Perforating internal root resorption (IRR): a closer look

Dr. Joseph Stern explores IRR from causes to treatment

Introduction

Confusion surrounding root resorption is common within the general dental community. This is likely due to the numerous subtypes — such as internal, external, cervical, and apical resorption — and the wide variety of potential causes, including trauma, pressure, infection, inflammation, and systemic factors. Much of this confusion appears to stem from the terminology used to describe the location and etiology of root resorption. This article focuses on perforating internal root resorption (IRR), exploring its causes, diagnosis, and successful nonsurgical treatment, utilizing cone beam computed tomography to assess the extent of the lesion and bioceramics to fill the defect effectively.

Root resorption: defined

Root resorption is defined as the loss of dental hard tissues as a result of clastic activities, which can occur as a pathologic or physiologic process depending on the location and timing of the resorptive process.¹ While most internal and external resorption is pathologic in nature, the resorption associated with the primary dentition is most often a normal physiologic process.² The primary theory for what initiates internal root resorption (IRR) is multinucleated giant cells located in the granulation tissue that form in response to infected coronal pulp tissue. These odontoclasts are believed to be responsible for the resorption of the lining of the pulp space.

A second theory suggests that the granulation tissue arises from the vascular system, outside of the pulp space. Damage and/or loss of the predentin and odontoblastic layer must occur prior to the resorptive process.³ Trauma is suspected as an initiating cause, possibly supported by continuous stimulation from infection. Iatrogenic causes of continued inflammatory excitation of the coronal pulp include overheating the tooth.^4-8

IRR is insidious and often progresses without symptoms. Pain and/or swelling may not occur until the process perforates the root, at which time the prognosis for a successful outcome becomes more questionable. As long as the apical portion of the pulp retains vital tissue, the resorptive process continues.

Another requirement for continued resorption is bacterial infection, as a microbial stimulus is required for the continuation of IRR.⁷ When and/if the pulp tissue becomes necrotic, before perforation, the process can be self-limiting. Usually, internal root resorption is first observed at a routine radiographic exam. Because it begins in the pulp space, the lesion is contiguous with the space. It can be confirmed if two acute-angled radiographs, taken from extreme mesial and distal positions, show no separation between the lesion and the pulp space. Cone beam computed tomography (CBCT) can help make this differential diagnosis between external and internal resorption.

Treatment protocol

Our treatment of IRR follows the standard protocol for nonsurgical endodontics. The root canal space is debrided and decontaminated to the apical constriction and, subsequently, filled. Interrupting the vital tissue pathway at the apex arrests the resorptive process. Extra care, mechanically and chemically, may be in order to remove tissue from the undercut areas that are created by the resorptive process. Creating a straight-line access to the resorptive defect is often not feasible, as this would require removal of more dentin, further weakening the root structure.

It is interesting to note that internal resorption can be perceived as a misplaced periapical lesion found inside the root canal rather than at the apex. Both are caused by the presence of bacteria and the triggering of resorptive cells. Both form in a symmetrical manner. However, the periapical lesion has surrounding vital tissue, which allows these lesions to grow in size, unlike IRR, which is self-limiting. Because active IRR requires a pulp space that is partially vital and partially necrotic, vitality testing is unreliable. One cannot be sure whether the pulp tissue at the time of diagnosis is necrotic and, therefore, the resorptive process is arrested, or vital tissue remains, and the IRR is ongoing. Regardless, if perforation has occurred, the external lesion has a life of its own, and treatment is essential.

Differential diagnosis

While external root resorption comes in many forms, such as transient surface resorption, pressure resorption, external inflammatory root resorption, invasive cervical root resorption, and replacement resorption (ankylosis), internal root resorption is uniquely different. The differential diagnosis is made by taking multiple radiographs at different angles.^9,10 Utilizing the buccal object rule, a lesion of internal origin will remain close to the canal regardless of the angle, while a lesion of external origin will move away from the canal depending on the angle of the radiograph (Figures 1A and 1B).

