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Articles de revues sur le sujet « Bone resorption »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 25 juillet 2025

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1

Carron, CP, DM Meyer, VW Engleman, et al. "Peptidomimetic antagonists of alphavbeta3 inhibit bone resorption by inhibiting osteoclast bone resorptive activity, not osteoclast adhesion to bone." Journal of Endocrinology 165, no. 3 (2000): 587–98. http://dx.doi.org/10.1677/joe.0.1650587.

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Osteoclasts are actively motile on bone surfaces and undergo alternating cycles of migration and resorption. Osteoclast interaction with the extracellular matrix plays a key role in the osteoclast resorptive process and a substantial body of evidence suggests that integrin receptors are important in osteoclast function. These integrin receptors bind to the Arg-Gly-Asp (RGD) sequence found in a variety of extracellular matrix proteins and it is well established that the interaction of osteoclast alpha v beta 3 integrin with the RGD motif within bone matrix proteins is important in osteoclast-me

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Flatten, Jana, Thomasz Gedrange, Christoph Bourauel, Ludger Keilig, and Anna Konermann. "The Role of Bone and Root Resorption on the Biomechanical Behavior of Mandibular Anterior Teeth Subjected to Orthodontic Forces: A Finite Element Approach." Biomedicines 12, no. 9 (2024): 1959. http://dx.doi.org/10.3390/biomedicines12091959.

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Aims: This study was conducted to systematically evaluate the biomechanical impact of varying degrees of root and bone resorption resulting from periodontitis and orthodontic tooth movement (OTM) on the mandibular anterior teeth. The objective was to determine whether these distinct resorption patterns exert a specific influence on tooth displacement and strain patterns. Methods: A finite element (FE) model of an idealized anterior mandible from the first premolar in the third to the fourth quadrant was developed without bone or root resorption and a constant periodontal ligament (PDL) thickne

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Chu, Pei-Wen, Yu-Hsu Chen, Chien-Hui Chen, and Shau-Kwaun Chen. "Inflammatory environments disrupt both bone formation and bone resorption." Journal of Immunology 204, no. 1_Supplement (2020): 224.46. http://dx.doi.org/10.4049/jimmunol.204.supp.224.46.

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Abstract Inflammation has been associated with bone diseases such as osteoporosis and osteoarthritis. Bone loss were reported in the patients of several inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease. However, how inflammation influence bone metabolism remains elusive. The bone loss in inflammatory environments are widely considered as the results of osteoclast overactivation which leads to excessive bone resorption. We previously discovered that osteoclasts induced from RAW macrophage treated with RANKL exhibited different cell pr

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Towhidul Alam, A. S. M., Christopher L. H. Huang, David R. Blake, and Mone Zaidi. "A hypothesis for the local control of osteoclast function by Ca2+, nitric oxide and free radicals." Bioscience Reports 12, no. 5 (1992): 369–80. http://dx.doi.org/10.1007/bf01121500.

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Several important conclusions have recently emerged from in vitro studies on the resorptive cell of bone, the osteoclast. First, it has been established that osteoclast function is modulated locally, by changes in the local concentration of Ca2+ caused by hydroxyapatite dissolution. It is thought that activation by Ca2+ of a surface membrane Ca2+ receptor mediates these effects, hence providing a feedback control. Second, a number of molecules produced locally by the endothelial cell, with which the osteoclast is in intimate contact, have been found to affect bone resorption profoundly. For in

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Borggaard, Xenia G., Dinisha C. Pirapaharan, Jean-Marie Delaissé, and Kent Søe. "Osteoclasts’ Ability to Generate Trenches Rather Than Pits Depends on High Levels of Active Cathepsin K and Efficient Clearance of Resorption Products." International Journal of Molecular Sciences 21, no. 16 (2020): 5924. http://dx.doi.org/10.3390/ijms21165924.

