References

Hülsmann M. Dens invaginatus: aetiology, classification, prevalence, diagnosis, and treatment considerations. Int Endod J. 1997; 30:79-90 https://doi.org/10.1046/j.1365-2591.1997.00065.x
Alani A, Bishop K. Dens invaginatus. Part 1: classification, prevalence and aetiology. Int Endod J. 2008; 41:1123-1136 https://doi.org/10.1111/j.1365-2591.2008.01468.x
OehlerS FA. Dens invaginatus (dilated composite odontome). I. Variations of the invagination process and associated anterior crown forms. Oral Surg Oral Med Oral Pathol. 1957; 10:1204-1218 https://doi.org/10.1016/0030-4220(57)90077-4
Gallacher A, Ali R, Bhakta S. Dens invaginatus: diagnosis and management strategies. Br Dent J. 2016; 221:383-387 https://doi.org/10.1038/sj.bdj.2016.724
Grahnen H, Lindahl B, Omnell K. Dens invaginatus. A clinical roentgenological and genetical study of permanent lateral incisors. Odontologisk Revy. 1959; 10:115-137
Bishop K, Alani A. Dens invaginatus. Part 2: clinical, radiographic features and management options. Int Endod J. 2008; 41:1137-1154
Vaidyanathan M, Whatling R, Fearne JM. An overview of the dens invaginatus with case examples. Dent Update. 2008; 35:655-663 https://doi.org/10.12968/denu.2008.35.10.655
Caries-risk assessment and management for infants, children, and adolescents.Chicago, IL, USA: AmericanAcademy of Pediatric Dentistry; 2020
Parnell AG, Wilcox JD. Frequency of palatal invagination in permanent maxillary anterior teeth. ASDC J Dent Child. 1978; 45:392-395
Gotoh T, Kawahara K, Imai K Clinical and radiographic study of dens invaginatus. Oral Surg Oral Med Oral Pathol. 1979; 48:88-91
Cameron AC, Widmer RP. Handbook of Paediatric Dentistry, 4th edn. : Elsevier; 2013
Kidd E, Fejerskov O. Changing concepts in cariology: forty years on. Dent Update. 2013; 40:(4)277-8 https://doi.org/10.12968/denu.2013.40.4.277
Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's Clinical Periodontology, 11th edn. : Elsevier; 2012

Comprehensive management of a child with multiple dens invaginatus

From Volume 50, Issue 6, June 2023 | Pages 522-525

Authors

LKN Premathilaka

BDS

MD in Restorative Dentistry, Senior Registrar in Restorative Dentistry, Faculty of Dental Sciences, University of Peradeniya, Sri Lanka

Articles by LKN Premathilaka

Email LKN Premathilaka

S Vasantha

BDS

MS in Restorative Dentistry, Consultant in Restorative Dentistry, National Dental Teaching Hospital, Sri Lanka

Articles by S Vasantha

EMUCK Herath

BDS

MS in Restorative Dentistry, FDSRCS(Paed), Professor in Paediatric Dentistry, Faculty of Dental Sciences, University of Peradeniya, Sri Lanka

Articles by EMUCK Herath

Abstract

‘Dens invaginatus’ (DI) is a developmental anomaly of teeth, where an infolding of the enamel occurs into the dentine, creating a pocket or a dead space, as a result of the invagination of the enamel organ into the dental papilla prior to calcification. DI have been reported in 0.3–10% of the population. This case describes the comprehensive management of a 9-year-old child with multiple dens invaginatus.

CPD/Clinical Relevance: Early diagnosis and early intervention of DI is important to avoid dental caries, pulpitis and pulp death.

Article

‘Dens invaginatus’ (DI) is a developmental anomaly of teeth, in which an infolding of the enamel occurs into the dentine, creating a pocket or a dead space, as a result of the invagination of the enamel organ into the dental papilla prior to calcification.1,2

DI can be classified depending on the degree of enamel infolding. The most widely accepted classification (Table 1) was developed by Oehlers in 1957.3 Several other terms such as ‘dens in dente’, ‘dilated composite odontome’, and ‘gestant anomaly’ also have been used in the literature to describe this condition.2 DI has been reported in 0.3–10% of the population.1


Type I The invagination is minimal and enamel lined, it is confined to the crown of the tooth and does not extend beyond the level of the cemento-enamel junction
Type II The invagination is minimal and enamel lined and extends into the pulp chamber, but remains within the root canal with no communication with the periodontal ligament
Type IIIA The invagination extends through the root and communicates laterally with the periodontal ligament space through a pseudo foramen. There is usually no communication with the pulp, which lies compressed within the root
Type IIIB The invagination extends through the root and communicates with the periodontal ligament at the apical foramen. There is usually no communication with the pulp

