Management of Acute Dental Trauma

©2001 Dr. Ira R. Luskin Diplomate AVDC
Etiology, Pathophysiology and Clinical Signs

There are numerous traumatic causes, which lead to oral injury of both soft tissue and hard tissue. The anterior teeth are often affected by blunt trauma from Frisbee catching, cage biting, running into immobile objects and “tug of war” between disproportionately sized animals. The damage often seen to the animal is acute dental fractures, gingival lacerations and in the worst-case scenario, partial or complete dental avulsions. The animal attempting to chew on hard objects like bones and sticks, on the other hand, often injures the posterior teeth. The carnassial upper fourth premolar and lower first molar, due to their prominent cusp tips, are often affected.

Micro-fractures are created in the cusp enamel due to the intense shearing forces that the cheek teeth are capable of creating. These lead to the crown subsequently fracturing and exposing the pulp chamber. Depending on the depth and angle of the fracture and the length of time of exposure, one can see various clinical signs. In the case of near exposure of the pulp chamber, there is no evidence of bleeding from the tooth. There might be sensitivity present on percussion or palpation of the tooth. The pulp is visible as a pink spot however a thin layer of dentin protects it from bacterial contamination. Once the fracture goes deeper, the pulp then becomes exposed and there is acute bleeding and sensitivity. If the exposure duration is greater then 2-3 weeks in young animals, one might see a pulpal "mushroom" of hyperplastic tissue. This extrudes out of the chamber, bleeds and is very sensitive. In older animals, in contrast to this hyperplastic reparative state, the pulp dies and becomes necrotic. There is no obvious pain and the entry into the chamber becomes black and is slightly recessed.

Teeth that are traumatized don’t always exhibit fractures of the crown. Quite often there is enough resilience in the periodontium or supporting structures to prevent damage to the crown. The problem, however, often presents itself that the blood supply that enters the tooth apically can be damaged by radical deviation of the longitudinal dental axis. The ensuing pulpitis can be characterized by tooth hemorrhage and edema. This creates pressure within the canal that forces the blood into the dentin tubules. Initially the crown, either partially or in its entirety, turns pink. As the process progresses, the blood pigment in the tubules breaks down to form hemosiderin and then the tooth crown turns gray. A mature tooth undergoing pulpitis usually dies.

Internally the pulpal and root canal contents undergo necrolysis, which then drains out the apex into the surrounding tissue. This process leads to periapical abscessation, which causes the breakdown of the supporting bone and the formation of fistulous tracts. If the upper fourth premolar or molar are involved, the tract will drain out laterally and form a “gum boil” on the non-attached gingiva. In addition, the upper fourth premolar and molar can drain into the maxillary sinus and develop into a suborbital fistula. Canine tooth drainage occurs at the level of the tooth's apex, which is usually ventral or dorsal to the second premolar and fistulates laterally on the non-attached gingiva. The lower canines can also fisulate submandibularly through the skin. Dental disease must always be the primary rule out for these chronic non-healing tracts.

Based on the above discussion, it becomes evident that the treatment plan is predicated on the type of injury and its duration. With non-vital dental fractures and intact crowns that exhibit irreversible pulpitis, the treatment of choice is preservation of the dental structure, albeit, a root canal therapy. If the underlying bone is severely compromised with infection then the tooth should be extracted. These procedures are beyond the scope of this lecture.

Vital Pulpectomy and Pulp Capping

Vital pulpectomy and pulp capping best treat recent dental fractures with pulp chamber exposure. The most important issue affecting this therapy's success is the age of the patient and the length of time of pulpal exposure. In general, animals that are two years old and younger, with exposures of the pulp less than two weeks in duration, can be treated successfully. In addition, older patients undergoing a crown reduction to disarm the canine teeth, or those showing a hyperplastic pulp secondary to a cusp fracture, can also undergo this treatment. Besides age and duration affecting success, the animals that are started immediately on an antibiotic and bactericidal flushing agents, have a more favorable treatment prognosis

The objective of this procedure is to remove the contaminated or infected portion of the pulp and to stimulate the remaining healthy part to form a reparative protective layer of dentin. Placing on the freshly debrided pulp tissue a layer of calcium hydroxide, as a pulp capping, does this. Calcium hydroxide is very basic and serves as an irritant thereby stimulating the odontoblasts lining the pulp chamber to lie down dentin.

Procedure

An injectable antibiotic is given and a radiograph is taken to check for any subgingival fractures, which may lead to complications. The teeth are cleaned and the affected tooth is prepped. For crown reductions, either a sterile tapered fissure bur or a diamond disc is used in a water-cooled drill. The crown of the canine tooth is cut off at 90 degrees at the level of the lateral incisor. Depending on the size of the canal and the species, a number 1/2 to 2 sterile round bur is used in a high-speed handpiece to remove 5-8mm of the coronal pulp.

One should avoid pushing dentine shavings into the chamber since this will increase pulpal hemorrhage. The canal is flushed with sterile saline and the blunt end of a sterile paper point is gently introduced into the pulp chamber and allowed to stay there for 3-5 minutes for hemostasis. Never use any electro or chemical cautery to control the bleeding since this will impair the creation of reparative dentin. Normal pulp usually stops bleeding after 5 minutes. If it continues to bleed, then a further removal of 1-2 millimeters of pulp should be done. If bleeding persists, than a light coating of calcium hydroxide on a paper point placed in the canal may stop it. A paper point soaked in a 1:10,000 epinephrine solution placed on the cut pulp, can also be used for hemostasis if the above measures are not successful.

A full layer of calcium hydroxide powder is then placed directly on the pulp with either a flat plastic filling instrument or a retrograde amalgam carrier. The blunt end of another paper point is used to lightly pack the powder into the chamber, leaving about 5 mm for the subsequent materials. Using a spoon escavator, the walls of the cavity prep are debrided and any loose powder is removed. A hard setting calcium hydroxide cement, like Dycal, is mixed on a paper pad and then introduced with a ballpoint applicator or a needle tip Centrix syringe. The Dycal layer is about 1-2mm thick. Any excess material is again removed from the wall of the pulp chamber prior to the final cavity restoration.

A pear-shaped bur, size 330, is used to create a slight undercut or a retentive shelf for the composite restoration. The so prepared cavity is rinsed, and then with a phosphoric acid, etched. The acid gel is thoroughly rinsed and dried. An enamel-dentin bonding agent can be used prior to the composite for a greater adhesion and cavity seal. The chemical cured composite material is packed into the cavity with a plastic instrument and finished with either a fine diamond or sanding discs. Radiographs should be taken 6 months to one year later and checked for evidence of a thicker dentin wall, a dentinal bridge at the CaOH interface and a normal apex with no lysis.