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Until recently, it was well-accepted that osteoclasts resorb bone according to the resorption cycle model. This model is based on the assumption that osteoclasts are immobile during bone erosion, allowing the actin ring to be firmly attached and thereby provide an effective seal encircling the resorptive compartment. However, through time-lapse, it was recently documented that osteoclasts making elongated resorption cavities and trenches move across the bone surface while efficiently resorbing bone. However, it was also shown that osteoclasts making rounded cavities and pits indeed resorb bone

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Datta, Harish K., Iain MacIntyre, and Mone Zaidi. "The effect of extracellular calcium elevation on morphology and function of isolated rat osteoclasts." Bioscience Reports 9, no. 6 (1989): 747–51. http://dx.doi.org/10.1007/bf01114813.

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Osteoclasts are large multinucleate cells unique in their capacity to resorb bone. These cells are exposed locally to high levels of ionised calcium during the process of resorption. We have therefore examined the effect of elevated extracellular calcium on the morphology and function of freshly disaggregated rat osteoclasts. Cell size and motility were quantitated by time-lapse video recording together with digitisation and computer-centred image analysis. In order to assess the resorptive capacity of isolated osteoclasts, we measured the total area of resorption of devitalised cortical bone

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Fuller, Karen, Barrie Kirstein, and Timothy J. Chambers. "Regulation and enzymatic basis of bone resorption by human osteoclasts." Clinical Science 112, no. 11 (2007): 567–75. http://dx.doi.org/10.1042/cs20060274.

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Although much has been learned recently of the mechanisms that regulate osteoclastic differentiation, much less is known of the means through which their resorptive activity is controlled. This is especially so for human osteoclasts. We have recently developed an assay that allows us to measure resorptive activity while minimizing confounding effects on differentiation by optimizing osteoclastogenesis, so that measurable resorption occurs over a short period, and by relating resorption in each culture during the test period to the resorption that had occurred in the same culture in a prior con

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Feng, Shi, Zhiyong Zhang, Lei Shi, et al. "Temporal Bone Resorption." Journal of Craniofacial Surgery 26, no. 2 (2015): e185-e187. http://dx.doi.org/10.1097/scs.0000000000001452.

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Taguchi, Takafumi, and Yoshio Terada. "Subperiosteal Bone Resorption." New England Journal of Medicine 370, no. 21 (2014): e32. http://dx.doi.org/10.1056/nejmicm1308814.

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Aspenberg, P., and P. Herbertsson. "PERIPROSTHETIC BONE RESORPTION." Journal of Bone and Joint Surgery. British volume 78-B, no. 4 (1996): 641–46. http://dx.doi.org/10.1302/0301-620x.78b4.0780641.

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Zhong, Qing, Takashi Itokawa, Supriya Sridhar, et al. "Effects of glucose-dependent insulinotropic peptide on osteoclast function." American Journal of Physiology-Endocrinology and Metabolism 292, no. 2 (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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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 (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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Franco, Leonardo, and Mario Alejandro Ortíz Salazar. "Biochemical markers of bone metabolism." Revista Estomatología 18, no. 1 (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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Klein, Gordon L. "The Role of Bone in Muscle Wasting." International Journal of Molecular Sciences 22, no. 1 (2020): 392. http://dx.doi.org/10.3390/ijms22010392.

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This review describes the role of bone resorption in muscle atrophy as well as in muscle protein anabolism. Both catabolic and anabolic pathways involve components of the proinflammatory cytokine families and release of factors stored in bone during resorption. The juxtaposition of the catabolic and anabolic resorption-dependent pathways raises new questions about control of release of factors from bone, quantity of release in a variety of conditions, and relation of factors released from bone. The catabolic responses involve release of calcium from bone into the circulation resulting in incre

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Duka, Milos, Zoran Lazic, and Marija Bubalo. "Effect of local administration of platelet-rich plasma and guided tissue regeneration on the level of bone resorption in early dental implant insertion." Vojnosanitetski pregled 65, no. 6 (2008): 462–68. http://dx.doi.org/10.2298/vsp0806462d.

