Relevant bibliographies by topics / Osteoclast

Academic literature on the topic 'Osteoclast'

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Published: 4 June 2021
Last updated: 14 March 2023

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Journal articles on the topic "Osteoclast"

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Yu, Anna Xiao-Dan, Jian Xiao, Shi-Zheng Zhao, Xiang-Peng Kong, Kenneth Kin-Leung Kwan, Brody Zhong-Yu Zheng, Kevin Qi-Yun Wu, Tina Ting-Xia Dong, and Karl Wah-Keung Tsim. "Biological Evaluation and Transcriptomic Analysis of Corylin as an Inhibitor of Osteoclast Differentiation." International Journal of Molecular Sciences 22, no. 7 (March 29, 2021): 3540. http://dx.doi.org/10.3390/ijms22073540.

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Corylin, a flavonoid isolated from the fruit of Psoralea corylifolia, has an osteogenic effect on osteoblasts in vitro and bone micromass ex vivo. However, the effect and mechanism of corylin in regulating osteoclastogenesis remain unknown. By using murine bone marrow macrophages as the osteoclast precursor, corylin was found to inhibit the receptor activator of nuclear factor (NF) κB ligand (RANKL)-induced osteoclast differentiation via down-regulating osteoclastic marker genes. In parallel, F-actin formation and osteoclast migration were diminished in corylin-treated cultured osteoclasts, and subsequently the expressions of osteoclastic proteins were suppressed: the suppression of protein expression was further illustrated by transcriptomic analysis. Furthermore, corylin inhibited the nuclear translocation of p65, giving rise to a restraint in osteoclastic differentiation through the attenuation of transcription factors nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor of activated T cells c1 (NFATc1). There was no obvious change in apoptosis when the RANKL-induce osteoclasts were cultured in the presence of corylin. The finding supports the potential development of corylin as an osteoclast inhibitor against osteoporosis.
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Alatalo, Sari L., Jussi M. Halleen, Teuvo A. Hentunen, Jukka Mönkkönen, and H. Kalervo Väänänen. "Rapid Screening Method for Osteoclast Differentiation in Vitro That Measures Tartrate-resistant Acid Phosphatase 5b Activity Secreted into the Culture Medium." Clinical Chemistry 46, no. 11 (November 1, 2000): 1751–54. http://dx.doi.org/10.1093/clinchem/46.11.1751.

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Abstract Background: Osteoclasts secrete tartrate-resistant acid phosphatase (TRAP; EC 3.1.3.2) 5b into the circulation. We studied the release of TRAP 5b from osteoclasts using a mouse in vitro osteoclast differentiation assay. Methods: We developed and characterized a polyclonal antiserum in rabbits, using purified human osteoclastic TRAP 5b as antigen. The antiserum was specific for TRAP in Western analysis of mouse osteoclast culture medium and was used to develop an immunoassay. We cultured mouse bone marrow-derived osteoclast precursor cells for 3–7 days with or without clodronate in the presence of vitamin D and analyzed the number of osteoclasts formed and the amount of TRAP 5b activity released into the culture medium. Results: TRAP 5b activity was not secreted from osteoclast precursor cells. Addition of clodronate-containing liposomes decreased in a dose-dependent manner the number of osteoclasts and TRAP 5b activity released in 6-day cultures. The amount of TRAP 5b activity in the medium detected by the immunoassay correlated significantly with the number of osteoclasts formed (r = 0.94; P <0.0001; n = 120). Conclusions: The TRAP 5b immunoassay can be used to replace the laborious and time-consuming microscopic counting of osteoclasts in the osteoclast differentiation assay and to test the effects of potential therapeutic agents on osteoclast differentiation, enabling fast screening of large amounts of potential therapeutic agents.
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Combs, Charlotte E., Karen Fuller, Hashethra Kumar, Anthony P. Albert, Grisha Pirianov, James McCormick, Ian C. Locke, Timothy J. Chambers, and Kevin M. Lawrence. "Urocortin is a novel regulator of osteoclast differentiation and function through inhibition of a canonical transient receptor potential 1-like cation channel." Journal of Endocrinology 212, no. 2 (November 14, 2011): 187–97. http://dx.doi.org/10.1530/joe-11-0254.

