Abstract
For the last 70 years, the phenomenon of pre-eruptive intracoronal resorption (PIR) has been described in the literature, including a number of case reports illustrating the challenges clinicians face in diagnosing and managing these resorptive defects. Pre-eruptively affected teeth can be difficult to access and posteruptively they are difficult to diagnose because the defects resemble caries. Many times, these defects are not detected until after eruption, when the majority are diagnosed as dental decay and teeth are often subjected to surgical tooth restoration. The purposes of this paper are to report a case of nonprogressive PIR that was detected early, treated with a preventive glass ionomer sealant, and monitored for 44 months, and to propose an alternative approach to management of nonprogressive defects that may help preserve tooth structure.
Keywords: TOOTH ABNORMALITIES, PRE-ERUPTIVE CORONAL RESORPTION, PREVENTIVE DENTISTRY
Pre-eruptive intracoronal resorption (PIR) is a resorptive defect, often well-defined, located in dentin just beneath the dentinoenamel junction in the occlusal surface of the crown. Although these radiolucencies resemble caries and may occasionally be referred to as ‘pre-eruptive caries’, they are unlikely to be infected with cariogenic microorganisms, as the teeth are completely encased in their crypt.1 However, soon after eruption, microorganisms can enter through an exterior opening and decay is likely to superimpose the resorptive defect.2 Posteruptively, these defects are radiographically indistinguishable from caries1,3,4 and subsequently, the teeth are often subjected to surgical tooth restoration.
Intracoronal dentin radiolucencies in erupted teeth with apparently intact enamel are sometimes referred to as ‘hidden’ or ‘occult’ caries because clinically the occlusal surface appears intact and the lesion or defect can only be detected radiographically. Dentinal caries is capable of developing even where the enamel defect is too small to detect clinically.3,5 Diagnosis is difficult, as these dentin radiolucencies may represent fissure caries, PIR, or PIR with caries superimposed. It has been suggested that at least half of all occult caries lesions originate as PIR.1 Despite knowing that an occult lesion began as a PIR, diagnosis cannot be made with certainty and these lesions are often presumed to be carious and treated as such.
PIR has been reported as having a subject prevalence of three percent to six percent and a tooth prevalence of 0.5 percent to two percent, depending on the tooth type and the type of radiograph utilized for detection.1,4,6 One study (using bitewing radiographs), however, reported a subject prevalence as high as approximately 27 percent.7 They are most often found on either the permanent mandibular first molar or the permanent maxillary first molar1,4,6 but have also been reported in premolars and canines.1–4,6–12 The prevalence for the primary dentition is unknown. No association has been found between pre-eruptive intracoronal defects and race, gender, medical conditions, systemic factors, or fluoride supplementation.1,4,6,13 Current clinical and histological evidence support the hypothesis that these defects are acquired as a result of coronal resorption.1–4,6,7,9–16 Histologically, the soft tissue from a pre-eruptive lesion often reveals resorptive cells such as osteoclasts and macrophages situated in the scalloped margins of the lesion.1,2,4,7,10–15 It is thought that these resorptive cells originating from the surrounding bone, may enter the dentin through a break in the reduced enamel epithelium, poorly coalesced enamel fissures, or cementoenamel junction.1,2,5–10,16
Clinical management of PIR is based largely on the extent of the defect at the time of detection and the anticipated eruption time of the affected tooth.4,6 It is also important to consider the progressive nature of the defect, patient compliance, and caries risk. In unerupted teeth with extensive or rapidly progressing lesions, surgical exposure of the crown and immediate intervention may be necessary to avoid pulpal involvement.1,6,11,14 Some defects may undergo rapid progression without any warning signs and may only be diagnosed after collapse or large destruction of the crown.7,9,10 However, many lesions may enlarge only minimally while in the pre-eruptive state; hence, it may be possible to wait for the tooth to erupt before restoring it.1 Moskovitz and Holan15 reported a nonprogressive lesion that remained unchanged dimensionally for nearly seven years. McEntire et al.12 suggested that, for some small lesions, clinicians may choose to closely monitor them and restore the tooth if progression is noted.
The purposes of this paper are to report a case of nonprogressive PIR that was detected early, and to propose an alternative approach to management of nonprogressive defects that may help preserve tooth structure.
