Case Report

Pre-eruptive resorption of dentinin the primary andpermanent dentitions:case reports and literature reviewW. Kim Seow, BDS, MDSc, DDSc, PhD, FRACDS Donna Hackley, DDS

I ntracoronal radiolucencies in unerupted teeth havebeen reported as early as 1941.1 Since then, manycase reports have appeared in the dental literature

(Table 1), although the prevalence of such defects re-main unknown. These defects, which are usually dis-covered incidentally on routine dental radiographs,2-2B

are often reported in dentin only, although in advancedcases the enamel also may be involved. The defects mayresemble dental decays‘ 7, 8,12,15 in both clinical and radio-graphic appearance, thus prompting many authors torefer to them as "pre-eruptive caries."

As shown in Table 1, the most commonly involvedteeth are the mandibular second premolars,7,1~,~7, ~9 man-dibular permanent second molars,s, 14,16,18, 20, 22-24 andthird molars,9,11, is although the mandibular permanentfirst molars1°,1s as well as mandibular caninesTM also havebeen described as teeth showing intracoronal resorp-tion. In the affected teeth, it is of interest to note thatwhile the location of the defects at the time of detectionusually is described as occlusal, radiographic examina-tion often reveals the defects to be situated mainly onthe mesial aspects of the crown in the case of the man-dibular second molars,7, s, is, 2324 and on the distal part ofthe occlusal in the case of the mandibular premolars14,24 and the permanent first molars.~°, ~s

Speculation and controversy surround the possibleetiology of these defects. As listed in Table 2, authorspropose that these defects may originate as a develop-

TABLE . CASES OF PRE-FRUPTIVF DENTIN DEFECTS

REPORTED IN THE LITERATURE

TABLI! 2. POSSIBLE I~TIOLOGY OF DENTIN DEFECTS

1. Localized developmental anomaly of dentin

2. Acquired pathology:

A. Apical inflammation of primary teeth

B. Dental caries

C. Coronal resorption

3. Resorption superimposed on existingdevelopmental anomaly

Author / Year Teeth Affected

Skillen, 1941

Goldman, 1954

Browne, 1954

Luten, 1958

Muhler, 1957

Blackwood, 1958

Wooden & Kuftinec, 1974

Skaff & Dilzell, 1978

Baddour & Tilson, 1979

Mueller et al, 1980

Walton, 1980

Nickel & Wolske, 1980

Giunta & Kaplan, 1981

Coke & Belanger, 1981

Grundy et al, 1984

Baab et al, 1984

Wood & Crozier, 1986

Rankow et al, 1986

Brooks, 1988

DeSchepper et al, 1988

Rubinstein et al, 1989

Ignelzi et al, 1990

Taylor et al, 1991

Holan et al, 1994

Seow & Hackley (present cases)

3rd Mmand

not mentioned

3rd Mmand (3 cases)

1st Mrnand1St PMmax2nd PMmax2nd Mmand

2nd PMmand

2nd Mmand (2 cases)

3rd Mmax1st PMmand

1St Mmand (2 cases)

3rd Mmand

2nd PM .... d

2nd PMmand

2nd Mmand (3 cases)

3rd Mmax1st Mma× (4 cases),

1st Mmand (7 cases)

2rid Mmand (3 cases)

2nd PMmand (2 cases)

Cmand" 2nd Mmand

2nd PMmand

2nd Mmand2nd PM~a~a

2nd Mmand

2nd MmandC~a, 2nd Mm~d’

2ndPMmand2nd Mmand2nd Mma~d (primary)

Pediatric Dentistry- 18:1, 1996 American Academy of Pediatric Dentistry 67

mental anomaly16-22 in which sections of the tooth arenot mineralized properly. Alternatively, they may beacquired after full coronal development as a result ofresorption.18'22 Etiological factors suggested in thepathogenesis of these acquired defects include apicalinflammation of primary teeth, dental caries, and coro-nal resorption. Apical inflammation of primary teethmay cause disruption of the protective dental epithe-lium of the permanent successor and allow invasion ofnormal vascular or inflammatory resorptive cells toenter the crowns of unerupted teeth. However, dentinresorption also had been reported in permanent teeththat did not have primary predecessors such as the per-manent second and third molars, hence other etiologi-cal factors are likely.

