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Książki na temat „Bone disease”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 10 marca 2023

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1

McKillop, James H. Benign and malignant bone disease. Edinburgh: Churchill Livingstone, 1990.

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2

R, Reid I., red. Metabolic bone disease. London: Baillière Tindall, 1997.

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3

Lecka-Czernik, Beata, i John L. Fowlkes, red. Diabetic Bone Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-16402-1.

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4

Diel, Ingo J., M. Kaufmann i G. Bastert, red. Metastatic Bone Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78596-2.

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5

Roodman, G. David, red. Myeloma Bone Disease. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-554-5.

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6

Randall, R. Lor, red. Metastatic Bone Disease. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-5662-9.

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7

Roodman, G. David. Myeloma bone disease. New York: Humana, 2010.

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8

D, Tiegs Robert, red. Metabolic bone disease. Philadelphia: Saunders, 1989.

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9

D, Tiegs Robert, red. Metabolic bone disease. Philadelphia: Saunders, 1990.

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10

J, Maricic Michael, i Gluck Oscar S. 1949-2003, red. Bone disease in rheumatology. Philadelphia: Lippincott Williams & Willkins, 2005.

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11

V, Avioli Louis, i Krane Stephen M, red. Metabolic bone disease and clinically related disorders. Wyd. 2. Philadelphia: W.B. Saunders Co., 1990.

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12

Yamaguchi, Masayoshi. Osteocalcin: Production, regulation, and disease. Hauppauge, N.Y: Nova Science Publishers, 2011.

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13

Singer, Frederick R., i Stanley Wallach, red. Paget’s Disease of Bone. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-2307-5.

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14

Patel, Vinood B., i Victor R. Preedy, red. Biomarkers in Bone Disease. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7693-7.

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15

Preedy, Victor R., red. Biomarkers in Bone Disease. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7745-3.

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16

G, Ward William, i Peabody Terrance D, red. Orthopedic management of metastatic disease. Philadelphia: W.B. Saunders, 2000.

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17

Paul, Grech, red. Diagnosis of metabolic bone disease. London: Chapman and Hall Medical, 1985.

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18

S, Tam Cherk, Heersche Johannes N. M i Murray Timothy M, red. Metabolic bone disease: Cellular and tissue mechanisms. Boca Raton, Fla: CRC Press, 1988.

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19

Orthopaedic management of metastatic bone disease. St. Louis: Mosby, 1988.

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20

Hukkanen, Mika V. J., 1962-, Polak Julia M, Hughes Sean i Royal Postgraduate Medical School, red. Nitric oxide in bone and joint disease. Cambridge, UK: Cambridge University Press, 1998.

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21

Mone, Zaidi, red. Skeletal development and remodeling in health, disease, and aging. Boston, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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22

A, Morris H., Need A. G i Nordin B. E. C, red. Metabolic bone and stone disease. Wyd. 3. Edinburgh: Churchill Livingstone, 1993.

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23

C, Nordin B. E., Need A. G i Morris H. A, red. Metabolic bone and stone disease. Wyd. 3. Edinburgh: Churchill Livingstone, 1993.

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24

Conference on Skeletal Biology and Medicine (4th 2011 New York, N.Y.). Skeletal biology and medicine II: Bone and cartilage homeostasis and bone disease. Redaktor Zaidi Mone. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2011.

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25

Musculoskeletal disease: Staged for rapid comprehension. Chicago: Year Book Medical Publishers, 1985.

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26

C, Stevenson John, red. New techniques in metabolic bone disease. London: Wright, 1990.

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27

E, Bonucci, i Motta Pietro M, red. Ultrastructure of skeletal tissues: Bone and cartilage in health and disease. Boston: Kluwer Academic Publishers, 1990.

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28

I, Tovey F., i Stamp T. C. B, red. The measurement of metabolic bone disease. New York: Parthenon Pub. Group, 1995.

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29

Rachel, Ives, i ScienceDirect (Online service), red. The bioarchaeology of metabolic bone disease. Amsterdam: Elsevier/Academic Press, 2008.

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30

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

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31

W, Weissman Barbara N., red. Imaging of arthritis and metabolic bone disease. Philadelphia, PA: Mosby/Elsevier, 2009.

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32

J, Diel I., Kaufman M. 1946-, Bastert G. B i European Symposium on Calcified Tissues (3rd : 1993 : Heidelberg, Germany), red. Metastatic bone disease: Fundamental and clinical aspects. Berlin: Springer-Verlag, 1994.

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33

Avioli, Louis V., i Stephen M. Krane. Metabolic Bone Disease: Volume II. Elsevier Science & Technology Books, 2013.

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34

Avioli, Louis V., i Stephen M. Krane. Metabolic Bone Disease: Volume 1. Elsevier Science & Technology Books, 2013.

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35

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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36

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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37

Gikas, Panagiotis D., i Timothy W. R. Briggs. Metastatic bone disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.002007.

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♦ Metastatic pathological fractures rarely unite, even if stabilized♦ Never rush to fix a pathological fracture; traction or splintage will suffice while investigations are performed and surgical intervention discussed♦ When surgery is indicated for spinal metastases, both decompression and stabilization are generally required♦ Implants should allow immediate weight-bearing and last the lifetime of the patient♦ Always use a multidisciplinary team.

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38

Metabolic bone disease. Philadelphia: Saunders, 1991.

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39

Martin. Metabolic Bone Disease. Elsevier, 1988.

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40

Myeloma Bone Disease. Humana, 2012.

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41

(Editor), R. Coleman, i Robert D. Rubens (Editor), red. Metastatic Bone Disease. Taylor & Francis Ltd, 1992.

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42

Roodman, G. David. Myeloma Bone Disease. Humana Press, 2010.

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43

Bone disease in rheumatology. Philadelphia, PA: Lippincott Williams & Wilkins, 2005.

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44

Diagnosis Metabol Bone Disease. Lippincott Williams & Wilkins Publishers, 1998.

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45

Handbook of cancer-related bone disease. BioScientifica, 2010.

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46

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

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47

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

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48

Anderson, Paul. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2017.

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49

Anderson, Paul. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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50

Javaid, Kassim. Paget’s disease of bone. Redaktorzy Patrick Davey i 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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