Background: Amelogenesis imperfecta (AI) is a group of genomic developmental disorders that can affect the structure and clinical appearance of the enamel of all or almost all teeth. They can affect both the primary and permanent dentition. Not only are patients aesthetically compromised by the altered enamel, but in severe cases the exposed dentin can exacerbate carious lesions. This case report shows an all-ceramic restoration in a young female patient.
Case report: At the time of presentation to the Department of Prosthodontics at the University Hospital of Münster, the patient was 28 years old. Since 2010, carious lesions had been repeatedly treated with composite fillings due to the diagnosis of amelogenesis imperfecta (hypoplastic type 1). As the fillings had to be replaced regularly and the patient had already suffered a moderate loss of bite height of approximately 4 mm, a bite augmentation was planned by crowning all teeth with all-ceramic crowns.
The new bite height was first tested with long-term PMMA temporaries. After preparation of all teeth, these were placed in 6 blocks and worn for 3.5 months. The patient showed no problems after the wearing period. Therefore, the new bite height was transferred to all-ceramic crowns for the final restoration. Monolithic zirconia crowns were used in the posterior and mandibular anterior regions, and zirconia frameworks were veneered in the maxillary anterior region to improve aesthetics.
Discussion: A few cases of restorations in patients with amelogenesis imperfecta have been described in the literature. In less severe forms, composite abutments or veneers can be used to treat the enamel malformation. As enamel may be completely absent in type 1, crowns are the treatment of choice. A full crown prevents future substance loss and provides the best possible protection for the remaining tooth substance. With modern all-ceramic restorations, highly aesthetic results can be achieved even in severe initial conditions.
Keywords: amelogenesis imperfecta, all-ceramic crowns, hereditary disease