Management of invasive cervical resorption using a surgical approach followed by an internal approach after 2 months due to pulpal involvement.

Invasive cervical resorption (ICR) is an aggressive and invasive form of external tooth resorption that commences in the cervical region which can be managed using either a nonsurgical, surgical or a combination of nonsurgical and surgical approach. The restoration of resorptive defects having a coronal and radicular extent can be challenging as a single material cannot be used to restore the entire defect. This case presented with Heithersay's Class 3 ICR lesion in tooth #12, which was managed initially using a surgical approach and restoration of ICR defect with a combination of resin modified glass ionomer cement, composite resin and mineral trioxide aggregate (MTA). However, the patient presented with pulpal symptoms 2 months later which warranted a root canal therapy. An internal approach was then used to debride and remove remnant fibro-osseous tissue. The defect was then repaired with MTA. A 1 year follow-up demonstrated adequate periapical healing and no pathologic changes around the restored resorptive defect.

INTRODUCTION

Invasive cervical resorption (ICR) is an uncommon aggressive type of external tooth resorption.[1] Though the exact etiology is not clear, it is believed that the damage to the protective cementum layer at the cervical region leads to exposure of the underlying dentine to odontoclasts.[23] Orthodontic treatment, dental trauma, intracoronal bleaching, and surgical procedures have been documented as potential predisposing factors for ICR.[3]

ICR is usually asymptomatic and is detected when the tooth displays a pink discoloration in the cervical region or on routine radiographic examination.[14] The pulp usually remains protected by a thin layer of dentine and predentine probably due to the presence of an anti-inflammatory invasion factor in predentine. The involvement of pulp occurs at a very late stage following which symptoms may ensue.[1] The predentine layer lacks arginine-glycine-aspartic acid peptides and this apparently reduces the attachment of odontoclasts, thus preventing resorption.[5] Clinically, the pink cervical discoloration is due to the highly vascular granulation tissue showing through the resorbed overlying dentine and enamel.[36] Radiographically, ICR appears as an irregular radiolucency with ragged margins or presents a “moth-eaten” image.[2] The root canal outline can usually be traced on the radiograph due to the noninvolvement of the pulp in the early stages.[3] Three-dimensional (3D) imaging techniques, like cone-beam computed tomography (CBCT), can indicate the exact extent of an ICR lesion and proximity of the lesion to the pulp space.[789] Heithersay's[10] clinical classification can act as a guide in the diagnosis of ICR lesions. Figure 1 illustrates the various treatment options for the management of ICR lesions.[2411]

Figure 1

Treatment options for management of invasive cervical resorption

This report presents a case of Class 3 ICR lesion in tooth #12 that was managed using a surgical approach followed by an internal approach, 2 months later, after the patient presented with pulpal symptoms.

CASE REPORT

A 21-year-old female patient was referred to the department of Conservative Dentistry & Endodontics due to pink discoloration seen in her maxillary right lateral incisor (tooth #12) [Figure 2a]. The medical history was noncontributory. The patient had history of orthodontic treatment about a year prior. On clinical examination, pink discoloration on the labial surface of the crown in the cervical region was seen and a “catch” was detected [Figure 2b] with subsequent bleeding. The tooth was nontender to percussion and gave a positive response to electric and thermal pulp testing. Radiographic examination showed an irregular radiolucency having a mottled appearance involving the coronal dentine and extending to the coronal third of the root [Figure 2c]. Axial CBCT (Planmeca ProMax 3D, Planmeca Oy, Helsinki, Finland) slices revealed the extent and encircling nature of the lesion [Figure 2d]. Though the lesion appeared to be in close approximation to the pulp space, some amount of intervening dentine was present. Coronal CBCT slices and 3D CBCT reconstruction images revealed compartmentalization of the lesion, with presence of bone like tissue in the lower compartment [Figure 2e–g]. The diagnosis was Heithersay's Class 3 ICR lesion. The patient was presented with two treatment options: (a) Surgical approach combined with nonsurgical internal approach which would warrant an intentional root canal therapy or (b) surgical approach only and root canal therapy in case of pulp exposure during the surgical approach or if the tooth becomes symptomatic at a later date. The patient opted for the second approach.

