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Relevant bibliographies by topics / Bone disease / Journal articles

Journal articles on the topic 'Bone disease'

To see the other types of publications on this topic, follow the link: Bone disease.

Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Jain, Ekta, Rajpal S. Punia, Amrita Bhattacharya, and Sudhir Garg. "Hydatid Disease of The Bone." Annals of Pathology and Laboratory Medicine 6, no. 12 (December 24, 2019): C133–135. http://dx.doi.org/10.21276/apalm.2596.

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2

Terpos, Evangelos. "BONE DISEASE." HemaSphere 6 (April 2022): 6. http://dx.doi.org/10.1097/01.hs9.0000829544.33044.41.

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3

Smergel, Eleanor M., and Marie A. Capitanio. "Bone disease." Current Opinion in Pediatrics 2, no. 1 (February 1990): 9–16. http://dx.doi.org/10.1097/00008480-199002000-00003.

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4

Chivima, Brenda. "Bone disease." Nursing Standard 28, no. 10 (November 6, 2013): 61. http://dx.doi.org/10.7748/ns2013.11.28.10.61.s51.

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5

Lipkin, Edward W. "METABOLIC BONE DISEASE IN GUT DISEASES." Gastroenterology Clinics of North America 27, no. 2 (June 1998): 513–23. http://dx.doi.org/10.1016/s0889-8553(05)70016-9.

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6

Zeng, Zhipeng, Xuchang Zhou, Yan Wang, Hong Cao, Jianmin Guo, Ping Wang, Yajing Yang, and Yan Wang. "Mitophagy—A New Target of Bone Disease." Biomolecules 12, no. 10 (October 4, 2022): 1420. http://dx.doi.org/10.3390/biom12101420.

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Bone diseases are usually caused by abnormal metabolism and death of cells in bones, including osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Mitochondrial dysfunction, as an important cause of abnormal cell metabolism, is widely involved in the occurrence and progression of multiple bone diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma. As selective mitochondrial autophagy for damaged or dysfunctional mitochondria, mitophagy is closely related to mitochondrial quality control and homeostasis. Accumulating evidence suggests that mitophagy plays an important regulatory role in bone disease, indicating that regulating the level of mitophagy may be a new strategy for bone-related diseases. Therefore, by reviewing the relevant literature in recent years, this paper reviews the potential mechanism of mitophagy in bone-related diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma, to provide a theoretical basis for the related research of mitophagy in bone diseases.

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7

Duursma, SA, JA Raymakers, and HJJ Verhaar. "Osteoporosis, osteomalacia and Paget’s disease of bone." Reviews in Clinical Gerontology 7, no. 2 (February 1997): 127–36. http://dx.doi.org/10.1017/s0959259897000142.

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Three diseases of bone are common in the elderly: osteoporosis, osteomalacia and Paget’s disease of bone. Osteoporosis is the result of bone loss, caused by a change in factors that regulate bone cell metabolism. The process of bone loss itself, resulting in osteoporosis, does not cause symptoms. It is the consequences of osteoporosis, fractures and bone deformity, that patients complain of. Osteomalacia is a defect in the process of mineralization of bone, nearly always due to vitamin D deficiency. In contrast to osteoporosis, patients with osteomalacia may have complaints of bone pain and muscle weakness. Page’s disease of bone is probably caused by a slow virus, which initially affects osteoclasts, followed by stimulation of osteoblasts. The process of increased bone cell turnover itself does not usually cause complaints. However, it results in deformation of bones and joints causing a painful secondary osteoarthritis. Pain resulting from high bone cell turnover responds remarkably quickly to treatment. In exceptional cases local pain in the long bones occurs. In an earlier review the problems of origin, diagnosis and treatment of osteoporosis were discussed. This paper focuses on diagnostic procedures and therapeutic regimens.

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8

Bandeira, Francisco, Natalie E. Cusano, Barbara C. Silva, Sara Cassibba, Clarissa Beatriz Almeida, Vanessa Caroline Costa Machado, and John P. Bilezikian. "Bone disease in primary hyperparathyroidism." Arquivos Brasileiros de Endocrinologia & Metabologia 58, no. 5 (July 2014): 553–61. http://dx.doi.org/10.1590/0004-2730000003381.

