Saudi Endodontic Journal

: 2018  |  Volume : 8  |  Issue : 1  |  Page : 44--49

Dens invaginatus: A review and case series

Nesrine Tebbeb1, Dhia Zaabar2, Sonia Zouiten1, Abdelatif Boughzala1,  
1 Department of Dental Medicine, EPS Farhat Hached, Sousse, Tunisia
2 Department of Anesthesiology, Hospital IBN JAZZAR, Kairouan, Tunisia

Correspondence Address:
Dr. Nesrine Tebbeb
Sidi Abdallah Street, Chebba 5170


Dens invaginatus (DI) (dens in dente) is a developmental anomaly resulting from an invagination in part of variable depth of the enamel organ into the dental papilla in the surface of the crown before calcification of the dental tissues. This anomaly usually involves the upper lateral incisors. These teeth are frequently expressed by an unusual form of crown and accentuation in the cingulum or a cusp. They are a target for caries leading to pulp necrosis and apical pathosis, so the diagnosis and early prevention measures are important. When treatment is necessary, conservative, endodontic, and periodontal possibilities are very effective. Surgical interventions are only rarely indicated. The present paper deals with the treatment of series cases with DI.

How to cite this article:
Tebbeb N, Zaabar D, Zouiten S, Boughzala A. Dens invaginatus: A review and case series.Saudi Endod J 2018;8:44-49

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Tebbeb N, Zaabar D, Zouiten S, Boughzala A. Dens invaginatus: A review and case series. Saudi Endod J [serial online] 2018 [cited 2021 Mar 6 ];8:44-49
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Dens invaginatus (DI), known more commonly as “dens in dente,” is an unusual anomaly of development resulting in a deepening of the enamel organ into the dental papilla in the surface of the crown before calcification of the dental tissues.[1] This anomaly is often bilateral. The prevalence of DI has been reported between 1.3% and 9.6% in population.[2],[3],[4] The etiology is still unknown and unclear. Many theories such as alterations in tissue pressure, local discrepancy in the cellular hyperplasia, trauma, genetic factor, or infection have been suggested.[1]

Hallett (1953) published the first classification of invaginated teeth. Four types of invagination were suggested based on clinical and radiological criteria.[5]

In 1957, Oehlers [6] classified the occurrence of the anomaly into three types:

Type I: an enamel-lined minor form occurring within the confines of the crown, not extending beyond the amelocemental junction;Type II: an enamel-lined form which invades the root but remains confined as a blind sac. It may or may not communicate with the dental pulpType III: a form which penetrates through the root perforating at the apical area showing a “second foramen” in the apical or in the periodontal area. There is no immediate communication with the pulp. The invagination may be completely lined by enamel, but frequently cementum will line the invagination.

According to Oehlers' classification, Ridell et al. reported that Type I is most common (79%), followed by Type II (15%) and Type III (5%).[7] The same study found that 85% of upper lateral incisors presented invagination with 3.3% are Type III.

Unfortunately, the classification of Oehlers maybe in majority of cases underestimates the complexity of the invagination because this classification is based on a two-dimensional (2D) radiograph. However, it still uses distinction between incomplete (Type I and II) and complete (Type III) invaginations, which is important as the management of each is potentially different.

Actually, with the increase availability of 3D imaging, the classification and the management of the invagination may overcome the limitations caused by the conventional radiograph.[8]

The purpose of this article was to present four clinical cases of invagination and discuss the treatment decisions and outcomes with different types.

 Case Reports

Case 1

A 25-year-old male with noncontributory medical history was referred to the Department of Dentistry in the University Hospital Farhat Hached, Sousse, Tunisia, by his general dentist to treat his first upper right molar.

