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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;

^* 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

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				H. Seedorf, M. Klaften, F. Eke, H. Fuchs, U. Seedorf, and M. Hrabe de Angelis A Mutation in the Enamelin Gene in a Mouse Model J. Dent. Res., August 1, 2007; 86(8): 764 - 768. [Abstract] [Full Text] [PDF]