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Background/Aim. Osseointegration is a result of cellular migration, differentiation, bone formation, and bone remodeling on the surface of an implant. Each of these processes depends on platelets and blood coagulum. Platelet-rich plasma (PRP) is used to improve osseointegration and stability of implants. The aim of the research was to test the influence that PRP and guided tissue regeneration in bone defects have on bone defect filling and the level of bone resorption in early implant insertion. Methods. This experimental study included 10 dogs. A total of 40 BCT implants were inserted, 4 in e

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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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Barberán M., Marcela, Patricia Díaz G., Claudio Liberman G., and Maritza Garrido P. "Marcadores de recambio óseo en mujeres postmenopáusicas: utilidad clínica." Revista Hospital Clínico Universidad de Chile 27, no. 1 (2016): 55–63. http://dx.doi.org/10.5354/2735-7996.2016.71118.

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Bone metabolism is a dynamic process, which includes formation and resorption. Osteoblast and osteoclast are responsible of replacing 20% of bone each year. Bone Markers are fragments of bone matrix; these peptides are released in the process of formation and resorption, later accumulated in body compartments (bone and blood) and finally excreted in the urine, reflecting bone dynamic. The international Federation of Osteoporosis and the International Federation of Laboratory and Clinical Chemistry recommend the use of these two markers (one representing bone formation and the other bone resorp

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Klein, Gordon L. "Transforming Growth Factor-Beta in Skeletal Muscle Wasting." International Journal of Molecular Sciences 23, no. 3 (2022): 1167. http://dx.doi.org/10.3390/ijms23031167.

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Transforming growth factor-beta (TGF-β) is part of a family of molecules that is present in many body tissues and performs many different functions. Evidence has been obtained from mice and human cancer patients with bony metastases and non-metastatic disease, as well as pediatric burn patients, that inflammation leads to bone resorption and release of TGF-β from the bone matrix with paracrine effects on muscle protein balance, possibly mediated by the generation of reactive oxygen species. Whether immobilization, which confounds the etiology of bone resorption in burn injury, also leads to th

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Calle, Yolanda, Gareth E. Jones, Chris Jagger, et al. "WASp deficiency in mice results in failure to form osteoclast sealing zones and defects in bone resorption." Blood 103, no. 9 (2004): 3552–61. http://dx.doi.org/10.1182/blood-2003-04-1259.

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Abstract No defects related to deficiency of the Wiskott-Aldrich Syndrome protein (WASp) have been described in osteoclasts. Here we show that there are significant morphologic and functional abnormalities. WASp-null cells spread over a much larger surface area and are highly polykaryotic. In their migratory phase, normal cells assemble clusters of podosomes behind their leading edges, whereas during the bone resorptive phase multiple podosomes are densely aggregated in well-defined actin rings forming the sealing zone. In comparison, WASp-null osteoclasts in either phase are markedly depleted

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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 (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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Ueland, Thor. "GH/IGF-I and bone resorption in vivo and in vitro." European Journal of Endocrinology 152, no. 3 (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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Fuller, K., J. M. Owens, and T. J. Chambers. "Macrophage inflammatory protein-1 alpha and IL-8 stimulate the motility but suppress the resorption of isolated rat osteoclasts." Journal of Immunology 154, no. 11 (1995): 6065–72. http://dx.doi.org/10.4049/jimmunol.154.11.6065.

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Abstract Cells of the osteoblastic lineage play a major role in the regulation of osteoclastic bone resorption. Recent studies have demonstrated production of chemokines by osteoblastic cells. Although these phagocyte-stimulating and proinflammatory cytokines act as chemoattractants and activators for other members of the hemopoietic lineage, their actions on osteoclasts have not been characterized. We found that macrophage inflammatory protein-1 alpha (MIP-1 alpha) and IL-8 inhibited bone resorption by rat osteoclasts, primarily through reduction in the proportion of osteoclasts resorbing bon

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Moonga, BS, OA Adebanjo, HJ Wang, et al. "Differential effects of interleukin-6 receptor activation on intracellular signaling and bone resorption by isolated rat osteoclasts." Journal of Endocrinology 173, no. 3 (2002): 395–405. http://dx.doi.org/10.1677/joe.0.1730395.

