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CLINICIAN’S CORNER Nonsurgical management of a nonvital tooth with orthodontically induced external root resorption and extensive periapical pathology Vasudev Ballal,a Mala Kundabala,b and K. Seetharama Bhatc Manipal, Karnataka, India The purpose of this article is to report a rare case of orthodontically induced external root resorption of a maxillary left central incisor with a large periapical radiolucency; it was treated successfully with a conservative approach that included the use of calcium hydroxide. The tooth was nonvital and had grade III mobility. It was treated endodontically for 2 years with an interim filling of calcium hydroxide mixed with propylene glycol. After 2 years, the postoperative intraoral periapical radiograph showed good periapical healing with complete resolution of periapical radiolucency. There was a significant reduction in the mobility of the tooth, from grade III to grade I. (Am J Orthod Dentofacial Orthop 2008;134:149-52) O rthodontically induced inflammatory root resorption is an unfortunate consequence of orthodontic tooth movement.1 There is no single explanation why a certain tooth resorbs severely. Resorption of permanent teeth was first mentioned by Bates2 in 1856, when he stated the cause to be the traumatization of the periodontal membrane. Before the reports by Ketcham3,4 in 1927 and 1929, little attention was paid to root resorption associated with orthodontic treatment because it was considered a normal phenomenon in permanent teeth. He indicated that 21% of 500 patients whose teeth were examined radiographically after orthodontic treatment had distinct evidence of root resorption of the permanent teeth. He stated that root resorption occurred in only 1% of people who do not receive orthodontic therapy. Rudolph,5 in 1936, reported that the incidence of root resorption in permanent teeth was as high as 74% after orthodontic therapy. Based on animal experiments, Becks and Weber6 reported that the amount of resorption in permanent teeth after orthodontic treatment was not directly due to the orthodontic treatment itself but, rather, primarily to concurrent metabolic upsets. Orthodontically induced inflammatory resorption is distinct from other types of root resorption. It is an extremely complex, sterile inflammatory process, brought on by various disparate components including forces, tooth roots, bone, cells, surrounding matrix, and biological messengers.7-10 It was reported that adequate endodontic treatment can be effective on the resorption process.11 Treatment of extensive resorption can require surgical intervention, and extraction might be necessary in extreme cases.12 Various materials, including calcium hydroxide, antibiotic or corticosteroid paste, and calcitonin paste have been used to prevent or treat external root resorption.13-15 Biologically, an active material such as calcium hydroxide is effective for the treatment of external root resorption.16 It might arrest resorption and stimulate the formation of a new calcified barrier in the defect; this allows for conventional canal obturation. In this article, we describe a successful endodontic therapy that included the use of calcium hydroxide mixed with propylene glycol to treat external resorption with a large periapical radiolucency and grade III mobility of a maxillary left central incisor after orthodontic treatment. a CASE REPORT Reader, Department of Conservative Dentistry and Endodontics, Manipal College of Dental Sciences, Manipal, Karnataka, India. b Professor, Department of Conservative Dentistry and Endodontics, Manipal College of Dental Sciences, Mangalore, Karnataka, India. c Emeritus professor, Department of Conservative Dentistry and Endodontics, Manipal College of Dental Sciences, Manipal, Karnataka, India. Reprint requests to: Vasudev Ballal, Department of Conservative Dentistry and Endodontics, Manipal College of Dental Sciences, Manipal, Karnataka, India; e-mail, drballal@yahoo.com. Submitted, April 2007; revised and accepted, May 2007. 