PEDIATRIC DENTISTRY/Copyright @1986 byThe American Academy of Pediatric Dentistry

Volume 8 Number 1

External resorption in an unerupted second permanentmolar: case report

William K. Duncan, DDS, MEd Mark L. Helpin, DMDJames E. Fleming, DMD Bruce P. McCoy, DMD

AbstractThe literature on radiolucent lesions in unerupted

permanent teeth is reviewed with particular attention toetiology. A case is presented which demonstrates severecoronal destruction of a mandibular second permanentmolar. Histological evidence also is presented to confirmdiagnosis of external resorption. Based on previousliterature and the results of this case, the authorsconclude that there are apparently 2 types of radiolucentlesions affecting unerupted permanent teeth.

There is a process of resorption which can affect

the coronal portion of unerupted permanent pre-molars and molars. When detected on radiographs,it initially presents a radioIucency which suggestsdental caries. This process, if undetected, can be dev-astating to the developing permanent tooth.

Literature Review

The literature includes many reports of resorptionof an unerupted tooth and a number of terms havebeen used to describe the process.l-s In 1941 Skillendescribed what he called "intra-follicular caries.’’1

Muhler referred to the condition as "dental caries ofpermanent teeth in situ" or "preeruptive caries", 2 aterm which was used frequently. The term caries dentiprofunda cum origine incognita was used by Woodenand Kufti~ec.3 More recent literature has labeled thesedefects as "lesions resembling caries", "caries-like re-sorption", or "dentin radiolucencies.’’4-7

Much of the confusion about the terminology ofthe lesion stems from its uncertain etiology. Preerup-tive radiolucent lesions of the coronal portion of une-

rupted permanent teeth have been attributed to acarious process, internal or external resorption, or adevelopmental inclusion or defect. The first reportsinvolved unerupted premolars. This led to the pos-tulation that these defects were actually a form ofdental caries initiated by chronic periapical inflam-mation associated with primary molars2 or by an an-achoretic effect through imperfectly formed dentinaltubules. 3

Kronfeld believed that histological examination ofthese lesions would reveal osteoclasts and Howship’slacunae,s These findings then would establish re-sorption rather than caries as the process involved.6,8

Skillen reported that microscopic examination of anunerupted third molar did, in fact, demonstrate os-teoclasts along surface lamellae in areas of cavita-tion. 1 Mueller, in 1980, stated that he believed theprocess involved was external resorption, althoughhe thought the etiology was not as important as ar-resting the process and providing pulpal protection.5

Skaff and Dilzell stated that it was impossible to con-clude without histological evidence whether the de-fects were caries or a form of resorption.4

The most recent theory proposed for these radiol-ucent lesions is one postulating developmental ori-gin. Walton originally proposed a developmentaltheory based on the histological examination of ma-terial excavated from teeth of 2 patients. 6 This ex-amination revealed necrotic connective tissue andnumerous globular fragments resembling dystrophiccalcification. He stated that this process probably rep-resented the developmental inclusion of uncalcifiedenamel matrix which later became necrotic. He fur-ther suggested that these lesions would not increasein size before eruption. The histological examination

PEDIATRIC DENTISTRY: March 1986/Vol. 8 No. 1 45

of one tooth also revealed the presence of bacteriathroughout the lesion, a condition he attributed tocontamination during the operative procedure.

Giunta and Kaplan7 presented an even strongercase for a developmental theory because they wereable to extract the involved teeth for orthodontic pur-poses and submit the entire tooth for histological ex-amination. They refuted the resorptive process theorybased on finding no lacunae or scalloped border andno evidence of reparative dentin. Their histology didreveal necrotic material suggestive of early dentin andenamel matrix overlying the defect. They concludedthat the lesion was not an inclusion of the enamelmatrix, but rather a developmental hypoplastic lesionof both dentin and enamel.

Case ReportA six-year-old Caucasian male presented for rou-

tine dental treatment. Medical and dental historieswere unremarkable and routine treatment was rec-ommended at that time. The oral examination re-vealed hard tissues, soft tissues, and occlusion withinnormal limits. Bite-wing radiographs (Fig 1) were un-remarkable. The patient received routine preventivecare and was placed on recall. He was seen periodi-cally for the next 4 years for bite-wing radiographs,sealants, and other preventive procedures when anoral examination revealed the mandibular left per-manent second molar erupting through soft tissuewith an apparent enamel defect. A panoramic radio-graph with 4 periapical radiographs were taken. Theperiapical radiographs of the mandibular right andmaxillary left and right posterior areas revealed nor-mal condition. The panagraph and mandibular left

posterior periapical radiograph revealed severe de-struction of the coronal portion of the erupting per-manent second molar (Figs 2, 3). No history of painor traumatic injury was revealed. After discoveringthis lesion, the previous bite-wing radiographs werereexamined. No part of the lesion in question couldbe seen on these radiographs.

Consultations regarding treatment alternatives wereobtained with the departments of endodontics, pros-thodontics, and orthodontics. Although heroic effortsmay have saved this tooth, it was decided in con-junction with the parent that the tooth be removed.Inferior alveolar block with buccal infiltration anes-thesia was obtained. A 0.5 cm buccal flap was madeto expose the crown and the tooth was sectioned inthe furcation area. Several small pieces of the crownand mesial and distal root sections then were deliv-ered atraumatically. All portions of the tooth wereplaced in sterile water and subsequently submittedfor histological examination. The area was irrigatedand cleaned and silk sutures placed. Seven days later,healing had progressed and the sutures were re-moved.

