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Bibliographies thématiques / Bone resorption / Livres

Livres sur le sujet « Bone resorption »

Pour voir les autres types de publications sur ce sujet consultez le lien suivant : Bone resorption.

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 10 mars 2023

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1

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

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2

Bronner, Felix, Mary C. Farach-Carson et Janet Rubin, dir. Bone Resorption. London : Springer-Verlag, 2005. http://dx.doi.org/10.1007/b136184.

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3

Harvey, Wilson. Prostaglandins in bone resorption. Boca Raton, Fla : CRC Press, 1988.

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4

Pierce, Angela Mary. Cellular mechanisms in bone and tooth resorption : Morphological studies in rats and monkeys. Stockholm : Kongl. Carolinska Medico Chirurgiska Institutet, 1988.

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5

Brown, R. James. Histological and compositional responses of bone to immobilization and other experimental conditions : Semi-annual report. San Francisco, Calif : Institute of Chemical Biology, University of San Francisco, 1985.

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6

Arun, Shanbhag, Rubash Harry E et Jacobs Joshua J. 1956-, dir. Joint replacement and bone resorption : Pathology, biomaterials, and clinical practice. New York : Taylor & Francis, 2005.

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7

Maria, Bijvoet Olav Leonardus, dir. Bisphosphonate on bones. Amsterdam : Elsevier, 1995.

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8

Åkesson, Louise. Panoramic radiography in the assessment of the marginal bone level. Malmö : Department of Oral Radiology, Faculty of Odontology, Lund University, 1991.

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9

Fleisch, Herbert. Bisphosphonates in bone disease : From the laboratory to the patient. Bern : H. Fleish, 1993.

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10

Jonasson, Grethe. Mandibular alveolar bone mass, structure and thickness in relation to skeletal bone density in dentate women. Göteborg : Department of Orthodontics, Faculty of Odontology, The Sahlgrenska Academy at Göteborg University, 2005.

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11

Loomer, Peter Michael. The direct effects of Porphyromonas Gingivalis 2561 on bone formation and mineral resorption in vitro. [Toronto : University of Toronto, Faculty of Dentistry], 1997.

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12

Fleisch, Herbert. Bisphosphonates in bone disease : From the laboratory to the patient. 3^e éd. New York : Parthenon Pub. Group, 1997.

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13

Fleisch, Herbert. Bisphosphonates in bone disease : From the laboratory to the patient. 2^e éd. New York : Parthenon Pub. Group, 1995.

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14

Fleisch, Herbert. Bisphosphonates in bone disease : From the laboratory to the patient. 4^e éd. San Diego : Academic Press, 2000.

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15

D, Rubens R., et European Conference on Clinical Oncology (5th : 1989 : London, England), dir. 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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16

Congress, European Society for Medical Oncology. Disodium pamidronate (APD) in the treatment of malignancy-related disorders : An international symposium held during the 13th Congress of the European Society for Medical Oncology (ESMO), Lugano, Switzerland, October 1988. Toronto : Hogrefe & Huber, 1990.

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17

Peter, Burckhardt, dir. Disodium pamidronate (APD) in the treatment of malignancy-related disorders. Toronto : Huber, 1989.

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18

Meyer, James L. I loved a boy : Confessions of a Roman Catholic priest. Royal Oak, Mich : Van Antwerp and Beale Publishers, 2007.

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19

Meyer, James L. I loved a boy : Confessions of a Roman Catholic priest. Royal Oak, Mich : Van Antwerp and Beale Publishers, 2007.

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20

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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21

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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22

Mundy, Gregory R. Bone remodeling and its disorders. London : Martin Dunitz, 1994.

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23

Mundy, Gregory R. Bone remodeling and its disorders. London : Martin Dunitz, 1995.

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24

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

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25

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

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26

Harvey, Wilson, et Alan Bennett. Prostaglandins in Bone Resorption. CRC Press, 2020. http://dx.doi.org/10.1201/9780429279195.

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27

Harvey, Wilson, et Alan Bennett. Prostaglandins in Bone Resorption. Taylor & Francis Group, 2020.

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28

Harvey, Wilson, et Alan Bennett. Prostaglandins in Bone Resorption. Taylor & Francis Group, 2020.

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29

Harvey, Wilson, et Alan Bennett. Prostaglandins in Bone Resorption. Taylor & Francis Group, 2020.

