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Case report: Idiopathic pre-eruptive coronal resorption of a maxillary permanent canine.


Idiopathic coronal resorption of a tooth prior to eruption into the oral cavity resembles a carious lesion in appearance. Therefore, it is easily misdiagnosed. Pre-eruptive resorptive lesions often remain unobserved because they cannot be detected until the tooth has erupted [Brooks, 1988]. Hence, clinical identification of idiopathic coronal resorption has been difficult. Thus, radiographic records are useful to provide an accurate diagnosis of pre-eruptive lesions during a routine recall visit. However, pre-eruptive intra-coronal radiolucencies are characteristically noted as accidental findings on radiographs of unerupted teeth, where they frequently appear as distinct radiolucencies within the coronal dentine, immediately adjacent to the amelodentinal junction. Therefore, the radiological appearance of external resorption of a crown has to be distinguished from pre-eruptive radiolucent lesions such as caries, internal resorption and hypoplasia [Wood and Crozier, 1985; Rankow et al., 1986; Brooks, 1988].

The reported prevalence of affected subjects is between 1.56% and 27.3% and tooth prevalence is 0.5% to 2.1%. [Seow et al., 1999a and b; Nik and Rahman, 2003; Ozden and Acikgoz, 2009]. Usually, a single tooth is affected in an individual but two or more lesions have also been reported [Seow, 1998]. Most of these lesions have been found in the permanent dentition; however, the occurrences of these lesions in the primary dentition [Seow and Hackley, 1996] and an association with supernumerary teeth [Ozden and Acikgoz, 2009] have also been reported in the literature. In the permanent dentition the most commonly involved teeth have been the mandibular first permanent molars, followed by the maxillary first permanent molars, the mandibular second premolars, and then the mandibular second permanent molars. In one study it has been reported that 106 (46.9%) of 226 unerupted and impacted teeth with coronal resorption were maxillary permanent canines [Stafne and Slocumb, 1944]. These results were based on subjects of various ages.

Coronal resorption is manifested histologically by degeneration of the enamel and dentine of the coronal portion of the tooth, which is ultimately replaced by vascular connective tissue it occurs because of a defect in the enamel organ of an unerupted tooth [Stafne and Austin, 1945; Blackwood, 1958; Owens et al., 1988]. The irregular resorption begins in localised areas of the enamel and subsequently involves the dentine of the unerupted tooth. These features were considered to describe an external resorptive process [Blackwood, 1958]. Intra-coronal or internal resorptive lesions appear radiographically as a well-circumscribed radiolucency in dentine [Luten, 1958; Seow, 1998; Nik and Rahman, 2003] and from histological findings they resemble globular fragments of dystrophic calcifications, remnants of necrotic dentine and aggregates of pre-collagenous fibres [Walton, 1980].

Seow and her co-workers [1999 a and b] speculated that resorptive cells from the surrounding bone get into the dentine through a breach in the external covering of the developing tooth. The majority of previous studies [Stafne and Austin, 1945; Browne, 1954; Blackwood, 1958; Luten, 1958; Grundy et al., 1984; Brooks, 1988; Owens et al., 1988] have supported the hypothesis that pre-eruptive lesions are resorptive in nature. However, the aetiology of this condition remains unclear; although several hypotheses [Skillen, 1941; Blackwood, 1958; Browne, 1954; Kronfeld, 1955; Muhler, 1957; Luten, 1958; Wooden and Kuftinee, 1974; Walton, 1980; Giunta and Kaplan, 1981; Grundy et al., 1984; Brooks, 1988; Ignelzi et al., 1990; Holan et al., 1994; Seddon et al., 1996; Seow et al., 1999 a and b] have been proposed, see Table 2. The purpose of this report is to describe an erupted right maxillary permanent canine with pre-eruptive coronal resorption with an emphasis on the initial clinical management.





Case report

An orthodontic consultant referred a 13 years 7 months old Caucasian male because of gingival hyperplasia associated with his maxillary right canine tooth. A review of the patient's previous medical history indicated that he was healthy except that he suffered from hay fever and asthma.