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This study investigated the role of urocortin (UCN), a member of the corticotrophin-releasing factor (CRF) family of peptides, in osteoclast maturation and function. We found that 10−7 M UCN significantly (P<0.05) suppressed osteoclast differentiation from bone marrow precursor cells in culture and reduced the expression of several osteoclastic markers. Furthermore, UCN potently suppressed osteoclast bone resorption, by significantly inhibiting both the plan area of bone resorbed by osteoclasts and actin ring formation within osteoclasts at 10−9 M (P<0.05), with complete inhibition at 10−7 M (P<0.001). UCN also inhibited osteoclast motility (10−7 M) but had no effect on osteoclast survival. Osteoclasts expressed mRNA encoding both UCN and the CRF receptor 2β subtype. Pre-osteoclasts however, expressed CRF receptor 2β alone. Unstimulated osteoclasts contained constitutively active cation channel currents with a unitary conductance of 3–4 pS, which were inhibited by over 70% with UCN (10−7 M). Compounds that regulate calcium signalling and energy status of the cell, both crucial for osteoclast activity were investigated. The non-selective cation channel blockers, lanthanum (La3+) and gadolinium (Gd3+), inhibited actin ring formation in osteoclasts, whereas modulators of voltage-dependent Ca2+ channels and KATP channels had no effect. These findings show for the first time that UCN is a novel anti-resorptive molecule that acts through a direct effect on osteoclasts and their precursor cells.
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Fong, E. L. S., E. L. Prabha, and T. Carney. "POS0348 DEVELOPING A WHOLE MOUNT FLUORESCENT OSTEOCLAST ACTIVITY ASSAY USING THE ELF97 PHOSPHATASE SUBSTRATE TO VISUALISE AND QUANTIFY IN SITU OSTEOCLAST ACTIVITY IN ZEBRAFISH (DANIO RERIO)." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 427.3–428. http://dx.doi.org/10.1136/annrheumdis-2022-eular.5402.

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BackgroundOsteoporosis is a mineral bone disease arising from the predominance of osteoclastic bone resorption. Bisphosphonates which inhibit osteoclasts are commonly used in osteoporosis treatment, but are not without severe adverse effects like osteonecrosis of the jaw. The mechanisms behind the development of such phenomena is not well understood. Bone homeostasis is achieved through an intimate cross-talk between osteoclasts and osteoblasts. Thus, it is important to visualise activities of these cells simultaneously in situ. Currently, there are means to visualise osteoclast shape and numbers with tartrate-resistant alkaline phosphatase (TRAP) staining but no practical and accurate methods to quantify osteoclast activity in situ.ObjectivesThis investigation aims to establish the use of ELF97, a substrate of TRAP, to visualise and quantify osteoclast activity. This provides vital clues to mechanisms of various bone disorders. TRAP dephosphorylation of ELF97 results in a detectable fluorescent product at areas of osteoclast activity.MethodsOsteoclastic activity was initiated in zebrafish by inducing crush injuries in tail fin rays. Colocalisation of ELF97 fluorescence with osteoclast-specific DsRed in transgenic zebrafish, visualised under confocal microscopy, is used to further establish the specificity of ELF97 to sites of osteoclastic activity. Quantification is established by comparing fluorescence between wild type, osteoclast-deficient mutants and bisphosphonate-treated zebrafish. The utility of ELF97 will also be investigated in terms of the stability of the florescent product.ResultsThe investigation revealed that ELF97 and DsRed fluorescence were found commonly at crush sites with osteoclastic activity. Wild type zebrafish had greater fluorescence compared to osteoclast-deficient (p<0.0001) and bisphosphonate-treated zebrafish (p<0.0001) after 7 and 14 days post-crush, revealing that fluorescence from ELF97 corresponds to expected osteoclastic activity. Fluorescence of tail fins treated with ELF97 did not diminish over a period of 21 days of storage, demonstrating its stability.ConclusionELF97 is thus a useful means to visualise osteoclast activity, potentially crucial in more advanced investigations to understand bone disorders. It could be used in combination with other cellular markers in whole biological samples to study and experimentally manipulate bone remodelling.Disclosure of InterestsNone declared
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Niida, Shumpei, Masato Kaku, Hitoshi Amano, Hisahiro Yoshida, Hiroshi Kataoka, Satomi Nishikawa, Kazuo Tanne, Norihiko Maeda, Shin-Ichi Nishikawa, and Hiroaki Kodama. "Vascular Endothelial Growth Factor Can Substitute for Macrophage Colony-Stimulating Factor in the Support of Osteoclastic Bone Resorption." Journal of Experimental Medicine 190, no. 2 (July 19, 1999): 293–98. http://dx.doi.org/10.1084/jem.190.2.293.