The most affected teeth are the maxillary lateral incisors, maxillary central incisors, and rarely the premolar and canine teeth.4 It may affect the mandibular teeth, deciduous teeth and supernumerary teeth.4 In 43% of cases, DI has occurred bilaterally implying the necessity to assess the contralateral tooth.5

Affected teeth may present with a deepened cingulum pit, grooved palatal enamel, increased mesio-distal or labio-lingual diameter, incisal notching in association with a labial groove, pronounced talon cusp and a peg or conical morphology.6

Early diagnosis and early intervention of DI is imperative as, if left undiagnosed, bacterial accumulation within the invagination may result in development of caries and consequently pulpitis and pulp death.7

The following case describes the comprehensive management of a child patient presented with multiple dens invaginatus.

Case report

A 9-year-old girl presented to the restorative unit at the National Dental Teaching Hospital (NDTH), Sri Lanka after being referred from the outpatient department of the same hospital, for the management of a discharging sinus over the chin. She was medically fit and healthy otherwise.

On examination, a discharging sinus was evident over the lower border of the anterior mandible, to the left from the midline (Figure 1).

Figure 1. Pretreatment extra-oral view showing the discharging sinus.

Intra-orally, a mucosal laceration was seen on upper labial mucosa in relation to UL1. The patient's gingivae, in relation to the upper and lower anterior teeth, showed signs of inflammation.

The patient's UL1crown had abnormal morphology with a labial developmental groove extending from a notch at the incisal edge to an enamel projection in the cervical region (Figure 2). Palatally, it had two deep pits on either side of a talon cusp, which did not create any occlusal interference (Figure 3). While, UR1 and UR2 had only deep palatal pits. On eruption, a deep palatal pit was noticed in UL2 too. LL1 crown also was wider than the norm mesio-distally and had multiple enamel projections and multiple deep pits affected by enamel caries (Figure 4). It was tender to pressure and was grade I mobile.

Figure 2. Anterior re-treatment intra-oral view.
Figure 3. Pre-treatment view of the upper arch.
Figure 4. Pre-operative view of the lower arch.

Her dmft (decayed, missing, filled primary teeth) was 11 and DMFT (decayed, missing, filled permanent teeth) was 05 out of 13 permanent teeth. According to the Caries Risk Assessment Tool (CAT) for children above the age of 6 years of the American Academy of Paediatric Dentistry (AAPD),8 the child was found to have high risk for dental caries.

UL2 was in a crossbite with LL3, and there was a developing crossbite in URE and LR6 (Figure 2).

Pulp sensibility testing was carried out using an electric pulp tester, and findings were within the normal range except for LL1, which was non-responsive.

Following insertion of a gutta percha (GP) point through the sinus opening, a lower standard occlusal radiograph and an intra-oral peri-apical (IOPA) radiograph were taken, and LL1 was identified as the source of infection (Figures 5 and 6). A dental panoramic tomograph (DPT) was taken to investigate the status of remaining other teeth (Figure 7). UL1 and LL1 were identified with complex root canal anatomy simulating Oehler's class III type dens invaginatus. A bifid cingulum was seen in UR1, UR2 and UL2. A cone beam computed tomograph (CBCT) was not taken because the patient could not afford it.

Figure 5. Pre-treatment lower standard occlusal view.
Figure 6. Pre-treatment intra-oral peri-apical radiograph of LL1.
Figure 7. Pre-operative dental panoramic tomograph (DPT).

Following informed consent from the parents, canals (two root canals and a single invagination) in LL1 were cleaned and dressed with non-setting calcium hydroxide and iodoform paste (Metapex, Meta Biomed, Korea). One week later, both canals were re-dressed with non-setting calcium hydroxide for the purpose of disinfection.

The preventive phase of treatment was initiated by educating the parents regarding the disease condition and its possible complications. Oral hygiene instructions and dietary advice were given thereafter. Odontoplasty of UL1 and LL1 was carried out in order to remove the enamel projections to facilitate plaque removal. The entire dentition was treated with fluoride varnish (FluoritopSR varnish, India) and fissure sealant (Clinpro sealant, 3M ESPE, USA) was placed on the deep pits in UR1, UR2, UL1 and UL2 and in the deep fissures of UR6 and LL6 under rubber dam.

Following an orthodontic opinion, enameloplasty of LLC was carried out to correct the crossbite of UL2 and LLC. Fluoride varnish application was carried out thereafter.

Carious teeth were restored with glass ionomer cement (Fuji IX, GC Corp, Japan). Then, the URC was extracted because it was grossly carious and mobile. ULD showed root resorption of more than two-thirds of its length, and the root formation of the permanent successor UL4 had started. Therefore, ULD was extracted to facilitate the eruption of UL4.

