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Dentinogenesis imperfecta: full-mouth rehabilitation using implants and sinus grafts – a case report

From Volume 39, Issue 7, September 2012 | Pages 498-504

Authors

DW Seymour

BChD, MFDS RCSEd

Specialist Registrar in Restorative Dentistry, Leeds Dental Institute, Clarendon Way, Leeds, LS2 9LU, UK

Articles by DW Seymour

M F W-Y Chan

BDS, MDSc, FDS(Rest Dent) RCPS(Glasg), DRD, MRD RCSEd

Consultant in Restorative Dentistry, Leeds Dental Institute, Clarendon Way, Leeds, LS2 9LU, UK

Articles by M F W-Y Chan

PJ Nixon

BChD(Hons), MFDS RCSEd, MDentSci, FDS RCSEd(Rest Dent)

Consultant in Restorative Dentistry, Leeds Dental Institute, Clarendon Way, Leeds, LS2 9LU, UK

Articles by PJ Nixon

Abstract

This case report outlines one possible treatment modality to manage the developmental abnormality dentinogenesis imperfecta (DI). In this case, the patient's dentition is restored using a combination of full-coverage crowns for the remaining teeth and implant-supported crowns to replace missing teeth in a re-organized occlusal scheme. The case also demonstrates the effective use of the sinus graft procedure with simultaneous placement of dental implants. This paper also aims to make the reader aware of the current thinking behind treatment delivered to this group of patients, focusing on full-mouth rehabilitation using a combination of implant-supported and conventional metal ceramic crowns.

Clinical Relevance: For the general dental practitioner this case outlines the prevalence and cause of DI. It demonstrates how early diagnosis and appropriate referral has an impact on future treatment.

Article

Dentinogenesis imperfecta (DI) is a genetically determined developmental defect of dentine. The condition is broadly grouped into three categories:1

The prevalence of DI is 1:8000. Type I occurs as part of osteogenesis imperfecta, which is caused by mutations in collagen (Type 1 collagen alpha 1 and alpha 2 chains) genes. The inheritance pattern of DI type II and type III is autosomal dominant. Mutations in the DSPP gene have been identified in both types of DI occurring as an isolated trait. Research indicates that Type II and Type III are different expressions of the same gene.3

Histologically, the dentine appears normal. However, the scalloping at the dentino-enamel junction is missing. This scalloping acts to hold the two tooth structures together mechanically; in its absence enamel is easily chipped off the dentine.4,5 Clinically, teeth appear bluish-brown and opalescent. The enamel tends to chip and wear away, exposing the malformed abnormal dentine which wears rapidly. Radiographically, the crowns are bulbous while the roots are short and thin. The pulp chambers are wide initially but obliterate soon after eruption.

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