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We demonstrated previously that a single injection of recombinant human macrophage colony-stimulating factor (rhM-CSF) is sufficient for osteoclast recruitment and survival in osteopetrotic (op/op) mice with a deficiency in osteoclasts resulting from a mutation in M-CSF gene. In this study, we show that a single injection of recombinant human vascular endothelial growth factor (rhVEGF) can similarly induce osteoclast recruitment in op/op mice. Osteoclasts predominantly expressed VEGF receptor 1 (VEGFR-1), and activity of recombinant human placenta growth factor 1 on osteoclast recruitment was comparable to that of rhVEGF, showing that the VEGF signal is mediated through VEGFR-1. The rhM-CSF–induced osteoclasts died after injections of VEGFR-1/Fc chimeric protein, and its effect was abrogated by concomitant injections of rhM-CSF. Osteoclasts supported by rhM-CSF or endogenous VEGF showed no significant difference in the bone-resorbing activity. op/op mice undergo an age-related resolution of osteopetrosis accompanied by an increase in osteoclast number. Most of the osteoclasts disappeared after injections of anti-VEGF antibody, demonstrating that endogenously produced VEGF is responsible for the appearance of osteoclasts in the mutant mice. In addition, rhVEGF replaced rhM-CSF in the support of in vitro osteoclast differentiation. These results demonstrate that M-CSF and VEGF have overlapping functions in the support of osteoclastic bone resorption.
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Moreaux, Jerome, Dirk Hose, Alboukadel Kassambara, Thierry Reme, Philippe Moine, Guilhem Requirand, Hartmut Goldschmidt, and Bernard Klein. "Osteoclast-gene expression profiling reveals osteoclast-derived CCR2 chemokines promoting myeloma cell migration." Blood 117, no. 4 (January 27, 2011): 1280–90. http://dx.doi.org/10.1182/blood-2010-04-279760.

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Abstract Multiple myeloma is characterized by the clonal expansion of malignant plasma cells (multiple myeloma cells [MMCs]), in the bone marrow. Osteolytic bone lesions are detected in 80% of patients because of increased osteoclastic bone resorption and reduced osteoblastic bone formation. MMCs are found closely associated with sites of increased bone resorption. Osteoclasts strongly support MMC survival in vitro. To further elucidate the mechanisms involved in osteoclast/MMC interaction, we have identified 552 genes overexpressed in osteoclasts compared with other bone marrow cell subpopulations. Osteoclasts express specifically genes coding for 4 CCR2-targeting chemokines and genes coding for MMC growth factors. An anti-CCR2 monoclonal antibody blocked osteoclast chemoattractant activity for MMC, and CCR2 chemokines are also MMC growth factors, promoting mitogen-activated protein kinase activation in MMC. An anti-insulin growth factor-1 receptor monoclonal antibody completely blocked the osteoclast-induced survival of MMC suppressing both osteoclast and MMC survival. Specific a proliferation-inducing ligand or IL-6 inhibitors partially blocked osteoclast-induced MMC survival. These data may explain why newly diagnosed patients whose MMC express high levels of CCR2 present numerous bone lesions. This study displays additional mechanisms involved in osteoclast/MMC interaction and suggests using CCR2 and/or insulin growth factor-1 targeting strategies to block this interaction and prevent drug resistance.
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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 (June 1, 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 bone, a pattern of inhibition previously observed in response to macrophage CSF (M-CSF). MIP-2, RANTES, MIP-1 beta, and monocyte chemotactic protein-1 were without effect on resorption. MIP-1 alpha and IL-8, but not the other chemokines, also stimulated osteoclastic motility and increased the osteoclast spread area in a dose-dependent manner, over the same concentration range as that which inhibited bone resorption. In addition, MIP-1 alpha induced osteoclast orientation in a gradient of the chemokine, and stimulated osteoclast migration. We detected no effect of chemokines on osteoclast formation or survival. Our data suggest that chemokines can promote osteoclast orientation and migration, processes that might be involved in chemotaxis; it seems appropriate that resorptive functions should be suppressed during migration. Because chemokines are proinflammatory, their actions on osteoclasts might represent mechanisms by which bone resorption is modulated by the inflammatory process when this occurs in bone. However, given that chemokines are increasingly recognized to be multifunctional and that they are produced by cells of the osteoblastic lineage, they may also be components of the physiologic regulation of bone resorption.
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Perkins, S. L., and S. J. Kling. "Local concentrations of macrophage colony-stimulating factor mediate osteoclastic differentiation." American Journal of Physiology-Endocrinology and Metabolism 269, no. 6 (December 1, 1995): E1024—E1030. http://dx.doi.org/10.1152/ajpendo.1995.269.6.e1024.

