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 Table of Contents  
CLINICAL REPORT
Year : 2009  |  Volume : 9  |  Issue : 1  |  Page : 47-50

Restoring function and esthetics in a patient with amelogenesis imperfecta


Department of Prosthodontics, Govt. Dental College and Hospital, Nagpur, India

Date of Web Publication23-Jun-2009

Correspondence Address:
Saee Deshpande
I-7 Sagar Palace, Laxminagar, Nagpur - 22
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-4052.52867

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  Abstract 

Amelogenesis Imperfecta (AI) is a group of hereditary defects of enamel, unassociated with any other generalized defects. Al results in poor development or complete absence of the enamel of the teeth caused by improper differentiation of the ameloblasts. This report describes the diagnosis and treatment of a young male patient with AI using contemporary restorative strategies. Initially, the tooth surfaces were treated with a professional cleaning along with conservative restorative treatment. Later, full mouth rehabilitation with metal-ceramic crowns was done. The treatment resulted in improved function, esthetics and self-confidence of the patient.

Keywords: Amelogenesis Imperfecta, Full Mouth Rehabilitation


How to cite this article:
Deshpande S, Parkhedkar R D, Sarin S. Restoring function and esthetics in a patient with amelogenesis imperfecta. J Indian Prosthodont Soc 2009;9:47-50

How to cite this URL:
Deshpande S, Parkhedkar R D, Sarin S. Restoring function and esthetics in a patient with amelogenesis imperfecta. J Indian Prosthodont Soc [serial online] 2009 [cited 2019 May 21];9:47-50. Available from: http://www.j-ips.org/text.asp?2009/9/1/47/52867


  Introduction Top


Amelogenesis imperfecta (AI) has been defined 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 imperfecta [2],[3],[4],[5],[6] using a combination of clinical, radiographic, histological, and genetic criteria. [7],[8] On the clinical and radiographic basis alone, three broad groups can be distinguished: (1) hypoplasia, in which the enamel is reduced in quantity but is relatively well-mineralized; (2) hypocalcification, in which enamel is formed in relatively normal amounts but is poorly mineralized; and (3) hypomaturation, in which the final stages of the mineralization process are abnormal. Clinical features distinguish the hypoplastic and hypocalcified types. [9] In the hypoplastic forms, the enamel does not develop to its normal thickness. In the hypocalcified 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 hypocalcification 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],[10],[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 disorder, and the intra-oral situation at the time the treatment plan is developed. This clinical report describes the treatment of a 23-year-old with amelogenesis imperfecta using porcelain metal- ceramic fixed partial dentures (FPDs).


  Case Report Top


Diagnosis

A 23-year-old male patient presented with esthetic and functional inadequacy of permanent teeth, along with considerable tooth sensitivity. He was very self- conscious about the appearance of his teeth. Detailed medical, dental, and social history was obtained. The enamel of all his teeth was hypoplastic and yellow-brown in color. The surfaces of the teeth were rough, and the enamel was either not visible or very thin over the crowns of all teeth. The dentin, where it was exposed, was brown and hypersensitive [Figure 1],[Figure 2],[Figure 3].

Differential diagnosis

Thorough dental, medical and family history was taken to differentiate it from dental fluorosis. The patient was not drinking water high in fluoride content. The enamel was not only discolored but also weak and prone to wear. He had no systemic ailments. The patient was questioned about the presence of similar abnormalities in his family including parents, brothers, sisters, and grandparents. He stated that his cousin who lived in a distant city was the only one to have such an appearance to her teeth. Therefore, the patient was diagnosed with hereditary Al.

Photographs and a panoramic radiograph [Figure 4] were obtained prior to treatment. No other abnormalities were observed.

The patient's oral hygiene was unsatisfactory, along with many carious teeth and old restorations. The initial level of gingivitis was observed and recorded. The patient reported he was reluctant to brush because of the sensitivity of his teeth.

His left mandibular first molar required root canal therapy. Amalgam restorations were placed on premolars and molars, which were carious.

Diagnostic casts were made, as were facebow and protrusive records. Casts were mounted in centric relation in a semi-adjustable articulator (Whip Mix Corp., USA). It was determined that the patient had 3 to 4 mm of interocclusal distance and no loss of facial height; therefore, the articulator's vertical dimension was not altered. Diagnostic preparations on the casts were done to evaluate the amount of tooth reduction to correct the contour and alignment. Maxillary left lateral incisor and mandibular right canine were rotated and out of the arch. Intentional endodontic therapy was done on them in anticipation of pulp exposure during preparation. His right maxillary and mandibular third molars were out of occlusion and left ones were not erupted fully. The patient was not willing for disimpaction surgery, so it was decided not to restore them and get them extracted whenever symptomatic. Canine-protected occlusal scheme was developed through a diagnostic waxing.

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. Using diagnostic models, along with clinical and radiographic findings, the treatment plan was formulated.

The patient was informed about the restorative procedure and all other treatment alternatives including the differences in costs, the levels of tooth structure removal, the expected clinical longevity, the time period necessary to conclude the treatment, and the possible esthetic result.

Treatment Procedure

Following a dental prophylaxis and oral hygiene instructions, the patient was placed on a 0.12% chlorohexidine gluconate (Periogard Oral Rinse, Colgate Oral Pharmaceuticals, Canton, Mass) oral rinse, with a recommended use of twice daily.

