• Title of article

    Different enamel and dentin mineralization observed in VDR deficient mouse model

  • Author/Authors

    Zhang، نويسنده , , Xueming and Rahemtulla، نويسنده , , Firoz and Zhang، نويسنده , , Ping and Beck، نويسنده , , Preston and Thomas، نويسنده , , Huw F.، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2009
  • Pages
    7
  • From page
    299
  • To page
    305
  • Abstract
    Vitamin D plays an important role in the bone mineralization process. Enamel and dentin are two mineralized tissues of different origins that combine to form teeth, but the mechanism by which vitamin D regulates these tissues remains unclear. We hypothesized that vitamin D affects enamel and dentin mineralization through different mechanisms. ive mine enamel and dentin mineralization in a vitamin D receptor (VDR) deficient mouse model by micro-computerized tomography (micro-CT) and scanning electronic microscopy (SEM). s ld type mice (VDR+/+) and VDR deficient (VDR−/−) littermates were sacrificed at 70.5 days old, and their mandibles were dissected. Micro-CT was used to compare mineral density (MD) of enamel and dentin of the two groups at different levels along the axis of mandibular incisors. SEM was employed to examine the ultrastructure of incisors at the levels corresponding to the levels used for the micro-CT studies. Furthermore, an accelerated eruption procedure was performed to exclude the effect of delayed eruption on enamel and dentin mineralization. s ent distribution patterns of enamel and dentin MD were observed between VDR+/+ and VDR−/− groups. Early enamel maturation, mineralization, and hypomineralization in dentin were observed in the VDR deficient mice. sion n D may affect the mineralization of dentin systemically, and enamel mineralization may be regulated locally.
  • Keywords
    Dentin and mineralization , Vitamin D receptor , Enamel
  • Journal title
    Archives of Oral Biology
  • Serial Year
    2009
  • Journal title
    Archives of Oral Biology
  • Record number

    1805099