0889-5406/$34.00 Copyright © 2008 by the American Association of Orthodontists. doi:10.1016/j.ajodo.2007.05.014 A 25-year-old woman was referred to the Department of Endodontics, Manipal College of Dental Sciences, Manipal, Karnataka, India, complaining of excessive mobility of her maxillary left central incisor. She had undergone orthodontic treatment for 5 years and immediately after that observed the mobility of her tooth and was referred to the Department of Endodontics. The intraoral periapical radiograph showed extensive external root resorption with a large periapical 149 150 Ballal, Kundabala, and Bhat American Journal of Orthodontics and Dentofacial Orthopedics July 2008 Fig 2. Postoperative radiographs: A, after 2 years of treatment; B, after 2.5 years, showing complete periapical healing. Fig 1. A, Preoperative intraoral periapical radiograph of tooth 21; B, preoperative orthopentamograph. radiolucency of the maxillary left central incisor and severe vertical bone loss on its distal aspect (Fig 1, A). On vitality testing with an electric pulp tester (Parkell Electronics Division, Farmingdale, NY), the tooth responded negatively, confirming the diagnosis of nonvitality. The tooth was not tender to percussion, the surrounding hard and soft tissues were normal, and oral hygiene was fair. The tooth exhibited grade III mobility in a labiopalatal direction. The adjoining teeth, the maxillary right central incisor and left lateral incisor, responded positively to vitality testing with the electric pulp tester and were within normal vital pulp range. The panoramic radiograph showed extensive vertical and horizontal bone loss extending up to the second molar (Fig 1, B). Almost all the rest of the teeth showed apical root resorption and responded positively to vitality testing and were within the normal vital pulp range. Because the left central incisor had a negative response to vitality testing, root canal treatment was advised. The tooth was stabilized with a wire-composite splint because it had grade III mobility; a rubber dam was placed for the split-dam technique, and the access cavity was prepared. Working length was determined by using the technique of Ingle and Bakland.17 Cleaning and shaping of the root canal was done by the step-back technique. Apical enlargement of the canal was done up to International Standards Organization (ISO) size no. 35 and coronal enlargement up to ISO size no. 55 using K files (MANI, Tochigi City, Japan). The canal was irrigated with 2.5% sodium hypochlorite solution and saline solution. Calcium hydroxide powder (Ramam Research, Kolkata, India) was mixed with propylene glycol, made into a paste, and placed in the root canal as the interim filling by using a lentulo spiral. The access cavity was temporarily sealed with Cavit (3M ESPE, St Paul, Minn). The tooth was relieved from occlusion by selective grinding. The patient returned every 3 weeks, and the calcium hydroxide dressing was replaced. The response of the tooth to the endodontic treatment was assessed regularly every 3 months by intraoral periapical radiographs. Good periapical healing with an acceptable periapical stop was evident after 2 years, with new bone-like tissue formation (Fig 2, A). The canal was then irrigated with 17% aqueous solution of EDTA to remove the remnants of the calcium hydroxide, and the canal was obturated with gutta percha cones by using AH Plus sealer (Dentsply Maillefer, Ballaigues, Switzerland) with the lateral compaction and vertical condensation technique. The access cavity was then sealed with glass ionomer cement (Fuji II, GC Corporation, Tokyo, Japan), and the splint was removed. Mobility had improved from grade III to grade I. The patient was advised to return every 6 months for evaluation. A follow-up radiograph taken 2.5 years posttreatment show good healing (Fig 2, B). The rest of the teeth continued to respond positively to vitality testing, in spite of the root resorption and mild mobility. Ballal, Kundabala, and Bhat 151 American Journal of Orthodontics and Dentofacial Orthopedics Volume 134, Number 1 DISCUSSION This appears to be the first case reported in the literature of orthodontically induced inflammatory root resorption with a large periapical lesion that was treated conservatively with calcium hydroxide. The risk of severe root resorption after orthodontic treatment is much greater for the maxillary incisors.18 The reasons for root resorption after orthodontic procedures are multifactorial. One factor might be hypo-function of the teeth during normal occlusion.19 But in our patient, the tooth was functional during normal occlusion. Another important factor is the magnitude and duration of force applied. Extremely heavy forces should always be avoided because they can cause great resorptive activity.20 This might be the probable cause for the severe apical root resorption in this patient. Longer orthodontic treatment was shown to increase the incidence and extent of root resorption.8 The patient’s 5 years of orthodontic treatment might also be a cause for her extensive resorption. According to Fuss et al,21 apical root resorption is a complication of orthodontic treatment, with injury originating from