Saudi Endodontic Journal

CASE REPORT
Year
: 2013  |  Volume : 3  |  Issue : 3  |  Page : 132--138

Revascularization of an impacted, immature dilacerated permanent maxillary central incisor associated with odontoma and a supernumerary tooth


Priya Subramaniam1, Krishna Kumar1, Ramakrishna Tangaturi2, Girish Kadalagere Lakshmana Babu1,  
1 Department of Pedodontics and Preventive Dentistry, The Oxford Dental College and Hospital, Bangalore, India
2 Department of Oral and Maxillofacial Surgery, The Oxford Dental College and Hospital, Bangalore, India

Correspondence Address:
Priya Subramaniam
Department of Pedodontics and Preventive Dentistry, The Oxford Dental College and Hospital, Hosur Road, Bomanahalli, Bangalore 560 068, Karnataka
India

Abstract

To intentionally replant an impacted immature permanent maxillary central incisor in the mixed dentition period followed by revascularization in order to achieve apical root closure. A 9-year-old boy presented with retained maxillary left primary incisors. Radiographic evaluation revealed the presence of a supernumerary tooth and an odontoma associated with an impacted permanent maxillary left central incisor, having root dilaceration. Treatment included surgical removal of mesiodens and odontoma. The impacted dilacerated permanent central incisor was removed and intentionally replanted, followed by revascularization of pulp. During the follow-up, root end closure with narrowing of canal space was observed, patient has been asymptomatic and the tooth remains vital. Revascularization of the immature reimplanted tooth showed continued root development and thickening of the lateral dentinal walls through deposition of new hard tissue and narrowing of the canal space.



How to cite this article:
Subramaniam P, Kumar K, Tangaturi R, Babu GK. Revascularization of an impacted, immature dilacerated permanent maxillary central incisor associated with odontoma and a supernumerary tooth.Saudi Endod J 2013;3:132-138


How to cite this URL:
Subramaniam P, Kumar K, Tangaturi R, Babu GK. Revascularization of an impacted, immature dilacerated permanent maxillary central incisor associated with odontoma and a supernumerary tooth. Saudi Endod J [serial online] 2013 [cited 2019 Nov 20 ];3:132-138
Available from: http://www.saudiendodj.com/text.asp?2013/3/3/132/121506


Full Text

 Introduction



Impacted or clinically missing permanent maxillary incisors can have a major impact on dental and facial aesthetics of a young individual. Factors contributing to impaction include developmental anomalies such as malposition, dilaceration, ankylosis, tumors, odontoma, dentigerous cysts, presence of supernumerary teeth, and systemic genetic interrelation such as cleidocranial dysostosis and hypopituitarism. [1]

Supernumerary teeth are the most common disorder of odontogenesis resulting from hyperactivity of dental lamina, dichotomy, spontaneous gene mutation, or environmental factors. [2],[3] Four major types of supernumerary teeth are recognized based on their morphology and location: Conical, tuberculate, supplemental, or odontoma. [2] Conical mesiodens is usually peg shaped, develops root formation ahead of or at an equivalent stage to that of the central incisor. [2],[4],[5] The conical supernumerary may be noninverted or inverted. [6] When noninverted, it may remain unerrupted and lie palatal to the permanent incisors.

Odontomas are developmental anomalies resulting from the growth of completely differentiated epithelial and mesenchymal cells that give rise to functional ameloblasts and odontoblasts. These cells in turn form variable amounts of enamel, dentin, and pulpal tissue of the odontoma. They are usually associated with overly retained primary and unerupted permanent teeth. The exact etiology of odontomas is unknown, but local trauma, infection, inheritance, and genetic mutation are reported to be possible causes of odontomas. [7]

The incidence of odontogenic tumors is estimated to be between 0.002 and 0.1% and varies greatly in different population groups. [8] In most cases, odontomas are asymptomatic and the presence could be suspected due to the delay in tooth eruption or via routine radiographic examinations.

