NEWSLETTERS

After completion of Orthodontic Treatment - a "pink" maxillary central incisor

Published: December 2014

Bulletin #39 – December 2014

After completion of Orthodontic Treatment - a "pink" maxillary central incisor

An orthodontic colleague and former student of mine received a call from a dentist regarding a young female patient whose orthodontic treatment he had successfully completed a year earlier. The treatment had involved the extraction of 4 premolar teeth and, because of poor cooperation, it had taken 4 years to complete. There were no apparent complications and all seemed well.

Now, at age 17, a specialist endodontist has advised the extraction of the patient’s vital left maxillary central incisor tooth.

sss.Fig. 1 jpg_1

Fig. 1. Intraoral views of the patient at 1 year post-orthodontic treatment. The arrows point to the affect tooth and clearly show the pink discoloration and gingival inflammation.


The reason for the harsh verdict was that the tooth had become discolored, with a pink area in the labial cervical region (Fig. 1), which had just been diagnosed as extensive invasive cervical root resorption (ICRR).1-5 The pink hue seen in the cervical area showing through the enamel, in this patient, is due to the blood vessels within the lesion and thus appears similar to the pink hue seen in a resorbing deciduous tooth which is due to shed naturally. The tooth was otherwise symptomless, although there was some inflammation of its labial and distal gingiva.

sss.Fig. 2 ceph and pan_1

Fig. 2. The pre-treatment lateral cephalogram and panoramic view of the patient.

My orthodontic colleague was most distressed at hearing the disturbing news and immediately sought out the patient’s records to see if there were any clues of the initiation of the condition that could have been detected during the active orthodontic treatment. He examined the initial pre-treatment clinical photographs and radiographs (Fig. 2). Mid-treatment radiographs had not been elicited and, at the end of the treatment, the patient had failed to attend the session which had been planned for acquiring the final photographic and radiographic records. From the history of the patient, recorded before the commencement of treatment, it had been noted that the child had received a severe blow to the front of the mouth some years earlier, but no further details were remembered and neither had any treatment been instituted.

sss.Fig._3_pre_tx_p.a

Fig. 3. The pre-treatment periapical view of the anterior teeth shows no sign of pathology.

Figure 3 shows a pre-treatment periapical view of the maxillary anterior region, which shows nothing untoward in the outline and texture of the left central incisor. With the benefit now of “20:20 hindsight”, a case could be made for the distal shadow at the CEJ being considered a very early ICRR lesion, but it can be more strongly argued that this is typical interproximal radiographic “burnout”. In stark contrast, the new periapical radiograph (Fig. 4a) shows a very broad and long radiolucent area, with a “woolly” appearance in the distal two-thirds of the tooth in the cervical region, extending to the middle of its crown and to a considerable way down the root. A gap in the integrity of the mesial outline of the tooth in the CEJ area can be seen (arrow), presumably signifying the portal of entry of the initial resorptive lesion into the body of the tooth.

sss._Fig._4

Fig. 4a. The periapical radiograph showing the wide extent of the ICRR lesion and its “woolly” appearance. Note also the presence of a normal lamina dura and the absence of periapical pathology.

Fig. 4b. The extracted tooth and the pink spot excavated by the dentist, to show the severely undermining ICRR process extending down the root and into the crown. It is surprising that the tooth did not fracture during the extraction procedure

ICRR is a phenomenon that seems to be largely unknown within the orthodontic profession, because it is not seen frequently and is often confused with ankylosis, because it too will not permit the affected tooth to respond to orthodontic forces. Occurrence of the condition in an impacted tooth is characterized by non-response of the tooth to extrusive mechanics. In an erupted tooth with ICRR, one may witness a failure for passive eruption and, thus, the tooth becomes progressively infraoccluded in relation to the adjacent teeth. This did not occur in this particular patient because of the presence of a premolar-premolar lingual bonded twistflex wire splint.

From the radiograph (Fig. 4a), it was concluded that the lesion was very extensive, affecting a large portion of the middle section of the crown and the root, to a level apical to the crestal bone. Since the lesion would not now permit the tooth to respond to orthodontic extrusion (forced eruption) it was effectively declared unrestorable and this was the basis on which the decision of the endodontist to extract the tooth was made.

sss.Fig._6_Maryland

Fig. 5. The root of the ICRR-affected incisor was amputated, the pulp chamber filled with composite material and the restored crown bonded to the two adjacent teeth as an immediate and temporary rehabilitation expedient.

The dentist extracted the tooth and was more than curious as to the character and extent of the ICRR lesion. Accordingly, he took the extracted tooth, identified the lesion in the mid-labial cervical area of the root and proceeded to carefully open the undermined enamel in the cervical area of the crown of the tooth, where it displayed the large crater that had been burrowed into it by the resorptive process (Fig. 4b). Subsequently, he sectioned of the root portion and restored the crown with composite material, before bonding it to the two adjacent incisors, as a temporary Maryland bridge (Fig. 5).

The question arises as to whether there were alternative treatment options available for this patient, aside from extraction. Was the patient’s right maxillary central incisor doomed once the identity of the lesion and its extent had been determined?