Additionally, with IRR, the outline of the root canal is usually distorted and appears contiguous with the resorptive defect, while with external resorption, the root canal outline appears normal and can usually be seen running through the radiolucent resorptive defect, as there remains a thin layer of dentin separating the canal from the resorptive area^9-10 (Figures 2A-2D).

The radiographic appearance of IRR is a fairly uniform radiolucent enlargement of the root canal. There would only be alveolar bone loss adjacent to the resorption if the resorption perforates into the PDL. The best and most accurate tool we have for diagnosing IRR and determining the path of the perforating lesion is cone beam computed tomography (CBCT). It is best to use a limited field of view (FOV), as opposed to the larger FOV used with other disciplines in dentistry. A smaller FOV increases image resolution, while at the same time providing a lower effective radiation dose to the patient. It is worth noting that in Case 2, one cannot visualize the resorptive defect from just looking at the periapical radiograph. It has been shown in countless studies that CBCT gives a more accurate diagnosis and better visualization of periapical pathology.^11-13

Case report 1

A 41-year-old male presented with a chief complaint of pain and swelling adjacent to tooth No. 10. The patient reported a history of trauma as a teenager, though he had not experienced issues until the recent onset of pain and swelling. Clinical examination revealed tenderness on the buccal gingiva around tooth No. 10, with sensitivity to percussion and biting. A small, fluctuant intraoral swelling was noted near the apex of tooth No. 10, and the tooth did not respond to vitality testing. Radiographic examination showed a large perforating internal resorptive defect near the apical third of the root (Figure 3A). CBCT (Veraviewepocs 3D R100; J. Morita) revealed significant alveolar bone loss adjacent to the defect, extending along the entire mesial side of the apical half of the root of tooth No.10 and reaching the root of tooth No. 9 (Figures 3B and 3C).

A diagnosis of pulpal necrosis with acute apical abscess was made. All treatment options, including extraction with replacement by an implant or bridge, were discussed. The patient, motivated to retain the tooth, opted for root canal therapy and repair of the resorptive defect. Informed consent was obtained.

First visit

The patient was anesthetized with 1.7 mL of 4% articaine with 1:100,000 epinephrine (Septocaine^®; Septodont^®, Lancaster, Pennsylvania) via labial infiltration. Rubber dam isolation was achieved, and the tooth was accessed using a No. 2 surgical length carbide round bur. Necrotic pulp was encountered. Working length was established with a Root ZX^® apex locator (Morita, Tokyo, Japan), and the canal was instrumented to a size 35 .04 Vortex Blue^® rotary file (Dentsply Tulsa Dental, Johnson City, Tennessee). Care was taken to ensure that the files passed through the resorptive defect and entered the apical portion of the canal. The canal was irrigated with 5.25% sodium hypochlorite, and the EndoActivator^® (Dentsply, Tulsa, Oklahoma) was used to sonically agitate the irrigant to promote thorough disinfection of the resorptive defect. The canal was dried with paper points, and calcium hydroxide (Ultracal™ XS, Ultradent Products Inc, South Jordan, Utah) was syringed into the canal and the defect. The tooth was then temporarily restored with Cavit^® (3M ESPE, Neuss, Germany).

Second visit

Two weeks later, the patient returned for completion of the endodontic treatment, reporting that all symptoms had subsided. Clinical examination confirmed that the swelling had resolved. Calcium hydroxide was removed from the canal through instrumentation, irrigation, and activation with the EndoActivator. The canal was dried with paper points, and excess irrigant was removed using surgical suction with a micro-tip. A master gutta-percha cone was placed to the working length and confirmed with radiographic examination (Figure 3D). The canal was coated with EndoSequence^® BC (bioceramic) sealer (Brasseler USA, Savannah, Georgia) to ensure sufficient sealer filled the resorptive defect. It was then obturated with gutta percha and BC sealer using the technique of warm vertical condensation (Figure 3E). The lingual access opening was restored with TPH Spectra^® ST composite (Dentsply Sirona, Charlotte, North Carolina), and the patient was scheduled for recall to monitor healing.

