July 2017
Volume 13, Issue 7

Peer-Reviewed

Invasive Cervical Root Resorption

An emerging diagnostic entity

Brooke Blicher, DMD | Rebekah Lucier Pryles, DMD

For many practicing clinicians, resorptive dental diseases remain complex, mysterious, and enigmatic. Historically, these conditions were presented during training as being limited to either external or internal resorption. Traditional thought dictated that internal resorption occurred in vital teeth and was related to direct pulpal trauma (Figure 1). Conversely, external resorption was thought to be limited to instances involving necrotic teeth (Figure 2); involving trauma to the periodontal ligament by external forces, pressure from erupting teeth, or developing pathology (Figure 3); or following orthodontic treatment that initiates osteoclast-mediated resorption of cementum and dentin near the apex.1 While many practitioners rely on their educational foundation alone to diagnose and treat their patients, the astute clinician scientist adapts his or her knowledge and treatment to changing evidence.

During the past 2 decades, a growing body of data describing a unique external resorptive dental disease located in the cervical area of vital teeth has been presented in the dental literature, adding a third distinct resorptive entity to our diagnostic options (Figure 4). Although the nomenclature utilized to describe this condition is often subjective to the author, the term “invasive cervical root resorption” (ICRR) will be utilized here because it is the terminology used by Dr. Geoffrey S. Heithersay, the author of the seminal literature that fostered our modern-day understanding of ICRR as a distinct diagnostic entity.2,3,4 To provide clinicians with a better understanding of this unique pathologic entity, this article will review the clinical and radiographic characteristics of ICRR as well as its etiology, pathophysiology, and treatment.

Background

Understanding ICRR’s uniqueness among other resorptive dental diseases requires a foundational understanding of resorption. Regardless of its manifestation, resorption is a loss of hard tooth structure caused by immune-mediated clastic cells. In normal conditions, the clastic behavior of these cells is prevented by the intact unmineralized layers present in both cementum and dentin. The disruption of these layers by trauma, infection, and other etiologies permits attachment of clastic cells and destruction of tooth structure.1 The cells responsible for ICRR originate from the attached, or junctional, epithelium at the base of the gingival sulcus. Given its sulcular source, these lesions are frequently noted in the cervical area of teeth. Exceptions, however, are noted in areas of attachment loss or in newly erupting teeth where the periodontal attachment is apically located (Figure 5 and Figure 6). The cells attach to tooth structure in areas of precementum loss, thereby permitting invasion of fibrovascular tissue, followed by degradation of the mineralized root structures.2 Unless prevented by epithelial downgrowth into or bacterial contamination of the defect, in later stages, some degree of osseous ingrowth from neighboring bone may occur.5 Though similar histologically to replacement resorption, wherein osseous ingrowth occurs following loss or damage to the periodontal ligament, osseous repair of ICRR is localized to the portal of entry of the resorptive lesion.5 The predentin that surrounds the pulp, like intact precementum, serves a protective role in preventing extension of the resorbing tissues directly into the pulp space until cavitation or breakdown of the predentin otherwise allows pulpal involvement.1 Consequently, ICRR lesions oftentimes encircle the pulp without direct contact and spread apically or coronally throughout the dentin.2

Etiology

Several etiologic factors have been associated with the development of ICRR; however, direct causation has yet to be proven. The most commonly reported predisposing factors include a history of orthodontic treatment, traumatic dental injuries, orthognathic surgery, periodontal treatment, intracoronal restorations, and nonvital bleaching.3 Most of these factors are thought to damage the cementum in the cervical region of the tooth by causing direct physical or chemical trauma. Oral habits involving force on the teeth, such as a history of woodwind instrument practice, might predispose a patient to the condition in a similar manner as orthodontics because the anterior maxillary teeth are subject to potentially damaging, excessive force.6 The use of systemic bisphosphonate medications has also been associated with ICRR development, including a proposed mechanism of action on clastic cells and altered bone turnover.7 In addition, a potential viral etiology has been proposed for the development of ICRR. Feline odontoclastic resorption is common in cats secondary to infection with Feline Herpesvirus 1 (FeHV-1), and it has a marked clinical resemblance to ICRR found in the human dentition. A small scale study on patients presenting with multiple ICRR lesions found that 100% of subjects tested positive for FeHV-1, suggesting a potential viral etiology of ICRR in humans.8 Lastly, a familial relationship has been reported among patients diagnosed with ICRR, indicating a genetic component is also likely.9 Like many other conditions, however, there may be some idiopathic origin to ICRR, as cases have been reported with no association to the aforementioned factors.3