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Macrophage colony-stimulating factor (M-CSF) is essential for differentiation of osteoclasts and macrophages from a common bone marrow precursor. Using ST-2 stromal cell/murine bone marrow coculture, we studied the effects of increasing amounts of M-CSF on differentiation of macrophages and osteoclasts. Addition of exogenous M-CSF caused a dose-dependent 98% decrease in tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells, accompanied by a 2.5-fold increase in nonspecific esterase-staining macrophages. Similar decrease in osteoclastic functional activity, including 125I-labeled calcitonin binding and calcitonin-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production, were observed. Addition of exogenous M-CSF beyond 6 days in coculture had a decreasing ability to inhibit osteoclast formation, suggesting that M-CSF exerts its effects early in osteoclast differentiation, during the proposed proliferative phase of osteoclast formation. Similarly, early addition of neutralizing anti-M-CSF inhibited osteoclast formation, with diminishing effects beyond day 9. These results suggest that local high concentrations of M-CSF may influence the early determination of terminal differentiation into either macrophages or osteoclasts.
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Kameda, Takashi, Hiroshi Mano, Tatsuhisa Yuasa, Yoshihisa Mori, Koshi Miyazawa, Miho Shiokawa, Yukiya Nakamaru, et al. "Estrogen Inhibits Bone Resorption by Directly Inducing Apoptosis of the Bone-resorbing Osteoclasts." Journal of Experimental Medicine 186, no. 4 (August 18, 1997): 489–95. http://dx.doi.org/10.1084/jem.186.4.489.

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Estrogen deficiency causes bone loss, which can be prevented by estrogen replacement therapy. Using a recently developed technique for isolation of highly purified mammalian osteoclasts, we showed that 17 β-estradiol (E2) was able to directly inhibit osteoclastic bone resorption. At concentrations effective for inhibiting bone resorption, E2 also directly induced osteoclast apoptosis in a dose- and time-dependent manner. ICI164,384 and tamoxifen, as pure and partial antagonists, respectively, completely or partially blocked the effect of E2 on both inhibition of osteoclastic bone resorption and induction of osteoclast apoptosis. These data suggest that the protective effects of estrogen against postmenopausal osteoporosis are mediated in part by the direct induction of apoptosis of the bone-resorbing osteoclasts by an estrogen receptor– mediated mechanism.
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Cheng, Yin, Haixia Liu, Jing Li, Yujie Ma, Changheng Song, Yuhan Wang, Pei Li, Yanjing Chen, and Zhiguo Zhang. "Evaluation of culture conditions for osteoclastogenesis in RAW264.7 cells." PLOS ONE 17, no. 11 (November 17, 2022): e0277871. http://dx.doi.org/10.1371/journal.pone.0277871.

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Osteoclasts are the only multinucleated cells in vivo responsible for bone resorption and are vital for regulating bone remodeling and maintaining bone mass. The RAW264.7 cell line is widely used to study osteoclastic differentiation and biological molecular mechanism. However, protocols for inducing osteoclast formation in RAW264.7 cells vary considerably between laboratories, hindering the replication of results. Therefore, we tested the influence of culture conditions on osteoclast differentiation, including cell density and receptor activator of nuclear factor kappa-B ligand (RANKL) concentrations with or without macrophage colony-stimulating factors (M-CSF). Tartrate-resistant acid phosphatase (TRAP) staining was used to detect the morphology of osteoclasts. qPCR was used to detect gene expression of osteoclast-specific gene marker cathepsin K (CTSK), osteoclast transcription factors c-Fos and nuclear factor of activated T cells, cytoplasmic 1 (NFATc1). The bone resorption function was evaluated by a scanning electron microscope (SEM). RANKL treatment increased multinucleated osteoclasts formation and increased CTSK, c-Fos and NFATc1 gene expression. Compared with RANKL treatment, M-CSF significantly decreased multinucleated osteoclasts formation, reduced CTSK gene expression and had little effect on c-Fos and NFATc1 gene expression. Concerning bone resorption activity, RANKL treatment increased bone resorption pits on bovine bone slices. Significantly higher levels of osteoclastogenesis were observed with RAW264.7-cell density of 2×104 cells/well in 24-well plates. Our results suggest that the addition of 50 ng/ml M-CSF has no positive effect on osteoclastogenesis. RANKL treatment and cell density contribute to osteoclast formation, and the optimal conditions are beneficial when exploring osteoclast function and mechanism.
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Dissertations / Theses on the topic "Osteoclast"

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O'Brien, Elizabeth Ann. "Regulation of osteoclast activity : differential adhesion of osteoclasts to the bone surface." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343930.

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Stephens, Sebastien. "Novel Osteoclast Signalling." Thesis, Griffith University, 2010. http://hdl.handle.net/10072/365823.

