title: Enamel defects associated with coeliac disease: putative role of antibodies against gliadin in pathogenesis.
abstract: Enamel defects in the permanent teeth of patients with coeliac disease (CD) are often reported as an atypical manifestation, sometimes being suggestive of an undiagnosed atypical disease. We proposed to explore the pathogenesis of these oral defects, which are poorly studied. Sequence analyses of proteins from gluten (gliadins) and of proline-rich enamel proteins (amelogenin and ameloblastin) suggested the presence of common antigenic motifs. Therefore, we analyzed, by ELISA and western blotting, the reactivity of sera from patients with CD against gliadin and enamel-derived peptides. Correlation analyses between the levels of specific antibodies against gliadin and enamel derived peptides and inhibition experiments confirmed the presence of cross-reactive antibodies. Immunoblot analysis revealed that the most prominent component in enamel matrix derivative (of approximately 18.6 kDa), identified by an amelogenin-specific antibody, is recognized by sera from patients with CD; in addition, several fractions of pure gliadin were recognized by amelogenin-specific antibody. In agreement, sera from mice immunized with enamel matrix-derived proteins generated antibodies that recognized a peptide (of approximately 21.2 kDa) derived from gliadin. In conclusion, antibodies against gliadin generated in patients with CD can react in vitro with a major enamel protein. The involvement of anti-gliadin serum in the pathogenesis of enamel defects in children with untreated CD can be hypothesized on the basis of these novel results.
authors.affiliation: Cátedra de Inmunología, Instituto de Química Biológica, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay.
authors.forename: Florencia
authors.initials: F
authors.lastname: Muñoz
authors.forename: Natalia
authors.initials: N
authors.lastname: Del Río
authors.forename: Cecilia
authors.initials: C
authors.lastname: Sóñora
authors.forename: Inés
authors.initials: I
authors.lastname: Tiscornia
authors.forename: Alicia
authors.initials: A
authors.lastname: Marco
authors.forename: Ana
authors.initials: A
authors.lastname: Hernández
mesh_terms: D000293:Adolescent; D000328:Adult; D053523:Amelogenin / Q000276:immunology*; D000595:Amino Acid Sequence; D000818:Animals; D015153:Blotting, Western; D016022:Case-Control Studies; D002446:Celiac Disease / Q000097:blood / Q000276:immunology*; D003429:Cross Reactions; D003744:Dental Enamel Hypoplasia / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D003746:Dental Enamel Proteins / Q000276:immunology*; D005260:Female; D005903:Gliadin / Q000276:immunology*; D006801:Humans; D008297:Male; D051379:Mice; D008875:Middle Aged; D020539:Sequence Analysis, Protein; D018709:Statistics, Nonparametric; D055815:Young Adult
chemical_list: C490889:AMBN protein, human; D053523:Amelogenin; D003746:Dental Enamel Proteins; D005903:Gliadin