Journal of Conservative Dentistry
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Year : 2018  |  Volume : 21  |  Issue : 1  |  Page : 109-113
Dens invaginatus with necrotic pulp in a right maxillary lateral incisor with preserved vitality

Multidisciplinary Department of Medical-Surgical and Dental Specialities, Second University of Naples, Naples, Italy

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Date of Submission16-Feb-2017
Date of Decision11-Oct-2017
Date of Acceptance30-Jan-2018
Date of Web Publication19-Feb-2018


Dens invaginatus (DI) is a dental malformation occurring in several morphologic types. Consequently, treatment of teeth affected by DI can get complicated because of the complex root canal anatomy. The aim is to describe how to manage a rare report of a DI with necrotic pulp held within the vital pulp of a maxillary lateral incisor. Oral fistula was found on the buccal mucosa of the apex of the vital maxillary lateral incisor with a DI having necrotic pulp. Endodontic treatment of the maxillary lateral incisor and of the tract canal of DI was realized. Clinical disappearance of oral sinus tract was observed after 10 days. On the contrary, the disappearance of radiolucent area occurred after 6 months. A proper and prompt diagnosis is necessary to carry out effective prevention protocols or prevent consequences generating nonrecoverable endo-perio diseases.

Keywords: Dens in dente; dens invaginatus; dental malformation; endodontic treatment; periapical lesion

How to cite this article:
Alessandro L, Fabrizio DF, Gennaro D, Dario DS, Eugenio G, Letizia P, Luigi F, Felice F. Dens invaginatus with necrotic pulp in a right maxillary lateral incisor with preserved vitality. J Conserv Dent 2018;21:109-13

How to cite this URL:
Alessandro L, Fabrizio DF, Gennaro D, Dario DS, Eugenio G, Letizia P, Luigi F, Felice F. Dens invaginatus with necrotic pulp in a right maxillary lateral incisor with preserved vitality. J Conserv Dent [serial online] 2018 [cited 2022 Aug 16];21:109-13. Available from:

   Introduction Top

Dens invaginatus (DI) also known as “dens in dente” was analyzed in a whale's tooth by Ploquet in 1794 and later identified in a human tooth by the dentist Socrates in 1856. DI represents an unusual developmental anomaly involving an early invagination of enamel and dentin that may deeply extend into both the pulp cavity and the roots, sometimes reaching the apex before calcification occurs.[1],[2],[3]

The case described in this study is a rare report of a DI with necrotic pulp held within the vital pulp of a maxillary lateral incisor.

