|Year : 2008 | Volume
| Issue : 6 | Page : 72-75
Nonsurgical treatment of periapical lesion associated with type III dens invaginatus using calcium hydroxide: A case report
R Kalaskar1, AR Kalaskar2
1 Department of Pedodontics, Sharad Pawar Dental College, Wardha, Maharashtra, India
2 Department of Oral Diagnosis Medicine and Radiology, VSPM Dental College and Research Center, Nagpur, Maharashtra, India
Plot No. 68, Banerjee Layout, Bhagwan Nagar, Nagpur 27, Maharashtra
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Dens invaginatus is a developmental malformation of teeth, probably resulting from an infolding of the papilla during tooth development. It predisposes the tooth to develop caries and periapical pathosis. Root canal therapy may present many problems because of the complex anatomy of the teeth. The purpose of this case report is to describe the endodontic treatment of an Oehlers type III dens invaginatus that perforated into the apical area. Calcium hydroxide powder mixed with normal saline, was used as an intracanal medicament. This eradicated the pathogenic microorganisms in the invagination and preserved the vitality of the tooth, allowing gutta-percha obturation in the invagination.
Keywords: Calcium hydroxide, dens invaginatus, maxillary central incisor, periapical lesion
|How to cite this article:|
Kalaskar R, Kalaskar A R. Nonsurgical treatment of periapical lesion associated with type III dens invaginatus using calcium hydroxide: A case report. J Indian Soc Pedod Prev Dent 2008;26, Suppl S2:72-5
|How to cite this URL:|
Kalaskar R, Kalaskar A R. Nonsurgical treatment of periapical lesion associated with type III dens invaginatus using calcium hydroxide: A case report. J Indian Soc Pedod Prev Dent [serial online] 2008 [cited 2021 Apr 19];26, Suppl S2:72-5. Available from: https://www.jisppd.com/text.asp?2008/26/6/72/43536
| Introduction|| |
Dens invaginatus (DI), the condition alternatively called dens in dente, invaginated odontome, and dense telescope, is a rare developmental anomaly resulting from the invagination of enamel organ into the dental papilla before calcification has occurred.  The depth of invagination varies from a slight enlargement of the cingulum pit to a deep infolding that extends to the apex.  The reported prevalence rate of DI varies from 0.04 to 10%. It primarily affects the permanent dentition, especially the maxillary lateral incisor, but it may also occur, in decreasing order of incidence, in the central incisor, canine, and premolars. , Bilateral occurrence is not uncommon and there are cases of double and triple invaginations and also reports of occurrence in deciduous teeth.  The etiology of DI remains controversial; the following explanations have been proposed:
- Kronfeld  proposed that DI is caused by a focal failure of growth of the internal enamel epithelium, leading to the proliferation of the surrounding normal epithelium with eventual engulfment of the static area.
- Oehlers  proposed that distortion of the enamel organ occurs during tooth development and results in protrusion of a part of the enamel organ.
- Other theories include infection, trauma, and genetics, but none have been proven or widely accepted. ,,
Historically, DI has been classified into three major types:
Type I - exhibits an invagination that is confined to the crown.
Type II - extends below the cementoenamel junction and ends in a blind sac that may or may not communicate with the adjacent dental pulp.
Type III - extends through the root and perforates in the apical or lateral radicular area, without any immediate communication with the pulp. This perforation provides direct communication from the oral cavity to the intraosseous periradicular tissues and often produces inflammatory lesions in the presence of a vital pulp. 
Clinically, the morphology of DI may appear normal or the tooth may have a larger mesiodistal dimension at the cervical area than at the incisal area. Mild invagination exhibits only a palatal pit, which is often clinically unnoticed. However, when the crown is large and has a prominent cingulum with a palato-gingival groove, DI is assumed to be present. ,, Radiographically, the invagination may vary in size and shape and may present a radiopaque ribbon-like structure with a density equal to that of enamel extending from the cingulum into the root canal to the root apex, simulating a tooth within tooth. In extensive invagination the crown is almost invariably malformed, with a wide apical foramen. These features are often apparent in the radiograph even before the tooth erupts. ,,,
Histologically, the structure of DI shows intact dentine without irregularities, and strains of vital connective tissue or even fine canals connecting the dental pulp and the hypomineralized internal enamel. The internal enamel exhibits complex rod shapes and its surface also presents the typical honeycomb pattern, but no perikymata. ,
The invagination is usually separated from the pulp chamber by a relatively thin wall, and often it communicates with the pulp chamber through fine canals, causing pulp diseases even in the absence of caries. Abscess formation, cyst formation, tooth discoloration, periapical granuloma, and open apex have already been reported with DI. ,
The following case report describes the nonsurgical treatment of a periapical lesion associated with type III DI using calcium hydroxide, preserving pulpal vitality of the concerned maxillary right central incisor.
