INTRODUCTION AND REVIEW OF THE LITERATURE
Orthodontic tooth movement is dependent on changes to the local environment, including vascular changes, recruitment of inflammatory mediators and alveolar socket remodelling.1 In most instances, orthodontic tooth movement occurs without significant damage to the teeth and surrounding periodontium. Rarely, pulpal side effects may occur, including altered pulpal respiration rate, internal root resorption, pulpal obliteration by secondary dentin and pulpal necrosis.2 While it is understood that alterations in the neurovascular bundle are necessary for successful orthodontics, the key clinical question is to understand the point at which these changes become pathologic and clinically significant. Furthermore, it would be useful for the clinician to be able to predict which patients are more susceptible to pathologic changes, as well as have the ability to implement measures to prevent them from occurring. This article will describe the common pulpal changes that occur with orthodontics. A case of pulpal necrosis that developed during orthodontic treatment will be discussed and possible reasons for the necrosis will be examined.
Studies have determined that the risk of pulp damage in the average orthodontic patient is minor.3 There are conditions, however, that predispose a patient to an increased likelihood of pulpal damage during orthodontic treatment. In a study comparing impacted canines to non-impacted canines, 21% of impacted canines displayed radiographic pulpal obliteration, 25% of them did not respond to electric pulp testing, and 3% of these teeth required root canal treatment. All of the control canines had normal pulpal responses and none required root canal treatment.4 Another study suggested that teeth with advanced periodontal bone loss are more susceptible to pulpal necrosis following orthodontic treatment, as these teeth have a limited ability to mitigate the forces on the neurovascular bundle.5
Most alterations in pulpal blood flow that result from orthodontic treatment are reversible, unless the pulp has been previously irritated by caries, restorations or trauma.6 The literature supports that teeth with closed apical foramina that have a history of trauma or caries, and that are subjected to heavy and prolonged orthodontic forces, are more susceptible to irreversible pulpal changes or necrosis than teeth with no history of such insult.6,7 Teeth with incomplete apical foramina are not immune to adverse sequelae during orthodontic tooth movement; however they are more resistant to these changes.6
Of the force vectors that can be applied to teeth during orthodontic movement, intrusion is thought to have the most significant effect on the pulp due to the concentration of force at the apex.2 In a study examining alterations in pulpal blood flow from physiologic forces of intrusion, it was demonstrated that pulpal blood flow was not altered during the application of varying levels of intrusive force.2 Another study comparing histological changes of the pulp following intrusive and extrusive forces found that there was no difference between these groups, and there were only minor histological changes relative to the control group.8 Studies have also shown that changes in pulpal blood flow that occur as a result of orthodontic force normalize after 72 hours.9,10 From reviewing the literature, it can be concluded that there are transient changes in pulpal blood flow that occur with tooth movement; however, orthodontic tooth movement with a physiologic force application does not lead to pathologic changes in pulpal blood flow or necrosis.
Although the literature indicates that normal, healthy teeth subjected to orthodontic forces should have transient and reversible pulpal changes, rarely irreversible pulpal side effects occur. We will review a case of a patient who experienced pulpal
CASE REPORT
A healthy, 41-year-old male was referred by his general practitioner for an orthodontic evaluation. His main concern was his ‘bite’. In particular, he felt minimal contact between the teeth of the second and third quadrant. Based on a thorough examination and review of diagnostic records, the following diagnosis was made: Left Class II malocclusion associated with posterior crossbites, crowding, asymmetry, midline discrepancy, lateral open bite, missing teeth 14,24,34,44 and gingival recession at 33, 35 and 43, 45. (Figures 1-5)
It was recommended that the patient consider orthodontic treatment with fixed appliances. Intermaxillary elastics would be prescribed to improve upon the occlusion and a temporary anchorage device (TAD) was recommended in quadrant 3 to allow for mesial movement of teeth 35, 36, 37. Free gingival grafting at 33, 35 and 43, 45 was advised by a periodontist. The goals of treatment were as follows: 1) Align the teeth and consolidate spaces, 2) correct the right posterior crossbite, 3) correct the left lateral open bite and 4) create of a left functional malocclusion, accepting the left posterior crossbite and an Angle Class II canine relationship.
The patient consented to treatment and proceeded to have fixed upper lingual and lower labial appliances placed on June 18, 2010. Overall treatment progress was uneventful. Grafts were completed on two separate occasions dated August, 2010 and January, 2011. A review of the progress photos on May 2011 revealed slight discoloration of tooth 13 (Figure 6, 7). 13 was otherwise asymptomatic. A TAD was placed on July 25, 2011 without incident and a panoramic radiograph was prescribed to confirm its’ proper placement. Thickening of the periodontal ligament space at tooth 13 was evident (Figure 8).
In August, 2011, the patient presented for a routine cleaning with his general dentist and reported discomfort when he pressed against the apex of tooth 13. No other symptoms such as hot, cold or percussion sensitivity were present. A referral was made to an endodontist and pulp testing deemed this tooth to be necrotic. Root canal therapy was completed on September 15, 2011 (Figures 9, 10).
DISCUSSION
Irreversible pulpal changes are very rare with orthodontic movement of normal, healthy teeth. In this case, there was no obvious reason why this patient experienced pulpal necrosis of the 13 during orthodontic treatment; there was no reported history of trauma to 13, no existing restoration, no obvious pulpal obliteration on the radiograph, and no periodontal bone loss. Moreover, the orthodontic forces used were biologic, the distance this tooth had to travel was minimal and there was absence of traumatic occlusion. Interestingly, the patient reported that his primary maxillary canines were extracted as a child, which may be indicative of ectopic eruption or impaction of his permanent canines. However, without access to his previous dental records it is difficult to make this conclusion.
In the treating endodontist’s report, it was indicated that the apex of the 13 may have been close to the cortical bone. It is plausible that this may have compressed the apical blood supply or caused a fenestration at the apical level, thus challenging the blood supply to the tooth and contributing to its’ pulpal necrosis. It is difficult to determine whether the apex of 13 was compressed against the cortical plate prior to orthodontic treatment, hence starting off with a compromised blood supply, or if the orthodontic movement caused this to occur. Although cortical compression may have been a factor in contributing to pulpal necrosis of 13, it is not possible to make this conclusion with a great degree of certainty. Perhaps with the use of cone beam computed tomography, this could have been more accurately demonstrated.
Given the review of the literature and the case report, the following recommendations can be made for patients who will have orthodontic treatment, with relation to pulpal necrosis:
1. A detailed history of the dentition should be taken, wi
th specific attention given to any history of dental trauma.
2. On radiographic examination, teeth should be examined for evidence of pulpal obliteration as these teeth are at a higher risk of irreversible pulpal changes during orthodontic treatment.
3. Patients who have risk factors for pulpal necrosis with orthodontic treatment (impacted teeth, teeth with a history of trauma, caries or restorations, teeth with periodontal bone loss, teeth with evidence of pulpal obliteration) should be informed about the risk of pulpal damage during treatment.
4. Orthodontic forces should be light and continuous, respecting physiologic boundaries.
5. Care should be taken to ensure that the intended orthodontic tooth movement does not challenge the apical blood supply (e.g. compressing the root apex against the cortical plate).
6. Pulpal symptoms that arise during orthodontic treatment should be treated appropriately and swiftly.
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