Thereafter, endodontic treatment of LL1 was completed, as the extra-oral sinus had healed completely (ie 5 weeks after the initiation of endodontic treatment) (Figures 8 and 9). Subsequently, poor quality glass ionomer restorations were replaced with resin composite and veneering of UL1 was performed using resin composite (Figures 1012).

Figure 8. Extra-oral view after healing of the sinus
Figure 9. Intra-oral peri-apical view of LL1 after the endodontic treatment.
Figure 10. Anterior post-treatment intra-oral view.
Figure 11. Post-treatment view of the upper arch.
Figure 12. Lower arch post-treatment view.

A referral was then made to the orthodontic unit for the management of space loss and potential crowding.

Discussion

In majority of cases, teeth affected by dens invaginatus (DI) show no signs or symptoms of malformation. Hence, unless it is detected by a radiograph by chance, or extensive malformations have resulted in an abnormal clinical crown morphology, these remain undiagnosed.4

Teeth affected by DI may present with a deepened cingulum pit, grooved palatal enamel, increased mesio-distal or labio-lingual diameter, incisal notching in association with a labial groove, pronounced talon cusp and a peg or conical morphology.6

Clinical examination should be assisted by radiographs. The infolding of the enamel may be more radiopaque than the surrounding tooth structure, making the identification easy. The radiographic image may vary from a narrow undilated fissure to a tear-shape loop pointing to the main body of the pulp.6,9,10 The application of methylene blue dye to the palatal side of the tooth also may be useful as penetration of the dye can act as a radiopaque marker.6

A peri-apical view is the image of choice to identify DI lesions, and may need two images of different angulations.4 CBCT also facilitates assessment of the affected teeth prior to treatment.4

Once DI is identified in a particular tooth, it is prudent to assess the contralateral tooth because in 43% of cases, DI has occurred bilaterally.4,5

Early diagnosis and early intervention of DI is imperative because if left undiagnosed, bacterial accumulation within the invagination could result in the development of caries, and consequently pulpitis and pulp death.7

In this case, the presence of an extra-oral sinus over the chin, with an abnormal morphology of LL1, which was non-responsive to the sensibility test, led to the identification of LL1 as the source of infection. Upon radiographic assessment, the source of infection was confirmed and LL1 and UL1 were found to have Oehler's class III type dens invaginatus. Oehler's class I type dens invaginatus was evident in UR1, UR2 and UL2.

As the child presented with an extra-oral discharging sinus originating from LL1, root canal treatment in LL1 was initiated at the emergency phase of the treatment and was dressed with non-setting calcium hydroxide and iodoform for the purpose of disinfection.

Obturation using warm gutta percha technique is the treatment of choice to ensure filling of the canals in teeth affected by dens invaginatus teeth.7 If endodontic treatment fails, or if there is any difficulty in canal negotiation, surgical endodontic treatment and retrograde obturation may be necessary. As the last option, extraction can be considered. In this case, endodontic treatment of LL1 was completed using the warm gutta percha technique. To improve aesthetics, UL1 was veneered using resin composite.

As prevention is the most important aspect in the management of dental caries,12 the patient and parents were advised to reduce the frequency and amount of sugar consumption, and brushing instructions were given, including appropriate use of fluoridated dentifrices. Fluoride varnish application was carried out at 3-monthly intervals.

Sealing of the fissures of all permanent molars in children at high risk is recommended by the AAPD guidelines.8 Hence, UR6 and LR6 were sealed with resin sealants and it was planned to seal the premolars when they had fully erupted. Further, the palatal invaginations of UR1, UR2 and UL2 were sealed with resin sealants to reduce the risk of caries incidence.

It is well documented, that developmental anomalies of teeth, such as cervical enamel projections and enamel pearls, can result in localized periodontal attachment loss.13 Therefore, odontoplasty of UL1 and LL1 was carried out to facilitate plaque control.

Early loss of primary molars can result in adverse outcomes, such as buccal crowding and impaction of permanent successors. In this patient, early loss of the primary molars resulted in space loss for the permanent successors. For the management of this potential crowding, the patient was referred for an orthodontic opinion.

The maintenance phase was aimed at monitoring plaque control, existing restorations, recurrent caries and teeth with dens invaginatus as well as providing professional fluoride therapy and sealing the fissures of premolars when they had erupted fully.

Conclusion

Providing dental care to a child with multiple dens invaginatus, together with multiple dental caries, poses a significant challenge to a clinician. However, the basic restorative paradigm should be applied when managing a child with multiple dental queries.