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The effects of the related cytokines interleukin-6 (IL-6), leukemia inhibitory factor (LIF) and oncostatin-M on bone resorption and cytosolic Ca(2+) signaling were compared in isolated rat osteoclasts. In the traditional disaggregated osteoclast (pit) assay, IL-6 and LIF, but not oncostatin-M, conserved the bone resorption otherwise inhibited by high extracellular [Ca(2+)] (15 mM). It produced a paradoxical, concentration-dependent stimulation of resorption by elevated extracellular Ca(2+). In the micro-isolated single osteoclast resorption assay, IL-6, high [Ca(2+)] or IL-6 plus high [Ca(2+)]

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Lin, Xiaoping, Xiaozhe Han, Toshihisa Kawai та Martin A. Taubman. "Antibody to Receptor Activator of NF-κB Ligand Ameliorates T Cell-Mediated Periodontal Bone Resorption". Infection and Immunity 79, № 2 (2010): 911–17. http://dx.doi.org/10.1128/iai.00944-10.

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ABSTRACTActivated T and B lymphocytes in periodontal disease lesions express receptor activator of NF-κB ligand (RANKL), which induces osteoclastic bone resorption. The objective of this study was to evaluate the effects of anti-RANKL antibody on periodontal bone resorptionin vitroandin vivo. Aggregatibacter actinomycetemcomitansouter membrane protein 29 (Omp29) andA. actinomycetemcomitanslipopolysaccharide (LPS) were injected into 3 palatal gingival sites, and Omp29-specific T clone cells were transferred into the tail veins of rats. Rabbit anti-RANKL IgG antibody or F(ab′)2antibody fragments

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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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Zaidi, Mone. "Modularity of osteoclast behaviour and “mode-specific” inhibition of osteoclast function." Bioscience Reports 10, no. 6 (1990): 547–56. http://dx.doi.org/10.1007/bf01116615.

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This study is part of an attempt to understand the role of specific cellular activities in the bone resorptive process. Experiments were performed whereby known pharmacological agents were used to inhibit individual modes of osteoclastic activity, such as motility and secretion. The effects of such treatments on bone resorption were assessed by quantitative scanning electron microscopy. The compounds included colchicine, which was used to inhibit osteoclast motility; molybdate ions which were used to selectively inhibit the catalytic activity of secreted acid phosphatase, and omeprazole which

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Zhang, Jian, Fei Peng, Zhuang Liu, et al. "Cranioplasty with autogenous bone flaps cryopreserved in povidone iodine: a long-term follow-up study." Journal of Neurosurgery 127, no. 6 (2017): 1449–56. http://dx.doi.org/10.3171/2016.8.jns16204.

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OBJECTIVEThe aim of this study was to investigate the long-term therapeutic efficacy of cranioplasty with autogenous bone flaps cryopreserved in povidone iodine and explore the risk factors for bone resorption.METHODSClinical data and follow-up results of 188 patients (with 211 bone flaps) who underwent cranioplasty with autogenous bone flaps cryopreserved in povidone-iodine were retrospectively analyzed. Bone flap resorption was classified into 3 types according to CT features, including bone flap thinning (Type I), reduced bone density (Type II), and osteolysis within the flaps (Type III). T

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Yehudina, Ye.D., and I.Yu. Golovach. "LABORATORY ASPECTS AND CLINICAL SIGNIFICANCE OF BONE TURNOVER MARKERS." Annals of Mechnikov Institute, no. 3 (October 2, 2019): 7–18. https://doi.org/10.5281/zenodo.3469393.