Examination. Clinically, his oral hygiene was satisfactory and there was a soft tissue overgrowth between his maxillary right lateral incisor and first premolar. Enamel fragments were embedded in a pedunculated soft tissue overgrowth of normal to slightly erythematous colour (Fig. 1). It was apparent that the enamel and dentine of the canine had been almost totally resorbed (Fig. 1). A periapical radiograph (Fig. 2) showed no evidence of a retained primary canine. While a panoramic radiograph (Fig. 3), which had been taken about a year previously, revealed a coronal radiolucency resembling a carious lesion on the permanent canine with evidence of a retained primary canine.


Following excisional biopsy under local analgesia, the histopathological examination of the soft tissue specimen from the crown was reported to be consistent with granulation tissue. A hard tissue fragment of dentine was colonised by a large aggregate of actinomyces like filamentous bacteria and neutrophilic infiltrates, intermixed with scanty inflamed granulation tissue and stratified squamous mucosa. There was evidence of polypoid squamous mucosa with a mildly hyperplastic epithelium. There was no evidence of dysplasia or malignancy. The overall features were said to be consistent with dental caries. The clinical and radiographic features plus the histopathological findings led to a diagnosis of idiopathic pre-eruptive coronal resorption.

Treatment objectives were devised so as to improve the aesthetics, prevent further loss of tooth structure, maintain the space and improve the periodontal health. As part of the treatment plan, the alternatives were explained to the child and his parents. These included monitoring any further eruption; retain alveolar bone height and width for placement of an implant in the future, or space closure with an orthodontic fixed appliance if the root needed to be extracted. After considering all of the treatment options, a mutual decision was made to monitor the tooth for up to 12 months; the parents understood that this would temporarily compromise the aesthetics in the anterior region.


During the follow-up period there has been no evidence of a sinus, or abscess clinically and no periapical pathology was found on any radiographs. However, after 18 months there was evidence of a sinus in relation to tooth 13, a periapical radiograph revealed an apical radiolucency (Fig. 4). As a consequence of the periapical infection, the prognosis of tooth 13 was considered to be poor even though the resorptive process had apparently ceased. Furthermore, the loss of bone and the chronic infection would be likely to compromise the success of any future implant. Therefore tooth 13 will only be retained whilst orthodontic treatment planning is being conducted, it should then be extracted as part of a long-term orthodontic treatment plan. This information was conveyed to the parents who favoured this approach.


The coronal enamel and dentine resorption defect was evident radiographically before exfoliation of the primary canine (Fig. 3). In spite of the radiolucent area being identified preeruptively no active treatment could have knowingly been proposed. It has been reported that in unerupted teeth the resorptive process commences adjacent to the defective enamel epithelium [Blackwood, 1958], and progresses in an irregular manner from an isolated area within the enamel and subsequently continues to progress towards the dentine. Eventually, in order for complete crown resorption, the connective tissue has to be in direct contact with the enamel and maintain a vascular communication with the peripheral vessels. It has been reported that the tooth structure destroyed by this resorptive process is usually replaced by bone [Brooks, 1988]. The internal resorption begins at the junction of the pulp and dentine, and is at the expense of the dentine and so results in widening of the pulp chamber [Skillen, 1941; Browne, 1954; Muhler, 1957; Blackwood, 1958; Wooden and Kuftinee, 1974; Grundy et al., 1984; Brooks, 1988; Seddon et al., 1996; Seow et al., 1999 a and b; Nik and Rahman, 2003]. Lesions of intra-coronal resorption may appear radiographically to be similar to external resorption, which is commonly found in chronically unerupted or impacted teeth [Stafne and Austin, 1945].

The histopathological examination revealed that the soft tissue taken from this erupted tooth consisted of granulation tissue with bacterial invasion, while there could have been post-eruption contamination; such an appearance suggests that the histopathological appearance represents a carious lesion that occurred post-eruptively [Walton, 1980]. Brooks [1988] reported that long-term inflammation of the primary teeth might induce granulation tissue proliferation and an osteoclastic response. Furthermore, it is thought that this kind of resorptive process does not apply to the type of resorption found in permanent molars, because they do not have a primary predecessor similarly it does not apply to any permanent tooth in patients who have hypodontia where the primary predecessor is congenitally missing. This phenomenon may explain the different prevalence figures for the different tooth types. Nevertheless, Kronfeld [1955] gave an opinion that caries could not occur prior to eruption of a tooth.