At the clinical examination, a fortuitously unusual anatomy in his maxillary left (#22) and right (#12) lateral incisor was detected. It presented weird crown morphology as talon cusps and a decayed cavity on the palatal face, which represent an entrance to invagination [Figure 1]a.{Figure 1}

The initial periapical radiographic examination revealed that both teeth showed a radiopaque projection entering the root canal, lined by enamel not extending beyond the cementoenamel junction and a complete root development without apical radiolucency [Figure 1]b and [Figure 1]c. The teeth were asymptomatic and responded normally to pulp sensitivity test with no pain on palpation or percussion. The diagnosis of Type I Oehlers' DI with a normal pulp was established. The treatment plan was to eliminate the decayed cavity of the invagination and to seal it with composite [Figure 2]a and [Figure 2]b.{Figure 2}

Case 2

A 35-year-old female patient with no contributory medical history consulted the Department of Dentistry in the University Hospital of Farhat Hached, Sousse, Tunisia. She suffered from the discoloration of her upper right central incisor (#11) but asymptomatic [Figure 3]a. The tooth did not represent carious cavity or periodontal pocket. She did not report a history of trauma. The occlusal examination did not show any occlusal dysfunction. The radiological examination demonstrated radiolucent pocket parallel to the principal canal, communicate with it and no communication with the periodontal area. The extremity of this pocket was beyond the cementoenamel junction. The root was fully formed with large periapical radiolucency [Figure 3]b.{Figure 3}

The tooth did not respond to the thermal vitality test and sensitive to percussion. So, we established the diagnosis of invagination Type II Oehlers' DI with a pulp necrosis and symptomatic apical periodontitis.

After isolation using rubber dam, the access cavity was completed and the invagination was eliminated with the Endo Z bur 25 mm (Dentsply Maillefer, Canada) and opened to the principal canal. The working length was taken and the canal was debrided by crown down technique with Revo-S sequence (Micro-Mega, BESANCON Cedex France) to get the diameter of 25 mm and 6% conicity of SU file. The canal irrigation was done with 2.5% sodium hypochlorite. After drying the canal with sterile paper points, calcium hydroxide (Produits dentaires SA, Vevey, Switzerland) medication was applied and the canal was sealed with a temporary filling Cavit (3M ESPE AG, Seefeld, Germany). Two weeks later, the canal was disinfected using 2.5% sodium hypochlorite, dried with paper points, and obturated by lateral condensation using gutta-percha (Pearl Dent Co., Ltd., Ho Chi Minh City, Vietnam) and zinc oxide eugenol sealer (Produits dentaires SA, Vevey, Switzerland) [Figure 4]a. After 1 week, the access cavity was sealed with composite filling (Nexcomp, META BIOMED Co., Ltd, Korea). The 1-year follow-up showed asymptomatic tooth with complete healing of the periapical radiolucency [Figure 4]b. The patient was referred to a specialist of fixed prosthesis to resolve the esthetic problem.{Figure 4}

