From Volume 40, Issue 2, March 2013 | Pages 114-119
Teeth with periapical lesions can undergo successful orthodontic treatment, but conventional protocols indicate that such teeth should be endodontically stabilized prior to such treatment. A case report is presented where such endodontic stabilization was not possible, yet a chronic periapical lesion resolved as orthodontic treatment progressed. This paper will discuss the possible causes of the initial lesion, and reasons why it resolved without endodontic treatment.
Conventional protocols indicate that teeth with periapical lesions should be endodontically stabilized prior to orthodontic treatment, since the movement of such teeth may otherwise cause a delay in the healing process. Furthermore, areas of root resorption resulting from both orthodontic movement and periapical lesions are repaired by newly formed cementum in the majority of cases.1
The following is a report of an adult orthodontic patient who presented with a Class II division 1 malocclusion, complicated by a deep overbite causing extensive trauma to the anterior palatal soft tissues. One of the upper central incisors initially had an extensive chronic periapical radiolucency, however, during the course of the orthodontic treatment, this lesion resolved without endodontic treatment. The report will discuss the possible implications of the occlusion in the development and subsequent resolution of this periapical lesion.
A 46-year-old woman was referred to the Orthodontic Department of Peterborough and Stamford Hospital by her general dentist, with a complaint of prominent and spaced upper incisor teeth. Clinical examination (Figures 1–3) revealed:
Radiographic examination (Figures 4–6) showed:
Treatment was aimed to correct the antero-posterior and vertical skeletal relationship, and therefore relieve the traumatic overbite and lip incompetence, using orthognathic surgery. However, conventional pre-surgical orthodontics was contra-indicated by the patient's reduced dental and periodontal support. Therefore, a 7mm mandibular advancement osteotomy was performed without the benefit of pre-surgical orthodontic alignment and arch co-ordination. Mini-plate bone fixation was utilized, and intra-operative intermaxillary fixation was achieved using a combination of intermaxillary fixation screws and orthodontic mini-implants, as described by Gibbons and Cousley.2
A simultaneous free gingival graft to the anterior palatal area was considered, but it was felt that the palatal tissues would benefit from an initial post-operative healing period in order to optimize the chance of graft survival.
Two months after surgery, the patient's dentist attempted endodontic treatment of UL1. A test cavity was prepared without local anaesthetic which confirmed UL1 to be non-vital. Unfortunately, owing to the root sclerosis, no entry could be gained into the root canal, and therefore the tooth could not undergo any formal endodontic instrumentation, irrigation or application of medication into the root canal. The access cavity was restored and the patient warned that the prognosis for UL1 appeared hopeless.
Post-operatively, it was considered that limited orthodontic treatment should be undertaken to improve the occlusal contacts, and consequently upper and lower arch fixed appliances were fitted after three months (Figure 7). As UL1 was asymptomatic, it was decided to retain this tooth temporarily, include it in the fixed appliance and then consider prosthetic replacement after orthodontics. This tooth remained asymptomatic as the treatment proceeded and, surprisingly, the associated buccal sinus was noted to resolve as treatment progressed. In addition, the upper incisor's palatal attached gingivae showed marked improvement following surgery, and the mobility of these teeth diminished.
After approximately one year of orthodontics (15 months post-operatively), a follow-up periapical radiograph of UL1 revealed the unexpected finding of complete bony in-fill of the periapical radiolucency (Figure 8). Furthermore, there did not appear to be progressive root resorption and, consequently, this tooth appeared to have a much better prognosis. Further clinical and radiographic examinations six months later showed no recurrence of the periapical radiolucency or buccal sinus.
One reason why UL1 lost vitality and developed radiographic sequelae may have been a previous episode of acute trauma. This would explain why the adjacent central incisor had undergone root canal treatment. This would be concordant with current literature, which has reported that an increased overjet and inadequate lip coverage are major risk factors for incisor trauma. As well as causing acute symptoms, incisor trauma can also lead to more chronic pathological changes, such as pulp obliteration.3 This may explain the root canal sclerosis seen in UL1.
However, of particular interest in this case is the resolution of the periapical lesion without endodontic treatment. It is possible that the attempted access cavity preparation of UL1 could have resulted in a micro-exposure of the root canal and established some drainage, which may have contributed to healing of the periapical lesion. Reports in the literature indicate that teeth with obliteration of the root canal do still maintain a patent microscopic canal space that is not usually visible radiographically.4 Furthermore, there are cases where establishing drainage of the root canal relieves the pressure from a periapical lesion, with changes in the periapical tissues allowing the host defences to initiate healing.5 However, in this case no irrigant or medication was used in the root canal, no repeat drainage was carried out, and the tooth did not undergo any formal endodontic preparation.
