Purpose: to review the aetiology, classification, diagnosis and management of teeth affected with dens invaginatus.
•Developmental dental anomaly where there is invagination of the enamel organ into the dental papilla before completion of calcification; which creates a pocket of organic material underneath enamel surface.
•Bacterial contamination and propagation in the irregularity which leads to early caries and later on pulpal necrosis.
•Necrosis in immature teeth disturbs root formation, and teeth might present with wide open or “blunderbuss” open apices.
•Many theories proposed (infection, trauma, developmental disturbances and genetic factors) but definite cause could not be identified.
•Genetic factors theory is supported by the fact that DI has a familial tendency.
Classification by Oehler:
•Class I : Partial, confined to crown, involves enamel and dentine (does not cross CEJ)
•Class II : Partial, beyond the crown and into the root, beyond CEJ, may or may not involve the pulp (does not communicate with PDL)
•Class III a : through the root and communicate with PDL with a second foramen on the lateral aspect but no involvement of the pulp itself
•Class III b : complete invagination; through the root, communicate with PDL at the apical foramen
•Affects 0.3 – 10 % •43% Bilateral
•Lateral incisors > Maxillary central Incisors “rarely premolars and canince”
•Mostly symptomatic, littler external deformity
•Patients might present with symptoms of irreversible pulpitis or apical periodontitis
•Radiolucent pockets underneath the cingulum and incisal edges
•If extensive, appears as a fissure
•Communication with PDL may be evident laterally or at the apex
•If a patient develops pulpal pathology a butterfly-like peri-apical radiolucency may be seen corresponding to 2 sites of inflammation
Class I Lesions:
•Palatal surface should be sealed as soon as a lesion is detected
•If pulpal necrosis is evident, root canal treatment should be performed, and the whole lesion should be incorporated in the access cavity
Class II Lesions:
•A deeper defect is present, showing an intact enamel surface; therefore, it’s not advisable to seal these lesions
•Invagination should be thoroughly debrided using ultrasonic and hypochorites
•If tooth does not show signs of pulpal pathology, restoration is advisable without accessing the root canal
•Dressing the invagination with a material that promotes hard tissue formation due to its close proximity to the pulp (MTA, CaOH)
Class III Lesions:
•If tooth is asymptomatic à only seal
•More conservative approach is advised
•In cases where the invagination becomes infected, pulp may still be healthy
•Invagination could be treated alone or in combination with root canal system
•Instrumentation with files is useless as it’s lined with enamel and cementum; use ultrasonic alloy tips fpr debriding these lesions •invagination will communicate with the periodontal ligament space and will need obturating with MTA to promote healing of the peri-radicular tissues
•Long term review
Teeth affected with dens invaginatus lesions are predisposed to developing pulpal disease. The resulting endodontic treatment is complex due to the unpredictable and aberrant internal anatomy of teeth affected with these lesions. Although CBCT, modern endodontics and surgical endodontics have improved the man- agement of such anomalies, early identification and prophylactic treatment of these lesions is imperative in preventing pulpal pathology from developing and avoiding complex and specialised endodontic treatment.