Figure 2

(a) The preoperative clinical view of invasive cervical resorption lesion in tooth #12, (b) a “catch” detected in the cervical region, (c) preoperative periapical radiograph, (d-g) cone beam computed tomography scan demonstrating the extent of invasive cervical resorption lesion

A full thickness labial mucoperiosteal flap was reflected following local infiltration anesthesia. Granulomatous tissue was seen involving the labial surface and part of the distoproximal surface [Figure 3a]. A small cotton pellet dipped in 90% trichloroacetic acid (TCA) was applied on the tissue with gentle pressure for 1 min [Figure 3b]. Care was taken to squeeze the excess TCA from the cotton pellet with a gauze before application to avoid contact with adjacent bone. The necrotic tissue was scooped out with the help of a discoid excavator (Acharya Instruments, Manipal, Karnataka, India) [Figure 3c]. This procedure of application of TCA and removal of necrotic tissue was carried out till a sound dentinal base was seen [Figure 3d]. The area of osseous ingrowth was left untouched and the defect was refreshed with a round bur (Maillefer, Dentsply, Switzerland). No exposure of the pulp was evident at this stage. The resorptive defect extended from the cervical one third of the crown to the cervical one third of the root, involving the distoproximal line angle, with the defect becoming shallow toward the root. A combination of resin modified glass ionomer cement (RMGIC) (Fuji II LC; GC Corporation, Tokyo, Japan), composite resin (Tetric-N-Ceram, Ivoclar Vivadent, Liechtenstein), and MTA (Angelus, Londrina, Brazil) was used to restore the defect. After obtaining moisture control with absorbable gelatin sponge (Gelfoam, Pfizer, USA), a “framework” with RMGIC was created by building the distal proximal surface and the cervical portion of the tooth, resulting in two cavities: Coronal and radicular [Figure 3e]. The axial wall of the coronal cavity was also lined with RMGIC. MTA was mixed and packed in the radicular cavity and the coronal cavity was restored with composite resin [Figure 3f]. The flap was sutured back [Figure 3g] and the patient was called for follow up after 1 week for suture removal. The postoperative radiograph revealed the nonrestored osseous compartment and an infiltrative channel present mesially alongside the canal in the coronal one third of the root [Figure 3h]. At a 1 month recall, the patient was asymptomatic and the probing depth was normal with no gingival recession. However, after 2 months, the patient presented with pain in relation to tooth #12. The tooth was sensitive to percussion and did not respond to electric and thermal pulp testing. The diagnosis was pulp necrosis with symptomatic apical periodontitis. Hence, it was decided to initiate a root canal therapy for tooth #12.

Figure 3

(a) Granulomatous tissue seen following flap reflection, (b) application of 90% trichloroacetic acid, (c) removal of necrotic tissue, (d) sound dentinal base, (e) resin modified glass ionomer cement framework, (f) restoration of radicular cavity with mineral trioxide aggregate and coronal cavity with composite resin, (g) suturing of flap, (h) immediate postoperative radiograph, (i) postoperative radiograph after obturation and sealing of invasive cervical resorption defect with mineral trioxide aggregate, (j) radiographic follow-up after 1 year

Access cavity preparation was done and the canal was negotiated. A small communication with the external root surface was probed with an endodontic explorer (DG-16, Hu-Friedy, Chicago, USA) in the cervical region with no evidence of bleeding. A long shanked endodontic excavator (31W Endo excavator, Hu-Friedy, Chicago, USA) was used to check for the presence of any granulomatous tissue. Long shank burs (Munce Discovery Burs, CJM Engineering, Inc., Santa Barbara, CA, USA) were used at slow speed in the cervical region through the access cavity, under magnification and illumination (STAC loupes ×3.5, Analytical Medical Technologies, India), for thorough debridement and removal of osseous tissue. Cleaning and shaping of the canal was carried out and calcium hydroxide (Ca-Excel, Ammdent, India) intracanal medicament was placed in the canal. Calcium hydroxide powder (Deepti Dental, India) mixed with saline, to a thick consistency was carried with an amalgam carrier (GDC, India) and packed in the cervical defect, to limit its solubility. After 1 week, calcium hydroxide was removed and root canal obturation was carried out. MTA was mixed as per the manufacturer's instructions and condensed into the resorptive defect. A moist cotton pellet was placed in the pulp chamber and the access cavity was temporized (Cavit, ESPE, Seefeld, Germany). After 48 hours, the MTA was checked for set and the access cavity was restored with composite resin (Tetric-N-Ceram, Ivoclar Vivadent, Liechtenstein). Some amount of unintentional extrusion of MTA, beyond the confines of the defect was observed [Figure 3i]. At a 1 year follow-up, clinically, the periodontal status of tooth #12 was good and probing depths were within normal limits. The follow-up radiograph [Figure 3j] showed complete periapical healing and adequate sealing of the resorptive defect with no changes in the surrounding osseous tissue. There was no progression in the extent of the infiltrative line on the mesial aspect.

