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Livros sobre o tema "Osteoclasts"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 6 de julho de 2024

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1

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

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2

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

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3

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

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4

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

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5

National Institute on Aging/National Institute of Dental Research Workshop on Human Models of Skeletal Aging (1994 Washington, D.C.). National Institute on Aging/National Institute of Dental Research Workshop on Human Models of Skeletal Aging: Washington, DC, March 1-2, 1994. Editado por Robey Pamela Gehron 1952-, Sherman Sherry, National Institute of Dental Research (U.S.) e National Institute on Aging. New York, NY: Springer International, 1995.

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6

Maria, Bijvoet Olav Leonardus, Lipton Allan e 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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7

D, Rubens R., e 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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8

Shorey, Seema. Differences in the degree to which osteoclasts from different parts of the skeleton employ cathepsin K and matrix metalloproteinases for bone resorption. Ottawa: National Library of Canada, 2002.

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9

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

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10

David, Evered, Harnett Sara e Ciba Foundation, eds. Cell and molecular biology of vertebrate hard tissues. Chichester, UK: Wiley, 1988.

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11

H, Helfrich Miep, e Ralston Stuart, eds. Bone research protocols. Totowa, N.J: Humana Press, 2003.

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12

H, Helfrich Miep, e Ralston Stuart, eds. Bone research protocols. Totowa, N.J: Humana Press, 2003.

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13

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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14

service), ScienceDirect (Online, ed. Osteoimmunology: Interactions of the immune and skeletal systems. Amsterdam: Academic, 2011.

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15

R, Arnett Timothy, e Henderson Brian, eds. Methods in bone biology. London: Chapman & Hall, 1998.

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16

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

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17

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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18

Graziano, Victor M. A. The ferret: A potential in vitro small animal model for the study of osteogenesis and osteoclasis. [Toronto: University of Toronto, Faculty of Dentistry], 1998.

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19

Poore, Charles T. Osteotomy and Osteoclasis for Deformities of the Lower Extremities. Creative Media Partners, LLC, 2018.

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20

Gabet, Yankel, Drorit Neumann, Ari Elson, Noam Levaot e Natalie A. Sims. Developmental Biology and Regulation of Osteoclasts. Frontier Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-867-2.

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21

Brown, Alexander J. Osteoclasts: Morphology, Functions and Clinical Implications. Nova Science Publishers, Incorporated, 2012.

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22

Reeves, Cecelia. Osteoclasts: Cell Biology, Functions and Related Diseases. Nova Science Publishers, Incorporated, 2015.

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23

Yu, Hesheng. P2 purinoceptor-linked Ca2+ signaling and pH changes in osteoclasts. 1996.

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24

Bronner, Felix, Janet Rubin e Mary C. Farach-Carson. Bone Resorption. Springer London, Limited, 2006.

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25

Bronner, Felix, Janet Rubin e Mary C. Farach-Carson. Bone Resorption. Springer London, Limited, 2010.

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26

Anderson, Gail I. Osteoblast involvement in the formation and activation of osteoclasts in vitro. 1996.

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27

Chandra, Divya. To evaluate differences in mRNA expression of c-fms, EP2 and EP4 between large and small osteoclasts. 2001.

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28

Osteoblasts: Morphology, Functions and Clinical Implications. Nova Science Pub Inc, 2013.

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29

Ruabens, Robert D. The Management of Bone Metastases and Hypercalcaemia by Osteoclast Inhibition: An International Symposium Held During the 5th European Conference on. Hogrefe & Huber Pub, 1990.

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30

Zaidi, Mone. Osteoclast-Osteoblast. Jai Pr, 1999.

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31

Clarke, Noel W. Metastatic disease in prostate cancer. Editado por James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0068.

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Metastases are the predominant cause of morbidity and death from prostate cancer (CaP). The tendency for cells to migrate from the primary site, enter the vascular/lymphatic circulation, and implant/grow at secondary sites is the principal discriminator of aggressive form indolent disease. But this process is poorly understood. Cells enter the circulation in increasing number as the disease progresses, impinging on endothelial surfaces, particularly in red bone marrow where they bind and transmigrate, forming early cell colonies. This requires chemo-attractants and nutrients enabling cellular survival. Established metastases thrive independently, disrupting local tissue, as characterized by progressive replacement of red bone marrow and disruption of skeletal architecture. Bone disruption includes massive overstimulation of both osteoblasts and osteoclasts, inducing synchronous over-production of abnormal bone and gross osteolysis.