Diagnosis

Most cases of ICRR are asymptomatic and clinically undetectable. Lesions are often found incidentally via routine radiographic exam, when investigating for pathology on neighboring teeth, or even when retracting the gingiva by cord placement for restorative work. When lesions are felt with the explorer, subtle cavitation or a chalky surface is generally noted just beneath the gingival margin. More progressive lesions may present with frank, often subgingival, cavitation with solid margins. These defects are often filled with soft tissue that bleeds readily upon probing. Because the predentin layer that surrounds the dental pulp prevents invasion of ICRR until the lesions have reached a very late stage, more often than not, pulp sensitivity testing remains normal, and pulpitis or necrosis is infrequently noted, even among very progressive lesions. Further symptoms of periodontal ligament inflammation, such as percussion or palpation sensitivity, and periodontal pocketing are usually absent.10

Occasionally, lesions will present in a clinically obvious manner. Figures 7 through 10 present a case where the patient noted a pink discoloration in the cervical portion of his right lateral incisor. Although pulp sensitivity was normal, a perforating lesion was found to be clinically detectable along the distofacial aspect of the tooth. While historical precedent dictates that pink teeth are an indicator of internal resorption, the majority of teeth with visible pink discoloration of the coronal tooth structure are now correctly diagnosed with ICRR.

Due to the principles of anatomic noise and the fact that two-dimensional radiographs are subject to a significant amount of overlap, routine radiographic imaging, whether by bitewing x-ray or periapical image, is oftentimes not sensitive enough to properly diagnose ICRR. Lesions are oftentimes not detectable on traditional radiography until a significant amount of mineralized tooth structure is lost. Cone-beam computed tomography (CBCT) imaging can be especially useful in the detection of pathology in the very early stage, although as the technology is not yet used as a screening tool, lesions are often imaged incidentally during treatment planning scans or investigation for other pathology. Periodontal bone breakdown is not typically present adjacent to the portal of entry of the ICRR lesion.10

When detectable radiographically, early ICRR lesions resemble Class V caries. When lesions are present on the buccal or lingual/palatal aspects of a tooth, they may overlap with the pulp chamber space on bitewing or periapical radiographs, creating an irregular shape to the pulp chamber. As ICRR develops, the lesions progress toward pulpal structures without causing direct pulp exposure. In the majority of lesions, even among those that are extensive, the para-pulpal hard tissues appear intact and a thin radiopaque line is often noted marking the border between the lesion and the pulp.2

ICRR lesions are classified according to their extent of invasion, with Class 1 lesions presenting as small and well-defined lesions localized to the cervical area of dentin only; Class 2 lesions presenting as slightly larger, but still well-defined lesions localized to the cervical area and approaching the pulp; Class 3 lesions presenting as larger and less well-defined lesions extending into the coronal third of root structure; and Class 4 lesions presenting as those that extend beyond the coronal third of the root.2 Class 1 and Class 2 lesions may present with a more well-defined radiolucency, especially when present on the mesial or distal aspect of a tooth, whereas Class 3 and Class 4 lesions tend to present with less well-defined margins and classically thin projections into root structure around the central root canal space.2 Figure 11 depicts the classification scheme.11

Treatment

ICRR research indicates that treatment of early lesions can be performed quite predictably; however, more extensive lesions may not be amenable to intervention. Treatment of the defects requires surgical exposure, debridement, treatment of the defect with trichloroacetic acid (TCA), and restorative care.4 As with any surgical care, access to the defect must be considered. For example, lesions located on the buccal roots are more accessible surgically, whereas interproximal, palatal, or lingual lesions are relatively inaccessible and therefore may not be easily and successfully treated. Application of TCA for 1 to 4 minutes removes residual clastic cells, preventing recurrence of resorption and treatment failure. TCA is extremely caustic and reactive upon contact with orofacial soft tissues, thus extreme care must be taken to avoid any spill, and a glycerol backdrop is suggested to protect the surrounding periodontium. After TCA application, the area should be rinsed with sterile water or saline and dried, then a suitable restorative material (eg, a resin-modified glass ionomer cement) should be placed to repair the defect. Depending on the location of the defect, appropriate soft tissue surgical procedures with respect to flap design and suturing should be utilized.4 Class 1 lesions are manageable without endodontic treatment, whereas Class 2 and Class 3 lesions often require root canal treatment in conjunction with the repair procedure.4

While the previously discussed techniques may effectively manage Class 1 through Class 3 lesions, this technique is not appropriate for the management of Class 4 lesions. Class 4 lesions typically have a very poor prognosis because the extent of the volume requiring removal would render a tooth non-restorable, therefore no endodontic or surgical treatment is advised.4 Empirically, these lesions can remain asymptomatic without pathologic effects on adjacent bone for many years, and perhaps even undergo some degree of osseous repair.5 Consequently, the option to follow up rather than move forward with extraction is oftentimes the most advisable course.