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<strong>Introduction.</strong> With an aging population, there is a marked increase in prevalence of metabolic bone diseases, especially osteoporosis. A serious complication of osteoporosis is non-traumatic bone fractures, which significantly impair quality of life and are associated with comorbid conditions and high mortality. Diseases associated with impaired bone remodeling require timely diagnosis, treatment and monitoring. The consequent public health and socioeconomic burden warrant timely diagnosis, treatment and follow-up of these disorders. Knowing the limitations of radiological tech

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Ishii, Takenobu, Montserrat Ruiz-Torruella, Kenta Yamamoto, et al. "Locally Secreted Semaphorin 4D Is Engaged in Both Pathogenic Bone Resorption and Retarded Bone Regeneration in a Ligature-Induced Mouse Model of Periodontitis." International Journal of Molecular Sciences 23, no. 10 (2022): 5630. http://dx.doi.org/10.3390/ijms23105630.

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It is well known that Semaphorin 4D (Sema4D) inhibits IGF-1-mediated osteogenesis by binding with PlexinB1 expressed on osteoblasts. However, its elevated level in the gingival crevice fluid of periodontitis patients and the broader scope of its activities in the context of potential upregulation of osteoclast-mediated periodontal bone-resorption suggest the need for further investigation of this multifaceted molecule. In short, the pathophysiological role of Sema4D in periodontitis requires further study. Accordingly, attachment of the ligature to the maxillary molar of mice for 7 days induce

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Mathis, Katlynn M., Kathleen M. Sturgeon, Renate M. Winkels, Joachim Wiskemann, Mary Jane De Souza, and Katherine H. Schmitz. "Bone resorption and bone metastasis risk." Medical Hypotheses 118 (September 2018): 36–41. http://dx.doi.org/10.1016/j.mehy.2018.06.013.

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Toledo, Sílvia Regina Caminada, Indhira Dias Oliveira, Oswaldo Keith Okamoto, et al. "Bone deposition, bone resorption, and osteosarcoma." Journal of Orthopaedic Research 28, no. 9 (2010): 1142–48. http://dx.doi.org/10.1002/jor.21120.

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Puspitadewi, Susi R., Lindawati S. Kusdhany, Sri Lelyati C. Masulili, Pitu Wulandari, Hanna B. Iskandar, and Elza I. Auerkari. "The Role of Parathyroid Hormone in Alveolar Bone Resorption on Postmenopausal Women." Open Dentistry Journal 14, no. 1 (2020): 82–87. http://dx.doi.org/10.2174/1874210602014010082.

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Background: Postmenopausal women exhibit reduced bone mineralization, which causes bone resorption, including that of alveolar bone. Parathyroid hormone has been shown to play a role in alveolar bone resorption. Objective: This study aims to analyze relationships between parathyroid hormone and other factors that may contribute to alveolar bone resorption in postmenopausal women. Methods: This cross-sectional study included 82 postmenopausal women aged 50–74 years, who resided in Central and East Jakarta, Indonesia. Subjects' data were obtained through questionnaires, dental examinations, and

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Shen, Shufeng, Yong Hu, Zhentao Chu, and Weixin Dong. "Bone resorption of vertebral bodies at the operative segment after prevail cervical interbody fusion: A case report." Medicine 102, no. 37 (2023): e35231. http://dx.doi.org/10.1097/md.0000000000035231.

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Background: We report an interesting case of bone resorption of vertebral bodies at the operative segment after Peek Prevail cervical interbody fusion. Instability of cervical vertebrae is likely to occur due to increased stress in Peek Prevail implant body for bone resorption. The finite element analysis was used to clarify the biomechanical effects of bone resorption and stress distribution in Peek Prevail implant body. Methods: We reported the case of a 48-year-old male patient who underwent Peek Prevail cervical interbody fusion and exhibited bone resorption 1 month after the surgery in X-

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Richardson, Kimberly K., Wen Ling, Kimberly Krager, et al. "Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice." International Journal of Molecular Sciences 23, no. 2 (2022): 675. http://dx.doi.org/10.3390/ijms23020675.