Case 3

A 27-year-old female with a noncontributory medical and family history complaining of recurrent abscess and fistula in her upper left vestibule consulted the dental emergency clinic. Clinical examination revealed discolored upper left lateral incisor (#22), no response to thermal vitality test, and sensitivity to percussion [Figure 5]a. Periodontal probing around the tooth revealed no deep pockets. Radiological examination revealed that this tooth presented an invagination Type II (Classification of Oehlers), large periapical radiolucency, incomplete root development, and an open apex [Figure 5]b and [Figure 5]c. The diagnosis established was pulp necrosis and symptomatic periapical abscess. A cone beam computed tomography (CBCT) was advised which showed the exact size of the periapical radiolucency, especially the destruction of the palatal cortical bone [Figure 6]. The decision was root canal preparation. Rubber dam was placed. The access cavity was opened. Because the canal was very large, we used stainless steel K-file number 50, 55, and 60 (FKG Dentaire SA, Switzerland). Irrigation with 2.5% sodium hypochlorite was done. The working length was measured radiographically and recorded for reference. The canal was filled with calcium hydroxide paste (Metapaste, Meta Biomed, Korea) and the access cavity was temporarily sealed with Cavit. The patient returned with a cellulitis, and we opened the tooth to drain and prescribed amoxicillin 2 g/day for 6 days (3M ESPE AG, Seefeld, Germany). Two days later, the canal was disinfected using 2.5% sodium hypochlorite and filled with the calcium hydroxide. After 10 days, she returned with the same symptoms and had a cellulitis for a second time. Because she suffered from a recurrent cellulitis, our decision was to create the apical plug, to obturate the rest of the canal with gutta-percha, and to surgically enucleate the periapical lesion. A small pieces of ETIK collagen (Acteon Pierre Roland, Mérignac, France) were packed against the bone into the periapical defect to create a matrix for the placement of mineral trioxide aggregate “MM-MTA” (MICRO-MEGA ® SA5-12, BESANCON cedex France). The MM-MTA was compacted against the barrier with pluggers to create an apical plug approximately 4 mm thickness. The rest of the canal was filled with warm gutta-percha injection Obtura™ and zinc oxide eugenol sealer [Figure 7]a. The coronal cavity was sealed with Cavit (3M ESPE AG, Seefeld, Germany). A radiograph to confirm the obturation was taken. The surgical enucleation of the cyst was successfully done the next day [Figure 7]b and [Figure 7]c, and 1 week after, the access cavity was sealed with composite resin. The follow-up done after 3, 6, and 12 months [Figure 8] demonstrated a radiographic decrease in the periapical radiolucency. The tooth was asymptomatic and clinically functional.{Figure 5}{Figure 6}{Figure 7}{Figure 8}

Case 4

A 30-year-old female patient who did not have any medical problem was referred to the Department of Dentistry, University Hospital Farhat Hached, Sousse, Tunisia, by her general dentist because of large periapical radiolucency extending to the apex of tooth #22 and abnormal canal morphology. The diagnosis was a pulp necrosis and symptomatic periapical abscess. The access cavity was opened to drain 2 days before. The tooth appeared as a peg-shaped microdont. Periodontal probing depth was normal and did not show a response to thermal test. Panoramic and retroalveolar radiograph showed that the tooth had Oehlers Type III DI, distal and mesial canal communicated with large periapical radiolucency and internal resorption perforated [Figure 9]a. A small tooth was observed in the pulp chamber surrounded by a radiopaque enamel border in the crown. A CBCT scan of the tooth was ordered to obtain a more accurate diagnosis [Figure 9]b and [Figure 9]c. Infolding of the enamel and dentin was clearly visible and distinct from the pulp chamber and was divided into two distinct areas. At the middle level of the root, an internal resorption was perforated with a defect communicated with the periapical radiolucency. This periapical radiolucency measured 15 mm × 14 mm × 12 mm and was responsible for thinning and breaking of the palatal cortical.{Figure 9}

Because of the complexity of the case and the difficulty of treating this tooth, the extraction was decided.


The growth of the dental papilla occurs as an alteration in cloche step and results of a deep folding of the enamel organ (different levels can go until the apex to the periapical region). The result is a partial invagination of the enamel organ with variable deeps, leading to a very complex root canal system. The mineralization of the enamel and dentin leads to a coronal formation in the tooth like a fissure or a cusped on the palatal face. The invagination is in continuity with the oral cavity which is a septic atmosphere.[9],[10],[11] The enamel is thin and lesser mineralization or even absent in the invagination. Studies described interruptions on the surface which facilitate the penetration of the irritants in the pulp. It can contain conjunctive tissues of dental papilla and its necrosis became nutrition to the bacteria. However, other studies described the invagination as uniform and regular with the absence of communication with the pulp.[8],[12],[13]

The clinical diagnostic in most cases detected DI by routine oral examination. Often, it is difficult to locate the entrance. The use of magnification or application of methylene blue to the palatal portion helps identify it.[14]

Its clinical appearance varies considerably. In some cases, the absence of any significant clinical signs of the anomaly may be easily overlooked it.[8]