Histological FindingsHistological examination revealed a decalcified

specimen consisting of a vital molar. The tooth wascomposed chiefly of dentin which exhibited regularlydistributed dentinal tubules. The radicular portion ofthe tooth was covered by a uniform, thin layer ofcementum. The pulp chamber and canals containedessentially normal pulpal tissue. The pulpal tissuesupported a peripheral-most layer of odontoblastswhich were oriented perpendicular to the inner wallsof the pulp chamber and pulpal canals. No evidenceof inflammation was noted within the pulpal tissue.The coronal dentin exhibited a front of active resorp-

FIG 1. Bite-wing radiographs.FIG 2. Panoramic radiograph.FIG 3. Mandibular left posterior periapical radiograph.

46 EXTERNAL RESORPTION/UNERUPTED TEETH: Duncan et al.

tion. The front was perpendicular to the long axis ofthe tooth and advancing in a pulpal direction. Alongthis plane, multinucleated giant cells resided withinHowship's lacunae-like areas (Fig 4). These cells weretherefore interpreted as odontoclasts. In some areas,these resorptive foci exhibited evidence of osteoden-tin repair.

Discussion

It would appear from the histological evidence pre-sented in this and previous reports1-3-7-8 that thereare 2 etiologies causing radiolucent defects in une-rupted permanent teeth, one being a resorptive processand the other a developmental defect.

The authors agree with Kronfeld that caries cannotoccur in the unerupted tooth,8 but that it could be acomplicating factor posteruptively. This conclusion issupported by the histology findings presented. Therewas no pulpal inflammation seen in the tooth in thisreport and no bacteria were seen in dentin tubules,which is typical of the caries process.

A form of resorption is the likely etiology for manyof the reports in the literature and certainly for thecase presented here. This conclusion is based on thehistological finding of odontoclasts, lacunae, and os-teodentin repair. The histology described in the de-velopmental theory (dystrophic calcification andnecrotic enamel matrix) was not observed. In con-junction with the histological differences between aresorptive and a developmental lesion is the inherentclinical course of the lesion. Giunta and Kaplan7

radiographically observed a defect for 2 years. Duringthis time the defect appeared to remain unchanged

FIG 4. Multinucleated giant cells in lacunae along the front ofresorption (H & E stain 200x).

in size. The process of resorpion is innately an in-vasive one. The lesion described in the present reportwas quite large at the time of its discovery. Althoughthe authors have no corroboration, they assume thislesion started incipiently and progressed to its finalsize.

After concluding that the present case was resorp-tive in etiology, the question of whether the processwas internal or external resorption remained. Internalresorption initiates in the pulp of the crown or rootand progresses toward the external surfaces of thetooth. Initial evidence of internal resorption seen onradiographs is usually limited to the root.9 Althoughthe etiology may not be known, the process of inter-nal resorption almost always is associated with aninflammatory hyperplasia of the pulp and most oftenthe tooth is nonvital9-10 External resorption affectsthe crown of the unerupted tooth, frequently with asmall opening through the enamel with gross cavi-tation of the underlying dentin.1-2-4-8-10 Pulpal tissuesusually are not involved due to the deposition of sec-ondary dentin.10 In the present report, the resorptionwas located coronally and progressed toward the pulp.The pulp was vital and not associated with the re-sorption front. Therefore, the diagnosis of externalresorption was made.

Dr. Fleming is in private practice in Jackson, Mississippi; Drs. Dun-can and Helpin are associate professors, Dept, of Pediatric Den-tistry; and Dr. McCoy is an instructor, Dept, of Oral Pathology/Oral Radiology, University of Mississippi School of Dentistry. Re-print requests should be sent to: Dr. William K. Duncan, Dept, ofPediatric Dentistry, University of Mississippi School of Dentistry,2500 N. State St., Jackson, MS 39216.

1. Skillen WG: So-called "inrra-follicular caries." Ill Dent J 10:307-8, 337, 1941.

2. Muhler JC: The effect of apical inflammation of the primaryteeth on dental caries in the permanent teeth. J Dent Child24:209-10. 1957.

3. Wooden EE, Kuftinec MM: Decay of unerupted premolar.Oral Surg 38:491-92, 1974.

4. Skaff DM, Dilzell WW: Lesions resembling caries in une-rupted teeth. Oral Surg 45:643-46, 1978.

5. Mueller BH, Lichty GC, Tallerico ME, Bugg JL: "Caries-like"resorption of unerupted permanent teeth. J Pedod 4:166-72,1980.

6. Walton JL: Dentin radiolucencies in unerupted teeth: reportof two cases. J Dent Child 47:183-86, 1980.

7. Giunta JL, Kaplan MA: "Caries-like" dentin radiolucency ofunerupted permanent tooth from developmental defects. JPedod 1:249-55, 1981.

8. Kronfeld R: Histopathology of the Teeth and Their Surround-ing Structures. Philadelphia; Lea & Febiger, 1955 pp 283-84.

9. Ashrafi MH, Sadeghi EM: Idiopathic multiple internal resor-pion: report of a case. J Dent Child 47:196-99, 1980.

10. Sullivan HR, Jolly M: Idiopathic resorption. Aust Dent J 2:193-99, 1957.

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