Molar odontogenesis in the trisomic 16 mouse

Abstract

Stocks used were male and female monozygotes for Robertsonian translocation specific for chromosomes 16 and 17 Rb(16.17)7Bnr and males and females homozygous for Robertsonian translocation for chromosomes 6 and 16 Rb(6.16)24Lub to produce double heterozygotes characterized as Rb(16.17)Bnr/Rb(6.16)24Lub. This study was based on 156 fetuses, of which 70 were normal (euploid/ controls) and 86 were affected trisomies identified grossly by decreased size, shortened faces (flattened snouts), oedema, petechiae, open eyelids and dysplastic ears. Confirmation of trisomics included karyotyping metaphasic spreads. Throughout the five gestational days studied (14–18), trisomic fetuses exhibited developmental delays of up to 24 h. In general, tooth organs were smaller, hypocellular, hypoplastic and had a decreased blood supply. These differences were progressive and more pronounced in the later periods of odontogenesis, especially in the morpho- and histodifferentiation stages.