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32

Lories, Rik J., e Georg Schett. Pathology: bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0010.

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Axial spondyloarthritis is associated with different types of skeletal damage. Inflammation at the affected sites is linked with both loss of trabecular bone and new bone formation on the cortical side, potentially leading to joint or spine ankylosis. Both aspects of the disease can result in a significant burden for the patient. Bone loss is directly linked to proinflammatory cytokines and activation of osteoclasts. Control of inflammation is therefore the best strategy to prevent loss of bone. The nature of the new bone formation process is less defined. A prominent role for developmental signalling pathways has been proposed. Current therapies have limited or no impact on this process. However, emerging data suggest that early control of disease activity may be part of a window of opportunity to prevent structural damage, as biomechanical factors and instability following inflammation may also play a role.

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33

Hall, Brian K. Bone, Volume II: The Osteoclast. CRC, 1991.

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34

Hall, Brian K. Bone, Volume II: The Osteoclast. Taylor & Francis Group, 1991.

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35

Bone Research Protocols (Methods in Molecular Medicine). Humana Press, 2003.

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36

Helfrich, Miep H., e Stuart H. Ralston. Bone Research Protocols. Humana Press, 2016.

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37

Helfrich, Miep H., e Stuart H. Ralston. Bone Research Protocols. Humana Press, 2010.

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38

Choi, Yongwon, Mark Horowitz, Joseph Lorenzo, Hiroshi Takayanagi e Georg Schett. Osteoimmunology: Interactions of the Immune and Skeletal Systems. Elsevier Science & Technology Books, 2015.

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39

Choi, Yongwon, Mark Horowitz, Joseph Lorenzo, Hiroshi Takayanagi e Georg Schett. Osteoimmunology: Interactions of the Immune and Skeletal Systems. Elsevier Science & Technology Books, 2015.

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40

Choi, Yongwon, Mark Horowitz, Joseph Lorenzo e Hiroshi Takayanagi. Osteoimmunology: Interactions of the Immune and Skeletal Systems. Elsevier Science & Technology Books, 2010.

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41

Folkins, Alia. Coloring Book - You Will Get Better - Osteoclast. Independently Published, 2021.

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42

Folkins, Alia. Coloring Book - You Will Get Better - Osteoclast. Independently Published, 2021.

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43

Poore, Charles T. Osteotomy and Osteoclasis for Deformities of the Lower Extremities. Franklin Classics Trade Press, 2018.

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44

Henderson, Brian, e T. Arnett. Methods in Bone Biology. Springer, 2013.

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45

Osteoimmunology Interactions Of The Immune And Skeletal Systems Ii. Springer, 2009.

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46

Lees, Rita L. Osteoclast heterogeneity: The importance of cell size and phase of activity. 2000.

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47

Sprague, Stuart M., e James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Editado por David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.

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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.

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48

Sheraly, Aly R. The use of gastric proton pump inhibitors to modulate osteoclast-mediated resorption of calcium phosphate cements. 2005.

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49

J. Singh, Parminder, e Rohit Kotnis. The musculoskeletal system: structure and function. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.0003.

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♦ Structure of bone is comprised of cells, matrix, and water♦ Bone consists broadly of three surfaces (periosteal, endosteal, and Haversian) and two membranes (periosteum and endosteum)♦ The blood supply of bone is derived from four main routes (nutrient, metaphyseal, epiphyseal, and periosteal arteries)♦ There are three main types of cells in bone (osteoblast, osteocyte, and osteoclast)♦ The matrix is a composite material consisting of an organic and an inorganic component♦ Two types of bone formation are intramembranous and endochondral ossification♦ The skeleton is also involved in the vital homeostasis of calcium and phosphate.

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50

Bijvoet, O. L. M. Osteoclast Inhibition in the Management of Malignancy-Related Bone Disorders: An International Symposium Held During the 15th International Cancer Co. Hogrefe & Huber Pub, 1992.

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