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Bone disease in severe primary hyperparathyroidism (PHPT) is described classically as osteitis fibrosa cystica (OFC). Bone pain, skeletal deformities and pathological fractures are features of OFC. Bone mineral density is usually extremely low in OFC, but it is reversible after surgical cure. The signs and symptoms of severe bone disease include bone pain, pathologic fractures, proximal muscle weakness with hyperreflexia. Bone involvement is typically characterized as salt-and-pepper appearance in the skull, bone erosions and bone resorption of the phalanges, brown tumors and cysts. In the radiography, diffuse demineralization is observed, along with pathological fractures, particularly in the long bones of the extremities. In severe, symptomatic PHPT, marked elevation of the serum calcium and PTH concentrations are seen and renal involvement is manifested by nephrolithiasis and nephrocalcinosis. A new technology, recently approved for clinical use in the United States and Europe, is likely to become more widely available because it is an adaptation of the lumbar spine DXA image. Trabecular bone score (TBS) is a gray-level textural analysis that provides an indirect index of trabecular microarchitecture. Newer technologies, such as high-resolution peripheral quantitative computed tomography (HR-pQCT), have provided further understanding of the microstructural skeletal features in PHPT.

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9

Eriksen, Erik Fink, and Bente Langdahl. "Bone changes in metabolic bone disease." Acta Orthopaedica Scandinavica 66, sup266 (January 1995): 195–201. http://dx.doi.org/10.3109/17453679509157690.

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10

Brandenburg, V. M., and J. Floege. "Adynamic bone disease--bone and beyond." Clinical Kidney Journal 1, no. 3 (May 16, 2008): 135–47. http://dx.doi.org/10.1093/ndtplus/sfn040.

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11

Ryan, P. J., and Ignac Fogelman. "Bone scintigraphy in metabolic bone disease." Seminars in Nuclear Medicine 27, no. 3 (July 1997): 291–305. http://dx.doi.org/10.1016/s0001-2998(97)80030-x.

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12

Choi, Yong Jun, Young Bae Sohn, and Yoon-Sok Chung. "Updates on Paget’s Disease of Bone." Endocrinology and Metabolism 37, no. 5 (October 31, 2022): 732–43. http://dx.doi.org/10.3803/enm.2022.1575.

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Paget’s disease of the bone is a prevalent bone disease characterized by disorganized bone remodeling; however, it is comparatively uncommon in East Asian countries, including China, Japan, and Korea. The exact cause still remains unknown. In genetically susceptible individuals, environmental triggers such as paramyxoviral infections are likely to cause the disease. Increased osteoclast activity results in increased bone resorption, which attracts osteoblasts and generates new bone matrix. Fast bone resorption and formation lead to the development of disorganized bone tissue. Increasing serum alkaline phosphatase or unique radiographic lesions may serve as the diagnostic indicators. Common symptoms include bone pain, bowing of the long bones, an enlarged skull, and hearing loss. The diagnosis is frequently confirmed by radiographic and nuclear scintigraphy of the bone. Further, bisphosphonates such as zoledronic acid and pamidronate are effective for its treatment. Moreover, biochemical monitoring is superior to the symptoms as a recurrence indicator. This article discusses the updates of Paget’s disease of bone with a clinical case.

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13

Harinarayan, CV. "Thyroid bone disease." Indian Journal of Medical Research 135, no. 1 (2012): 9. http://dx.doi.org/10.4103/0971-5916.93417.

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14

Crawford, Doreen, and Annette Dearmun. "Brittle bone disease." Nursing Children and Young People 28, no. 7 (September 12, 2016): 17. http://dx.doi.org/10.7748/ncyp.28.7.17.s18.

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15

Papadakis, Stamatios A., Eleni C. Babourda, Lubna Khaldi, Stefanos Papadakis, Thomas Mitsitsikas, and George Sapkas. "Vanishing Bone Disease." Orthopedics 31, no. 3 (March 1, 2008): 1–7. http://dx.doi.org/10.3928/01477447-20080301-31.