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When you say osteoporosis, people think of their grandma’s brittle bones, but scientists think of the osteoclast. When you say cancer, people think of death, but before this, many succumb to the osteoclast. The fact is all these things are true yet it is even truer to say that each disease in fact also has more of the other – osteoporosis and death, and cancer and brittle bones. However, the commonality is undeniably the osteoclast. Scratching the surface of the osteoclast reveals that it is the basis of a diversity of bone-related disorders yet the osteoclast itself is, even given the large amount of effort devoted to it to this day, an ill- defined cell. Not surprisingly, deaths related to osteoporotic fractures and skeletal pain due to metastases to bone remain far higher than ideal. Today’s dogma describes the osteoclast as a multinucleated cell derived from the haematopoietic cell lineage that is capable of bone resorption. It is suspected that it is through multiple signalling mechanisms, that this bone-resorbing activity is augmented in certain bone diseases eventually causing osteolysis or the break down of bone. Currently, it still stands that any way to advance our understanding of the osteoclast will provide stepping stones for eventual treatments and perhaps cures for these diseases. Thus the goal of this thesis was to better characterise the osteoclast. For this, four different projects were undertaken; analysis in the osteoclast of (1) the chemokine MCP-1, (2) the RhoGTPase family, (3) DMSO and (4) genes dependent on RANKL (by array). Project results are summarised in order.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Wilkinson, Debbie Isabelle. "Visualisation of osteoclast membrane domains." Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158808.

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Osteoclasts polarise upon activation and form four distinct membrane domains; the basolateral domain, the sealing zone, the functional secretory domain and the ruffled border. The ruffled border is the resorptive organelle of the cell and provides a large surface area for the release of protons and enzymes into the space beneath the osteoclast. Defects in osteoclast formation or function can lead to diseases such as osteopetrosis. Ruffled border formation is a critical event in osteoclast function but the process by which it and other membrane domains form is only partially understood. Vesicular trafficking is essential for the tight regulation of the osteoclast membrane domains and it has been shown previously that treatment with pharmacological inhibitors causes disruption of trafficking. The aims of this PhD were to increase our understanding of vesicular trafficking in osteoclasts and to optimise ways of visualising osteoclast membrane domains. My studies of patients with osteoclast-poor osteopetrosis identified defects in RANKL as a cause of the defect. This in turn has identified a potential therapy of recombinant RANKL for patients with this form of the disease. Although purification of wild type or mutant RANKL was not completely successful, it did suggest that the mutant forms of RANKL were not functional. I have used pharmacological inhibitors to study osteoclast membrane domains, and found that transmission electron microscopy is an essential tool for studying membrane changes following pharmacological inhibition at the ultrastructural level. I also established that the study of vesicular trafficking to analyse formation of membrane domains can make excellent use of immuno-electron methods. Furthermore, genetic diseases associated with defective ruffled border formation such as XLA and osteopetrosis provide useful tools to further analyse the dynamics involved in the formation and maintenance of the ruffled border, as well as revealing more about the diseases themselves.
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Zaidi, Mone. "Novel mechanisms of osteoclast regulation." Thesis, University of London, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411434.

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Gu, Xiaomei Everett Eric T. "Physiopathology of osteoclast in bone." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1870.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Curriculum of Oral Biology." Discipline: Oral Biology; Department/School: Dentistry.
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Barnes, Calvin Langston Toure. "C-mpl Expression in Osteoclast Progenitors: A Novel Role for Thrombopoietin in Regulating Osteoclast Development." Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06262006-123750/.

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A new paradigm has evolved in which multiple regulatory interactions between the skeletal and hematopoietic systems have been identified. Previous studies have demonstrated that megakaryocytes (MK) play a dual role in skeletal homeostasis by stimulating osteoblast proliferation and simultaneously inhibiting osteoclast (OC) development. Here we identify a novel regulatory pathway in which the main MK growth factor, thrombopoietin (TPO), directly regulates osteoclastogenesis. To study the role of TPO in OC development, spleen or bone marrow (BM) cells (2x10[exponent]6 cells/ml) or BM macrophages (BMM, 1x10[exponent]5 cells/ml) from C57BL/6 mice , as a source of OC precursors, were cultured with M-CSF (30 ng/ml) and RANKL (50 ng/ml) to induce OC formation. TPO (0.1-1000 ng/ml) and/or primary MK (0-0.5%), derived from C57BL/6 fetal livers, were titrated into these cultures and OC were identified as tartrate resistant acid phosphatase positive (TRAP+) giant cells with >3 nuclei. There was a significant, up to 15-fold reduction in OC formed when MK were added to all OC generating cultures, p < 0.001. Moreover, if OC generating cultures did not contain MK or MK progenitors, TPO treatment significantly enhanced OC formation up to six-fold, p < 0.01. This data demonstrates that MK are responsible for the inhibition of OC formation and that in cultures containing MK or MK progenitors such as BM or spleen cells, that TPO acts indirectly to inhibit OC formation by stimulating megakaryopoiesis, whereas in the absence of MK or MK progenitors TPO directly enhances OC formation. This conclusion is further supported by Real-Time PCR data which demonstrates that OC progenitors express c-mpl, the TPO receptor, albeit at low levels when compared to expression of c-mpl on MK. Finally, we have begun to dissect the c-mpl signaling pathway in OC progenitors. We have found that TPO induces tyrosine phosphorylation of several specific cellular proteins in the JAK/STAT pathway. Thus, TPO acts in a somewhat paradoxical manner by inhibiting OC formation through the stimulation of MK, while simultaneously playing a direct role in enhancing osteoclastogenesis.
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Hale, Annette Julie. "The characterisation of the Pagetic osteoclast." Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359919.