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30

Harvey, Wilson, et Alan Bennett. Prostaglandins in Bone Resorption. Taylor & Francis Group, 2019.

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31

Harvey, Wilson, et Alan Bennett. Prostaglandins in Bone Resorption. Taylor & Francis Group, 2020.

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32

Bone resorption, metastasis, and diphosphonates. New York : Raven Press, 1985.

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33

Shanbhag, Arun, Harry E. Rubash et Joshua J. Jacobs, dir. Joint Replacement and Bone Resorption. CRC Press, 2005. http://dx.doi.org/10.1201/b14138.

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34

Rubash, Harry E., Arun Shanbhag et Joshua J. Jacobs. Joint Replacement and Bone Resorption. Taylor & Francis Group, 2019.

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35

OGURA, HIDEAKI. Pharmacological Approach to the Study of the Formation and the Resorption Mechanism of Hard Tissues. MEDICO DENTAL MEDIA INTERNATIONAL, 1994.

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36

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

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37

Anderson, Paul, Borje Edgar Christopher Nordin et Howard Arthur Morris. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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38

Anderson, Paul, Borje Edgar Christopher Nordin et Howard Arthur Morris. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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39

Anderson, Paul, Howard A. Morris et B. E. Christopher Nordin. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2017.

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40

Anderson, Paul, Borje Edgar Christopher Nordin et Howard Arthur Morris. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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41

Rubash, Harry E., Arun Shanbhag et Joshua J. Jacobs. Joint Replacement and Bone Resorption : Pathology, Biomaterials and Clinical Practice. Taylor & Francis Group, 2005.

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42

(Editor), Arun Shanbhag, Harry E. Rubash (Editor) et Joshua J. Jacobs (Editor), dir. Joint Replacement and Bone Resorption : Pathology, Biomaterials and Clinical Practice. Informa Healthcare, 2005.

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43

Rubash, Harry E., Arun Shanbhag et Joshua J. Jacobs. Joint Replacement and Bone Resorption : Pathology, Biomaterials and Clinical Practice. Taylor & Francis Group, 2005.

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44

Mansfield, Ian David. The synthesis of novel agents which inhibit tumour-stimulated bone resorption. 1999.

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45

The relationship between bone mineral density and selected variables : An epidemiological perspective. 1990.

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46

Javaid, Kassim. Paget’s disease of bone. Sous la direction de Patrick Davey et David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0274.

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Paget’s disease of bone is an uncommon bone disorder with increased bone resorption and disorganized bone formation of woven bone. Its cause is unclear; there is a clear genetic component but additional environmental factors are important, given the reduction in severity and prevalence in the UK. Paget’s disease is usually asymptomatic and detected by an unexplained raised alkaline phosphatase on routine biochemistry. Symptoms include focal bone pain, including headache. Other symptoms include bone deformity and complications such as fracture and nerve conduction. Paget’s disease can sometimes present with immobilization-associated hypercalcaemia or high-output cardiac failure, and rarely can transform to an osteosarcoma. This chapter addresses the clinical features, diagnosis, and management of Paget’s disease of bone.

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47

Effects of prostaglandin Eb2s on chick bone rudiments in vitro : Studies on bone resorption and formation. Ottawa : National Library of Canada, 1990.

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48

Wordsworth, B. P. Skeletal dysplasias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0150.

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Bone is metabolically active throughout life and metabolic disturbances may have wide-ranging consequences that are not restricted to altering its mechanics. The study of some genetic bone diseases has already provided remarkable insights into the normal regulation of bone metabolism. Skeletal dysplasias are developmental disorders of the chondro-osseous tissues commonly resulting in short stature, which is often disproportionate. The underlying mutations are often in the structural genes encoding components of the matrix but may also involve growth factors or cell signalling. In contrast, the dysostoses tend to affect single bones or groups of bones, reflecting the transient nature of the many different signalling factors to which they are responsive during development. Abnormalities of bone density (high or low) may be due to primary deficiency of bone matrix synthesis (e.g. osteogenesis imperfecta and hypophosphatasia) but may also reflect an imbalance between bone formation and resorption. This may be caused by abnormalities of bone formation (e.g. hyperostosis/sclerosteosis and osteoporosis pseudoglioma syndrome) or bone resorption (e.g. classic osteopetrosis and fibrous dysplasia).

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49

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0144.

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Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.

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50

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0144_update_001.

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Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.

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