| Case Report|| |
An 11-year-old child reported to the Department of Pediatric Dentistry, Sharad Pawar Dental College, Wardha, with the chief complaint of pain and swelling in the upper anterior region for 1 month. Intraoral examination revealed an enlarged crown of the maxillary right central incisor with the presence of incisal notches. The palatal surface showed a pronounced cingulum, along with a fissure in the central region [Figure 1]. The maxillary right permanent central incisor was tender to vertical percussion and showed positive response to thermal testing [cold test (Polfofluorange Pharma Dental Handelsges)] and electric pulp testing (Parkell Farmingdate). The responses of the adjacent teeth were within normal limits. The tooth was not associated with trauma, caries, or periodontal pocket. The labial mucosa in relation to 11 showed diffuse swelling. An intraoral periapical radiograph of permanent right central incisor revealed enamel invagination (with a density equal to that of enamel) extending from the cingulum to the apical region, simulating a tooth within tooth. The root was dilated and was associated with a periapical lesion approximately 5 × 5 mm in diameter [Figure 2]. The patient was informed about the complexity of the conservative endodontic therapy as well as the likely need for a surgical approach. A size 10 K-type file was used to explore the enamel invagination. The invagination was widened carefully to prevent exposure of the remaining vital pulp tissue in the body of the tooth. Necrotic tissue was removed from the invagination and the working length was estimated as being 1 mm short of the radiographic apex [Figure 3]. The canal was enlarged to size 35 using K-type files in a step-back technique. During instrumentation, the canal was copiously irrigated with 3 % sodium hypochlorite (Vishal Dentocare Pvt Ltd, Ahmedabad). The canal was dried with sterile paper points and filled with calcium hydroxide powder mixed with normal saline (0.9% w/v; Core Pharmaceuticals). The access cavity was sealed with zinc oxide eugenol cement. At recall after a week, the tooth was asymptomatic and the soft tissue in relation to the tooth was healthy. The intracanal dressing was removed, a fresh paste of calcium hydroxide was placed into the canal, and the access cavity was sealed with zinc oxide eugenol cement. The second recall visit was made after 6 weeks in order to check for any redevelopment of the sinus tract, swelling, or mobility or pain on percussion of the tooth. The maxillary right central incisor was asymptomatic, without any signs or symptoms of reinfection. During these visits, saline was used to irrigate the canal. After the 6 weeks' observation period, root canal obturation was done using gutta-percha points by the lateral condensation method (Hygenic, Akron, OH, USA). The access cavity and incisal notching were restored with composite resin (Charisma, Heraeus Kulzer). The patient was recalled after 6 months, when an intraoral periapical radiograph was taken and revealed complete resolution of the periapical lesion [Figure 4].
| Discussion|| |
Several treatment options exist for the treatment of type III DI, depending on the internal anatomy and the condition of the pulp. These options include preventive restoration, root canal treatments, combined root canal and surgical treatments, intentional replantation, and extraction. ,
As would be expected, before eruption of the tooth the lumen of the invagination is filled with soft tissue similar to dental follicle (i.e., reduced enamel epithelium with a fibrous connective tissue). After eruption, microorganisms invade the invagination and cause inflammation of the tissue. Initially the pulp probably remains uninfected; however, the infection may reach the pulp through the apical opening, i.e., via a retrograde route or through channels existing between the invagination and the pulp. , Inflammatory sequelae related to the invagination can often be avoided by early diagnosis and prophylactic treatment, i.e., the cingulum pit should be closed using composite resin as soon as the tooth passes the gingival margin during the course of eruption. However periodic follow-up examinations, including pulp sensitivity testing and radiographic evaluation, are mandatory to avoid serious periradicular complications. ,,
In a vital tooth that has a DI and periapical pathology, the invagination should be treated endodontically, similar to a normal root canal treatment, to preserve the pulp vitality in the remainder of the tooth. The present case report describes a type III invagination associated with a periapical lesion in a vital maxillary right central incisor, which was successfully treated endodontically, similar to the case reported by Cole et al. ,  Zillich et al. ,  and Eldeeb. 