At 1-year, 2-year, and 5-year recall visits, the patient was asymptomatic, and radiographs showed complete healing with full restoration of bone and lamina dura adjacent to the resorptive defect (Figures 3F and 3H). The patient expressed satisfaction with the outcome, having retained a tooth originally planned for extraction.

Case report 2

A 56-year-old male presented with a chief complaint of vague discomfort in the left mandible. The patient reported that the discomfort had been intermittent for more than 6 months but had recently worsened. Clinical examination revealed pain to percussion on tooth No. 19. No swelling was observed, and the tooth was not sensitive to palpation or biting. Radiographic and CBCT (Veraviewepocs 3D R100; J. Morita) examination revealed a crowned tooth No.19 with perforating internal root resorption near the apical end of the mesial root, accompanied by periapical pathology extending distally to involve the distal root and coronally toward the furcation (Figures 4A-4D). A diagnosis of pulpal necrosis with symptomatic apical periodontitis was made.

The prognosis for treating the tooth with root canal therapy was discussed, along with alternative options such as extraction and replacement with an implant or bridge. Due to financial constraints, the patient opted for endodontic treatment rather than extraction. It was also explained that follow-up treatment, including an apicoectomy of the mesial root, might be necessary if the lesion persists. Informed consent was obtained.

First visit

The patient was anesthetized with 1.7 mL of 3% mepivacaine (Carbocaine, Dentsply Pharmaceutical, York, Pennsylvania) via left inferior alveolar nerve block and 1.7 mL of 4% articaine with 1:100,000 epinephrine (Septocaine; Septodont, Lancaster, Pennsylvania) via buccal infiltration. After achieving rubber dam isolation, access was made through the porcelain-fused-to-metal (PFM) crown using a combination of a round diamond bur and a No. 2 surgical length carbide round bur. Necrotic pulp was encountered. Working length was established with a Root ZX apex locator (Morita, Tokyo, Japan). The canals were instrumented to a size 35 .04 Vortex Blue rotary file (Dentsply Tulsa Dental, Johnson City, Tennessee) and irrigated with 5.25% sodium hypochlorite. The EndoActivator (Dentsply, Tulsa, Oklahoma) was used to sonically agitate the irrigant to ensure thorough disinfection of the resorptive defect. The canals were dried with paper points, and calcium hydroxide (Ultracal XS, Ultradent Products Inc, South Jordan, Utah) was syringed into the canals and defect. The tooth was then temporarily restored with Cavit (3M ESPE, Neuss, Germany).

Second visit

The patient returned after 3 weeks for completion of endodontic treatment. He reported that all symptoms had subsided. Calcium hydroxide was removed from the canals with instrumentation, irrigation, and activation with the EndoActivator. The canals were dried with paper points, and excess irrigant was removed using a surgical suction with a micro-tip. The canals were coated with BC sealer to allow for sufficient amounts of sealer to fill the resorptive defect and were then obturated with gutta percha and BC (bioceramic) sealer using the technique of warm vertical condensation (Figure 4E). The occlusal access opening was restored with TPH Spectra ST composite (Dentsply Sirona, Charlotte, North Carolina), and the patient was put on a recall schedule to monitor healing. The patient returned at the 16-month point for endodontic treatment of tooth No. 18. At a 16-month recall visit, the patient was completely asymptomatic on tooth No.19. And radiographic/CBCT examination revealed complete healing of the lesion adjacent to the resorptive defect on tooth No. 19 (Figures 4F and 4G). At the 3-year recall, the patient was asymptomatic on both teeth Nos.18 and 19.

Conclusion

Two cases of extensive perforating internal root resorption (IRR) successfully treated nonsurgically are presented. A discussion of the biologic process of IRR, combined with the importance of accurate diagnosis, underscores that a nonsurgical approach should be the primary treatment plan in such cases. The advent of bioceramic sealers has enabled a more standardized and effective endodontic approach for managing perforating internal resorption. Additionally, the use of CBCT during the diagnostic planning phase is crucial for accurately visualizing the full extent of the lesion.

A version of this article appeared in New York State Dental Journal.