Odontomas have been classified as benign odontogenic tumors and are subdivided into complex or compound odontomas morphologically. The calcified dental tissues in compound odontoma are arranged in an orderly pattern resembling miniature tooth structures, whereas complex odontoma has an amorphous and disorderly pattern. Compound odontomas commonly occur in the incisor canine region of the maxilla, and complex odontomas are frequently located in the premolar and molar region of both jaws. [9]

Dilaceration refers to an angulation, or a sharp bend or curve, in the root or crown of a formed tooth. It commonly occurs as a result of trauma to the primary predecessors whose apices lie close to the permanent tooth germ. [9] Tooth dilaceration may present as noneruption of the affected tooth, prolonged retention of the primary predecessor, apical fenestration of the labial cortical plate, or it can be completely asymptomatic. Clinically, a dilacerated tooth can be appreciated on palpation in the labial sulcus or hard palate, and it has a characteristic appearance on a radiograph. [10]

Management options that have been proposed for impacted permanent incisors in the mixed dentition are: (1) Extraction or surgical removal of impacted supernumerary tooth and further observation till the permanent incisors erupts, (2) surgical repositioning, and (3) orthodontic correction. [11],[12],[13],[14],[15],[16] Extraction of the tooth was carried out in a rare case report of a compound odontoma associated with a developing supernumerary tooth and an unerupted dilacerated maxillary primary incisor. [16]

Treatment modalities for management of immature permanent teeth include revascularization, apexogenesis using calcium hydroxide, apexification with either calcium hydroxide or mineral trioxide aggregate, custom made roll cone technique and periapical surgery. Recent advances have led to a paradigm shift from conventional replacement procedures to regenerative protocols. In an earlier report of a 13-year-old patient, a necrotic immature mandibular second premolar with periapical involvement was treated with antimicrobial agents and the root canal was left empty. Radiographic examination showed complete apical closure following 30 months of treatment. [17] Treatment of thin, fragile blunderbuss canals in young permanent teeth is a challenge. Various authors have demonstrated the regenerative process in immature, nonvital teeth by revascularization induced maturogenesis. [17],[18],[19],[20] A disinfected canal, having a matrix for tissue growth with excellent coronal seal has been shown to favor revascularization. [19] There is potential for stem cells to allow tissue regeneration in immature permanent teeth. [20]

The following case report represents an intentionally replanted impacted immature permanent maxillary central incisor in the mixed dentition period followed by revascularization in order to achieve apical root closure.

 Case Report



A boy aged 9 years presented to the Department of Pedodontics and Preventive Dentistry with retained maxillary left primary incisors and lack of eruption of permanent central incisor. There was no significant medical history. There was no history of pain, swelling, or trauma to the orofacial region. There was no family history of unerupted teeth. Extraorally there was facial symmetry. Intraoral examination revealed a full complement of mixed dentition appropriate for his age, except for the presence of a retained maxillary left primary central incisor [Figure 1]. The contralateral maxillary permanent central incisor was present. No buccal or palatal swelling was palpable and the retained primary incisor was firm. There was no remarkable finding in relation to gingiva or soft tissue in that region. The boy was in need of orthodontic alignment of his teeth.{Figure 1}

Radiographic examination, showed an impacted maxillary permanent central incisor in close proximity to a calcified tooth-like mass and inverted mesiodens [Figure 2] and [Figure 3]. Based on clinical and radiographic findings, the presumptive diagnosis of an odontoma impeding the eruption of the right permanent central incisor was made. Treatment plan included surgical removal of both odontoma and mesiodens, followed by reimplantation of the permanent central incisor.{Figure 2}{Figure 3}

Under local anesthesia, the retained primary incisors were removed. A labial mucoperiosteal flap was raised and overlying bone was removed to expose the odotoma [Figure 4]. Both odontoma and mesiodens were removed [Figure 5] and [Figure 6]. The odontoma was further subjected to histopathological examination. The impacted permanent central incisor was then carefully extracted with forceps [Figure 6]a. It had little bone support and exhibited root dilaceration in the apical third (5 mm) towards a distopalatal direction [Figure 6]b. The apical root end closure was incomplete and the apical opening was about 2 mm wide. The tooth was immediately reimplanted. The surgical wound was closed primarily with sutures and the tooth stabilized for 3-4 weeks, using a semirigid splint. An immediate postoperative intraoral periapical radiograph revealed a large root canal space of about 5 mm wide at the cervical third, with thin dentinal walls [Figure 7].{Figure 4}{Figure 5}{Figure 6}{Figure 7}

The calcified tissue was fixed in formalin, embedded in paraffin, serially sectioned (5-mm thickness), and stained with hematoxylin and eosin (H and E). Histopathalogical examination with conventional light microscope confirmed the diagnosis of a compound odontoma [Figure 8].{Figure 8}