Pulp necrosis occurring in a tooth with the usual form of a type III DI can often be challenging to manage with endodontic therapy. The difficulties associated with the treatment of type III DI are closely related to the complexity of the root canals and the type and extent of the invagination. In most complex cases, the first challenge is posed by the location of root canal openings. A surgical microscope can be used for magnification and better lighting of the root canal system. Girish and McClammy,  Jung,  and Shoner and Wallace  recommended the use of ultrasonic cleaning for complex root canal systems in teeth with DI.
Failure of endodontic treatment is often associated with the persistence of microorganisms in the areas of the root canal system that are not accessible to the mechanical action of files. Therefore dressing with intracanal medicaments has been considered one of the most important steps for obtaining and maintaining a sterile root canal after mechanical instrumentation and before root canal obturation.  Calcium hydroxide is a material that has been used for a variety of purposes since its introduction into dentistry. In its pure form, calcium hydroxide has a high pH and its dental use relates chiefly to its ability to stimulate mineralization and also to its antibacterial property. Recent studies have recommended calcium hydroxide as a root canal medicament because of its low toxicity, bactericidal activity, biocompatibility, and tissue-dissolving property. , Souza et al. suggested that the action of calcium hydroxide beyond the apex may be four-fold: (1) anti-inflammatory action, through its hygroscopic action; (2) neutralization of acid products such as hydrophase; (3) activation of alkaline phosphatase; and (4) antibacterial action.  Numerous reports have described healing of periapical pathology with the use of intracanal calcium hydroxide medicament. , In addition to its antibacterial property, calcium hydroxide dressing also helps to build dentinal bridges and to maintain the vitality of the adjacent pulp in DI. 
Sodium hypochlorite dissolves residual necrotic tissue at a faster rate than calcium hydroxide. Thus, sodium hypochlorite can be used as an irrigation solution before application of intracanal calcium hydroxide dressings, so as to create a canal free of pulp remnants before obturation. 
For a more predictable result in large periapical lesions, the calcium hydroxide would have to be changed routinely at the first follow-up visit after 6 weeks.  Webber suggested that the calcium hydroxide dressings be changed as often as necessary. He also stated that dryness of the calcium hydroxide dressing at the apical half should be one of the deciding factors for changing the dressing. If the patient redevelops a sinus tract and / or symptoms in the early months of treatment, then too the dressing need to be changed.  Once the active infection subsides, the body's natural defense mechanisms start acting and brings about the healing of the periapical pathology.  Some authors have recommended obturation of the canals before healing of periapical pathology, whereas others prefer to wait till the periapical pathology has healed. ,,,, Kursat  obturated DI when the radiograph revealed significant healing of a large periapical lesion. In the present case report, the acute infection and sinus tract subsided by the second visit and hence root canal obturation was done before healing of the periapical pathology, which is in accordance with Oztan. 
Surgical treatment should be considered in cases of failure of endodontic treatment and in teeth which cannot be treated nonsurgically because of anatomical problems or failure to gain access to all parts of the root canal system. Extraction is indicated only in teeth with severe anatomical irregularities that cannot be treated nonsurgically or by apical surgery. 
A long follow-up is required to rule out recurrence of the lesion. In the present case, this was not possible and the patient could not be followed up after 6 months.
| Conclusion|| |
The clinician may come across different variations of dens invagination and should be alert to this possibility; he or she should therefore master a variety of techniques and be able to use different materials for the successful management of a complex DI. The present case report describes the successful endodontic management of a type III DI with a periapical lesion using calcium hydroxide, while preserving pulpal vitality.
