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Restoring function and esthetics in a patient with amelogenesis imperfecta: A clinical report

Tug rul Sari, DDS,a and Aslhan Usumez, DDS, PhDb Faculty of Dentistry, Selcuk University, Konya, Turkey
This clinical report describes the prosthodontic treatment for an 18-year-old man diagnosed with amelogenesis imperfecta. The aim of treatment was to reduce dental sensitivity and to restore esthetics and masticatory function. Metal-ceramic xed partial dentures were placed on posterior teeth to modify the occlusion, and porcelain laminate veneers were placed to improve the esthetics of the maxillary anterior teeth. Clinical examination 12 months after treatment revealed no evidence of disorders associated with the restored teeth or their supporting structures. (J Prosthet Dent 2003;90:522-5.)

melogenesis imperfecta (AI) has been dened as a group of hereditary enamel defects not associated with evidence of systemic disease.1 Investigators have demonstrated that it is possible to delineate at least 12 distinct types of amelogenesis imperfecta2-6 using a combination of clinical, radiographic, histological, and genetic criteria.7,8 On the clinical and radiographic basis alone, 3 broad groups can be distinguished: (1) hypoplasia, in which the enamel is reduced in quantity but is relatively well-mineralized; (2) hypocalcication, in which enamel is formed in relatively normal amounts but is poorly mineralized; and (3) hypomaturation, in which the nal stages of the mineralization process are abnormal. The clinical features distinguish the hypoplastic and hypocalcied types.9 In the hypoplastic forms, the enamel does not develop to its normal thickness. In the hypocalcied forms, the enamel thickness on the newly erupted teeth closely approaches that of normal teeth, but the enamel is soft, friable, and can easily be removed from the dentin. In contrast to hypoplastic types, the hypomaturation types develop enamel of normal thickness. The hypomaturation forms differ from hypocalcication in that the enamel is harder, with a mottled opaque white to yellow-brown or red-brown color, and tends to chip from the underlying dentin rather than wear away.6,9-11 According to Seow,12 the primary clinical problems of AI are esthetics, dental sensitivity, and loss of occlusal vertical dimensions. However, the severity of dental problems experienced by patients varies with each type of AI. Historically, treatment of patients has included multiple extractions and the fabrication of complete dentures.12 These options are psychologically harsh when the problem must be addressed in adolescent patients.13 The treatment plan for patients with AI is related to many factors including the age of the patient, the socioeconomic status of the patient, the type and severity of
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disorder, and the intraoral situation at the time the treatment plan is developed. This clinical report describes the treatment of an 18-year-old with amelogenesis imperfecta using porcelain laminate veneers in the anterior region and metal-ceramic xed partial dentures (FPDs) in the posterior region.

CLINICAL REPORT
An 18-year-old man was referred for treatment of attrition and considerable sensitivity of his teeth. He was very self-conscious about the appearance of his teeth. A detailed medical, dental, and social history was obtained. Photographs and dental radiographs were made. The patients maxillary right and left second premolars, mandibular right second premolar, and mandibular left second molar had been extracted due to caries. Tissue loss affected all teeth. The enamel layer was nearly absent in the occlusal portion of the molars, and enamel pit defects were present in the anterior teeth (Figs. 1-3). The exposed dentin was hypersensitive. It was concluded that the patient likely suffered from a hypomature type of AI. Diagnostic casts were made, as were face-bow and protrusive records. Casts were mounted in centric rela-

Post-graduate student, Department of Prosthodontics. Assistant Professor, Department of Prosthodontics.

Fig. 1. Pretreatment view of teeth in occlusion.


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Fig. 2. A and B, Pretreatment occlusal views. First molar teeth are highly affected.

Fig. 3. Panoramic radiograph. Radiodensities of enamel and dentin were similar.

tion in a semi-adjustable articulator. The patient had canine-protected occlusion. It was determined that the patient had 3 to 4 mm of interocclusal distance; therefore, the patients vertical dimension was not altered. A treatment plan was developed with the following aims: to reduce the reported sensitivity of the teeth, to improve the esthetics, and to restore masticatory function. Fabrication of metal-ceramic FPDs for maxillary and mandibular posterior teeth and porcelain laminate veneers for anterior teeth was planned. The patient was informed of the diagnosis and treatment plan, which he accepted. The facial surfaces of the maxillary anterior teeth were prepared. A 0.5-mm facial reduction was performed, creating a chamfer cervical nish line. The incisal portions of the teeth were prepared to allow overlap of the restoration. Self-limiting depth-cutting disks of 0.5-mm
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thickness (834-31-021; Gebr. Brasseler, Lemgo, Germany) were used to dene the depth of the cuts, and 1.4-mm chamfer diamond burs (6844-314-014; Gebr. Brasseler) were used to rene the preparations. All tooth preparations were completed without sharp line angles. Impressions for prepared teeth were made with silicone material (Speedex; Colte ` ne/Whaldent Inc, Cuyahoga Falls, Ohio). A denitive maxillary cast was formed and mounted in an articulator with trimmed dies of prepared teeth. All restorations were fabricated with IPS Empress 2 materials (Ivoclar Vivadent AG, Schaan, Liechtenstein) according to the manufacturers directions. After completion, the porcelain laminate veneers were evaluated for t on the prepared teeth. They were then luted with a resin luting agent (Variolink II high viscosity; Ivoclar Vivadent AG) in combination with a
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Fig. 4. Post-treatment occlusal views. A, Maxillary; B, mandibular.