Within 10 days, the patient was recalled for initiation of root end closure by revascularization. Under rubber dam isolation, access was gained to the root canal, and the necrotic contents of the canal were extirpated. Alternate irrigation with saline and 0.2% chlorhexidine solution was done along with minimal filing so as to prevent further weakening of root canal walls. An intracanal medicated dressing of metronidazole, ciprofloxacin, and minocycline was placed. [21] Following 1 week, the tooth was symptom-free and the canal was found to be dry. The revascularization process was then carried out. [22],[23]

The apical tissues beyond the confines of the root canal were gently stimulated with a sterile endodontic file to induce bleeding into the canal space. When frank bleeding was evident at the cervical portion of the root canal, a sterile moist cotton pellet was inserted at a depth of 3-4 mm into the canal. The bleeding was stopped at a level of 3 mm below the level of cement-enamel junction and left for 15 min so that the blood would clot at that level. The access opening was sealed with glass ionomer cement. Clinical and radiographic evaluation was done following 15 days, and at 1 month and 6 monthly intervals [Figure 9]a. The tooth was asymptomatic and responded to all vitality tests. At the end of 1 year, thickening of dentinal walls of the root canal, reduction in canal diameter, and closure of apical root end was observed. The patient has shown uneventful healing over a period of 2 years [Figure 9]b.{Figure 9}

 Discussion



The need for a careful surgical technique in such patients cannot be overemphasized and the surgical trauma and morbidity for young children should be considered. Careful manipulation of the root and socket under favorable preoperative, surgical, and postoperative conditions ensures survival of the cells of the periodontal ligament and promotes the reformation of a normal supporting apparatus. However, root resorption can be a major complication that can be exacerbated by pulp necrosis and infection. The occurrence of pulp necrosis is influenced by a number of factors, most importantly, maturity of the roots at the time of reimplantation. The chances of nonvitality are much lower when the treatment is initiated at a younger age due to the presence of a wide apical foramen.

An impacted immature incisor tooth germ in complete inversion was surgically repositioned using a closed-flap technique in a boy aged 6 years 8 months. Continued root formation and spontaneous eruption was observed over 51 months, without pulpal or periodontal complications. [24]

Revascularization is a process in which ingrowth of highly vascularized connective tissue occurs into the pulp space; or in which blood vessels already present in the pulp of the transplanted tooth anastomose with blood vessels from the periodontium. [25] It should be advocated to clinicians faced with pulp necrosis with an immature apex that is more than 1 mm wide on a radiograph. Since only the mesiodistal width of the root canal can be judged radiographically apices may seem closed, when they are open buccopalatally facilitating the occurrence of pulp revascularization. [26] The size of the apical opening must be sufficient to allow ingrowth of vital tissue. Kling et al., suggested that an apical opening greater than 1 mm mesiodistally was associated with successful revascularization of avulsed permanent teeth, and revascularization did not occur in teeth with a smaller apical opening. [27]

Relationships have been shown between the occurrence of pulp revascularization and the level of tooth development, the surgical procedure, the extra-alveolar time period, the type of tooth, and the level of oral hygiene. [28],[29],[30]

The key factor for the success of revascularization in necrotic, infected, and immature teeth is complete disinfection of the root canal space using copious irrigation, minimal instrumentation and placement of antibiotic pastes. [17],[18],[19],[20],[23],[28],[29],[30]

It is expected that necrotic infected immature teeth can be rendered to the same starting point as avulsed immature teeth with necrotic but uninfected pulps (i.e. severed blood supply as a result of avulsion). Mechanical instrumentation, an important step in root canal treatment, cannot be done in these teeth because the walls are very fragile and thin. Disinfection relies only on irrigation and intracanal medications. Various combinations of topical antibiotics have the ability to disinfect necrotic, infected root canals. One combination that is effective against the bacteria commonly found in infected root canals is the use of: (1) Ciprofloxacin; (2) metronidazole; and (3) cefaclor. [31]

Traditionally, calcium hydroxide has been used as the intracanal medication in apexification procedures. Though calcium hydroxide is a proven and effective medication, its effect is to create an environment conducive to the formation of a hard tissue bridge at the apex. However, because of its high alkalinity, tissue in immediate contact with it undergoes necrosis, leading to destruction of vital apical cells that have potential to differentiate into new pulp. Thus, with calcium hydroxide therapy, there is no possibility that the root canal walls will be strengthened. [32] Long-term calcium hydroxide as a root canal dressing may increase risk of root fracture. [32],[33]