In his series of articles published in 1999, Heithersay6, 7 noted that there is an increased prevalence of ICRR in patients who have had orthodontic treatment. This is by no means the only cause and he listed other associated etiologic factors, including trauma. The ICRR lesion itself is initiated at the external surface of the cervical area of the root of a tooth and its nutritional lifeline is from the periodontal membrane surrounding the tooth. It derives no nourishment from the pulp. As such, Heithersay considered that an appropriate treatment would be to orthodontically extrude the tooth to thus erupt the sub-gingival portal of entry out of the gingival tissues and into the oral cavity. In this way, the lesion would be effectively separated from its supply line (the PDL) and the resorptive cells would die. He suggested that the tooth could then be treated endodontically and an appropriate restoration made to replace the missing tooth structure.

There is unfortunately a flaw in this line of thought. The ICRR-affected tooth is prevented from responding to the extrusive orthodontic force by the resorptive process itself and, probably, by the bony tissue that is usually laid down in the lesion, in and around the resorption lacunae.8-10

On the other hand, if the specific area of the portal of entry of the lesion can be identified and accessed surgically with a periodontal flap, then the affected root surface may be minimally excavated and sealed with a glass ionomer or other cement. This needs to be done without any attempt made to remove all the mush. On the contrary, relating to the mush as if it were dental caries will inevitably result in iatrogenic pulp exposure and this would necessitate immediate root treatment. The reason the tooth is entirely asymptomatic is that the resorptive process is sterile, it stops short at the predentine line and continues on to encircle but not to penetrate the pulp. It seems that the resorptive process is prevented from advancing by the higher organic content of the predentine layer.10 There is therefore no pulpal inflammation, no pain, no stimulus to form secondary dentine and no direct justification for the initiation of emergency endodontic treatment.

With the integrity of the root surface restored by placement of the glass ionomer cement, the tooth is no longer restrained from responding to orthodontic extrusive force and an appropriate appliance placed on the teeth will then generate the needed movement and will be able to quickly bring the restored area of root to the surface. Extrusion should continue until the affected area of root is entirely supragingival and the tooth should then be prepared for crowning. It will therefore be obvious that this line of treatment can only be considered viable if the lesion is not too extensive,

Without doubt in the more advanced instances of invasive cervical root resorption, an elective root canal treatment will often need to be performed with the aim of providing adequate retention for the final crown and always assuming that the ICRR has left sufficient healthy root length to support the restoration.

One is permitted to wonder whether the orthodontist was responsible for the initiation of the ICRR lesion; whether ICRR is recognized by orthodontists for the progressive pathologic entity that it is and whether the profession-at-large is aware of the implications of the diagnosis. The fact that orthodontic treatment had been performed on the patient does not, of itself, mean that the treatment was the trigger that initiated the lesion. It is far more likely that trauma was the cause, as noted above. It should be recognized that trauma to the front teeth in a young child, whether during play, a fall, a fight at school, or other similar events, is a common occurrence. By and large, it is mild and forgotten by the next day ………. and consequently may be conspicuously absent from the patient’s history. The absence of any follow-up radiographs during the period of treatment, in a patient with a history of trauma and whose treatment is unnecessarily long, is a cause for concern.

ICRR is a condition that is seen routinely in endodontic practice and it must be assumed that an endodontist is aware of its implications regarding the prognosis of the tooth2-7. There can be little doubt that this is why this particular endodontist advised its extraction. He may or may not have been aware of the fact that an ICRR-affected tooth will not respond to orthodontic forces. However, did he consider the treatment option outlined above before prescribing extraction of the tooth? Perhaps he did but considered that the lesion too advanced for any conservative remedy.

References

1. See the monthly bulletin for March 2013 on this website

http://dr-adrianbecker.com/page.php?pageId=281&nlid=54

2. Patel S, Kanagasingam S, Pitt Ford T. External cervical resorption: a review. J Endod. 2009;35:616-625.

3. Patel S, Kanagasingam S, Pitt Ford T. External cervical resorption: a review. J Endod. 2009;35:616-625.

4. Neuvald L, Consolaro A. Cementoenamel junction: microscopic analysis and external cervical resorption. J Endod. 2000;26:503-508.

5. Iqbal MK. Clinical and scanning electron microscopic features of invasive cervical resorption in a maxillary molar. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007;103:e49-54.

6. Heithersay GS. Invasive cervical resorption: an analysis of potential predisposing factors. Quintessence Int. 1999;30:83-95.

7. Heithersay GS. Clinical, radiologic, and histopathologic features of invasive cervical resorption. Quintessence Int. 1999;30:27-37

8. Becker A, Abramovitz I, Chaushu S. Failure of treatment of impacted canines associated with invasive cervical root resorption. Angle Orthodontist, 2013, 83:870-876.

9. Becker A. The orthodontic treatment of impacted teeth. 3rd edition, 2012. Oxford: Wiley-Blackwell Publishers. Pages 197-206

10. Brosjo M, Anderssen K, Berg JO, Lindskog S. An experimental model for cervical resorption in monkeys. Endod Dent Traumatol. 1990;6:118-120.