In other cases, it can be investigated by unusual crown morphology such as protrusion cusp, greater buccolingual dimension, peg-shaped form, barrel-shaped form, conical shapes, and talon cusps. A deep foramen cecum might be considered as the first clinical sign indicating the presence of an invaginated tooth.[15],[16]

Conventional radiography helps in evaluating the complex morphology of the root canal system, but it only provides 2D representation of 3D structure.[17]

The invagination may not appear on retroalveolar radiograph when the standard parallel view is respected, so the angulations are important. If we suspect it, it is better to place the tube more mesially.[18]

The retroalveolar radiography provides an idea about the form of the crown and/or the root, the periapical lesion, the size of the pulp, and the apex.[19] The invagination could appear as a radiolucent pocket surrounded by a radiopaque enamel border as a deep enamel-lined fissure with its own opening into the periodontal ligament.[20],[21]

The use of more advanced images methods, such as CBCT, provides valuable information about dental anatomy and can be used before periapical surgery to assess the thickness of the cortical and cancellous bone and the inclination of roots in relation to the surrounding jaw. Periapical disease may be detected sooner using CBCT, revealing the actual size, extent, and its position.[22],[23]

There are a variety of treatment options: restoration, nonsurgical endodontic treatment, periapical surgery, and extraction. The morphologic and anatomic complexity often makes it difficult to perform diagnoses and to select treatment plans. Given these complexities, the endodontist must be aware that numerous treatment options are available for each case.

Early diagnosis and treatment is important for preventing pulp infection through the invagination. Sealing the invagination with a prophylactic restoration stops the penetration of the irritants to the root canal or the periapical area which is the treatment choice in this case. If there isn't an entrance to invagination or signs of pathosis, a follow up is recommanded.[1]

When pulps of young permanent teeth with incompletely formed roots are damaged, apexogenesis or apexification is indicated. A specific situation occurs when teeth have pulp necrosis and infection before the completion of root development or apical closure. The purpose of the treatment is to achieve the completion of root formation, to reduce the thickness of root canal walls, and to induce apical closure. The clinical approach for an immature permanent tooth with open apex and pulp inflammation comprises apexogenesis procedures, on the basis of the placement of calcium hydroxide pastes or even MTA barriers. Actually, the technique of pulp revascularization in immature teeth with an open apex becomes an excellent alternative. However, surgical treatment may be performed in cases in which the conventional method is not favored.[15],[18],[24],[25]

The communication of the invagination with periodontal ligament contributes to make successful cleaning, shaping, and filling difficult. The root presents a large and irregular volume improper with successful preparation. The use of hand file and sodium hypochlorite with the use of passive ultrasonic energy, the obturation with warm gutta-percha techniques including vertical condensation or thermoplastic filling techniques, has been recommended.[18],[26] In addition, if both the root canal and the invagination require treatment, a decision has to be made whether this is achieved with the lesion remaining separate to the root canal system or incorporated into it.

The authors found that the treatment of invagination and the pulp even apparently healthy is necessary because there is a close interrelationship and communication between them.[18]

However, it is possible to treat only the invagination and make a follow-up. If any complication occurs, consideration may need to be given to root canal treatment. If the teeth cannot be treated successfully nonsurgically with an orthograde root filling, a retrograde surgery is indicated in otherwise hopeless cases.[1],[18]

Finally, extraction should be performed if a tooth has abnormal anatomy and irregularities or has a major defect that is impossible to treat with nonsurgical or surgical procedure.[1]


DI is a rare tooth malformation and shows a range of morphological variation. Endodontic treatment of these teeth is a challenge for endodontist because of their varied shape which may include invaginated tooth structure making access and biomechanical preparation difficult.

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Conflicts of interest

There are no conflicts of interest.