Several previous studies have reported that the pre-eruptive lesions are resorptive in nature [Browne, 1954; Luten, 1958; Blackwood, 1958; Wooden and Kuftinee, 1974; Walton, 1980; Grundy et al., 1984; Brooks, 1988; Owens et al., 1988; Ignelzi et al., 1990]. The clinical management depends on the extensiveness of the lesions. The greater the extent of a lesion the more rapid will be the rate of resorption. Progressive resorption leads to loss of the protective epithelium so that there is an invasion of connective tissue into the enamel and dentine [Blackwood, 1958].

In the past the treatment recommended for an unerupted tooth was surgical exposure by removing the overlying soft tissue and curettage of the defects followed by lining with calcium hydroxide and restoration [Sullivan and Jolly, 1957; Wood and Crozier, 1985]. Multiple treatment options were considered and explained to the parents of the child reported herein, these included to monitor without any treatment and accept compromising the aesthetics, endodontic treatment followed by a post and core supported restoration; decoronisation of the tooth; and extraction followed by a resin bonded bridge as a temporary measure and to consider implants in the future. The parents were reluctant to have the tooth treated; they wanted it to be retained. Clinically it was considered impractical to retain the root because of the apparently progressive nature of the lesion; this further eliminated the option of extruding the remaining portion of the root prior to placement of a post-retained restoration. The basic principle behind the provision of treatment was that the prognosis of the tooth had to be good enough to retain the tooth for life and to avoid extraction of a sound tooth if space was required for orthodontic therapy. More recently it has been suggested that for the more progressive lesion, it is important to conserve the tooth by surgical exposure [Dowling et al., 1999]. Alternatively, if the lesion is thought to be slowly progressive, it should be allowed to erupt and then treatment can be commenced immediately upon eruption.


Teeth affected by idiopathic pre-eruptive coronal resorption can be retained if the problem is intercepted at an early stage and appropriate restorative procedures are performed. It is prudent to make an early diagnosis of the condition and to formulate short and long-term treatment plans, which may involve keeping the affected tooth to retain the alveolar bone height and width to allow for the option of planning an implant.


Blackwood HJJ. Resorption of enamel and dentine in the unerupted tooth. Oral Surg Oral Med Oral Pathol 1958; 11: 79-85.

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N.M. Manan, Paediatric Dentistry and Orthodontics Dept., Faculty of Dentistry, University of Malaya, Kuala Lumpur, Malaysia;

S.K. Mallineni, Paediatric Dentistry, Faculty of Dentistry, University of Hong Kong, Hong Kong SAR, China;

N.M. King, School of Dentistry, University of Western Australia, Australia.

Postal address: Prof. N.M. King, Paediatric Dentistry, School of Dentistry, Oral Health Centre of Western Australia, University of Western Australia, 17 Monash Avenue Nedlands, Perth, Western Australia, WA6009.

Table 1. Hypotheses for the aetiology of pre-eruptive intra-coronal
resorption reported in the literature.

Author                               Aetiological factors
Blackwood, 1958;
Brooks, 1988;
Browne, 1954;                        Internal /external resorption
Grundy et al., 1984

Giunta and Kaplan, 1981              Developmental abnormality
                                     in dentine

Holan et al., 1994                   Prolonged pre-eruptive period

Ignelzi et al., 1990; Luten, 1958    Developmental anomaly

Kronfeld, 1955                       Break down of reduced
                                     enamel epithelium

Muhler, 1957                         Apical inflammation of
                                     primary teeth

Seddon et al., 1996                  Impacted teeth

Seow et al., 1999 a and b            Ectopic position of
                                     particular tooth

Skillen, 1941; Wooden                Caries
and Kuftinee, 1974

Walton, 1980                         Developmental abnormality
                                     in enamel
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Author:Manan, N.M.; Mallineni, S.K.; King, N.M.
Publication:European Archives of Paediatric Dentistry
Article Type:Case study
Date:Apr 1, 2012
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