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Amelogenesis Imperfecta in a New Animal Model—a Mutation in Chromosome 5 (human 4q21)

¹ Department of Prosthetic Dentistry, University Hospital Hamburg-Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany;
² Department of Oral and Maxillofacial Surgery and
³ Department of Conservative Dentistry and Periodontology, University of Kiel, Arnold-Heller-Strasse 16, D-24105 Kiel, Germany;
⁴ GSF National Research Center for Environment and Health, Institute of Experimental Genetics, Ingolstaedter Landstrasse 1, D-85764 Oberschleissheim, Germany; and
⁵ Gene Mapping Centre, Max-Delbruck-Centre, Robert-Rössle-Str. 10, D-13092 Berlin;

View larger version (76K): [in a new window]   Figure 1. Toluidine-blue-stained non-decalcified sections. Regular structure of a tooth of a wild-type mouse (top). Enamel (E) of reduced width of a tooth of a heterozygotic ATE mutant (middle). Complete loss of the enamel of a tooth of a homozygotic ATE mutant (bottom). D, tubular dentin; A, crack (artefact).

View larger version (85K): [in a new window]   Figure 2. Scanning electron micrographs showing the intact enamel surface of the tooth of a wild-type mouse (top), the cracked enamel surface of the tooth of an heterozygotic ATE mutant (middle), and the loss of the enamel of a tooth of an homozygotic ATE mutant with exposed dentinal tubules (bottom).

View larger version (22K): [in a new window]   Figure 3. Chromatogram of pooled probes of 1st molars of homozygotic ATE1 mutants (a) and chromatogram of pooled probes of 1st molars of wild-type mice (b). The fluorescence was monitored with excitation at 297 nm and emission at 397 nm. The HP peak arose at 17.5 min after injection, followed by the LP peak. The HP and LP peaks in 1a are increased compared with those in 1b. Please note that the peaks appear to be of the same size, but that the scale of magnitude is different.