Fig. 5. A and B, Facial views of prostheses 12 months after insertion.

dentin adhesive (Syntac; Ivoclar Vivadent AG) and a bonding agent (Heliobond; Ivoclar Vivadent AG) with the use of rubber-dam isolation. Photo-polymerization was performed with a light polymerizing unit (Hilux 350; First Medica, NC) at 350 mW/cm2 for 40 seconds for incisal, mesial, and distal surfaces. After all the posterior teeth were prepared, impressions were made with vinyl polysiloxane material (Speedex; Colte ` ne/Whaledent Inc) in stock trays. From these impressions, casts were made and mounted in an articulator to produce metal-ceramic FPDs (Ivoclar Vivadent AG). The metal frameworks were evaluated intraorally to determine the marginal t. A metal trial insertion, prior to glazing of the ceramic material, enabled nal occlusal renement. The patients natural occlusal scheme (canine-protected occlusion) and anterior guidance were preserved in the denitive restorations to decrease lateral forces on the posterior dentition. The crowns were then completed in the laboratory and cemented with zinc-polycarboxylate cement (Poly F Plus; Dentsply DeTrey GmbH, Konstanz, Germany) (Fig. 4) according to manufacturers power/liquid ratio. The anterior porcelain laminate veneers and posterior metal-ceramic FPDs were satisfactory both esthetically
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and functionally at the end of 1 year of clinical service (Fig 5).

SUMMARY
This clinical report describes the use of metal-ceramic FPDs and porcelain laminate veneers for restoration of a hypomature type of amelogenesis imperfecta. Metal-ceramic FPDs were placed on the posterior teeth, and porcelain laminate veneers were placed on the maxillary teeth to improve the occlusion and esthetics.
REFERENCES
1. Winter GB, Brook AH. Enamel hypoplasia and anomalies of the enamel. Dent Clin North Am 1975;19:3-24. 2. Winter GB. Hereditary and idiopathic anomalies of tooth number structure and form. Dent Clin North Am 1969;13:355-73. 3. Winter GB, Lee KW, Johnson NW. Hereditary amelogenesis imperfectaa rare autosomal dominant type. Br Dent J 1969;127:157-64. 4. Witkop CJ Jr. Partial expression of sex-linked recessive amelogenesis imperfecta in females compatible with the Lyon hypothesis. Oral Surg 1967;23:174-82. 5. Rao S, Witkop CJ Jr. Inherited defects in tooth structure. Birth Defects Orif Artic Ser 1971;7:153-84. 6. Witkop CJ Jr, Kuhlmann W, Sauk J. Autosomal recessive pigmented hypomaturation amelogenesis imperfecta. Report of a kindred. Oral Surg Oral Med Oral Pathol 1973;36:367-82.

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7. Peters E, Cohen M, Altini M. Rough hypoplastic amelogenesis imperfecta with follicular hyperplasia. Oral Surg Oral Med Oral Pathol 1992;74:8792. 8. Haug RH, Ferguson FS. X-linked recessive hypomaturation amelogenesis imperfecta: report of case. J Am Dent Assoc 1981;102:865-7. zer F. Restoring function and esthetics in a patient with 9. Sengu n A, O amelogenesis imperfecta: a case report. Quintessence Int 2002;33:199204. 10. Fischman SL, Fischman BC. Hypoplastic amelogenesis imperfecta: report of case. J Am Dent Assoc 1967;75:929-31. 11. Ooya K, Nalbandian J, Noikura T. Autosomal recessive rough hypoplastic amelogenesis imperfecta. A case report with clinical, light microscopic, radiographic, and electron microscope observations. Oral Surg Oral Med Oral Pathol 1988;65:449-58. 12. Seow WK. Clinical diagnosis and management strategies of amelogenesis imperfecta variants. Pediatr Dent 1993;15:384-93. 13. Bouvier D, Duprez JP, Bois D. Rehabilitation of young patients with amelogenesis imperfecta: a report of two cases. ASDC J Dent Child 1996;63:443-7.

Reprint requests to: DR ASLIHAN USUMEZ FAKULTESI SELCUK UNIVERSITESI, DIS HEKIMLIGI PROTETIK DIS TEDAVISI ANABILIM DAL KAMPUS 42079 KONYA TURKEY FAX: 90-332-241-0065 E-MAIL: asli_u@hotmail.com Copyright 2003 by The Editorial Council of The Journal of Prosthetic Dentistry. 0022-3913/2003/$30.00 0

doi:10.1016/j.prosdent.2003.08.024

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