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Books on the topic 'Osteoclast'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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

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2

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

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3

Mattsson, Jan P. The osteoclast H⁺-ATPase: Isolation and initial characterization. Department of Biochemistry and Biophysics, Department of Cell Biology, University of Göteborg and Chalmers University of Technology, 1995.

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4

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

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5

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

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6

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

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7

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. Hogrefe & Huber, 1993.

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8

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. Hogrefe & Huber, 1990.

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9

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

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10

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

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11

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. Edited by Robey Pamela Gehron 1952-, Sherman Sherry, National Institute of Dental Research (U.S.), and National Institute on Aging. Springer International, 1995.

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12

Karhukorpi, Eeva-Kaisa. The mode of action of osteoclasts in bone resorption: An ultrastructural study of enzymes possibly involved. University of Oulu], Department of Anatomy, 1991.

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13

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

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14

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

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15

H, Helfrich Miep, and Ralston Stuart, eds. Bone research protocols. Humana Press, 2003.

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16

H, Helfrich Miep, and Ralston Stuart, eds. Bone research protocols. Humana Press, 2003.

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17

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

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18

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

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19

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

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20

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

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21

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

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22

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

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23

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

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24

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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25

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

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26

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

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27

Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by 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

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28

J. Singh, Parminder, and 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 vita

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29

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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30

Gabet, Yankel, Drorit Neumann, Ari Elson, Noam Levaot, and 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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31

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

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32

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

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33

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

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34

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

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35

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

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36

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

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37

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

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38

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

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39

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

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40

Clarke, Noel W. Metastatic disease in prostate cancer. Edited by 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

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41

Lories, Rik J., and 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 si

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42

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

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43

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

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44

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

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45

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

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46

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

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47

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

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48

Bone research protocols. 2nd ed. Humana Press, 2012.

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49

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

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50

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

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