Calcified Tissue International

, Volume 65, Issue 5, pp 352–353

Ethnic Difference in Contribution of Sp1 Site Variation of COLIA1 Gene in Genetic Predisposition to Osteoporosis

Authors

  • T.  Nakajima
    • Department of Molecular Biology, Institute of Gerontology, Nippon Medical School, Kawasaki-Tokyo, 211-8533, Japan
  • N.  Ota
    • Department of Molecular Biology, Institute of Gerontology, Nippon Medical School, Kawasaki-Tokyo, 211-8533, Japan
  • Y.  Shirai
    • Department of Orthopaedic Surgery, Nippon Medical School, Kawasaki-Tokyo, 211-8533, Japan
  • A.  Hata
    • Department of Public Health, Asahikawa Medical College, Asahikawa, 078-8510, Japan
  • H.  Yoshida
    • Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan
  • T.  Suzuki
    • Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan
  • T.  Hosoi
    • Tokyo Metropolitan Geriatric Hospital, Tokyo, 173-0015, Japan
  • H.  Orimo
    • Tokyo Metropolitan Geriatric Hospital, Tokyo, 173-0015, Japan
  • M.  Emi
    • Department of Molecular Biology, Institute of Gerontology, Nippon Medical School, Kawasaki-Tokyo, 211-8533, Japan
Article

DOI: 10.1007/s002239900711

Cite this article as:
Nakajima, T., Ota, N., Shirai, Y. et al. Calcif Tissue Int (1999) 65: 352. doi:10.1007/s002239900711

Abstract.

Osteoporosis, a condition characterized by low bone mineral density (BMD) leading to bone fragility [1], is a major public health concern in Japan as well as in other countries. Although genetic predisposition seems to be a factor in the pathogenesis of osteoporosis [2–4], the precise cohort of genes that may be involved is not well defined. The COLIA1 and COLIA2 genes encode polypeptide constituents of collagen type Iα1 and Iα2, respectively. Both are important candidates as genetic regulators of BMD, since mutations in either gene result in osteogenesis imperfecta, a disorder characterized by severe osteoporosis [5]. Some patients with adult osteoporosis also carry mutations in COLIA1 or COLIA2 genes [6].

Copyright information

© Springer-Verlag New York Inc. 1999