannou, J. Breckon, MC Meikle, JJ Reynolds, and PA Hill. "The effects of serine proteinase inhibitors on bone resorption in vitro." Journal of Endocrinology 178, no. 3 (September 1, 2003): 437–47. http://dx.doi.org/10.1677/joe.0.1780437.

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The aims of this study were to identify the role and sites of action of serine proteinases (SPs) in bone resorption, a process which involves a cascade of events, the central step of which is the removal of bone matrix by osteoclasts (OCs). This resorbing activity, however, is also determined by recruitment of new OCs to future resorption sites and removal of the osteoid layer by osteoblasts (OBs), which enables OCs to gain access to the underlying mineralized bone. The resorption systems we have studied consisted of (i) neonatal calvarial explants, (ii) isolated OCs cultured on ivory slices,
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Roy, Michèle, and Sophie Roux. "Rab GTPases in Osteoclastic Bone Resorption and Autophagy." International Journal of Molecular Sciences 21, no. 20 (October 16, 2020): 7655. http://dx.doi.org/10.3390/ijms21207655.

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Small guanosine triphosphate hydrolases (GTPases) of the Rab family are involved in plasma membrane delivery, fusion events, and lysosomal and autophagic degradation pathways, thereby regulating signaling pathways and cell differentiation and function. Osteoclasts are bone-resorbing cells that maintain bone homeostasis. Polarized vesicular trafficking pathways result in the formation of the ruffled border, the osteoclast’s resorptive organelle, which also assists in transcytosis. Here, we reviewed the different roles of Rab GTPases in the endomembrane machinery of osteoclasts and in bone disea
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