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The damaging effects of ionizing radiation (IR) on bone mass are well-documented in mice and humans and are most likely due to increased osteoclast number and function. However, the mechanisms leading to inappropriate increases in osteoclastic bone resorption are only partially understood. Here, we show that exposure to multiple fractions of low-doses (10 fractions of 0.4 Gy total body irradiation [TBI]/week, i.e., fractionated exposure) and/or a single exposure to the same total dose of 4 Gy TBI causes a decrease in trabecular, but not cortical, bone mass in young adult male mice. This damagi

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Hatton, R., M. Stimpel, and T. J. Chambers. "Angiotensin II is generated from angiotensin I by bone cells and stimulates osteoclastic bone resorption in vitro." Journal of Endocrinology 152, no. 1 (1997): 5–10. http://dx.doi.org/10.1677/joe.0.1520005.

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Abstract During bone resorption, osteoclasts are closely associated with endothelial cells. The latter are able to produce several agents that regulate bone resorption. In view of the increasing evidence that angiotensin II, which can be generated by endothelial cells, has actions outside the traditional renin-angiotensin system, we tested the effect of angiotensin II on bone resorption. Angiotensin II showed no effect either on osteoclast formation or on bone resorption by isolated osteoclasts. However, in co-cultures of osteoclasts with calvarial or MC3T3-E1 osteoblastic cells, and in osteoc

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Miyata, T., K. Notoya, K. Yoshida, et al. "Advanced glycation end products enhance osteoclast-induced bone resorption in cultured mouse unfractionated bone cells and in rats implanted subcutaneously with devitalized bone particles." Journal of the American Society of Nephrology 8, no. 2 (1997): 260–70. http://dx.doi.org/10.1681/asn.v82260.

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Advanced glycation end products (AGE) are formed in long-lived matrix proteins by a nonenzymatic reaction with sugar. The presence of AGE in beta 2-microglobulin-amyloid fibrils of dialysis-related amyloidosis, one of the characteristic features of which is an accelerated bone resorption around amyloid deposits, was recently demonstrated. This suggested a potential link of AGE in bone resorption and initiated this investigation of whether AGE enhance bone resorption. When mouse unfractionated bone cells containing osteoclasts were cultured on dentin slices, both AGE-modified beta 2-microglobul

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Thomson, B. M., G. R. Mundy, and T. J. Chambers. "Tumor necrosis factors alpha and beta induce osteoblastic cells to stimulate osteoclastic bone resorption." Journal of Immunology 138, no. 3 (1987): 775–79. http://dx.doi.org/10.4049/jimmunol.138.3.775.

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Abstract Antigen- or mitogen-stimulated leukocytes release bone-resorbing activity into culture supernatants in vitro. Among the agents likely to be present in such supernatants are monocyte-derived tumor necrosis factor (TNF-alpha) and lymphocyte-derived tumor necrosis factor (TNF-beta) (lymphotoxin), both of which have recently been shown to stimulate bone resorption in organ culture. To identify the mechanism of action of these agents, we compared bone resorption by isolated osteoclasts with bone resorption by osteoclasts cocultured with osteoblastic cells, and with bone resorption by osteo

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Iqbal, Jameel, and Mone Zaidi. "Bone resorption goes green." Cell 184, no. 5 (2021): 1137–39. http://dx.doi.org/10.1016/j.cell.2021.02.023.

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Buckland, Jenny. "BCLXL blocks bone resorption." Nature Reviews Rheumatology 5, no. 12 (2009): 656. http://dx.doi.org/10.1038/nrrheum.2009.220.

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MORIYAMA, HIROSHI, YOSHIO HONDA, CHENG CHUN HUANG, and MAXWELL ABRAMSON. "BONE RESORPTION IN CHOLESTEATOMA." Laryngoscope 97, no. 7 (1987): 854???859. http://dx.doi.org/10.1288/00005537-198707000-00016.

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Key Jr., L. L., W. C. Wolf, C. M. Gundberg, and W. L. Ries. "Superoxide and bone resorption." Bone 15, no. 4 (1994): 431–36. http://dx.doi.org/10.1016/8756-3282(94)90821-4.