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Lång, Johanna. "CCL11 and Effects on Pre-osteoclast Migration." Thesis, Umeå universitet, Institutionen för odontologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-143797.

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ABSTRACT  Periodontitis is a chronic inflammatory disease due to dental bacteria, and the disease is highly prevalent worldwide. Both environmental factors and genetic variation are confounding factors. Characteristic for disease development is degradation of gingival tissue and resorption of the alveolar bone due to inflammation. The cells that are capable to resorb bone is named osteoclasts and those are recruited and activated by numerous cytokines. Cytokines are small signal proteins responsible for cell communication and cell recruitment. Cytokines with chemotactic capacity are called chemokines. Patients with periodontitis have increased levels of chemokine ligand 2 (CCL2) and chemokine ligand 11 (CCL11) in serum. The aim of this study is to investigate whether CCL11 increases pre-osteoclast migration. Bone marrow was isolated from mouse long bones to achieve pre-osteoclasts for migration experiments. A migration plate, with membrane pore size 8-μm was used for the experiments. The cells were added on top of the membrane with the medium underneath. The cells were incubated at 37 °C, 5 % CO2 and the incubation time 5 hours. Migrated cells were fixed and stained for the osteoclast specific enzyme tartrate-resistant acid phosphatase (TRAP). Migrated cells were counted using a light microscope. The result showed that CCL11 had a statistical significant chemotactic effect on pre-osteoclasts and increase cell migration. By identification of chemokines, it might be possible to test chemokine antibodies to stop bone resorption in inflammatory bone destructive diseases as periodontitis.
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Combs, Charlotte Emma. "The role of urocortin in osteoclast physiology." Thesis, St George's, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517193.

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MacQuarrie, Robyn Melanie. "Arthroplasty-derived wear particles effect osteoclast differentiation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63539.pdf.

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Books on the topic "Osteoclast"

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Holt, Ian. Control of osteoclast activity. Manchester: University of Manchester, 1996.

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R, Rifkin Barry, and Gay Carol V, eds. Biology and physiology of the osteoclast. Boca Raton: CRC Press, 1992.

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Green, Philip Macey. An experimental study of the osteoclast and its role in bone remodelling. Birmingham: University of Birmingham, 1988.

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Tai, Victoria. The effects of leukotriene Bb4s on osteoclast formation and osteoclastic bone resorption and the role of osteoblastic cells in these processes. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Sutton, Michael Mark. The Influence of Microtubules and Microtubule-Based Structures on Osteoclast and CD4+ T Cell Function. [New York, N.Y.?]: [publisher not identified], 2022.

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Maria, Bijvoet Olav Leonardus, Lipton Allan, and International Cancer Congress (15th : 1990 : Hamburg, Germany), eds. Osteoclast inhibition in the management of malignancy-related bone disorders: An international symposium held during the 15th International Cancer Congress, Hamburg, Germany, August 1990. Seattle: Hogrefe & Huber, 1993.

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D, Rubens R., and European Conference on Clinical Oncology (5th : 1989 : London, England), eds. The Management of bone metastases and hypercalcaemia by osteoclast inhibition: An international symposium held during the 5th European Conference on Clinical Oncology (ECCO 5), London, September 1989. Toronto: Hogrefe & Huber, 1990.

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Yu, Hesheng. P2 purinoceptor-linked Ca2+ signaling and pH changes in osteoclasts. [Toronto: University of Toronto, Faculty of Dentistry], 1996.

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Felix, Bronner, Farach-Carson Mary C. 1958-, and Rubin Janet, eds. Bone resorption. London: Springer, 2005.

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Rodionova, N. V. Funkt͡s︡ionalʹnai͡a︡ morfologii͡a︡ kletok v osteogeneze. Kiev: Nauk. dumka, 1989.

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Book chapters on the topic "Osteoclast"

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Pavelka, Margit, and Jürgen Roth. "Osteoclast." In Functional Ultrastructure, 298–99. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_153.

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Schwab, Manfred. "Osteoclast." In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4277-2.