Arguably, it may be that correction of the traumatic overbite was a factor in promoting healing of the peri-radicular tissues. This in turn would suggest that production of a more favourable anterior occlusion, in combination with relief of the previous periodontal trauma, was responsible for the changes observed.
Animal studies in the 1970s examined the effects of increased occlusal force on the pulp, indicating that it may cause pulpal hyperaemia, pulpitis, pulp necrosis, pulp stones and breakdown of the periapical vessels.6 One study indicated the possibility that increased occlusal force over long periods might induce pulpal changes. Such changes consisted of a concentration of inflammatory cells, disruption of odontoblasts and deposition of secondary dentine.7 However, the link between occlusion alone and the development of pulpal pathology appears tenuous.
More recent studies have highlighted the role of occlusal trauma in periodontal destruction, and the notion of a co-destructive action between inflammation and such trauma. Acute trauma from occlusion occurs following an abrupt increase in load, such as biting unexpectedly on something hard. Chronic trauma from occlusion is more common, and of greater clinical significance.8 An investigation into the relationship of occlusal and periodontal status suggested that teeth with occlusal discrepancies had significantly deeper pocketing, more mobility and worse prognoses than teeth without such discrepancies.9 A follow-up study found that teeth with untreated occlusal discrepancies had a worse prognosis than teeth without such abnormalities. In addition, the progression of periodontal disease among teeth with treated occlusal discrepancies was not significantly different from teeth with no such interferences. Furthermore, this study found that similar results were obtained in patients with good oral hygiene. The authors felt these results indicated that untreated occlusal trauma is a catalyst for the progression of periodontal disease.10
Two reported cases have highlighted the possible detrimental effect of occlusal trauma on the healing of periapical lesions.11 In these cases, root canal treatment in anterior teeth failed initially, but healed after occlusal adjustment. The authors postulated that, whilst bacterial infection may not exist in all periapical lesions, it is more likely in longstanding ones. Occlusal trauma may lead such lesions to be broken down more easily than in non-infected sites. However, the authors felt that further study was required to clarify the relation between occlusal trauma and periapical healing.11
In this present case, could the pre-existing periodontal condition, together with the additional palatal soft tissue occlusal trauma, have lead to a perio-endo lesion, initiated from a primary periodontal infection? Similarities between the endodontic and periodontal microflora suggest that cross-infection between the root canal and periodontal pocket can occur. The main connections between these tissues are the periapical foramina. However, there are also accessory canals, and a third route for bacterial products is via the dentinal tubules. Whereas accessory canals are most frequent in the apical third of the root, the density of dentinal tubules is significantly lower in this region than in the mid-root and cervical areas. Usually the end of each tubule facing the periodontal ligament is covered with cementum. Some controversy exists whether removal of this cementum, such as during periodontal therapy, has a negative effect on the pulp by exposing the tubules to bacterial penetration. However, it is thought that a vital pulp maintains an outward flow of dentinal fluid upon removal of this layer, which may have a flushing action and reduce diffusion of bacterial products into the tooth.12 In the present case, the root canal appeared sclerosed, and as the tooth was non-vital then it would have lost this protective mechanism. Furthermore, trauma from the deep overbite may have contributed to continued patency of the tubules.
Animal studies have shown that orthodontic movement causes transient hyalinization of part of the periodontal ligament. This produces a temporary cell-free area, which evokes responses from the adjacent alveolar bone and root surface, and is then removed by inflammatory cells. Root resorption associated with removal of this hyaline region is followed by deposition of reparative cementum. No open dentinal tubules can be seen in this acellular cementum, which prevents communication between the pulpal and periodontal tissues.13 This would potentially explain resolution of the periapical lesion UL1 as the orthodontic treatment progressed, due to bacteria becoming entombed within the tubules preventing further external pathological responses.
Although the exact cause of the periapical lesion affecting UL1 is difficult to ascertain, this report attempts to explain some of the pathological processes that may have occurred. Furthermore, this case highlights the possible role that occlusal trauma may have as a co-destructive factor in the progression of periodontal disease, the development of a perio-endo lesion, and how subsequent orthodontic treatment may have lead to resolution of such a lesion. Figure 9 summarizes the possible causal and healing factors involved with this lesion.
However, the authors would still advise that, whenever possible, conventional protocols relating to endodontic stabilization of teeth prior to orthodontic treatment should be followed.