Maxillary and mandibular anterior and posterior teeth were prepared for metal-ceramic restorations. Mandibular anterior teeth exhibited gingival recession. Preparation margins in this area were kept supragingival to facilitate plaque control. Irreversible hydrocolloid impressions (Neocolloid, Zhermack, Italy) of the provisional restorations were obtained and poured in Type IV dental stone (Ultra-Rock, Kalabhai Dental, India). Laboratory-processed provisional restorations (DPI, Mumbai, India) were fabricated at existing occlusal vertical dimensions. They were evaluated intra-orally and adjusted for centric and eccentric contacts. They were cemented with zinc-oxide eugenol (Temp- NE, 3M,USA). The patient wore the provisional restorations for 2 weeks without complications.

A custom incisal guide table was fabricated from acrylic resin (Pattern Resin LS, GC America) to preserve the same anterior guidance of provisional restorations for fabrication of definitive restorations.

Gingival retraction was done using knitted cord (Ultradent products Inc., Salt Lake City, Utah) soaked in aluminum chloride (Visco Stat Clear Ultradent products Inc., Salt Lake City, Utah). Definitive impressions of the prepared maxillary and mandibular anterior teeth were obtained using vinyl polysiloxane impression material (Aquasil Putty and XLV, Dentsply, USA). Working casts were generated from Type IV die stone (Ultrarock, Kalabhai Dental, India) and mounted onto the articulator using interocclusal records (Take 1 Bite, Kerr Corp). Anterior FPDs were fabricated (Ceramco III, Dentsply Ceramco, Burlington, NJ) evaluated intra- orally, adjusted, and cemented (Ketac-CemMaxicap, 3M ESPE, St. Paul, Minn).

After establishing the anterior guidance, definitive impressions of the prepared maxillary and mandibular posterior teeth were obtained using vinyl polysiloxane impression material (Aquasil Putty and XLV, Dentsply, USA). Final casts were generated from Type IV die stone (Ultrarock, Kalabhai Dental, India) and mounted in the articulator using interocclusal records (Pattern Resin LS, GC America). Three posterior metal-ceramic crowns on maxillary and mandibular premolars and first molar and a full metal crown on second molars were fabricated (Ceramco III, Dentsply Ceramco), evaluated intra-orally, adjusted and cemented with glass-ionomer cement (Ketac-Cem Maxicap, 3M ESPE) [Figure 5],[Figure 6],[Figure 7].

A vacuum-formed maxillary night guard prescribed for nighttime use was fabricated, adjusted and placed. In addition to oral hygiene instructions, the patient was advised 0.12% chlorohexidine gluconate (Periogard Oral Rinse, Colgate Oral Pharmaceuticals, Canton, Mass) oral rinse, with a recommended use of twice daily.

Recall evaluations at 4-month intervals occurred for a period of 2 years, and the patient did not experience tooth sensitivity or any other complication associated with the oral rehabilitation. He was satisfied with the esthetic and functional outcome and showed improved self-confidence [Figure 8].


  Discussion Top


The prosthetic rehabilitation of Al patients has been previously presented in several case reports. [11],[13] The different materials and methods for restorative procedures currently available have made it both exciting and confusing for dental practitioners. It should be pointed out limitations exist, and the application of techniques is not universal. It has been reported that adhesive restorative techniques, overdentures, porcelain fused-to-metal crowns, fixed partial dentures, full porcelain crowns, and inlay/onlay restorations are all used for the prosthodontic treatment of AI patients. [7],[11] In the present case a porcelain fused to a precious metal alloy approach was utilized for the restoration. Both the marginal fit and the color acceptability of the restorations were satisfactory.

 
  References Top

1.
Winter GB, Brook AH. Enamel hypoplasia and anomalies of the enamel. Dent Clin North Am 1975;19:3-24.  Back to cited text no. 1
[PUBMED]    
2.
Winter GB. Hereditary and idiopathic anomalies of tooth number structure and form. Dent Clin North Am 1969;13:355-73.  Back to cited text no. 2
[PUBMED]    
3.
Winter GB, Lee KW, Johnson NW. Hereditary amelogenesis imperfecta: A rare autosomal dominant type. Br Dent J 1969;127:157-64.  Back to cited text no. 3
[PUBMED]    
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.  Back to cited text no. 4
[PUBMED]    
5.
Rao S, Witkop CJ Jr. Inherited defects in tooth structure. Birth Defects Orif Artic Ser 1971;7:153-84.  Back to cited text no. 5
    
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.  Back to cited text no. 6
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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;74:87-92.  Back to cited text no. 7
    
8.
Haug RH, Ferguson FS. X-linked recessive hypomaturation amelogenesis imperfecta: Report of case. J Am Dent Assoc 1981;102:865-7.  Back to cited text no. 8
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9.
Sengun A, Ozer F. Restoring function and esthetics in a patient with amelogenesis imperfecta: A case report. Quintessence Int 2002;33:199-204.  Back to cited text no. 9
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10.
Fischman SL, Fischman BC. Hypoplastic amelogenesis imperfecta: Report of case. J Am Dent Assoc 1967;75:929-31.  Back to cited text no. 10
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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.  Back to cited text no. 11
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12.
Seow WK. Clinical diagnosis and management strategies of amelogenesis imperfecta variants. Pediatr Dent 1993;15:384-93.  Back to cited text no. 12
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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.  Back to cited text no. 13
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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