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Crockett, Julie C., David J. Mellis, and Adam Taylor. "Transfection of Osteoclasts and Osteoclast Precursors." In Methods in Molecular Biology, 205–22. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-415-5_14.

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Reddy, Sakamuri V., and G. David Roodman. "Osteoclast Differentiation." In The Skeleton, 195–213. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-736-9_14.

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Krstić, R. V. "Knochengewebe. Osteoclast." In Die Gewebe des Menschen und der Säugetiere, 226–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-61380-7_111.

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Chambers, T. J. "The Osteoclast." In Handbook of Experimental Pharmacology, 353–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55742-2_19.

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Krstić, Radivoj V. "Bony Tissue. Osteoclast." In General Histology of the Mammal, 226–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70420-8_111.

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Orriss, Isabel R., and Timothy R. Arnett. "Rodent Osteoclast Cultures." In Methods in Molecular Biology, 103–17. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-415-5_8.

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Yang, Jingxuan, Xiaohong Bi, and Min Li. "Osteoclast Differentiation Assay." In Methods in Molecular Biology, 143–48. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8879-2_12.

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Lorenzo, Joseph A. "Osteoclast Precursor Cells." In Advances in Experimental Medicine and Biology, 77–82. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-72009-8_10.

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Conference papers on the topic "Osteoclast"

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Xuan, W., X. Feng, Y. Shi, F. Wang, M. Zhang, and W. Tan. "THU0066 Osteoclast differentiation gene expression profiling reveals ccl4 mediates rankl-induced osteoclast migration." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4255.

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Intemann, J., C. Wehmeyer, V. Kracke, E. Werbenko, P. Paruzel, I. Kramer, M. Kneissel, T. Pap, and B. Dankbar. "P081 Sclerostin affects rankl-mediated osteoclast differentiation." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.98.

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Hasegawa, Y., N. M. Nikolaidis, Y. Uehara, L. B. Pitstick, H. Wu, J. C. Gardner, J. G. Noel, E. J. A. Kopras, J. P. Bridges, and F. X. McCormack. "Osteoclast-Like Differentiation in Mouse Model of Silicosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5413.

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Oliveira, Leandro Gonçalves, Ana Cláudia Gonçalves Lima, Sebastião Alves Pinto, Barbara Elisabeth Schroff, André Maroccolo de Sousa, and Juarez Antônio de Sousa. "BREAST CARCINOMA WITH OSTEOCLAST-LIKE GIANT CELLS: A CASE REPORT." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2052.

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Introduction: Breast carcinoma with osteoclastic giant cells (OGCs) is rare. According to the WHO classification, breast tumors are designated “carcinoma with osteoclast-like giant cells” and are categorized under invasive carcinoma of no special type. This distinct subtype of breast carcinoma was first described in the French medical literature by Leroux in 1931 and Duboucher et al. in 1933. We reported a case study of a woman with OGCs with an invasive ductal and papillary carcinoma. Case Presentation: A 69-year-old female presented with left-sided breast lump. Ultrasound study documented the well-circumscribed retroareolar hypoechoic mass, measuring 3.5 cm in greatest dimension. Computed tomography scan and bone scan showed no evidence of distant metastasis. The patient underwent left breast mastectomy and sentinel lymph node biopsy. The tissue was fixed in 10% buffered formalin and embedded in paraffin. Hematoxylin and eosin–stained sections revealed a tumor composed of papillary intracystic carcinoma with a prominent OGC component. The background stroma revealed hemorrhage and hemosiderin deposition. Left axillary sentinel lymph node was free of malignancy (pN0). Tumor cells stained negative for estrogen receptor, progesterone receptor, and HERneu-2. Ki-67 positive was approximately 30%. After surgery, this patient received taxane-based chemotherapy for four cycles and post-mastectomy radiotherapy. Discussion: Breast carcinoma with OGCs is characterized by the presence of OGCs admixed with malignant epithelial cells. They often showed hyperchromatic nuclei that are atypical with occasional small nucleoli and fine chromatin structure. Mitotic figures are typically rare. The mechanism for the formation of OGCs is still unknown and is at least partially attributed to tumor-induced angiogenesis and inflammatory cytokines. To date, the influence of OGCs on the prognosis of patients is still controversial. We described an old woman with a triple-negative breast carcinoma with OGCs. She remains free of recurrence, with an 18-month follow-up.
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Intemann, J., C. Wehmeyer, DJ de Gorter, V. Kracke, P. Paruzel, I. Kramer, M. Kneissel, T. Pap, and B. Dankbar. "P082/O24 Sclerostin deficiency affects RANKL-mediated osteoclast differentiation." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.71.

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Hirayama, T., H. Taira, O. Kudo, I. Itonaga, T. Torisu, and Y. Fujikawa. "SAT0161 Menatetrenone acts directly on circulating human osteoclast precursors." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.648.