Although a bacteria-free canal is a prerequisite for tissue regeneration, tissue will not grow into an empty space. Rather, a scaffold is essential to aid the ingrowth of new tissue into the canal space. Induction of a blood clot, from the periapical tissues, may act as a scaffold for the ingrowth of new tissue into the root canal of the immature tooth. Blood clot also plays an important role in regeneration by releasing various growth factors like platelet derived growth factor (PDGF), platelet derived epithelial growth factor (PDEGF), and tissue growth factor (TGF b). [34]

Various possible reasons have been given to explain the apexogenesis or maturogenesis that occurs. These include the presence of mesenchymal stem cells residing in the apical papilla, also known as stem cells of apical papilla (SCAP). It has been hypothesized that SCAP can be the source of primary odontoblasts forming the root dentin [35] and are multipotent dental pulp stem cells. [29] An open apex provides a channel for SCAP and new blood vessels to proliferate into the pulp space over the blood clot matrix. [35] In the present case, the tooth had an open apex and the dilacerated root was shorter, which allowed new tissue to grow into the pulp space relatively quickly. The pulp was necrotic but may not have been infected, so it would have acted as a matrix into which the tissue could grow. In addition, the crown of the tooth was intact. At the beginning of treatment, it was not known whether the vital tissue was pulp. The growth factors and cells could have led to proliferation and differentiation of cells into odontoblasts, under the organizing influence of cells of Hertwig's epithelial root sheath (HERS). [19] The newly formed odontoblast lineages from stem cells in pulp tissue or apical papilla lay down atubular dentin at the apical end, as well as on lateral aspects of dentinal walls of the root canal, leading to apexogenesis. Whether the new vital tissue is truly pulp or pulp-like is of little consequence, as long as there is continued development of the root canal walls and apex. Reinforcement of dentinal walls occurs with deposition of hard tissue that will strengthen the root against fracture.

A limitation in determination of actual contents of the pulp space after revascularization procedures is that it is not possible to extract a functional tooth for histopathological analysis.

If the attempted revascularization procedure fails, the traditional option of apexification using calcium hydroxide or mineral trioxide aggregate remains, followed by a conventional root filling.

 Conclusion



Revascularization of the immature reimplanted tooth showed continued root development and thickening of the lateral dentinal walls through deposition of new hard tissue and narrowing of the canal space.