The location and appearance of ICRR lesions often resembles Class V caries or certain cases of perforating internal root resorption; therefore, these should be included in any differential diagnosis. The astute clinician must consider the entire clinical and radiographic picture, including potential etiologies, location, and most importantly, CBCT images to provide essential information for sifting through clinical data. ICRR lesions can be differentiated from carious lesions by the hard dental structures present, as long as a lesion that was originally ICRR has not been subject to secondary caries. Visualization of bleeding tissue during cavity preparation when a pulp exposure is not expected can be a clue that the true etiology is ICRR, and treatment should be modified accordingly to assure complete removal of any resorptive tissue by physical debridement and application of TCA. Lesions originating from internal root resorption will present with a radiographic appearance centered around the pulp space, although this can oftentimes occur in the cervical region of the tooth. Perforations in these cases will create adjacent PDL widening or bone loss that is not seen in ICRR cases.

Conclusion

ICRR is a unique diagnostic entity that is quite distinct from the traditional internal and other external varieties of root resorption. It’s unique pathophysiology makes accurate diagnosis absolutely essential for complete and successful management. Early lesions can be treated successfully by chemomechanical means, whereas late lesions oftentimes only require monitoring thanks to osseous remodeling. Modern research and technology have improved not only our understanding of ICRR, but the clinical and radiographic tools at our disposal, making it feasible for all clinicians to recognize ICRR in their practice.

References

1. Tronstad L. Root resorption—etiology, terminology and clinical manifestations. Endod Dent Traumatol. 1988;4(6):241-252.

2. Heithersay GS. Clinical, radiologic, and histopathologic features of invasive cervical resorption. Quintessence Int. 1999;30(1):27-37.

3. Heithersay GS. Invasive cervical resorption: an analysis of potential predisposing factors. Quintessence Int. 1999; 30(2):83-95.

4. Heithersay GS. Treatment of invasive cervical resorption: an analysis of results using topical application of trichloroacetic acid, curettage, and restoration. Quintessence Int. 1999;30(2):96-110.

5. Mavridou AM, Hauben E, Wevers M, Schepers E, Bergmans L, Lambrects P. Understanding external cervical resorption in vital teeth. J Endod. 2016;42(12): 1737-1751.

6. Gunst V, Huybrects B, De Almeida NA, Bergmans L, Van Meerbeek B, Lambrechts P. Playing wind instruments as a potential etiologic cofactor in external cervical resorption: 2 case reports. Int Endod J. 2011;44 (3):268-282.

7. Patel S, Saberi N. External cervical resorption associated with the use of bisphosphonates: a case series. J Endod. 2015;41(5):742-748.

8. von Arx T, Schawalder P, Ackermann M, Bosshardt DD. Human and feline invasive cervical resorptions: the missing link?—Presentation of four cases. J Endod. 2009; 35(6):904-913.

9. Neely AL, Gordon SC. A familial pattern of multiple idiopathic cervical root resorption in a father and son: a 22-year follow-up. J Periodontol. 2007;78(2): 367-371.

10. Frank AL, Torabinejad M. Diagnosis and treatment of extracanal invasive resorption. J Endod. 1998;24(7): 500-504.

11. Blicher B, Pryles RL, Lin J. Endodontics Review: A Study Guide. Chicago, IL: Quintessence; 2016.

About the Authors

Brooke Blicher, DMD
Upper Valley Endodontics, PC
White River Junction, Vermont
Assistant Clinical Professor
Department of Endodontics
Tufts University School of Dental Medicine
Boston, Massachusetts
Clinical Instructor
Department of Restorative Dentistry and Biomaterials Science
Harvard School of Dental Medicine
Boston, Massachusetts

Rebekah Lucier Pryles, DMD
Upper Valley Endodontics, PC
White River Junction, Vermont
Assistant Clinical Professor
Department of Endodontics
Tufts University School of Dental Medicine
Boston, Massachusetts

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