Although the dentin defects may resemble dentalcaries,5-17 little histopathological and microbiologicalevidence supports this hypothesis.22 It is likely that thebacteria found in the defects in erupted teeth in a fewreports7-"were from posteruptive colonization, and notthe cause of the lesions.

Most case reports support the hypothesis that thedefects are acquired as a result of coronal resorption.Histologic evidence for a resorptive etiology such asmultinucleated giant cells, osteoclasts, and chronic in-flammatory cells appears in several reports.h-16-20 Thetriggering factors for the resorption are unknown butare likely to be related to loss of integrity of the pro-tective reduced enamel epithelium that covers the de-veloping tooth. Although the radiographic appearanceoften suggests the areas of resorption to be localized in-ternally in dentin, the resorptive processes are likely tobe initiated externally rather than internally from thepulp for several reasons. First, in most cases, the den-tal pulps are reported to be unaffected and vital evenin the very deep defects.10-22Second, in some cases, anexternal soft tissue channel through the enamel hadbeen observed communicating with the internal den-tin defect.16 Third, overt external resorption of thecrown was observed in some cases.18

This study reports two cases of resorptive dentinaldefects, one in the primary dentition and other in thepermanent dentition. These twocases are interesting in that the firstdescribes the first reported case inthe primary dentition, and the sec-ond provides longitudinal radio-graphic evidence that the etiologyof the defect is acquired after com-plete coronal development and isnot the result of a developmentalaberration.

Case report 1: primarysecond molar

A 2 1/2-year-old white femalepresented to the emergency clinic ofChildren's Hospital, Boston with a

Fig 1. Case #1. Periapical radiographshowing a radiolucent defect in thedentin in the distal part of the occlusalof the second primary molar.

chief complaint of mandibular left facial swelling andmild fever of 2 days' duration. Her past medical his-tory was unremarkable. Her mother reported that themandibular left second primary molar had erupted 6weeks earlier, and that the surrounding soft tissues hadbeen inflamed and swollen since.

This moderately distressed child had diffuse facialswelling of approximately 3 cm diameter at the left angleof the mandible. The swelling was tender and warm topalpation, and the overlying skin appeared flushed.

Intraoral examination revealed a full, intact, normal-appearing primary dentition. No dental decay wasnoted, and the general oral hygiene was good. The gin-gival tissues surrounding the mandibular left secondprimary molar appeared severely inflamed and edema-tous. The tooth, which appeared intact, had a mobilityof 2+, and was slightly depressable. There were noclinically detectable defects on the enamel surface. Ra-diographs were not available.

The clinical impression was pericoronitis associatedwith the mandibular left second primary molar, and thepatient was placed on a course of oral Penicillin VK inconjunction with local irrigation with 50% hydrogenperoxide and warm moist packs. Five days later, theracial tenderness and erythema remained althoughthere was a reduction in the swelling. Intraorally, therewas buccal gingival swelling with apparent pocketing.The patient was continued on Penicillin VK.

The patient returned 12 days after the initial emer-gency visit. The persistence of the periodontal swell-ing and the development of a sinus tract opening onthe buccal mucosa prompted investigation of the lesionunder general anesthesia. A buccal flap raised in theregion of the mandibular primary molars revealed ex-tensive granulation tissue and a piece of bony seques-trum. A periapical radiograph (Fig 1) showed a largeradiolucent defect in dentin, and periapical radiolucen-cies around the open root apices.

The abscessed mandibular left second primary mo-lar was extracted and sent for pathological examination.Endodontic therapy was not attempted in view of theunknown etiology, which prevented a good estimate of

prognosis. Healing was uneventful.

Histopathological report

The exterior of the extractedtooth was examined under the dis-secting microscope. No obviousdefect communicating from thesurface to the interior of the toothcould be detected.

