Coronal Resorption in Unerupted Anterior Permanent Teeth: Cases with Different Aetiologies? A Review

Case 1 and pre-eruptive intra-coronal resorption

An unerupted tooth that is not directly exposed to the oral cavity is not at risk of the usual pathological processes that result in surface demineralization. In the presence of both a caries-favouring oral environment and a non-cleansable periodontal pocket associated with an unerupted tooth, it could be argued that demineralization could take place. However, the development of primary caries in an unerupted tooth has yet to be proven.^15,18 This makes it feature quite low down on the differential diagnosis list for Case 1 (Table 1). The insidious nature of PIR reported in the literature is highly reflective of the clinical and radiographic presentation of the UR3 in Case 1. Even though PIR has largely been reported in unerupted molars and premolars, a few reports highlight that the condition does not spare impacted canines.^{10,19,26,27,28} Furthermore, PIR has been associated with anomalies in the dentition, such as hypodontia. In this case, the patient presented with an impacted UR3 and developmentally absent maxillary laterals.²⁹

During dental development, the reduced enamel epithelium covers the crown of an unerupted tooth and protects it. It also separates it from the adjacent dental follicle, which contains vascular mesodermal tissue. This epithelial layer protects the enamel of an unerupted tooth from invasion by the nearby vascular channels within the connective tissue. Blackwood suggested that a breach in the reduced enamel epithelium followed by subsequent abnormal contact of the enamel with connective tissue leads to disruption in normal crown development and is believed to be the pathogenesis behind PIR.^9,18,22

An alternative pathogenesis for PIR was described by Seow: an ectopically positioned tooth may experience heightened localized pressure against the surface of the crown, precipitating resorption to ensue. This is thought to be mediated by resorption-inducing cells entering the dentine via enamel fissures or the cemento-enamel junction.^6,7,8,23 Azaz and Shteyer speculated damage at the level of the enamel and not the cemento-enamel junction as the starting point for resorption in impacted canines.²⁸ This is possible if the protective epithelium overlying the enamel of an unerupted tooth is destroyed, possibly by a local factor which then induces an inflammatory process.¹⁹

Similar to our management in Case 1, once a coronal radiolucency lesion has been identified in an unerupted tooth, many authors have advocated surgical exposure of the affected tooth with a view to gaining faster visual access, limiting the pathological process and conserving the tooth.^{6,10,18,23,26} However, after a certain point, PIR is not a fast progressing lesion, unlike dental caries.²² Interestingly, many papers evidence a lack of progression into the pulpal chamber. Despite extensive coronal resorption seen in PIR of unerupted teeth, pulpal infection does not occur at a histological level.^{6,7,9,16,21,22}

Cases in which poor-prognosis teeth have been extracted and examined under a microscope, unanimously describe a normal layer of dentine between the pulp and the resorptive lesion, with absence of pulpal inflammation and minimal secondary dentine deposition.^{9,15,16,17, 19, 20,22,25} The histological picture of PIR is strikingly different to that of dental caries: spindle-shaped fibroblasts, multi-nucleated giant cells and vascular connective tissue occupy the resorptive lesion. The epithelium, in areas of its deficiency, is often found to be replaced by multinucleated osteocytes thought to be responsible for the resorption.^9,17,20,22 Cross-contamination with oral microflora clouds the true presentation of a PIR lesion at a cellular level.¹⁶

In contrast to extracted teeth due to PIR, many papers have shown that affected teeth are not all destined for removal and can be retained with early interception and appropriate restorative procedures.^2,4,20,25 Pulpal regenerative techniques have been employed where possible,^{5,10,13,14,15,18,20,22} with some reports of very conservative management. This includes treating relatively large molar PIR lesions as fissure caries, sealing occlusal surfaces and monitoring closely long term,²⁵ while another example includes direct pulp capping,² and indirect pulp capping and restoration.⁴ Indeed, many cases from the paediatric literature place emphasis on careful curettage and pulpotomy, with successful short-term follow ups reported in scenarios where the pulp is believed not to have been directly affected.⁴ The most common restorative treatment modality appears to be either a calcium hydroxide lining or zinc-oxide eugenol base cement followed by a definitive restoration.^2,4,9,13,20