CASE REPORT
A four-year, three-month-old female patient presented for a dental examination and prophylaxis at a private practice. Her medical and dental histories were unremarkable. Beginning at two years old, she had been seen every six months for an oral examination, prophylaxis, fluoride treatment, and oral hygiene instruction. No clinical caries had ever been diagnosed, and there was no history of restorative treatment. A caries risk assessment indicated that the patient was at low risk. At four years, three months old, four periapical digital radiographs were obtained that revealed normal bone level and no interproximal caries. However, the unerupted permanent mandibular right first molar showed a well-defined, cup-shaped radiolucency adjacent to the dentinoenamel junction and located proximally to the center of the crown. The enamel appeared intact and of normal thickness and radiopacity (Figure 1A–B). As this tooth was in a pre-eruptive stage in a patient with no caries history, the radiolucent lesion was diagnosed as PIR. A decision was made to monitor the lesion, allow for further eruption, and re-evaluate in six months.
Figure 1.
(A) Periapical radiograph (arrow indicating lesion), and (B) intraoral photo taken at the initial visit, (C) periapical radiograph, and (D) clinical photo taken at the six-month follow-up.
At the six-month follow-up (Figure 1C–D), a periapical radiograph revealed neither progression nor any apparent change from the initial radiograph. The decision was made to surgically expose the tooth and examine the integrity of the dental enamel. In case the enamel was breached, a swab sample of the lesion would be collected for histological and molecular-microbiological investigation in an attempt to characterize the content of the lesion. Although it was highly unlikely that cariogenic microorganisms would be found in the unerupted tooth, such speculation should be confirmed. On the other hand, if the enamel was found to be intact, a glass ionomer (GI) sealant [(GC Fuji Triage), GC America, Alsip, Ill., USA] would be placed and monitoring of the tooth would continue. GI was selected because, compared to resin-based sealants, it is less sensitive to moisture, sets fast, releases fluoride, and requires none or minimal surface preparation (i.e. surface conditioning).
The patient returned for surgical exposure of the tooth in question, and a presurgical radiograph was obtained at the 11-month follow-up (Figure 2A). The area was prepared by deplaquing the adjacent erupted tooth and using a chlorhexidine (CHX) rinse. Although rubber dam isolation was not an option, as the tooth was still unerupted, appropriate measures were taken to achieve the best isolation possible. The procedure was performed by a pediatric dentist in a private practice setting using 40 percent nitrous oxide and 60 percent oxygen and 1.6 cc of four percent Septocaine® with 1:100,000 epinephrine (Novocol Pharmaceutical of Canada, Inc., Cambridge, Ontario, Canada) administered to the right inferior alveolar and long buccal nerves to achieve block anesthesia. After surgical exposure, a thorough visual and careful tactile evaluation with a sterile explorer was conducted. Independent evaluations by two dentists found the enamel surface ostensibly intact. The enamel appeared normal in color and texture. There were no enamel defects or hypoplasia. The pits and fissures were unmarred, and no clinical signs of caries were detected (Figure 2B). As planned, the tooth was cleansed with CHX, rinsed, dried and a GI sealant was applied to prevent potential ingress of cariogenic bacteria into susceptible pits and fissures. The nitrous oxide was turned off and 100 percent oxygen was administered for five minutes. Postsurgical radiographic and photographic images were obtained (Figure 2C–D).
Figure 2.
(A) Periapical radiograph and (B) intraoral photo at the time of surgical exposure; (C) periapical radiograph; and (D) clinical photo after GC Fuji Triage placement.
Eight weeks following surgery and sealant placement, the tissues and continued tooth eruption were within normal limits. Minor loss of sealant integrity and staining were noted at the mesial and distal margins (Figure 3A). To maintain the best possible seal, repair of the sealant was performed under cotton roll and dry angle isolation. The specific areas of the occlusal surface were microetched with sodium bicarbonate, rinsed thoroughly, and dried. GI was placed on the mesial and distal aspects of the existing sealant. A postoperative periapical radiograph was obtained (Figure 3B). A routine dental examination, prophylaxis, and radiographs two months later revealed no caries. The tooth appeared clinically and radiographically unremarkable, and the PIR defect showed no signs of change (Figure 3C–D).
Figure 3.
(A) Intraoral photo, and (B) periapical radiograph taken at the 13-month follow-up; (C) intraoral photo; and (D) periapical radiograph taken at the 15-month follow-up.
