Abstract
The sensitivity of teeth anterior to a fracture between the mental and mandibular foramina has been tested and followed up until reinnervation or 3 years has passed. This study assessed the reinnervation period, the number of denervated teeth, and their clinical importance. Fifty patients and 459 teeth were examined. Two hundred and seventy-three teeth were affected and had potentially impaired innervation. Tests after injury showed non-responsive teeth in 81% of affected teeth. Six weeks after injury, 19% of teeth were reinnervated; by 1 year after injury, 92% of initially non-responsive teeth were reinnervated. Most teeth (34%) were reinnervated from 6 weeks to 3 months. All 23/186 initially non-responsive, unaffected, contralateral corresponding teeth were reinnervated within 6 weeks. A year after injury, 95% of incisors, 91% of canines, 94% of premolars, and 82% of molars were reinnervated. Three years after injury, 8% of teeth remain denervated. During the second and third years, no reinnervation occurred, but clinical signs of pulp devitalisation of denervated teeth occurred in 18% or 1% of the initially non-responsive affected teeth. The results revealed the stability of pulp 1 year after injury. Denervated teeth should not be treated if no clinical or radiological signs of devitalisation exist.
Mandibular nerve injury is a common complication of mandibular fractures between the mental and mandibular foramina. As a consequence of nerve injury, disturbances of the skin and mucous membrane, and teeth sensitivity occur . Patients experience these disturbances at different intensities, but the condition gradually improves with time. Although it is known from clinical experience that teeth anterior to a fracture line can demonstrate disturbed sensitivity, the problem has not been addressed sufficiently in the literature .
Tooth sensitivity testing methods are based on pain, so it is impossible to differentiate vitality (a function of pulp vascularisation) from sensitivity (a function of innervation) . Tissue blood perfusion of the oral area can be detected using laser Doppler flowmetry (LDF) and pulse oximetry . The use of these physiometric tests for detecting tooth vitality is a valuable resource . C alil et al. concluded that further studies are required to assess their effectiveness and validity in determining pulp vitality in traumatized teeth. If the injury causes an interruption in pulp vascularisation, the result will be pulp tissue death (including the nerve); if only a nerve injury occurs, the vitality of the pulp will not be impaired. Some injuries damage the nerve without influencing the survival of the pulp. Terminal and electrical stimuli only assess the sensitivity of the pulp, so they are not indicated for the direct evaluation of vitality. A tooth that does not change colour and lacks necrotized pulp is vascularized; the innervation is thus of secondary importance. It is known from clinical experience that teeth anterior to the fracture line primarily demonstrate temporary disturbed sensitivity.
The incidence and natural history of post-traumatic sensory disturbances in the distribution of the inferior alveolar nerve (IAN) are insufficiently documented in the literature. This problem has been recognized and published studies include fractures and osteotomies that may or may not involve the mandibular canal in relation to specific methods and periods of fracture reduction . Only a few studies evaluate IAN disturbances by examining tooth sensitivity .
In tooth vitality investigations, the value of different stimuli in the detection of tooth vitality is debated. Some studies report electric stimuli to be 100% precise, although they cannot distinguish the quality of vitality . Other reports consider such stimuli to be unreliable . Others prefer vitality tests that measure electric amplitude without power , whereas some prefer a thermal vitality meter . It can be concluded that thermal and electric ‘vitality’ tests, history, and clinical and radiological findings should be secondary methods for detecting pulp status. Such status depends on many things, including age, general status, tooth size, past injuries, and pathological pulp changes .
The aims of this investigation were to evaluate IAN disturbances by assessing tooth sensitivity after mandibular fracture with the use of an electric tester and to determine the number of denervated teeth and the time period in which normalisation of tooth sensitivity or devitalisation occurred.
Material and methods
This prospective study used a sample derived from the population of patients with mandibular fractures treated at the Department of Oral and Maxillofacial Surgery in Zagreb between 2006 and 2009. Inclusion criteria were: the presence of a minimally displaced (<3 mm) mandibular fracture between the mental and mandibular foramina because these fractures place the IAN at direct risk of injury ; treatment with closed reduction and maxillomandibular fixation with elastics because late deleterious effects on the teeth and periodontal tissues from interdental wiring are uncommon 1 year after the removal of interdental wiring ; preoperative and postoperative panoramic radiographs as routine imaging, although it is possible to diagnose the interruption of IAN continuity with magnetic resonance imaging (MRI) ; and patients who accepted more follow-up examinations and pulp testing. The investigation included 50 patients with fractures between the mental and mandibular foramina. Anterior to the fracture line, these patients had affected teeth that initially seemed to be avital but actually were not, and they had potentially impaired innervation. The authors assumed that the lack of responsiveness to electric pulp testing was due to inferior dental nerve injury because there was no evidence of direct tooth trauma. Complete documentation was obtained for the patients and complete follow-up was carried out until reinnervation or 3 years had elapsed (in patients in whom reinnervation of all teeth did not occur). Patients with parasymphyseal fractures, teeth involved in the fracture line, carious teeth, teeth with prosthetic restorations, previously devitalized teeth, and teeth injured in the fractures were excluded from the study.