DISCUSSION

Orthodontic therapy was supposedly the predisposing factor that led to the development of ICR in the present case. Excess orthodontic forces in the cervical region can cause tissue necrosis which may trigger the differentiation of odontoclasts.[10]

Class 3 ICR lesions have been treated earlier by a nonsurgical approach using 90% TCA.[2] A success rate of 77.8% was reported using this technique. Ninety percent TCA causes coagulation necrosis of the granulation tissue making it avascular, thus facilitating its removal.[11] TCA also has the potential to deactivate tissue present in infiltrative channels and recesses.[3] Surgical or a combination of surgical and nonsurgical approach can be adopted when complete nonsurgical access to the coronal one third of the root is difficult.[12]

The lower compartment of the lesion showing osseous ingrowth was left untouched and no attempt was made to remove it with the bur during the initial surgical phase of treatment, to avoid excess bone removal from the alveolar crest. The debrided resorption defect comprised a coronal and radicular portion, involving the distal proximal line angle. The choice of restoration rested between composite resin, RMGIC and MTA. Periodontal reattachment is not possible with composite resin and less likely with RMGIC, while MTA has the ability to provide a biocompatible surface.[213] However, the entire defect could not be restored with MTA due to the coronal extent of the defect and due to inability of MTA to retain in the shallow radicular portion. Hence, a combination approach was used to restore the defect. The RMGIC framework divided the defect into coronal and radicular cavities. The radicular cavity served to retain the MTA and also prevented the exposure of the MTA to the oral environment. Constant contact of the MTA with the oral environment will result in its contamination, affecting the material properties and may also promote development of sub-gingival plaque.[13] The coronal cavity was lined with RMGIC due to close proximity of the defect to the pulp, followed by a composite resin restoration. Restoration of an ICR defect with a reverse sandwich technique using a combination of composite resin and RMGIC was suggested earlier in literature with the aim of obtaining ideal mechanical and biological properties and reinforcing weakened tooth structure.[6] The present case report combined RMGIC, MTA and composite resin with an objective of utilizing the beneficial properties of each of these materials.

The following could be suggested as the reasons for nonvitality of tooth #12, 2 months later: (i) Close proximity of the defect to the pulp or (ii) continuation of the resorption process due to nonremoval of the osseous ingrowth from the lower compartment of the lesion. Heithersay recommended routine pulpectomy for Class 3 ICR lesions to permit access to the encircling resorptive tissue.[11] If treatment option “a” (surgical approach combined with nonsurgical internal approach which would warrant an intentional root canal therapy) was selected in the present case, a re-intervention could have been avoided. Some authors termed fibro-osseous ingrowth of tissue as a repair process, while others have advocated complete removal or inactivation of this fibro-osseous tissue.[114] Failure to remove this tissue might result in reoccurrence. The direct deposition of osseous tissue onto the dentine makes it difficult to differentiate it from the underlying dentine. Selective removal of the fibro-osseous tissue with minimal damage to adjacent bone and underlying dentine should be done under magnification and good illumination.[3] Long shank Munce Discovery Burs facilitated the removal of osseous tissue through the access cavity, though ease of removal could have been enhanced during the surgical approach due to better accessibility.

The present case demonstrated adequate periapical healing and no pathologic changes in the osseous tissue around the restored resorptive defect, despite the extrusion of MTA. Although extrusion of MTA beyond the confines of the root is not advocated, an unintentional minor extrusion can still permit adequate healing due to the biologic properties of MTA, eliminating the need for further intervention.[15] A further follow-up is intended in the present case to assess the long-term prognosis of the restored ICR defect.

CONCLUSION

The authors recommend the thorough removal of resorptive tissue, including any fibro-osseous tissue, while treating a Class 3 ICR lesion, to prevent reoccurrence. This may entail adopting an intentional internal approach if the lesion is very close to the pulp or adopting a surgical approach or a combination of surgical and nonsurgical approach. A combination of materials can be used to restore ICR defects which have a coronal and radicular extent. Finally, future research is needed to device biocompatible materials with adhesive, reinforcing, and esthetic properties for restoring extensive ICR defects.

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Conflicts of interest

There are no conflicts of interest.