   Case Report Top

A 19-year-old Italian female with a noncontributory medical history presented to our observation for a medical examination. Through intraoral clinical examination, a fistula of the buccal mucosa in correspondence of apex of right maxillary lateral incisor was found (1.2) [Figure 1]a. The response to the electric pulp sensibility test of the right upper canine and the lateral and the central incisor was positive. The 1.2 appeared morphologically normal except for a deep pit on the lingual surface [Figure 1]b. Through periapical radiography, the dilated and amorphous central area was observed in the crown of 1.2, due to inner presence of a wide radiopaque development. The latter occupied the coronal space and got over the enamel cement junction, enclosing a radiolucent space that communicates with the periodontal space of the middle third of the root [Figure 1]c. The fistulography, performed through the insertion of a gutta-percha cone into the oral fistula and sinus tract, revealed the impact of gutta-percha's tip against the half of the lateral incisor root surface neighboring a radiolucent area. The radiographic diagnosis showed a DI of 1.2 [Figure 2]a and [Figure 2]b. The aim of the therapy was to try the endodontic treatment. The patient was informed about the diagnosis and the treatment plan; then, the agreement was signed by an informed consent form. After the administration of local anesthesia, under ×20, the pulp chamber of 1.2 was opened and the invagination orifice of malformation was localized [Figure 3]a. Subsequently, the design of the cavity was finished to surround the profile of the malformation. The DI appeared as a rounded shape malformation into the dental chamber, surrounded by vital and bloody pulp [Figure 3]b. The central hole of DI was recognized and enlarged using the Gates Glidden burs in succession from N° 1–3 to facilitate the gentle insertion of K-file 8 in the tract canal and to increase the diameter until the periodontal space was reached. The pulpal tissue of DI appeared necrotic and not bloody. Removal of vital pulp was necessary; thus, a pointed probe was used around the malformation to locate the access of the principal root canal [Figure 3]c. The working length was determined using a K-file 0.8 connected to an apex locator (Root ZX, Morita, Tokyo, Japan) followed by the confirmation of the periapical radiography. The endodontic treatment of dental root canals was carried out in a single session before the treatment of the pulpal tract of the inner malformation to avoid the spread of infectious processes. Canal systems' preparation includes both the enlargement and the shaping of the complex endodontic space using manual and mechanical instrumentation of ProTaper technique (Dentsply) and the disinfection using alternating irrigation solutions with ethylenediaminetetraacetic acid and sodium hypochlorite at 2% heated to 40°C. The filling of the canals was realized by mineral trioxide aggregate (MTA) obturation and three-dimensional gutta-percha obturation for DI canal and root canal systems, respectively; then, the vertical compaction technique with System B Heat Source (SybronEndo) and injection of thermoplastic gutta-percha by Obtura III (SybronEndo) were employed for the down packing and backfilling, respectively, to sealing the surrounding malformation space [Figure 3]d. Ten days after the end of the root canal therapy, clinical disappearance of oral fistula was observed [Figure 4]a. Then, the access cavity was restored by a vetroionomeric cement (3M Espe), used as a filling base, and an indirect composite restoration (A2 GandioSO, Voco) [Figure 4]b. After 6 months, the radiolucent area disappeared as shown by the periapical radiography, differently from the radiography at the end of endodontic treatment [Figure 5]a and [Figure 5]b. After 1 year, the patient required to improve her smile complaining about both the discoloration of the lateral incisor and the slope of the central incisor. A cervical gingivoplasty [Figure 6]a and a lithium silicate ceramic veneers on 1.2 associated with a reductive odontoplasty of central incisor were realized with great satisfaction of the patient [Figure 6]b.
Figure 1: (a) (Buccal view): Buccal fistula, (b) (palatal view): Accentuated lingual pit of the right maxillary lateral incisor, and (c) intraoral periapical radiograph

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Figure 2: (a) The gutta-percha cone inserted in oral fistula and (b) fistulography

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Figure 3: (a) Identification of the dens invaginatus invagination orifice, (b) dens invaginatus with a rounded shape surrounded by vital pulp of maxillary lateral incisor, (c) entrance of the dental root canal, and (d) seal of the peri-malformation space and of the canal tract of dental malformation

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Figure 4: (a) Clinical disappearance of the oral fistula and (b) Composite indirect restoration of the access cavity

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Figure 5: (a) Periapical radiography at the end of endodontic treatment and (b) periapical radiography after 6 months of endodontic treatment

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Figure 6: (a) Cervical gingivoplasty and (b) lithium silicate ceramic veneers on 1.2 and a reductive odontoplasty of the right maxillary central incisor

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   Discussion Top

Several theories have been put forward to explain the etiopathogenesis of DI.[1] Kronfeld suggested that the invagination results from a focal failure of the growth of the internal enamel epithelium, while the surrounding normal epithelium continues to proliferate engulfing the static area.[4] Conversely, Rushton proposed that the invagination is a result of rapid and aggressive proliferation, rather than a retardation, of a part of the internal enamel epithelium invading the dental papilla.[5] Fischer and Sprawson considered the infection to be responsible for the malformation.[6],[7] Growth pressure of the dental arch results in buckling of the enamel organ.[8] The “twin-theorie” suggested a fusion of two tooth germs.[9] Oehlers considered that distortion of the enamel organ during tooth development and subsequent protrusion of a part of the enamel organ would lead to the formation of an enamel-lined channel ending at the cingulum or occasionally at the incisal tip. Oehlers classified the DI into three types, in the light of the radiographic interpretation of the degree of invagination: Type I, Type II, and Type III.