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Pertot, Wilhelm-Joseph, and Jacques De´jou. "Bone and root resorption." Oral Surgery, Oral Medicine, Oral Pathology 74, no. 3 (1992): 357–65. http://dx.doi.org/10.1016/0030-4220(92)90076-3.

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van Niekerk, Gustav, Megan Mitchell, and Anna-Mart Engelbrecht. "Bone resorption: supporting immunometabolism." Biology Letters 14, no. 2 (2018): 20170783. http://dx.doi.org/10.1098/rsbl.2017.0783.

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Activation of the immune system is associated with an increase in the breakdown of various peripheral tissues, including bone. Despite the widely appreciated role of inflammatory mediators in promoting bone resorption, the functional value behind this process is not completely understood. Recent advances in the field of immunometabolism have highlighted the metabolic reprogramming that takes place in activated immune cells. It is now believed that the breakdown of peripheral tissue provides metabolic substrates to fuel metabolic anabolism in activated immune cells. We argue that phosphate, lib

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Teitelbaum, S. L. "Bone Resorption by Osteoclasts." Science 289, no. 5484 (2000): 1504–8. http://dx.doi.org/10.1126/science.289.5484.1504.

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Bonartsev, A. P., A. A. Muraev, R. V. Deyev, and A. V. Volkov. "Material-Associated Bone Resorption." Sovremennye tehnologii v medicine 10, no. 4 (2018): 26. http://dx.doi.org/10.17691/stm2018.10.4.03.

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Petrovic, M., and G. Cournot. "Barbiturate and bone resorption." Calcified Tissue International 56, no. 5 (1995): 408–9. http://dx.doi.org/10.1007/bf00301611.

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Chambers, T. J. "Prostaglandins and bone resorption." Clinical Materials 3, no. 4 (1988): 317. http://dx.doi.org/10.1016/0267-6605(88)90007-8.

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Miyahara, Tatsuro, Masakazu Takata, Sayuri Mori-Uchi, et al. "Stimulative effects of cadmium on bone resorption in neonatal pariental bone resorption." Toxicology 73, no. 1 (1992): 93–99. http://dx.doi.org/10.1016/0300-483x(92)90173-c.

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Park, Gyeong Do, Yoon-Hee Cheon, So Young Eun та ін. "β-Boswellic Acid Inhibits RANKL-Induced Osteoclast Differentiation and Function by Attenuating NF-κB and Btk-PLCγ2 Signaling Pathways". Molecules 26, № 9 (2021): 2665. http://dx.doi.org/10.3390/molecules26092665.

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Osteoporosis is a systemic metabolic bone disorder that is caused by an imbalance in the functions of osteoclasts and osteoblasts and is characterized by excessive bone resorption by osteoclasts. Targeting osteoclast differentiation and bone resorption is considered a good fundamental solution for overcoming bone diseases. β-boswellic acid (βBA) is a natural compound found in Boswellia serrata, which is an active ingredient with anti-inflammatory, anti-rheumatic, and anti-cancer effects. Here, we explored the anti-resorptive effect of βBA on osteoclastogenesis. βBA significantly inhibited the

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Georgess, Dan, Marlène Mazzorana, José Terrado, et al. "Comparative transcriptomics reveals RhoE as a novel regulator of actin dynamics in bone-resorbing osteoclasts." Molecular Biology of the Cell 25, no. 3 (2014): 380–96. http://dx.doi.org/10.1091/mbc.e13-07-0363.

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The function of osteoclasts (OCs), multinucleated giant cells (MGCs) of the monocytic lineage, is bone resorption. To resorb bone, OCs form podosomes. These are actin-rich adhesive structures that pattern into rings that drive OC migration and into “sealing-zones” (SZs) that confine the resorption lacuna. Although changes in actin dynamics during podosome patterning have been documented, the mechanisms that regulate these changes are largely unknown. From human monocytic precursors, we differentiated MGCs that express OC degradation enzymes but are unable to resorb the mineral matrix. We demon

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