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Abstract
Antecedentes: El esmalte dental, el tejido más duro del cuerpo, puede ser destruido por la caries, una enfermedad infecciosa y transmisible causada por bacterias. Cuando trastornos genéticos y hereditarios, como la amelogénesis imperfecta (AI), afectan la formación del esmalte, este se hace más vulnerable a sufrir dicha patología. Objetivo: Describir el tipo de caries presente en nueve individuos de ocho familias colombianas con diferentes fenotipos de AI. Métodos: Se realizó análisis clínico, de radiografías periapicales y panorámicas, y de fotografías. Se utilizó la clasificación de Witkop para los fenotipos de AI y la del Sistema Internacional de Valoración y Detección de Caries (ICDAS) para caries dental. Resultados: Los pacientes con AI, fenotipo hipoplásico, presentaron registros ICDAS 5 y 6. En algunos pacientes con AI, fenotipo hipocalcificado, se encontraron registros ICDAS 3 y 4 y desgastes dentales graves; mientras que en los pacientes con fenotipo hipomadurativo los registros ICDAS estuvieron entre 1 y 3. Conclusiones: El gran número de registros ICDAS 5 y 6 en pacientes con AI fenotipo hipoplásico parece estar relacionado con factores como rugosidad, sensibilidad y susceptibilidad a la fractura del esmalte. En pacientes con AI fenotipo hipocalcificado, los registros 3 y 4 posiblemente fueron causados por el esmalte poco mineralizado y poroso. Los desgastes parecen actuar como una forma de microabrasión que elimina el tejido cariado. En el fenotipo hipomadurativo se presentaron los registros más bajos, lo que parece deberse al gran contenido de proteína anormal que actúa como un protector de la disolución del esmalte por los ácidos.
Background: Dental enamel, the human hardest tissue, can be destroyed by tooth decay, an infectious and transmissible disease caused by bacteria. When genetic or heredity disorders such as imperfect amelogenesis (AI) affect the enamel formation, it makes it more vulnerable to the onset of caries or tooth decay. Objective: Describe the type of tooth decay present in nine individuals from eight Colombian families with different AI phenotypes. Methods: Clinical, radiographic (periapical and panoramic radiographs), and photographic analysis were performed. AI phenotypes were classified through Witkop’s index and so was ICDAS for dental caries. Results: Patients with hypoplastic phenotype of AI had ICDAS scores of 5 and 6. In some patients with hypocalcified phenotype of AI ICDAS 3 and 4 and severe dental wear were found. In addition, patients with hypomadurative phenotype had ICDAS scores 1-3. Conclusions: The larger number of ICDAS scores 5 and 6 in patients with hypoplastic AI appears to be due to factors such as roughness, sensitivity, and susceptibility to enamel fracture. In patients with hypocalcified AI ICDAS 3 and 4 were possibly caused by the porous and poorly mineralized enamel. Wear seems to act as a means of microabrasion to eliminate the carious tissue. The lowest ICDAS scores present in hypomadurative AI seem to be due to the high content of abnormal phenotype protein that acts as a dissolution protector of the enamel by acids.
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