1Hülsmann M. Dens invaginatus: Aetiology, classification, prevalence, diagnosis, and treatment considerations. Int Endod J 1997;30:79-90.
2Baumgart M, Hänni S, Suter B, Schaffner M, Lussi A. Dens invaginatus. Review of the literature and diagnostic and therapeutic guidelines. Rev Mens Suisse Odontostomatol 2009;119:706-14.
3Hamasha AA, Alomari QD. Prevalence of dens invaginatus in Jordanian adults. Int Endod J 2004;37:307-10.
4Bäckman B, Wahlin YB. Variations in number and morphology of permanent teeth in 7-year-old Swedish children. Int J Paediatr Dent 2001;11:11-7.
5Hallett GE. Incidence, nature, and clinical significance of palatal invaginations in the maxillary incisor teeth. Proc R Soc Med 1953;46:491-9.
6Oehlers 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.
7Ridell K, Mejàre I, Matsson L. Dens invaginatus: A retrospective study of prophylactic invagination treatment. Int J Paediatr Dent 2001;11:92-7.
8Alani A, Bishop K. Dens invaginatus. Part 1: Classification, prevalence and aetiology. Int Endod J 2008;41:1123-36.
9Heritier M. Anomalies dentaires. In: Anatomie Pathologique Des Dents et la Muqueuse Buccale. Paris: MASSON; 1989. p. 1-22.
10de Sousa SM, Bramante CM. Dens invaginatus: Treatment choices. Endod Dent Traumatol 1998;14:152-8.
11Bal S. Quel traitement pour quel type de dens in dente? Lere partie. Clinic 2012;33:127-37.
12Suruchi S, Rahul M, Anisha M. Dens invaginatus – A review and case report. Endodontology 2010;22:73-80.
13Baumgart M, Hänni S, Suter B, Schaffner M, Lussi A. Dens invaginatus. Schweiz Monatsschr Zahnmed 2009;119:697-714.
14Girsch WJ, McClammy TV. Microscopic removal of dens invaginatus. J Endod 2002;28:336-9.
15Tsurumachi T, Suguro H, Ogata H, Hatori K, Kobayashi C, Ogiso B. Endodontic treatment of bilateral dens evaginatus premolars with large periapical lesions. J Oral Sci 2009;51:475-9.
16Helvacioglu-Yigit D, Aydemir S. Endodontic treatment of type II dens invaginatus in a maxillary lateral incisor: A case report. Case Rep Dent 2012;2012:153503.
17Kato H. Nonsurgival endodontic treatment for dens invaginatus type III using cone beam computed tomography and dental operation microscope: A case report. Bull Tokyo Dent Coll 2013;54:103-8.
18Bishop K, Alani A. Dens invaginatus. Part 2: Clinical, radiographic features and management options. Int Endod J 2008;41:1137-54.
19Teman G, Lacan A, Suissa M, Sarazin L. Strategies des explorations en imagerie maxillofaciale. Paris: EMC Stomatologie; 2004. p. 8.
20White SC, Pharoah MJ. Oral Radiology: Principles and Interpretation. 2nd ed. St. Louis, MO: Mosby; 2000. p. 314-5.
21Gonçalves 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.
22Tyndall DA, Rathore S. Cone-beam CT diagnostic applications: Caries, periodontal bone assessment, and endodontic applications. Dent Clin North Am 2008;52:825-41, vii.
23Patel S, Dawood A, Ford TP, Whaites E. The potential applications of cone beam computed tomography in the management of endodontic problems. Int Endod J 2007;40:818-30.
24Schmitz MS, Montagner F, Flores CB, Morari VH, Quesada GA, Gomes BP. Management of dens invaginatus type I and open apex: Report of three cases. J Endod 2010;36:1079-85.
25Wayama MT, Valentim D, Gomes-Filho JE, Cintra LT, Dezan E Jr. 18-year follow-up of dens invaginatus: Retrograde endodontic treatment. J Endod 2014;40:1688-90.
26Alrejaie M, Ibrahim N, Malur M, AlFouzan K. Type II dens evaginatus of maxillary central incisor: An alternative approach. Saudi Endod J 2015;5:61-4.