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Journal of Dental Research
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Biological

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

H. Seedorf1, I.N. Springer2,*, E. Grundner-Culemann3, H.-K. Albers4, A. Reis5, H. Fuchs3, M. Hrabe de Angelis3 and Y. Açil2

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;

Correspondence: * corresponding author, springer{at}mkg.uni-kiel.de

Candidate genes for amelogenesis imperfecta (AI) and dentinogenesis imperfecta (DI) are located on 4q21 in humans. We tested our hypothesis that mutations in the portion of mouse chromosome 5 corresponding to human chromosome 4q21 would cause enamel and dentin abnormalities. Male C3H mice were injected with ethylnitrosourea (ENU). Within a dominant ENU mutagenesis screen, a mouse mutant was isolated with an abnormal tooth enamel (ATE) phenotype. The structure and ultrastructure of teeth were studied. The mutation was located on mouse chromosome 5 in an interval of 9 cM between markers D5Mit18 and D5Mit10. Homozygotic mutants showed total enamel aplasia with exposed dentinal tubules, while heterozygotic mutants showed a significant reduction in enamel width. Dentin of mutant mice showed a reduced content of mature collagen cross-links. We were able to demonstrate that a mutation on chromosome 5 corresponding to human chromosome 4q21 can cause amelogenesis imperfecta and changes in dentin composition.

Key Words: amelogenesis imperfecta (AI) • structure • collagen cross-links • pyridinoline • hydroxyproline

Journal of Dental Research, Vol. 83, No. 8, 608-612 (2004)
DOI: 10.1177/154405910408300805
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