Apexification procedure of immature non-vital permanent central incisors. By Edel Hughes BDS, Philip McLorinan BDS, Julie Kelly BDS and Anne Stevens BDS

Case history

An eight-year-old boy presented as a new patient to the Community Dental Services complaining of fractured central incisors six months previously, and repeated dental abscesses. Initially the child had attended Accident and Emergency where the fractured tooth fragments were re-cemented in place. The only treatment since the trauma had been antibiotics.

Clinical presentation

Clinical examination revealed mesial-incisal fractures of both central incisors involving the enamel and dentine. The UL1 had a buccal discharging sinus present. Radiographic investigation confirmed open apecies. Both teeth tested negative to ethyl chloride. (Fig 1)

Clinical management

It was decided that an apexification procedure was to be carried out. Consent was obtained and treatment started. Access was gained to both non-vital canals and rubber dam placed.

The necrotic pulp was extirpated. The canals were irrigated using chlorhexidine gluconate 0.2 per cent and dressed using non-setting calcium hydroxide. The access cavity was temporised using glass ionomer.

Initially, the buccal sinus to UL1 healed, however, four weeks into treatment buccal sinus appeared on UR1 and UL1. At this stage the canals were dressed with Ledermix paste for two weeks. Complete resolution occurred.

The patient was recalled and the canals irrigated and re-dressed with calcium hydroxide on a monthly and then three-monthly basis. Approximately 12 months from the time of re-infection an apical barrier was evident clinically and confirmed radiographically. (Fig 2)

A referral was made for the patient to attend a general dental practice where both canals were obturated using thermoplastic gutta percha and definitive restorations placed using composite.

Follow-up

The patient is now being kept under six-monthly review within the Community Dental Services for any clinical signs or symptoms and radiographic review at one year as per American Endodontic Guidelines.

Apical barrier formation

Apexification is a method of inducing apical closure through formation of mineralised tissue in the apical pulp region of a non-vital tooth with an incompletely formed root and open apex¹.

In this case, as with the majority, non-setting calcium hydroxide is the standard material of choice for it’s antibacterial and calcification inducing properties.

When the final radiograph was taken confirming apical barriers, it appeared as if there had been some development to the root length and apical closure to the UR1.

The calcified barrier had formed coronally to the apex of the UL1 suggesting that the calcium hydroxide has not been instrumented to the full working length of the canal.

It is hypothesised that some remnants of the epithelial root sheath of Hertwig may have remained vital and allowed some continued root development to the UR1.

Discussion

During root development some time after the crown develops the double layered epithelial root sheath of Hertwig proliferates apically to map out the shape of the future root². There has been some discussion as to the separate development of the coronal tooth and the root sheath, and that the root sheath may indeed be able to withstand significant insult during the trauma³.

In order to have continued to proliferate, some vital pulp tissue and Hertwig’s epithelial root sheath may have remained at the apex of the UR1. When the canal is disinfected and the inflammatory conditions reversed, the tissues can then proliferate. New research by Huang introduces the term revitalisation approach to achieve tissue generation and regeneration. New living tissue forms in the cleaned canal space, allowing continued root development⁴.

The study promotes haemorrhage induction in the canal to provide a scaffold to allow generation of live tissues and continued root formation. There have also been studies that suggest the use of triple antibiotic therapy in the canal for the purpose of disinfection. Because in traumatised teeth the crown is usually intact, it will take bacteria a long time to advance into the pulp space. If, in this time the new vital tissue fills the canal space, the ingress of bacteria will be stopped.

Conclusion

This case highlights the changing views on the apexification procedure and certainly highlights some theories that are traditionally limited to apexogenesis.

The case also demonstrates that complex restorative treatment is achievable within the community dental services with the correct case selection. The co-operation between community dentists and general dental services is also displayed, with the two working for the greater benefit of the patient.

Acknowledgements

Special thanks to the staff in the Carlisle Centre Community Dental Clinic, Belfast Trust; and to Philip McLorinan, practice owner and principal dentist, Dunmurry Dental Practice.

References

1. Non-vital immature permanent incisors: factors that may influence treatment outcome, Finucane D, Kinirons M.J, Endodontics and dental traumatology 1999; 15: 273-277

2. Oral Anatomy, Histology and Embryology, 3rd Ed, Berkovitz, Holland, Moxham

3. Continued apexigenesis of immature permanent incisors following trauma, R Welbury, AG Walton

4. G. T.-J Huang, Apexification: the beginning of its end, International Endodontic Journal

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