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16

Brown, Janet E., and Robert E. Coleman. "Metastatic Bone Disease." American Journal of Cancer 2, no. 4 (2003): 269–81. http://dx.doi.org/10.2165/00024669-200302040-00005.

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17

Galasko, Charles S. B. "Metastatic Bone Disease." American Journal of Cancer 3, no. 4 (2004): 265. http://dx.doi.org/10.2165/00024669-200403040-00006.

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18

Brown, Janet E., and Robert E. Coleman. "Metastatic Bone Disease." American Journal of Cancer 3, no. 4 (2004): 265. http://dx.doi.org/10.2165/00024669-200403040-00007.

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19

Carlson, Robert H. "Metastatic Bone Disease." Oncology Times 24, no. 10 (October 2002): 54. http://dx.doi.org/10.1097/01.cot.0000289558.82626.42.

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20

McCluggage, David. "Metabolic Bone Disease." AAV Today 1, no. 5 (1987): 208. http://dx.doi.org/10.2307/30133076.

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21

Fusaro, M., S. Giannini, D. Miozzo, M. Noale, G. Tripepi, M. Plebani, M. Zaninotto, et al. "DIALYSIS BONE DISEASE." Nephrology Dialysis Transplantation 29, suppl 3 (May 1, 2014): iii263—iii271. http://dx.doi.org/10.1093/ndt/gfu157.

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22

Diaz-Tocados, J. M., C. Herencia, J. M. Martinez-Moreno, A. Montes De Oca, M. E. Rodriguez-Ortiz, K. Gundlach, J. Buchel, et al. "CKD BONE DISEASE." Nephrology Dialysis Transplantation 29, suppl 3 (May 1, 2014): iii394—iii405. http://dx.doi.org/10.1093/ndt/gfu166.

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23

&NA;. "Metabolic bone disease." Current Opinion in Orthopaedics 3, no. 1 (February 1992): 126–30. http://dx.doi.org/10.1097/00001433-199202000-00024.

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24

Andersen, Mel, and David Hanley. "Metabolic bone disease." Current Opinion in Orthopaedics 4, no. 5 (October 1993): 1–2. http://dx.doi.org/10.1097/00001433-199310000-00001.

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25

Frassica, Frank J., and Franklin H. Sim. "Metastatic bone disease." Current Opinion in Orthopaedics 4, no. 6 (December 1993): 83–89. http://dx.doi.org/10.1097/00001433-199312000-00014.

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26

Sprague, Stuart M. "Renal bone disease." Current Opinion in Endocrinology, Diabetes and Obesity 17, no. 6 (December 2010): 535–39. http://dx.doi.org/10.1097/med.0b013e3283400945.

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27

Song, X. H., L. W. Ding, and H. Wen. "Bone hydatid disease." Postgraduate Medical Journal 83, no. 982 (August 1, 2007): 536–42. http://dx.doi.org/10.1136/pgmj.2007.057166.

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28

Menkes, Charles-Joel. "Metabolic bone disease." Current Opinion in Rheumatology 2, no. 1 (February 1990): 1–3. http://dx.doi.org/10.1097/00002281-199002010-00001.

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29

&NA;. "Metabolic bone disease." Current Opinion in Rheumatology 2, no. 1 (February 1990): 197–206. http://dx.doi.org/10.1097/00002281-199002010-00034.

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30

Menkès, Charlès-Joël. "Metabolic bone disease." Current Opinion in Rheumatology 3, no. 3 (June 1991): 449–51. http://dx.doi.org/10.1097/00002281-199106000-00017.

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31

&NA;. "Metabolic bone disease." Current Opinion in Rheumatology 3, no. 3 (June 1991): 536–53. http://dx.doi.org/10.1097/00002281-199106000-00028.

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32

&NA;. "Metabolic bone disease." Current Opinion in Rheumatology 4, no. 3 (June 1992): 442–54. http://dx.doi.org/10.1097/00002281-199206000-00024.