During the 20-month follow-up visit, a periapical radiograph and clinical evaluation of the tooth revealed no noticeable changes in the PIR defect, normal eruption into occlusion, an intact sealant, and no signs of caries (Figure 4).
Figure 4.
Periapical radiograph taken at the 20-month follow-up.
The patient returned for a routine examination 30 months after diagnosis. The GI sealant on the tooth showed some signs of wear. There was loss of sealant material at the margins with some staining, but clinically the tooth was free of caries (Figure 5A). Radiographically, the dimension of the PIR defect remained stable. However, the base of the defect appeared more radiopaque than previous radiographs, suggesting reparative dentin formation (Figure 5B).
Figure 5.
(A) Intraoral photo; (B) periapical radiograph; (C) weak, stained margins were removed; (D) Consepsis scrub applied, and (E) repaired sealant at the 30-month follow-up; (F) Periapical radiograph taken at 35 months; (G) clinical photo, and (H) periapical radiograph taken at the 44-month follow-up.
The GI sealant was repaired by isolating the tooth with cotton rolls and dry angles. The margins of the sealant were removed with a sterile one-half round bur. No clinical caries was detected (Figure 5C). Consepsis scrub (Ultradent Products Inc, South Jordan, Utah, USA) was used to disinfect the tooth surface (Figure 5D). The tooth was thoroughly rinsed, dried and re-isolated before the sealant was placed (Figure 5E).
At 35 months, the clinical and radiographic appearance of the PIR defect remained the same. The sealant was intact, and there was no change in the size of the defect. The patient remained caries-free (Figure 5F). At 44 months, the sealant remained intact, the radiograph continued to show no change regarding the PIR defect (Figure 5G), and the patient continued to be caries-free (Figure 5H).
DISCUSSION
This case report details the 44-month management and follow-up of a single tooth diagnosed with PIR. The management option employed demonstrated a proactive approach to minimize the risk of caries invasion and allow for stabilization of the existing pre-eruptive defect. When a clinician decides to monitor such a defect rather than treat it surgically, the placement of a sealant to protect the affected tooth from developing caries while it is being monitored is a logical approach.
It is well known that PIR defects are susceptible to post-eruptive bacterial colonization and development of caries, and it has been noted that decay is likely to superimpose on the resorptive defect soon after eruption.2–4,10,12 Application of a GI sealant helps prevent colonization of the fissure system. Even in the case of a clinically undetectable entrance to the lesion, a conventional GI sealant serves as a semipermeable membrane, delivering bioactive fluoride ions to encourage enamel and dentin remineralization.17,18
In this case, given the less-than-ideal conditions, a low-viscosity GI sealant was the most appropriate choice of material. In addition to its flowability and fluoride release, the bond of a GI sealant is moisture tolerant and, thus, provides the best possible seal in a potentially imperfect dry field.
The optimal time to place a sealant may be just prior to tooth eruption, as affected teeth are vulnerable to posteruptive microbial invasion. In this case, the surgical exposure was an appropriately timed intervention to allow sealant placement and maximize protection of the affected tooth. Additionally, surgical exposure allows for a clinical assessment of the tooth surface and, consequently, a more fully informed decision on whether to restore or monitor. It is not known if a sealant placed after surgical exposure is a more successful treatment than a sealant placed posteruptively and is, therefore, a limitation of this case study. The success of this alternative approach warrants further clinical research into optimal timing of sealant placement to achieve maximal preservation of tooth tissue.
Awareness of the PIR phenomenon, when the first set of intraoral radiographs are taken of a child with erupting dentition, may be the first step in preserving affected teeth. Clinicians should consider the progressive nature of the defect, the patient’s caries susceptibility, compliance with dental care, and the described preservative tooth management as a possible alternative to surgical tooth restoration.
ACKNOWLEDGMENTS
The authors wish to thank Dr. Megan Stowers, a pediatric dentist in private practice, West Bloomfield, Mich., USA, and Adjunct Clinical Instructor, Mott Children’s Health Center, Flint, Mich., USA, and Dr. Eduardo Bresciani, Assistant Professor, Department of Restorative Dentistry, Institute of Science and Technology, Paulista State University (UNESP), Sao Jose dos Campos, Sao Paulo, Brazil for their assistance with the literature review. We thank GC America for providing the complimentary materials used in this case.
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