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Pre-eruptive intracoronal resorption

Published: July 2013

Bulletin #24 July 2013

Pre-eruptive intracoronal resorption

In the March 2013 bulletin #20, I described the phenomenon of Invasive Cervical Root Resorption (ICRR) as a pathologic condition which is rapidly progressive and which, by the time it is recognized clinically, will usually result in extraction of the affected tooth. I pointed out that ICRR in an impacted tooth is a potent cause of failure to bring about resolution of the impaction and it is rarely diagnosed until investigation is under way to find out why the adjacent anchor teeth are all intruding and an open bite developing. To add to the confusion, ICRR is almost completely unrecognized by orthodontists and, until this year,1 totally absent from the orthodontic literature. As a distinct entity, it was brought to the notice of the dental profession by Heithersay only in 1999 and, while endodontists and dental traumatologists will find numerous articles on the subject in their specialist journals, orthodontists are completely ignorant of it and its clinical implications.

ICRR is frequently associated with a history of trauma to the affected tooth. It seems that the resorptive process begins at a pin-point site on the cervical area of the root, immediately beneath the gingival attachment, due to minute gaps in the protecting cementum layer covering the root surface. It then proceeds into the body of the root, extending both coronally and apically and also circum-pulpally, although it seems never to penetrate the pre-dentine layer, presumably due to its high organic content. Accordingly, it does not enter the pulp, at least not until very late in the progress of the lesion. Whether due to this or due to the fact that the process is non-inflammatory, the lesion is entirely silent, causing no pulpal inflammation and consequently no pain. With the passage of time during the resorption process, bone is deposited in the resorbing area and it is probably this or, perhaps, the loss of the integrity of the PDL in the immediate area, which makes the tooth resistant to orthodontic movement. This is regardless of whether the tooth is unerupted or fully erupted in the mouth.

Because the disease process is nourished by the blood supply of the periodontal ligament and not from the dental pulp, it can only be arrested by sealing it off from the PDL. By doing so, the clastic cells that comprise the mush within the lesion will die. Since this mush is definitely not dental caries, there is no concern that the resorption will continue. Accordingly, there is absolutely no merit in meticulously cleaning out the cavity, particularly when the area is difficult to access, as with an impacted tooth. Only enough diseased material to enable the sealing should be removed in the first instance, to arrest the resorption and to effectively release the tooth to move/erupt in response to the application of traditional orthodontic forces. The decision to restore the tooth and its lost tissue may be made at a much later and more convenient time and circumstance.

Pre-eruptive intracoronal resorption

This July 2013 bulletin focuses on another clinical pathologic resorptive condition which appears to be closely related to ICRR, insofar as it involves the resorption of dentine by the tissues (Fig. 1a, b). Here, however, the resorption occurs within the crown of an unerupted tooth, within a complete and unblemished dental follicle, does not extend into the root of the tooth until the crown is totally destroyed.2-4 Furthermore, the eruption mechanism of these teeth appears to be intact. 

Case 1:  A 10 year old boy


Fig. 1a. Partial panoramic view of the mandibular left side.

Fig. 1b. Annotations directly of the film point to a crown resorption lesion in an unerupted second molar, whose portal of entry was in the depth of the occlusal pit and has radiated downward into the dentine of the crown, in the 3 planes of space. Note the predentine bridge inhibiting the advance of the resorption process into the pulp.

Amelogenesis of the developing tooth within its crypt is responsible for the shape of the tooth and is characterized by the formation of cusps, pits and fissures. Sometimes, crevices, folds and pits on the occlusal or dens in dente on the palatal aspect of an incisor and, occasionally, a cusp tip or an incisal edge, may developmentally lack its protective enamel cover. This may have been the result of the presence of a minute gap in the integrity of the inner enamel epithelium, from which amelogenesis is initiated. This means that in these microscopically small areas, the outer surface of the crown is comprised of exposed dentine and, thus, becomes a high risk site for the development of early caries, within a short time after the tooth erupts. Pits and fissures are particularly prone and much of preventive pediatric dentistry is concerned with avoiding this eventuality.

In the pre-eruptive stage and while still hermetically sealed off within its protective dental follicle, the presence of these minute gaps in enamel formation also make the tooth vulnerable to the initiation of a resorptive process, which is very much akin to ICRR that occurs in the subgingival area at the unexposed neck of the tooth. The intracoronal resorption process attacks the unprotected dentine at this tiny site and devours its way into the crown of the tooth in a 3-dimensional front, undermining the enamel and gathering momentum as it goes. Accordingly the picture seen on a 2-dimensional plane film radiograph is of a semilunar radiolucency with its point of entry as the epicenter, although it is in fact a hemispherical lesion in 3-D (Fig. 1).

It is similar to ICRR in that the process is nourished from within the dental follicle and not from the dental pulp. The progress of the lesion is stopped short of the pulp by the predentine layer and it has no relation to caries. The resorptive process rapidly progresses through the dentine, but will only resorb the enamel more slowly and, therefore, much later, presumably due to its very much higher calcified structure. When the tooth erupts or when its crown is exposed surgically, the lesion loses its nutrient supply line and its vital elements necrose, to leave a similarly inert and dead mush within the crown of the tooth. Of itself, the dead mush is harmless, except that it may later be secondarily affected by dental caries. For this reason it needs to be treated soon after eruption and it is probably sufficient to use a composite fissure sealant, without the need to prepare the cavity or excavate the mush in any other way. This may offend the sensitivities of the pediatric dentist, but it should be remembered that complete excavation of the resorbed area may require widely opening the occlusal or other surface of the tooth and could well risk accidental pulp exposure – particularly given the extent of some of these incursions and the broad pulp chamber that is characteristic of a recently erupted tooth.