Several undecalcified sectionsprepared from the extracted sec-ond primary molar were exam-ined. Fig 2A shows a section takenfrom the center of the tooth. Exten-sive resorption of internal aspectsof the enamel and coronal and

68 American Academy ofPediatric Dentistry Pediatric Dentistry -18:1,1996

radicular dentin was observed. In some areas, the re-sorbed areas were filled in by calcified tissue resem-bling bone (Fig 2B). The pulp chamber was empty, pre-sumably as a result of abscess formation. At the distalpart of the crown, a tunnel that extended exteriorlyfrom near the cementoenamel junction and communi-cated with the pulp could have been the origin of theresorptive process. The enamel appeared normal inboth thickness and structure and no dental caries wasdetected. No communication was noted between pulpand resorption area, pulp and outer surface, or resorp-tion area and outer surface.

Case report 2: permanent second molarA healthy, 11-year-old white female was referred to

the first author by her orthodontist for management ofan intracoronal radiolucent defect on the crown of theunerupted mandibular right second permanent molar(Fig 3). The defect was discovered incidentally on apanoramic radiograph exposed for orthodontic assess-ment. As shown in Fig 3, the defect appeared to be lo-calized in the dentin on the mesial part of the crown.The root development was approximately two-thirds completed, and appeared normal. A periapicalradiograph of the tooth confirmed these findings. An-other panoramic ra-diograph exposed 28months previouslywas examined (Fig 4).No defect was evidenton the tooth at the ear-lier radiographic ex-amination.

The patient had anAngle's Class II, divi-sion 2 malocclusionwith maxillary archcrowding and trau-matic anterior deepoverbite. Other dentalanomalies had beendiagnosed earlier, in-cluding two congeni-tally missing mandibu-lar permanent incisors.Three years previ-ously, a mesiodens be-tween the maxillary in-cisors had beensurgically removed,along with a severelyankylosed maxillaryright second primarymolar associated witha deviated premolar. Aband-loop space main-tainer was inserted.

In view of the miss-

ing mandibular incisors, it was decided to preserve themandibular permanent second molar. Under generalanesthesia, a mucosal flap was raised, and theunerupted tooth exposed. When the intact enamel onthe mesial occlusal surface was removed, a large defectfilled with soft pink tissue was observed in the dentin.This tissue was removed by gentle curettage to reachthe floor of the cavity, which contained hard dentin. Nopulpal exposures were noted. The cavity was lined witha calcium hydroxide base and the defect was restoredwith glass ionomer cement. Because of the relativelydeep location of the unerupted tooth to the occlusalplane, the tooth was re-covered with the mucosal flapfor spontaneous eruption. The soft tissue fragmentswere removed from within the cavity, and soft tissuesections around the developing tooth were sent for his-tological examination.

Healing was uneventful, and the tooth eruptedthrough the mucosa approximately 9 months after thesurgery. It appeared normal in color, the restoration wasintact, and the tooth responded vital to hot and cold.Periapical radiographs showed close proximity of thefloor of the lesion to the pulp and normal root devel-opment. The tooth was followed over the next 2 yearsuntil full occlusal contact was achieved. All clinical and

Fig 2A. Case #1. Undecalcified mesiodistalsection of the second primary molar takenfrom approximately the center of the tooth.Extensive resorption of dentin was evident.In some areas, the resorbed areas were filledin by calcified tissue resembling bone (seeFig 2B). At the distal part of the crown, atunnel (arrowed) which extended exteriorlyfrom near the cementoenamel junction andcommunicated with the pulp may be theorigin of the resorptive process.

Fig 2B. Higher magnification (originalmagnification 75x) of boxed area in 2A,showing areas of bone replacement (arrow)in some resorbed parts of dentin.E: enamel D: dentin

Pediatric Dentistry - 18:1,1996 American Academy of Pediatric Dentistry 69

Fig 3. Case #2. Panoramic radiograph of 11-year-old female showing radiolucentdefect in the mesial part of the crown of the unerupted and partially developedright permanent second molar. A small notch (arrowed) on the mesial occlusal, justmesial to the mesial cusp tip may be discerned on the crown of the permanentsecond molar, and may represent the portal of entry of resorptive tissue. However,a similar notch is also evident on the contralateral tooth, which is normal. Thepatient also had two congenitally missing permanent mandibular incisors.

Fig 4. Case #2. Panoramic radiograph of the patient taken 28 months previous tothat in Fig 2. The crown of the right permanent second molar was fully formedwith no evidence of any defect. The patient had a mesiodens supernumerary,which was removed a year previously. The extracted maxillary right secondprimary molar had severely ankylosed. There was congenital absence of twomandibular permanent incisors.

radiographic features (Fig 5) indicated normal pulpvitality and occlusal function.