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33

Menkès, Charles-Joël. "Metabolic bone disease." Current Opinion in Rheumatology 5, no. 3 (May 1993): 329–31. http://dx.doi.org/10.1097/00002281-199305030-00011.

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34

&NA;. "Metabolic bone disease." Current Opinion in Rheumatology 5, no. 3 (May 1993): 388–401. http://dx.doi.org/10.1097/00002281-199305030-00020.

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35

Roberts, N. B., and A. Davenport. "Aluminium bone disease." BMJ 295, no. 6607 (November 7, 1987): 1209–10. http://dx.doi.org/10.1136/bmj.295.6607.1209-d.

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36

el Habib, R., and J. P. Eygonnet. "Aluminium bone disease." BMJ 295, no. 6610 (November 28, 1987): 1415–16. http://dx.doi.org/10.1136/bmj.295.6610.1415-d.

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37

Cunningham, John. "Posttransplantation Bone Disease." Transplantation 79, no. 6 (March 2005): 629–34. http://dx.doi.org/10.1097/01.tp.0000149698.79739.ef.

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38

Malcolm, A. J. "Metabolic bone disease." Current Diagnostic Pathology 8, no. 1 (February 2002): 19–25. http://dx.doi.org/10.1054/cdip.2001.0091.

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39

Joseph, James, and Ely Bartal. "Disappearing Bone Disease." Journal of Pediatric Orthopaedics 7, no. 5 (September 1987): 584–88. http://dx.doi.org/10.1097/01241398-198709000-00016.

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40

Sanderson, Ralph D., and Joshua Epstein. "Myeloma Bone Disease." Journal of Bone and Mineral Research 24, no. 11 (November 2009): 1783–88. http://dx.doi.org/10.1359/jbmr.090901.

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41

Whyte, Michael P., Mark C. Eddy, Michelle N. Podgornik, and William H. McAlister. "Polycystic Bone Disease." Journal of Bone and Mineral Research 15, no. 2 (February 18, 2010): 373. http://dx.doi.org/10.1359/jbmr.2000.15.2.373.

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42

Harvie, P., and D. Whitwell. "Metastatic bone disease." Bone & Joint Research 2, no. 6 (June 2013): 96–101. http://dx.doi.org/10.1302/2046-3758.26.2000154.

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43

Amerling, Richard. "Guideline Bone Disease." Blood Purification 36, no. 2 (2013): 132–35. http://dx.doi.org/10.1159/000353422.

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44

Viswanathan, Sreekanth, Wasim Khasawneh, Kera McNelis, Carly Dykstra, Randi Amstadt, Dennis M. Super, Sharon Groh-Wargo, and Deepak Kumar. "Metabolic Bone Disease." Journal of Parenteral and Enteral Nutrition 38, no. 8 (August 20, 2013): 982–90. http://dx.doi.org/10.1177/0148607113499590.

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45

Cunningham, John. "Renal bone disease." Medicine 35, no. 8 (August 2007): 450–52. http://dx.doi.org/10.1016/j.mpmed.2007.05.007.

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46

Veighey, Kristin, and John Cunningham. "Renal bone disease." Medicine 39, no. 7 (July 2011): 417–20. http://dx.doi.org/10.1016/j.mpmed.2011.04.014.

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47

Veighey, Kristin, and John Cunningham. "Renal bone disease." Medicine 43, no. 8 (August 2015): 465–68. http://dx.doi.org/10.1016/j.mpmed.2015.05.013.

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48

Phillips, Thomas, Kristin Veighey, and John Cunningham. "Renal bone disease." Medicine 47, no. 9 (September 2019): 580–84. http://dx.doi.org/10.1016/j.mpmed.2019.06.013.

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49

Sherman, K. P. "Metabolic bone disease." Orthopaedics and Trauma 26, no. 3 (June 2012): 220–25. http://dx.doi.org/10.1016/j.mporth.2012.04.003.

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50

Callander, Natalie S., and G. David Roodman. "Myeloma bone disease." Seminars in Hematology 38, no. 3 (July 2001): 276–85. http://dx.doi.org/10.1053/shem.2001.26007.

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