the pressure applied to the roots during tooth movement. Continuous pressure stimulates clast cells in the apical third of the roots; this can lead to significant shortening of the root. Usually, teeth are vital and asymptomatic unless the pressure applied is high enough to disturb the apical blood supply. This might be the reason for the nonvitality of this patient’s tooth. The large periapical radiolucency associated with the maxillary left central incisor might be attributed to the nonvitality of the tooth. Resorption might ultimately result in loss of teeth. However, with appropriate treatment, the prognosis for these teeth can be greatly improved. Such resorption usually needs surgical or nonsurgical endodontic intervention to stop the process.12,22 However, a conservative nonsurgical procedure should be attempted before a surgical process. The need for endodontic treatment in teeth with these resorptions depends on the extent of the damage on the affected roots and pulp vitality.23 Surgical intervention was not done for this patient because she was young and had healthy periodontal apparatus. Moreover, she had good oral and general health and was cooperative at the recall visits. Resorption was successfully managed by using calcium hydroxide. Propylene glycol was used as a vehicle for the calcium hydroxide because of its sustained release effect.24 Calcium hydroxide might have activated the undifferentiated progenitor cells in the surrounding mesenchyme to undergo mitotic division and differentiation into functional types of connec- tive tissue cells. Consequently, calcific healing occurred.22 The specific mechanism of action of calcium hydroxide is still debated. Several theories have been postulated for its biologic activity. Some suggest its high alkaline pH stimulates matrix formation by the formative cells.25 Others suggest that high pH neutralizes the acidic products of the resorptive cells.26 Furthermore, calcium hydroxide promotes healing because of its antibacterial properties.27 Seltzer and Bender28 stated that calcium hydroxide might activate ATPase, which might then enhance mineralization. Heithersay29 reported high hydroxyl ion concentration could be the factor that induces calcification. In our patient, calcium hydroxide, used as interim root canal filling, arrested the resoptive process and promoted good periapical healing. The purposes of dental splinting are to stabilize the mobile tooth for as long as required, ensure that there is no further injury, and protect the attachment apparatus to allow the periodontal fibers to regenerate.30 Hence, in this patient, a splint was placed to promote periodontal healing and also to facilitate the endodontic procedure. Although there was a residual grade I mobility of the maxillary left central incisor after 2 years, the patient understood the limitations of the treatment and yet was satisfied with the outcome. The reduction in the mobility could not be assessed regularly because the tooth was splinted. Thus, we had to rely on the total resolution of the periapical pathology with the new bone-like tissue formation that took 2 years. CONCLUSIONS Orthodontists should keep track of tooth movement and pulpal status of teeth that are prone to resorption clinically and radiographically at regular intervals during tooth movement by involving an endodontist. If root resorption is detected, a decision must be made about whether to continue, modify, or discontinue treatment. REFERENCES 1. Rygh P. Orthodontic root resorption studied by electron microscopy. Angle Orthod 1997;47:1-16. 2. Bates S. Absorption. Br J Dent Sci 1856;1:256. 3. Ketcham AH. A preliminary report of an investigation of apical root resorption of permanent teeth. Int J Orthodontia 1927;13: 97-127. 4. Ketcham AH. A progress report of an investigation of apical root resorption of vital permanent teeth. Int J Orthodontia 1929;15: 310-28. 5. Rudolph CE. A comparative study in root resorption in permanent teeth. J Am Dent Assoc 1936;23:822-6. 152 Ballal, Kundabala, and Bhat 6. Becks H, Weber H. The influence of diet on the bony system with special reference to the alveolar process and the labyrinthine capsule. J Am Dent Assoc 1931;18:197. 7. Owman-Moll P, Kurol J, Lundgren D. Continuous versus interrupted orthodontic force related to early tooth movement and root resorption. Angle Orthod 1995;65:395-401. 8. Kurol J, Owman-Moll P, Lundgren D. Time-related root resorption after application of controlled continuous orthodontic force. Am J Orthod Dentofacial Orthop 1996;110:303-10. 9. Harris EF, Kineret SE, Tolley EA. 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