References

1da Costa CT, Torriani DD, Torriani MA, da Silva RB. Central incisor impacted by an odontoma. J Contemp Dent Pract 2008;9:122-8.
2Garvey MT, Barry HJ, Blake M. Supernumerary teeth-an overview of classification, diagnosis and management. J Can Dent Assoc 1999;65:612-6.
3Russell KA, Folwarczna MA. Mesiodens-diagnosis and management of a common supernumerary tooth. J Can Dent Assoc 2003;69:362-6.
4Primosch RE. Anterior supernumerary teeth-assessment and surgical intervention in children. Pediatr Dent 1981;3:204-15.
5Mukhopadhyay S. Mesiodens: A clinical and radiographic study in children. J Indian Soc Pedod Prev Dent 2011;29:34-8.
6Nikhil S, Vineeta, Gupta P. Inverted mesiodens: A case report. J Indian Soc Pedod Prev Dent 1999;17:111-2.
7Owens BM, Schuman NJ, Mincer HH, Turner JE, Oliver FM. Dental odontomas: A retrospective study of 104 cases. J Clin Pediatr Dent 1997;21:261-4.
8de Oliveira BH, Campos V, Marcal S. Compound odontoma- diagnosis and treatment: Three case reports. Pediatr Dent 2001;23:151-7.
9Shafer WG, Hine MK, Levy BM. A Textbook of Oral Pathology, 4 th ed., Vol. 40 Philadelphia: W.B. Saunders Company; 1983. p. 308-11.
10Topouzelis N, Tsaousoglou P, Pisoka V, Zouloumis L. Dilaceration of maxillary central incisor: A literature review. Dent Traumatol 2010;26:427-33.
11Farronato G, Maspero C, Farronato D. Orthodontic movement of a dilacerated maxillary incisor in mixed dentition treatment. Dent Traumatol 2009;25:451-6.
12Pavlidis D, Daratsianos N, Jäger A. Treatment of an impacted dilacerated maxillary central incisor. Am J Orthod Dentofacial Orthop 2011;139:378-87.
13Lin YT. Treatment of an impacted dilacerated maxillary central incisor. Am J Orthod Dentofacial Orthop 1999;115:406-9.
14Cozza P, Marino A, Condo R. Orthodontic treatment of an impacted dilacerated maxillary incisor: A case report. J Clin Pediatr Dent 2005;30:93-7.
15Kuvvetli SS, Seymen F, Gencay K. Management of an unerupted dilacerated maxillary central incisor: A case report. Dent Traumatol 2007;23:257-61.
16Yeung KH, Cheung RC, Tsang MM. Compound odontoma associated with an unerupted and dilacerated maxillary primary central incisor in a young patient. Int J Paediatr Dent 2003;13:208-12.
17Iwaya S, Ikawa M, Kubota M. Revascularization of an immature permanent tooth with apical periodontitis and sinus tract. Dent Traumatol 2001;17:185-7.
18Weisleder R, Benitez CR. Maturogenesis: Is it a new concept? J Endod 2003;29:776-8.
19Banchs F, Trope M. Revascularization of immature permanent teeth with apical periodontitis: New treatment protocol? J Endod 2004;30:196-200.
20Huang GT. A paradigm shift in endodontic management of immature teeth: Conservation of stem cells for regeneration. J Dent 2008;36:379-86.
21Hoshino E, Kurihara-Ando N, Sato I, Uematsu H, Sato M, Kota K, et al. In-vitro antibacterial susceptibility of bacteria taken from infected root dentine to a mixture of ciprofloxacin, metronidazole and minocycline. Int Endod J 1996;29:125-30.
22Thibodeau B, Trope M. Pulp revascularization of necrotic infected immature permanent tooth: Case report and review of the literature. Pediatr Dent 2007;29:47-50.
23Jung IY, Lee SJ, Hargreaves KM. Biologically based treatment of immature permanent teeth with pulpal necrosis: A case series. J Endod 2008;34:876-87.
24Kim S, Kim J, Song JS, Choi HJ, Choi BJ, Kim SO. Continued root development of a surgically repositioned human incisor tooth germ. Oral Surg Oral Med Oral Pathol Oral Radiol 2013;115:e11-5.
25Skoglund A, Tronstad L, Wallenius K. A microangiographic study of vascular changes in replanted and autotransplanted teeth of young dogs. Oral Surg Oral Med Oral Pathol 1978;45:17-28.
26Duell RC. Conservative endodontic treatment of the open apex in three dimensions. Dent Clin North Am 1973;17:125-34.
27Kling M, Cvek M, Mejare I. Rate and predictability of pulp revascularization in therapeutically reimplanted permanent incisors. Endod Dent Traumatol 1986;2:83-9.
28Chueh LH, Huang GT. Immature teeth with periradicular periodontitis or abscess undergoing apexogenesis: A paradigm shift. J Endod 2006;32:1205-13.
29Murray PE, Garcia-Godoy F, Hargreaves KM. Regenerative endodontics: A review of current status and a call for action. J Endod 2007;33:377-90.
30Ding RY, Cheung GS, Chen J, Yin XZ, Wang QQ, Zhang CF. Pulp revascularization of immature teeth with apical periodontitis: A clinical study. J Endod 2009;35:745-9.
31Sato T, Hoshino E, Uematsu H, Noda T. In vitro antimicrobial susceptibility to combinations of drugs on bacteria from carious and endodontic lesions of human deciduous teeth. Oral Microbiol Immunol 1993;8:172-6.
32Andreasen JO, Farik B, Munksgaard EC. Long-term calcium hydroxide as a root canal dressing may increase the risk of root fracture. Dent Traumatol 2002;18:134-7.
33Rosenberg B, Murray PE, Namerow K. The effect of calcium hydroxide root filling on dentin fracture strength. Dent Traumatol 2007;23:26-9.
34Lacci KM, Dardik A. Platelet-rich-plasma: Support for its use in wound healing. Yale J Biol Med 2010;83:1-9.
35Huang GT, Sonoyama W, Liu Y, Liu H, Wang S, Shi S. The hidden treasure in apical papilla: The potential role in pulp/dentin regeneration and bioroot engineering. J Endod 2008;34:645-51.