  • Type I indicates a minor enamel-lined invagination that is restricted within the crown of the tooth and does not cross beyond the cementoenamel junction
  • Type II indicates the enamel-lined invagination extending into the pulp chamber but remains confined to the root canals without interaction with the periodontium
  • Type III is further subclassified into Type III A and Type III B.

    1. The invagination extends to the roots and communicates laterally, through a pseudoforamen, with the periodontal ligament without pulpal involvement
    2. The invagination extends into the root and communicates, through the apical foramen, with the periodontal ligament. The invagination is usually lined by enamel and in rare instances by cementum.[10]

DI mainly occurs in permanent dentition, even if several cases have been described in deciduous dentition and supernumerary teeth. The maxillary teeth are more commonly affected than mandibular teeth. Among permanent teeth, the maxillary lateral incisors are the most commonly affected teeth, as shown by the previous case, followed by central incisors, canines, and molars.[10] The upper lateral incisor can sometimes be a difficult element to treat endodontically because a narrow apical and pronounced curvature can be observed. Furthermore, the maxillary lateral incisor can often be characterized by abnormalities of form, of embryological basis, which can determine the need for endodontic, periodontal, or combined endo-perio treatment. The clinical appearance of the crown may vary ranging from a normal form to different unusual forms such as a greater labiolingual diameter, peg-shaped, barrel-shaped, and conical and talon cusp. The radiographic examination showed a radiopaque invagination of density equal to enamel and that extended from the cingulum to the root canal. The defects may vary in size and shape from a loop-like, pear-shaped, or slightly radiolucent structure to severe forms resembling a tooth within a tooth. In most cases, the invaginated tooth is occasionally highlighted in a radiography; furthermore, it usually shows no clinical symptoms; however, a deep foramen cecum susceptible to caries may be The first clinical sign indicating the existence of an invaginated tooth. The accentuated pit within the DI accumulates debris causing rapid initiation and progression of dental caries with subsequent involvement of the pulp, resulting in periapical pathology.[11],[12] The reported case involved a maxillary lateral incisor which showed an accentuated lingual pit. The unusual case described in this study reveals a tooth with preserved vitality containing a DI with necrotic pulp. A tooth with DI presents technical difficulties in clinical management and especially for the endodontic treatment, when necessary. The inaccessibility of the anomaly, its variable presentation, canal anomalies, and its proximity to the pulpal chamber are treatment challenges. Furthermore, partially developed roots and tortuous pit can complicate the treatment of DI. Treatment for Type I DI includes minimally invasive procedures and sealing of the defect with restorative materials. Bishop and Allani indicated that minor debridement with ultrasonic instruments and the use of sealants may be successful in Type I and Type II cases.[13] However, in most cases, the treatment requires further invasive procedures including root canal therapy due to the extension of the defect over a period of time. In cases where the pulp is involved, the treatment could range from conservative pulpotomy to a full root canal treatment, preferably using a dental endoscope.

In teeth with open apices, various restorative materials have been employed including calcium hydroxide, zinc oxide cement, MTA, and gutta-percha. Surgical treatments could be indicated in cases of DI with extensive infection in the periapical region, complex root canal anatomy, and incomplete root canal development. The reported case belongs to DI Type III A with a separate canal tract communicating with periodontal space.

