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Saving the traumatized tooth: Part 1
The Luxation Injury A mother drags her 7-year-old Spider-man into your office on a fully-scheduled day. While saving NY from the forces of evil, little Spidey smacked a central incisor on the edge of the coffee-table. Now it’s loose and “looks funny.” How do you treat the patient to restore function and comfort as well as minimize the possibility of future root resorption ... all without destroying the day’s schedule? by John I. Ingle, DDS, MSD
San Diego, CA Even when the teeth appear undamaged, sudden impact to dentition can cause injuries ranging from pulp concussion to tooth intrusion. Common to all luxation injuries is trauma to the neurovascular supply to the pulp and to the tooth’s supporting structures ... the periodontal ligament and alveolar bone. Injury to the PDL can be either a separation or a crushing injury.
Separation injury, also called “extrusion luxation”, occurs when the tooth is pulled away from the bony socket wall. Crushing injuries or “intrusive luxation,” occurs when the tooth is forced against the bone (Figure 1).
Of the two tissue injuries, crushing is more destructive and will take longer to heal.
The extent of the damage to the neurovascular supply exerts a major influence on the outcome of traumatic injuries. Severance of the blood supply leads to pulp necrosis (coagulation necrosis), which can become a fertile growth medium for bacteria. The end result is infection-related resorption (inflammatory resorption) that involves both the tooth and the surrounding bone. If sufficient damage has been done to the cementum and PDL, ankylosis-related resorption (replacement resorption) may gradually destroy the tooth.
Because the combination of pulpal and PDL trauma during a luxation injury can have such serious consequences for the injured tooth, treatment should be directed toward creating an environment in which the tooth is most likely to recover. Figures 1&2: There are two kinds of luxation injuries. Extrusive luxation results in displacement out of the alveolar socket (left). Intrusive luxation forces the tooth against the bony wall, resulting in a disappearance of the periodontal ligament space (right). Though extrusion appears more dramatic, intrusion is actually the more serious trauma and generally takes longer to heal. (Courtesy of Leif K. Bakland) 
Treatment of luxated teeth consists of
(1) repositioning the tooth if necessary;
(2) stabilizing the tooth if it is mobile in order to promote PDL repair; and
(3) monitoring the pulpal condition, and if the pulp undergoes necrosis, providing timely endodontic therapy.
The primary goal of treatment is to prevent root resorption. It has been shown that stabilization should be non-rigid to allow functional movement. This appears to reduce the risk of resorption. Furthermore, the splint should be in place only long enough to allow reorganization of PDL fibers ... 2 to 4 weeks is sufficient.
Pulp survival in mature, fully-formed teeth decreases with increasing luxation severity. The greater the injury to the pulp’s blood supply, the greater the likelihood of pulp necrosis. Of course, endodontic treatment is indicated in cases of pulp necrosis.
Reduction or severance of the blood supply to pulps in developing teeth is more complicated than in mature teeth. Pulp necrosis in an undeveloped tooth can result in a very weak tooth, one that’s prone to cervical root fracture. Apexification procedures in such teeth are done simply to induce a hard apical barrier to contain the root canal filling. The tooth will still be weak. In fact it appears that long term exposure to Calcium Hydroxide (as occurs in apexification procedures) weakens the tooth even further by making the dentin more brittle.
A better approach is to use the Calcium Hydroxide for only a short time (less than 1 month) to disinfect the root canal, and then fill the canal with Mineral Trioxide Aggregate.* 
Figures 3 &4: Splinting of luxated and replanted teeth. Absolute rigidity in the splint will encourage replacement resorption. So your objective is to stabilize the teeth while allowing some physiologic movement. Bond unfilled resin to small, etched areas of the teeth. Avoid etching interproximally. If there is a space between the teeth, a thin wire can be used to bridge the gap. (Courtesy of Leif K. Bakland) However, there’s also a more positive aspect to treating the developing tooth. Even though the original blood flow was stopped by the trauma, its large apical opening may allow reestablishment of the blood supply to the pulp tissue. Such revascularization is not likely in a tooth with an apical opening of less than 1 mm. Revascularization of a developing tooth is an important opportunity that must not be overlooked, because it can result in continued, normal root development. Therefore, luxated developing teeth should be continually monitored to detect return of pulpal activity. This is typically seen as a continuing reduction in pulp lumen size.
Management of a luxated tooth
There are three goals in treating a luxation injury. (1) Allow reestablishment of the PDL between the root and adjacent bone. (2) If the tooth is still developing, promote revascularization of pulp. (3) And prevent root resorption.
When the trauma has damaged the PDL (either by separation or crushing) your treatment can enhance reestablishment of the PDL between the root and the bone. If the tooth has been displaced, carefully reposition it. All luxated teeth should be functionally stabilized with a semi-rigid splint to promote PDL healing. Splinting is usually necessary for 2 to 4 weeks, depending on the severity of injury. Crushing injuries take longer to heal.
The splint used for dental injuries can be constructed by bonding unfilled resin= (not composite, which is too rigid) to small etched areas of the involved teeth. If there is a significant space between teeth, it can be spanned with thin, soft wire attached to the resin (Figure 2).
As mentioned, if the blood supply to a young developing tooth has been damaged, ideal outcome is revascularization and preservation of tooth vitality. In fact, young teeth stand a reasonably good chance of revascularizing, provided the injured pulp can be protected from bacteria. This means that any exposed dentin in a concomitant crown fracture must be sealed.
Careful and timely monitoring is essential. If revascularization does not take place, infection can lead to rapid, extensive inflammatory resorption. So after stabilization, the progress should be monitored periodically with an electronic pulp tester to test vitality** and with radiographs to check for continued root development (a certain sign of revascularization) or alternatively infection-related resorption, which indicates infection and necrosis.
Root resorption subsequent to trauma can be either infection-related (inflammatory) or ankylosis-related (replacement) resorption. Inflammatory ankylosis can be prevented or arrested by removing the tooth’s infected pulp and completing the root canal treatment (Figure 4). Unfortunately, replacement ankylosis currently does not respond to treatment. So if it occurs after a traumatic injury, the outlook for the tooth is bleak (Figure 8).
Though luxation injuries can cause considerable discomfort, the patient may not realize just how important proper treatment is to preserving the future of the tooth. In the next article of this series, we’ll look at what’s probably the most unsettling mishap from the patient’s point of view - Crown fractures with and without pulpal exposure.
= Ed: In Japan, the second most common use of C&B-Metabond, is for non-rigid splinting of mobile teeth. (The most common use of course, is cementation of indirect restorations.)
** Immediately after luxation injury, even vital teeth may not respond to pulp vitality tests. They should start reacting within 2 weeks.
* MTA - Dentsply/Tulsa Dental
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