Histopathological report

Sections of the soft tissues surrounding theunerupted tooth showed normal dental follicle. Thesoft tissue fragments taken from dentinal defectshowed uninflamed, loosely textured connective tissuecontaining nonproliferating nests of odontogenic epi-thelium, and lined on the inner aspect by a discontinu-ous, reduced enamel epithelium.

Discussion

Intracoronal defects ofunerupted teeth present chal-lenging problems of diagnosisand management. All previouscases have been described in thepermanent dentition. To the au-thors' knowledge, this reportdemonstrates the first case inthe primary dentition. The lackof diagnosis and reporting inthe primary dentition may bedue to the fact that routine ra-diographs in a young child areusually not attempted until ap-proximately 4-5 years of age. Bythis time, many defects that hadoriginated during the pre-erup-tive stages may have becomeindistinguishable from dentalcaries and usually are diag-nosed as such.

In this report, an affectedprimary molar presenting as anacute dental abscess suggeststhat internal noncarious defectsalways should be included inthe differential diagnosis of anabscess of unknown etiology. Itis most likely that in this case,the etiology of the defect is den-tin resorption, as demonstratedby the histopathological exami-nation of the tooth. However, alocalized developmental aberra-tion of dentin cannot be ruledout entirely. While the resorp-tion of the crown and partial re-pair by bone deposition hadprogressed over a relativelylong period of time, pulpal in-fection probably did not occuruntil after eruption when thetooth became exposed to theoral microflora.

In the case involving the per-manent second molar, radiographs suggested the den-tin defect was not present when the dental crown wascompletely formed, thus providing longitudinal evi-dence that the defect was acquired. To the authors'knowledge, this case is also the first in the literatureshowing such evidence.

The infection of the pulp in the first case and thepresence of soft tissue in the resorptive area in the sec-ond case indicate that communicating channel(s) be-tween the exterior, resorptive areas, and pulp werepresent, although these could not be identified readily

70 American Academy of Pediatric Dentistry Pediatric Dentistry - 18:1,1996

Fig 5. Case #2. Periapical radiograph of the second rightpermanent molar 2 years after surgical exposure andcurettage of the dentin defect. The tooth had erupted intofull occlusion, and root development had continuednormally. The pulp had remained vital.

even in histological sections. A break in the protec-tive external covering of the developing tooth crownmay allow resorptive cells to enter through these chan-nels to initiate the dentin resorption. Enamel, beingmuch harder than dentin, usually is not resorbed untilthe later stages.

In the second case, recognition that the dentindefect was resorptive in origin implied that it was likelyto be progressive and therefore necessary to control theprocess as soon as possible. Curettage of the defect, andfilling it with calcium hydroxide and restorative mate-rial were effective in preventing further resorptionuntil eruption. This method of management, which isachieved by either exposing or re-covering theunerupted tooth after restoration, is generally recom-mended for most cases as soon the defect is diagnosedradiographically.8-18-22 Waiting until full emergenceof the crown to achieve curettage may allow theresorption to extend to the pulp with complicationsfrom infection.

Dr. Seow is Associate Professor in Pediatric Dentistry, Universityof Queensland Dental School, Brisbane, Australia, and VisitingProfessor, Harvard School of Dental Medicine and Children'sHospital, Boston, Massachusetts. Dr. Hackley is Resident, Depart-ment of Dentistry, Children's Hospital, Boston.

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2. Goldman HM. Spontaneous intermittent resorption ofteeth. JADA 49:522-32, 1954.

3. Browne WG: A histopathological study of resorption insome unerupted teeth. Dent Record 74:190-96, 1954.

4. Muhler JC: The effect of apical inflammation of the primaryteeth on dental caries in the permanent teeth. J Den Children24:209-10,1957.

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9. Baddour HM, Tilson HB: A carious impacted third molar.Oral Surg 48:490,1979.

10. WaltonJL. Dentin radiolucencies in unerupted teeth: reportof two cases. ASDC J Dent Child 47:183-86, 1980.

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Pediatric Dentistry -18:1, 1996 American Academy of Pediatric Dentistry 71