The use of MTA as a filling material has become popular in cases of DI due to its advantageous characteristics such as sealing capacity, biocompatibility, and apical healing stimulation.[14] The so-called “one-step apexification technique” with MTA is an interesting alternative to treatments employing calcium hydroxide. In the present case, the use of MTA was used to fill the root canal of malformation after the removal of the necrotic pulp and to seal the wide orifice on radicular surface of tooth root. Some authors stated that endodontic treatment of the main canal is not necessary if there is no connection with the invaginated canal or when pulp necrosis is not detected.[15] In the case reported herein, the periapical radiography revealed two separate canals. The endodontic treatment of both tract canal of malformation and primary root canal was preferred to avoid both complications, in the case of a possible second surgical time, and a more complex endodontic treatment due to the formation of tertiary dentin, in the case of a second intervention.

   Conclusions Top

  • DI is a dental anomaly of embryological origin occurring in several morphologic types. Consequently, root canal treatment of teeth affected by DI can get complicated because of the complex root canal anatomy since residual infected pulpal tissues can be in inaccessible areas of the canal system
  • MTA obturation is a suitable technique to treat this kind of malformation
  • The formulation of a proper and prompt diagnosis in this report is necessary to carry out effective prevention protocols, when possible, or prevent consequences generating nonrecoverable endodontic, periodontal, or combined diseases.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.


The authors thank the dental technician, Mr. Roberto Della Neve, for the veneer restoration.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Schulze C. Developmental abnormalities of the teeth and the jaws. In: Gorlin RJ, Goldman HM, editors. Thoma's Oral Pathology. 6th ed. St. Louis: Mosby; 1970. p. 96-183.  Back to cited text no. 1
Jaramillo A, Fernández R, Villa P. Endodontic treatment of dens invaginatus: A 5-year follow-up. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:e15-21.  Back to cited text no. 2
Shadmehr E, Kiaani S, Mahdavian P. Nonsurgical endodontic treatment of a maxillary lateral incisor with dens invaginatus type II: A case report. Dent Res J (Isfahan) 2015;12:187-91.  Back to cited text no. 3
Kronfeld R. Dens in dente. J Dent Res 1934;14:49-66.  Back to cited text no. 4
Rushton MA. A collection of dilated composite odontomas. Br Dent J 1937;63:65-85.  Back to cited text no. 5
Fischer CH. To the question of the dens in dente. Dtsch tooth mouth Kieferheilkd 1936;3:621-34.  Back to cited text no. 6
Sprawson EC. Odontomes. Br Dent J 1937;62:177-201.  Back to cited text no. 7
Euler H. Anomalies, deformities and mutilations of human teeth. München, Germany: Lehmann; 1939. p. 62-7.  Back to cited text no. 8
Bruszt P. Etiology of dens in dente. SSO Schweiz Monatsschr Zahnheilkd 1950;60:534-42.  Back to cited text no. 9
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;10:1204-18.  Back to cited text no. 10
Nosrat A, Schneider SC. Endodontic management of a maxillary lateral incisor with 4 root canals and a dens invaginatus tract. J Endod 2015;41:1167-71.  Back to cited text no. 11
Patil S, Yadav N, Patil P. Non-syndromic occurrence of multiple dental and skeletal anomalies: A rare case report and brief literature review. J Clin Diagn Res 2014;8:ZD28-30.  Back to cited text no. 12
Bishop K, Alani A. Dens invaginatus. Part 2: Clinical, radiographic features and management options. Int Endod J 2008;41:1137-54.  Back to cited text no. 13
Brooks JK, Ribera MJ. Successful nonsurgical endodontic outcome of a severely affected permanent maxillary canine with dens invaginatus oehlers type 3. J Endod 2014;40:1702-7.  Back to cited text no. 14
Gonçalves A, Gonçalves M, Oliveira DP, Gonçalves N. Dens invaginatus type III: Report of a case and 10-year radiographic follow-up. Int Endod J 2002;35:873-9.  Back to cited text no. 15

Correspondence Address:
Prof. Lanza Alessandro
Multidisciplinary Department of Medical-Surgical and Dental Specialities, Second University of Naples, Via Luigi de Crecchio, 6, NA 80138
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCD.JCD_72_17

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


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