There is no evidence to assume that pre-eruptive intracoronal resorption has any adverse effect on the normal eruption mechanism and, indeed there are cases in which an effete lesion will only be discovered many months or years after the tooth has erupted ……………….. and be misdiagnosed as caries!

Four cases are presented here to illustrate some of the degrees of variation and extent of these lesions in different teeth.

Case 2: An 18 year old girl

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Fig. 2a. The initial periapical view of a dilacerate impacted central incisor, with a dark radiolucent shadow at the incisal edge.

Fig. 2b. In the panoramic view, the circumscribed appearance of the lesion can be more clearly seen.


Fig. 3a, b. In the 3-D screenshots from the cone beam CT, the surface outline of the anomaly on the crown surface can be seen.


Fig. 4. Consecutive transaxial cuts in the antero-posterior plane show the depth to which the resorption process has burrowed into the crown of the tooth.

Case 3:  A 12 year old boy


Fig. 5a, b. A normally developing dentition with the affected canine and its antimere in similar stages of development and eruption. The resorption process presumably began at a pin point location on the extreme tip of the cusp, undermining and resorbing the enamel although to a lesser extent than the dentine.


Fig. 6a. At exposure, it was revealed that the crown of the tooth comprised only the cervical half of the enamel wall which was extremely thin and unsupported by dentine.

Fig. 6b. An eyelet was bonded to the thin enamel wall at the time and ligated with a twisted steel ligature.

Fig. 6c. The occlusal view shows the mush within the hollowed out crown. This mush was left undisturbed and sequestrated from its lifeline to wither. At the same time, its presence within the cavity served to protect the exposed dentine beneath from thermal and tactile stimuli.


Fig. 7a,b.The flap was replaced and tightly sutured to cover the tooth as much as possible, with the expectation that it might nevertheless be quite sensitive to temperature extremes. At the same time, an auxiliary 0.014” stainless steel archwire, carrying a vertically directed “swinging gate” configuration in the canine area, was ligated in “piggy-back” fashion over the main arch.

Fig. 7c, d. The “swinging gate” raised in the lingual direction and ensnared by the twisted steel ligature attached to the canine eyelet. This produced a very light, wide ranging and efficient extrusive force on the canine.


Fig. 8a, b. 3 weeks later, the tooth had erupted, with the intra-coronal resorption mush still present and little or no sensitivity of the tooth to hot or cold.


Fig. 9a-d. The post-treatment outcome with a provisional composite restoration replacing most of the crown of the tooth.


Fig. 10. A periapical radiograph of the completed root canal treatment. Although the tooth was vital, there was inadequate tooth material available to support a permanent restoration and the root canal treatment was performed electively to facilitate a later post and crown restoration.

Case 4:  A 12 year old girl


Fig. 11. The initial panoramic view showing several missing teeth, in the late mixed dentition. There is a mandibular soldered lingual arch in place to maintain arch length. Both maxillary canines are unerupted with similarly developed root lengths. The eruptive state of the right canine is marginally more advanced, possibly as the result of having more space available to it. The left canine crown (arrow) is almost totally resorbed, with only thin slivers of enamel shell remaining.


Fig. 12. A series of 8 transaxial cuts through the affected tooth shows the complete destruction of the crown of the tooth, with the enamel as the last element to disappear. There is no resorption of the dentine/predentine immediately surrounding the pulp, which appears normal. The tooth is non-symptomatic and periapical pathology is notably absent.


Fig. 13. A similar series of axial cuts made (a) immediately apical to the lesion, (b) through the area of the lesion and (c) through the resorbed crown field, with only a thin enamel wall to partially outline the original circumference of the tooth. In particular, (b) shows the enamel perimeter and the unresorbed coronal dentine surrounding the pulp. The intervening black radio-opaque area shows the pattern of the circumpulpal resorption. This case is presented by courtesy of Dr. Miri Yisraeli-Shalish and Dr. Nimrod Dykstein, supervisors of graduate student Dr. Ioannis Zogakis.


1. Becker A, Abramovitz I, Chaushu S. Failure of treatment of impacted canines associated with invasive cervical root resorption. Angle Orthod. 2013 Jan 23. [Epub ahead of print]

2. Holan G, Eidelman E, Mass E. Pre-eruption coronal resorption of permanent teeth: report of 3 cases and their treatments. Journal of Pediatric Dentistry, 1994,16:373-377.

3. Davidovich E, Kreiner B, Peretz B. Treatment of Severe Pre-eruptive Intracoronal Resorption of a Permanent Second Molar. Journal of Pediatric Dentistry, 2005;27:74-77.

4. Rankow H, Croll TP, Miller AS Preeruptive Idiopathic Coronal Resorption of Permanent Teeth in Children. Journal of Endodontics , 1986;12:36-39.