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Monteiro, Karina Miranda, Francianne Rocha Fiel, Nyara Rodrigues Conde de Almeida, and Sandrelli dos Reis Carneiro. "GIANT CELL TUMOR OF THE BREAST WITH PULMONARY METASTASIS: A CASE REPORT." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1036.

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Giant cell tumor of soft tissue (GCT-ST) is an extremely uncommon tumor that resembles GCT of the bone in morphology and immunohistochemistry, usually occurs in the superficial and deep STs of the extremities, and the breast is a very rare location. It is composed of a mixture of round mononuclear cells and multinucleated osteoclast giant cells. It is classified as an intermediate-type fibrous tissue cell tumor, occasionally metastatic type, that has a benign clinical course when treated adequately by complete excision. Therefore, local recurrence or distant metastasis is extremely rare. A 36-year-old female patient was admitted to the Mastology Service with a 20-cm palpable nodule in the left breast, associated with ectasia without signs of lymphadenopathy; reports hypertension, hypothyroidism, and hysterectomy in 2006, due to uterine myomatosis. In relation to family history, her father had prostate cancer. On imaging examinations, a breast ultrasound was performed and showed a solid and hypoechoic node, lobulated contour with small cystic areas inside, with post acoustic phenomenon, located in the superolateral quadrant of the left breast. Mammography confirmed BIRADS 0. The biopsy revealed an atypical epithelial lesion with abundant osteoclast-like giant stromal cells. Computed tomography of the chest revealed nonspecific pulmonary nodules in the right upper lobe, the largest measuring 0.5 cm. Immunohistochemistry concluded histiocystic neoplasm rich in multinucleated giant cells — Ki-67 15%, AE1/AE3, and GATA-3 negative, CD68 positive. As clinical management, a simple left mastectomy was indicated. Anatomopathology showed a fibrohistiocytic neoplasm with abundant osteoclast-like multinucleated giant cells, measuring 10.5 cm.
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Sood, Shatakshi, Lisa Patel, Martyn Foster, Louise Jopling, Rob Van’t Hof, Iain Greig, Sam Williams, Iain Mcinnes, and Carl Goodyear. "SAT0045 A NOVEL SMALL MOLECULE, MBS2133, MODULATES OSTEOCLAST PRE-CURSOR METABOLISM TO INHIBIT OSTEOCLAST DIFFERENTIATION: AN ALTERNATIVE THERAPY FOR OSTEOLYTIC PATHOLOGY IN RA." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5482.

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Benabdoune, HA, P. Rondon, Q. Shi, JC Fernandes, H. Fahmi, and M. Benderdour. "THU0061 Regulation of osteoclast recruitment and activation by resolvin d1." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2934.

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Tanaka, Y., L. B. Pitstick, Y. Hasegawa, H. Wu, E. J. A. Kopras, and F. X. McCormack. "Pulmonary Osteoclast-Like Cells Contribute to Asbestos-Induced Pulmonary Fibrosis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4224.

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Reports on the topic "Osteoclast"

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Reddy, Sakamuri. Osteoclast Inhibitory Peptide-1 Therapy for Paget's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2010. http://dx.doi.org/10.21236/ada539193.

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Reddy, Sakamuri V. Osteoclast Inhibitory Peptide-1 Therapy for Paget's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada567774.

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Reddy, Sakamuri. Osteoclast Inhibitory Peptide-1 Therapy for Paget's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada553287.

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Reddy, Sakamuri V. Measles Virus Nucleocapsid (MJVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors. Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada484715.

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Reddy, Sakamuri V. Measles Virus Nucleocapsid (MVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors, Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada500887.

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Reddy, Sakamuri V. Measles Virus Nucleocapsid (MVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors, Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada462833.

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Reddy, Sakamuri V. Measles Virus Nucleocapsid (MVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors,Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada482539.

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Morgans, Alicia K., David F. Penson, Amy J. Graves, Parul Chaudhuri, and Daniel Sonnenburg. Osteoclast inhibitor treatment among men with metastatic castration-resistant prostate cancer. Science Repository OÜ, September 2018. http://dx.doi.org/10.31487/j.cor.2018.03.001.

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Morfin, C., and G. G. Loots. Characterizing the role of Mef2c in regulating osteoclast differentiation and energy metabolism. Office of Scientific and Technical Information (OSTI), April 2018. http://dx.doi.org/10.2172/1459127.

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Giachelli, Cecilia, Bruce Sangeorzan, Susan Lund, Steven Bain, Cameron Rementer, and Dewayne Threet. Engineered Osteoclasts for the Treatment and Prevention of Heterotopic Ossification. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612445.

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