| References|| |
|1.||Hülsmann M. Dens invaginatus: Aetiology, classification, prevalence, diagnosis and treatment considerations. Int Endod J 1997;30:79-90. |
|2.||Hovland EJ, Block RM. Nonrecognition and subsequent endodontic treatment of dens invaginatus. J Endod 1977;3:360-2. |
|3.||Rabinowitch BZ. Dens in dente: primary tooth: Report of a case. Oral Surg Oral Med Oral Pathol 1952;5:1312-4. |
|4.||Kronfeld R. Dens in dente. J Dent Res 1934;14:49-66. |
|5.||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. |
|6.||Fischer CH, Frage des Z. Dens in dente. Deutsche Zahn-, Mundund Kieferheilkunde 1936;3:621-34. |
|7.||Gustaffson G, Sundberg S. Dens in dente. Br Dent J 1950;88:83-8. |
|8.||Hosey MT, Bedi R. Multiple dens invaginatus in two brothers. Endod Dent Traumatol 1996;12:44-7. |
|9.||Takeda Y, Suzuki A, Shimono M. Multiple dens invaginatus and cranio-vertebral abnormality. Bull Tokyo Dent Coll 1991;4:165-9. |
|10.||Girsch WJ, McClammy TV. Microscopic removal of dens invaginatus. J Endod 2002;28:336-9. |
|11.||Tsurumachi T. Endodontic treatment of an invaginated maxillary lateral incisor with a periradicular lesion and a healthy pulp. Int Endod J 2004;37:717-23. |
|12.||Gotoh T, Kawahara K, Imai K, Kishi K, Fujiki Y. Clinical and radiographic study of dens invaginatus. Oral Surg Oral Med Oral Pathol 1979;48:88-91. |
|13.||Gound TG, Maixner D. Non surgical management of a dilacerated maxillary lateral incisor with type III dens invaginatus: A case report. J Endod 2004;30:448-51. |
|14.||Jung M. Endodontic treatment of dens invaginatus type III with three root canals and open apical foramen. Int Endod J 2004;37:205-13. |
|15.||Beynon AD. Developing dens invaginatus (dens in dente): A Quantitative microradiographic study and a reconsideration of the histogenesis of this condition. Br Dent J 1982;153:255-60. |
|16.||De Smit A, Demaut L. Non surgical endodontic treatment of invaginated teeth. J Endod 1982;8:506-11. |
|17.||Suchina JA, Ludington JR Jr, Madden RM. Dens invaginatus of a maxillary lateral incisor: Endodontic treatment. Oral Surg Oral Med Oral Pathol 1989;68:467-71. |
|18.||Stamfelj I, Kansky AA, Gaspersic D. . Unusual variant of type 3 dens invaginatus in a maxillary canine: A rare case report. J Endod 2007;33:64-8. |
|19.||Wells DW, Meyer RD. Vital root canal treatment of dens in dente. J Endod 1993;19:616-7. |
|20.||Ridell K, Mejàre I, Matsson L. Dens invaginatus: A retrospective study of prophylactic invagination treatment. Int J Paediatr Dent 2001;11:92-7. |
|21.||Cole GM, Taintor JF, James GA. Endodontic therapy of a dilated dens invaginatus. J Endod 1978;4:88-90. |
|22.||Zillich RM, Ash JL, Corcoran JF. Maxillary lateral incisor with two root and dens formation: A case report. J Endod 1983;9:143-4. |
|23.||Eldeeb ME. Non-surgical endodontic therapy of a dens invaginatus. J Endod 1984;10:107-9. |
|24.||Skoner JR, Wallace JA. Dens invaginatus: Another use for the ultrasonics. J Endod 1994;20:138-40. |
|25.||Chong BS, Pitt Ford TR. The role of intracanal medication in the root canal treatment. Int Endod J 1992;25:97-106. |
|26.||Bystrom A, Claesson R, Sundqvist G. The antibacterial effect of camphorated paramonochlorophenol, camphorated phenol and calcium hydroxide in the treatment of infected root canals. Endod Dent Traumatol 1985;1:170-5. |
|27.||Sjφgren U, Figdor D, Spεngberg L, Sundqvist G. The antimicrobial effect of calcium hydroxide as a short-term intracanal dressing. Int Endod J 1991;24:119-25. |
|28.||Souza V, Bernabe PF, Holland R, Nery MJ, Mello W, Otoboni Filho JA. Tratamento nao cururgico de dentis com lesos periapicais. Rev Brasil Odontol 1989;46:39-46. |
|29.||Caliskan MK, Türkün M. Periapical repair and apical closure of a pulpless tooth using calcium hydroxide. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;84:683-7. |
|30.||Oztan MD. Endodontic treatment of teeth associated with a large periapical lesion. Int Endod J 2002;35:73-8. |
|31.||Brad W Neville. Oral and maxillofacial pathology. 2 nd ed. Philadelphia: W.B. Saunders; 2004. p. 80-4. |
|32.||Andersen M, Lund A, Andreasen JO, Andreasen FM. In vitro solubility of human pulp tissue in calcium hydroxide and sodium hypochlorite. Endod Dent Traumatol 1992;8:104-8. |
|33.||Webber RT. Apexogenesis versus apexification. Dent Clin North Am 1984;28:669-97. |
|34.||Er K, Kustarci A, Ozan U, Ta?demir T. Nonsurgical endodontic treatment of dens invaginatus in a mandibular premolar with large periradicular lesion: a case report. J Endod 2007;33:322-4. |
|35.||Rotstein I, Stabholz A, Heling I, Friedman S. Clinical considerations in the treatment of dens invaginatus. Endod Dent Traumatol 1987;3:249-54. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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