An electric vitality tester was used for sensitivity testing (Digitest model No. D626D, Parkell). It consisted of an instrument casing with a battery. The tester contained a digital electric stimulus slide ranging from 0 to 64, with electrodes patched for examining tooth surface sensitivity and a connection cable applied to the patient’s lip. Teeth were dried and isolated with cotton, electrodes were moistened, and the lowest intensity stimulus that caused a reaction was marked as the level of sensitivity. In this investigation, initially sensitive teeth were noted as vital from this time onward, regardless of the presence of a later reaction. The eventual change in the level of sensitivity was not analysed. Teeth that did not react even at the highest level of electric stimulus were considered to be denervated.
Teeth were considered vital if they did not have any clear signs of avitality (e.g. colour change, pathological mobility, radiological periapical transparency, root resorption, or other clinical indicators and process symptoms). Teeth were selected for placement in the avital group based on clinical signs, not because of a negative electric test.
The sensitivity of all potentially endangered teeth was examined on admission (prior to therapy). Electric pulp testing was carried out on the contralateral, corresponding, unaffected teeth for control purposes. The sensitivity of all initially non-responsive teeth was examined 6 weeks, then 3, 4, 6 and 12 months after jaw fracture treatment. The teeth for which sensitivity was not verified (even 12 months after therapy) underwent an additional 2 years of testing as long as they did not show clear clinical signs of avitality.
Results
The sensitivity of 459 teeth was tested. Of these, 273 (60%) were affected anterior to the mandibular fracture between the mental and mandibular foramina and thus had potentially impaired innervation. Of the 459 teeth, 186 (41%) were unaffected, contralateral, corresponding teeth for control purposes. 222/273 (81%) of the affected and 23/186 of the unaffected, contralateral, corresponding teeth were initially non-responsive.
The number of reinnervated teeth increased with time. Six weeks after the injury, 19% were reinnervated. Roughly 85% of teeth were reinnervated after 6 months, and 92% of teeth were reinnervated 1 year after the injury. No reinnervation occurred later than 1 year following the injury ( Table 1 ).
| Time (months) | No | % |
|---|---|---|
| >1.5 | 42 | 18.9 |
| >3 | 117 | 52.7 |
| >4 | 156 | 70.3 |
| >6 | 188 | 84.7 |
| >12 | 205 | 92.3 |
| >36 | 205 | 92.3 |
When the reinnervation of teeth in a determined time period was analysed, most of the teeth were reinnervated in the period 6 weeks to 3 months after the injury (34%). Fewer teeth were reinnervated in the period 7–12 months after the injury (8%), and no teeth were reinnervated in the period 1–3 years after the injury.
The results were analysed for groups of teeth, because of the small number of samples for particular teeth. A year after injury, 95% of incisors, 91% of canines, 94% of premolars, and 81% of molars were reinnervated ( Table 2 ).
| Groups of teeth | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Incisors (86) | Canines (45) | Premolars (64) | Molars (27) | Total (222) | ||||||
| Time (months) | No | % | No | % | No | % | No | % | No | % |
| >1.5 | 21 | 24.4 | 10 | 22.2 | 8 | 12.5 | 3 | 11.1 | 42 | 18.9 |
| 1.5–3 | 33 | 38.4 | 16 | 35.5 | 18 | 28.1 | 8 | 29.6 | 75 | 33.8 |
| >4 | 10 | 11.6 | 9 | 20.0 | 16 | 25.0 | 4 | 14.8 | 39 | 17.5 |
| 5–6 | 11 | 12.8 | 3 | 6.7 | 13 | 20.3 | 5 | 18.5 | 32 | 14.4 |
| 7–12 | 7 | 8.1 | 3 | 6.7 | 5 | 7.8 | 2 | 7.4 | 17 | 7.7 |
| 13–36 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 |
| Total | 82 | 95.2 | 41 | 91.1 | 60 | 93.8 | 22 | 81 | 205 | 92.3 |
Most medial incisors (31%) were reinnervated by 6 weeks after injury or between 6 weeks and 3 months (31%). Only 7% of medial incisors were reinnervated between months 7–12. Most lateral incisors (46%), canines (36%), second premolars (31%), first molars (33%), and second molars (36%) were reinnervated in the period between 6 weeks and 3 months. The same number of first premolars (26%) was reinnervated during the period from 6 weeks to 3 months and the period from months 5–6. Most wisdom teeth were reinnervated during months 5–6. None of the second molars was reinnervated until 6 weeks after injury, but the same number was reinnervated during months 5 and 6 and from 7 to 12 months (1/11).
Three years after the injury, 17 of 222 teeth (8%) remained denervated. The most frequently denervated teeth were molars (19%), while the least frequently denervated teeth were the incisors (5%). Canines (4/45) and first premolars (3/35) were numerically the most frequently denervated teeth; as a percentage, however, third molars (29%) were the most frequently denervated teeth.
From 1 to 3 years after injury, 14/17 (82%) non-responsive teeth were denervated. This represents 6% of the initially non-responsive teeth (14/222). From 1 to 3 years after injury, 3/17 (18%) of denervated teeth were devitalized. Only three of 222 (1%) of the initially non-responsive teeth remained devitalized 3 years after the injury. The teeth that were devitalized included one lateral incisor from the 44 initially denervated lateral incisors (2%), one canine from the 45 initially denervated canines (2%), and one wisdom tooth from the 35 initially denervated wisdom teeth (3%).
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