In our case, the UR3 underwent root canal treatment by the GDP, a reasonable treatment approach towards suspected pulpal involvement in a permanent tooth in a patient who was an adult at that point. Historically, prompt endodontic treatment was advocated because lesions were usually discovered or made accessible once the radiographic coronal radiolucencies had become significantly large.^11,27 However, after a certain stage, progression can be minimal or arrest altogether.²² More recent reports have shown clinicians preferring to monitor PIR lesions for several years by adopting a protocol of delayed restorative treatment given the newly identified, slowly progressive nature.^4,25 Nonetheless, pulp regeneration is critical in teeth with immature apex formation because normal root development is desired. It can be argued that a tooth affected by PIR that achieves normal continued root development is more desirable than attempting to sustain pulp vitality in an affected tooth, particularly in the presence of hypodontia or premature loss of other teeth. Early and urgent referral by the orthodontist to a paediatric or restorative department will allow maximal chance of obtaining apexification; however, the literature seems to show that PIR-involved teeth continue to show normal and full root development.² It is worth noting that the canine and incisor described in our cases both showed completed root apexification before appearance of the coronal lesion, and referral to the GDP was deemed appropriate in Case 1.

Case 2 and invasive cervical root resorption

Both cases in this report involved impacted teeth, but it is suspected that the aetiology in Case 2 is different given the history of dental trauma. The involved tooth in Case 2 was beginning to cause intermittent pain unlike Case 1 in which the impacted UR3 remained asymptomatic despite demonstrating a larger radiolucency closer to the pulp. This suggests the pathogenic process was different in each. It could be that the UL1 had erupted more, and symptoms may have occurred as the pulpal tissue was exposed to the oral environment.

Table 2 considers possible diagnoses for Case 2, for which invasive cervical root resorption (ICRR) seems most likely. Hiethersay and Becker et al have described this form of external root resorption as rare, insidious and aggressive.^30,31 Orthodontics, closely followed by trauma were the most likely predisposing factors in the onset of ICRR.^31,32 It begins as a focal resorptive point in the cervical area under the epithelial attachment and spreads inwards to dentine both coronally and apically.^32,33 Heithersay also described a pink discolouration at the gingival margin is a tell-tell sign of ICRR.³³

Typically, it does not traverse into the pulp quickly and allows the tooth to remain asymptomatic while significant dentinal destruction takes place.³⁰ Symptoms arise only in the presence of pulpal or periodontal involvement, as seen in the female patient in Case 2.³³ The pathogenesis has been described as damage to the cementum at the cemento-enamel junction with subsequent exposure of the underlying dentine. Osteoclastic cells are signalled towards the dentine and initiate resorption.³⁰ A classification system (class I–IV) based on severity of the lesion has been described to provide a clinical guide for practitioners, serve as a research tool and to help assign either non-surgical or surgical treatment accordingly.³¹ ICRR is relatively uncommon, but is often mistaken as a form of internal root resorption when in reality it takes place external to the root surface.^10,31

It is difficult to pinpoint whether the trauma directly affected the development of the UL1 and resulted in coronal resorption, or whether it was the subsequent physical impaction of the UL1 that led to coronal resorption of the crown. The Children's Dental Health Survey 2013, revealed that 12% of 12-year olds in the UK had experienced traumatic damage to their maxillary permanent incisors by that age, reducing to a lower incidence of 10% in 15-year olds.³⁴ The likelihood of dental trauma in young people is often correlated with skeletal sagittal discrepancies, that is children with a retrognathic mandible, a class II skeletal pattern and proclined maxillary incisors.^35,36 Less commonly considered than the position of the teeth in the antero-posterior plane as a risk factor in dental trauma is the impact of a discrepancy in vertical face height.

A reduced vertical dimension may have been an important contributory factor for the prognosis of the UL1 following the trauma in Case 2. A relatively short height of the maxilla would imply that the developing UL1 was lying in relatively closer proximity to the root of the traumatized deciduous incisors within the anterior maxilla at the time of the trauma aged 4 years. Theoretically, there may have been greater chance of the developing permanent central incisor being adversely affected to a greater extent than compared to a patient with average or increased vertical dimensions.