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Artykuły w czasopismach 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

Jain, Ekta, Rajpal S. Punia, Amrita Bhattacharya i Sudhir Garg. "Hydatid Disease of The Bone". Annals of Pathology and Laboratory Medicine 6, nr 12 (24.12.2019): C133–135. http://dx.doi.org/10.21276/apalm.2596.

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2

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

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3

Smergel, Eleanor M., i Marie A. Capitanio. "Bone disease". Current Opinion in Pediatrics 2, nr 1 (luty 1990): 9–16. http://dx.doi.org/10.1097/00008480-199002000-00003.

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4

Chivima, Brenda. "Bone disease". Nursing Standard 28, nr 10 (6.11.2013): 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, nr 2 (czerwiec 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 i Yan Wang. "Mitophagy—A New Target of Bone Disease". Biomolecules 12, nr 10 (4.10.2022): 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 i HJJ Verhaar. "Osteoporosis, osteomalacia and Paget’s disease of bone". Reviews in Clinical Gerontology 7, nr 2 (luty 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 i John P. Bilezikian. "Bone disease in primary hyperparathyroidism". Arquivos Brasileiros de Endocrinologia & Metabologia 58, nr 5 (lipiec 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, i Bente Langdahl. "Bone changes in metabolic bone disease". Acta Orthopaedica Scandinavica 66, sup266 (styczeń 1995): 195–201. http://dx.doi.org/10.3109/17453679509157690.

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10

Brandenburg, V. M., i J. Floege. "Adynamic bone disease--bone and beyond". Clinical Kidney Journal 1, nr 3 (16.05.2008): 135–47. http://dx.doi.org/10.1093/ndtplus/sfn040.

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11

Ryan, P. J., i Ignac Fogelman. "Bone scintigraphy in metabolic bone disease". Seminars in Nuclear Medicine 27, nr 3 (lipiec 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 i Yoon-Sok Chung. "Updates on Paget’s Disease of Bone". Endocrinology and Metabolism 37, nr 5 (31.10.2022): 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, nr 1 (2012): 9. http://dx.doi.org/10.4103/0971-5916.93417.

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14

Crawford, Doreen, i Annette Dearmun. "Brittle bone disease". Nursing Children and Young People 28, nr 7 (12.09.2016): 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 i George Sapkas. "Vanishing Bone Disease". Orthopedics 31, nr 3 (1.03.2008): 1–7. http://dx.doi.org/10.3928/01477447-20080301-31.

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16

Brown, Janet E., i Robert E. Coleman. "Metastatic Bone Disease". American Journal of Cancer 2, nr 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, nr 4 (2004): 265. http://dx.doi.org/10.2165/00024669-200403040-00006.

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18

Brown, Janet E., i Robert E. Coleman. "Metastatic Bone Disease". American Journal of Cancer 3, nr 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, nr 10 (październik 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, nr 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 i in. "DIALYSIS BONE DISEASE". Nephrology Dialysis Transplantation 29, suppl 3 (1.05.2014): 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 i in. "CKD BONE DISEASE". Nephrology Dialysis Transplantation 29, suppl 3 (1.05.2014): iii394—iii405. http://dx.doi.org/10.1093/ndt/gfu166.

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23

&NA;. "Metabolic bone disease". Current Opinion in Orthopaedics 3, nr 1 (luty 1992): 126–30. http://dx.doi.org/10.1097/00001433-199202000-00024.

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24

Andersen, Mel, i David Hanley. "Metabolic bone disease". Current Opinion in Orthopaedics 4, nr 5 (październik 1993): 1–2. http://dx.doi.org/10.1097/00001433-199310000-00001.

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25

Frassica, Frank J., i Franklin H. Sim. "Metastatic bone disease". Current Opinion in Orthopaedics 4, nr 6 (grudzień 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, nr 6 (grudzień 2010): 535–39. http://dx.doi.org/10.1097/med.0b013e3283400945.

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27

Song, X. H., L. W. Ding i H. Wen. "Bone hydatid disease". Postgraduate Medical Journal 83, nr 982 (1.08.2007): 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, nr 1 (luty 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, nr 1 (luty 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, nr 3 (czerwiec 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, nr 3 (czerwiec 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, nr 3 (czerwiec 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, nr 3 (maj 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, nr 3 (maj 1993): 388–401. http://dx.doi.org/10.1097/00002281-199305030-00020.

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35

Roberts, N. B., i A. Davenport. "Aluminium bone disease." BMJ 295, nr 6607 (7.11.1987): 1209–10. http://dx.doi.org/10.1136/bmj.295.6607.1209-d.

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36

el Habib, R., i J. P. Eygonnet. "Aluminium bone disease." BMJ 295, nr 6610 (28.11.1987): 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, nr 6 (marzec 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, nr 1 (luty 2002): 19–25. http://dx.doi.org/10.1054/cdip.2001.0091.

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39

Joseph, James, i Ely Bartal. "Disappearing Bone Disease". Journal of Pediatric Orthopaedics 7, nr 5 (wrzesień 1987): 584–88. http://dx.doi.org/10.1097/01241398-198709000-00016.

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40

Sanderson, Ralph D., i Joshua Epstein. "Myeloma Bone Disease". Journal of Bone and Mineral Research 24, nr 11 (listopad 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 i William H. McAlister. "Polycystic Bone Disease". Journal of Bone and Mineral Research 15, nr 2 (18.02.2010): 373. http://dx.doi.org/10.1359/jbmr.2000.15.2.373.

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42

Harvie, P., i D. Whitwell. "Metastatic bone disease". Bone & Joint Research 2, nr 6 (czerwiec 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, nr 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 i Deepak Kumar. "Metabolic Bone Disease". Journal of Parenteral and Enteral Nutrition 38, nr 8 (20.08.2013): 982–90. http://dx.doi.org/10.1177/0148607113499590.

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45

Cunningham, John. "Renal bone disease". Medicine 35, nr 8 (sierpień 2007): 450–52. http://dx.doi.org/10.1016/j.mpmed.2007.05.007.

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46

Veighey, Kristin, i John Cunningham. "Renal bone disease". Medicine 39, nr 7 (lipiec 2011): 417–20. http://dx.doi.org/10.1016/j.mpmed.2011.04.014.

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47

Veighey, Kristin, i John Cunningham. "Renal bone disease". Medicine 43, nr 8 (sierpień 2015): 465–68. http://dx.doi.org/10.1016/j.mpmed.2015.05.013.

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48

Phillips, Thomas, Kristin Veighey i John Cunningham. "Renal bone disease". Medicine 47, nr 9 (wrzesień 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, nr 3 (czerwiec 2012): 220–25. http://dx.doi.org/10.1016/j.mporth.2012.04.003.

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50

Callander, Natalie S., i G. David Roodman. "Myeloma bone disease". Seminars in Hematology 38, nr 3 (lipiec 2001): 276–85. http://dx.doi.org/10.1053/shem.2001.26007.

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