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MeSH Review

Bone Diseases, Metabolic

 
 
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Disease relevance of Bone Diseases, Metabolic

 

Psychiatry related information on Bone Diseases, Metabolic

 

High impact information on Bone Diseases, Metabolic

  • Osteopenia associated with renal transplantation remains a problem in the cyclosporine era [11].
  • The importance of this regulatory mechanism for bone homeostasis is emphasized by the observation that mice deficient in IFN-beta signalling exhibit severe osteopenia (loss of bone mass) accompanied by enhanced osteoclastogenesis [12].
  • It appears that at present, serum BGP is the one bone protein that has the most promise for assisting in the diagnosis and management of high turnover metabolic bone disease states [13].
  • These results identify Fos as a key regulator of osteoclast-macrophage lineage determination in vivo and provide insights into the molecular mechanisms underlying metabolic bone diseases [14].
  • CONCLUSIONS--Long-term thyroid hormone use at thyroxine-equivalent doses of 1.6 micrograms/kg or greater was associated with significant osteopenia at the ultradistal radius, midshaft radius, hip, and lumbar spine [15].
 

Chemical compound and disease context of Bone Diseases, Metabolic

 

Biological context of Bone Diseases, Metabolic

 

Anatomical context of Bone Diseases, Metabolic

 

Gene context of Bone Diseases, Metabolic

  • By generating CD44(-/-) human TNF-transgenic (hTNFtg) mice, we show that destruction of joints and progressive crippling is far more severe in hTNFtg mice lacking CD44, which also develop severe generalized osteopenia [31].
  • Mice lacking the IRS-1 gene IRS-1(-/-) showed severe osteopenia with low bone turnover [26].
  • RESULTS: Eight- and 12-week-old IL-10-/- mice developed osteopenia of both cancellous and cortical bone, evidenced by lower femoral ash weight, cancellous bone area and surface, trabecular number, and decreased cortical bone area and width [21].
  • Unexpectedly, Cbfa1 transgenic mice showed osteopenia with multiple fractures [32].
  • In summary, we present Fhl2-deficient mice as a unique model for osteopenia due to decreased osteoblast activity [33].
 

Analytical, diagnostic and therapeutic context of Bone Diseases, Metabolic

References

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  19. The HIV protease inhibitor ritonavir blocks osteoclastogenesis and function by impairing RANKL-induced signaling. Wang, M.W., Wei, S., Faccio, R., Takeshita, S., Tebas, P., Powderly, W.G., Teitelbaum, S.L., Ross, F.P. J. Clin. Invest. (2004) [Pubmed]
  20. Administration of cyclooxygenase-2 inhibitor reduces joint inflammation but exacerbates osteopenia in IL-1 alpha transgenic mice due to GM-CSF overproduction. Niki, Y., Takaishi, H., Takito, J., Miyamoto, T., Kosaki, N., Matsumoto, H., Toyama, Y., Tada, N. J. Immunol. (2007) [Pubmed]
  21. Interleukin 10-deficient mice develop osteopenia, decreased bone formation, and mechanical fragility of long bones. Dresner-Pollak, R., Gelb, N., Rachmilewitz, D., Karmeli, F., Weinreb, M. Gastroenterology (2004) [Pubmed]
  22. Defective bone mineralization and osteopenia in young adult FGFR3-/- mice. Valverde-Franco, G., Liu, H., Davidson, D., Chai, S., Valderrama-Carvajal, H., Goltzman, D., Ornitz, D.M., Henderson, J.E. Hum. Mol. Genet. (2004) [Pubmed]
  23. Decreased cellular activity and replicative capacity of osteoblastic cells isolated from the periarticular bone of rheumatoid arthritis patients compared with osteoarthritis patients. Yudoh, K., Matsuno, H., Osada, R., Nakazawa, F., Katayama, R., Kimura, T. Arthritis Rheum. (2000) [Pubmed]
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  26. Insulin receptor substrate-1 in osteoblast is indispensable for maintaining bone turnover. Ogata, N., Chikazu, D., Kubota, N., Terauchi, Y., Tobe, K., Azuma, Y., Ohta, T., Kadowaki, T., Nakamura, K., Kawaguchi, H. J. Clin. Invest. (2000) [Pubmed]
  27. Pax5-deficient mice exhibit early onset osteopenia with increased osteoclast progenitors. Horowitz, M.C., Xi, Y., Pflugh, D.L., Hesslein, D.G., Schatz, D.G., Lorenzo, J.A., Bothwell, A.L. J. Immunol. (2004) [Pubmed]
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  31. CD44 is a determinant of inflammatory bone loss. Hayer, S., Steiner, G., Görtz, B., Reiter, E., Tohidast-Akrad, M., Amling, M., Hoffmann, O., Redlich, K., Zwerina, J., Skriner, K., Hilberg, F., Wagner, E.F., Smolen, J.S., Schett, G. J. Exp. Med. (2005) [Pubmed]
  32. Overexpression of Cbfa1 in osteoblasts inhibits osteoblast maturation and causes osteopenia with multiple fractures. Liu, W., Toyosawa, S., Furuichi, T., Kanatani, N., Yoshida, C., Liu, Y., Himeno, M., Narai, S., Yamaguchi, A., Komori, T. J. Cell Biol. (2001) [Pubmed]
  33. Fhl2 deficiency results in osteopenia due to decreased activity of osteoblasts. Günther, T., Poli, C., Müller, J.M., Catala-Lehnen, P., Schinke, T., Yin, N., Vomstein, S., Amling, M., Schüle, R. EMBO J. (2005) [Pubmed]
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  35. Antagonism of the osteoclast vitronectin receptor with an orally active nonpeptide inhibitor prevents cancellous bone loss in the ovariectomized rat. Lark, M.W., Stroup, G.B., Dodds, R.A., Kapadia, R., Hoffman, S.J., Hwang, S.M., James, I.E., Lechowska, B., Liang, X., Rieman, D.J., Salyers, K.L., Ward, K., Smith, B.R., Miller, W.H., Huffman, W.F., Gowen, M. J. Bone Miner. Res. (2001) [Pubmed]
  36. Zoledronic acid prevents osteopenia and increases bone strength in a rabbit model of distraction osteogenesis. Little, D.G., Smith, N.C., Williams, P.R., Briody, J.N., Bilston, L.E., Smith, E.J., Gardiner, E.M., Cowell, C.T. J. Bone Miner. Res. (2003) [Pubmed]
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