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The pathology and diagnosis of traumatically injured teeth

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01 December 2016, at 12:00am

THE TEETH OF OUR DOMESTIC DOG AND CAT PATIENTS can be damaged in a number of ways, and damage can be found in up to 25% of dogs and 10% of cats. 

Initially, owners may be unaware of the trauma; for instance, we commonly see dogs presented with acute dental fractures where owners have thrown stones which the dog has then caught, resulting in the damage. In these cases, the exposed pulp is likely to be obvious, often with haemorrhage at the fracture surface, and the animal is likely to be showing signs of discomfort.

As time progresses, and pulp tissue becomes necrotic and less sensitive, pain will often wane and the impetus for treatment can often be lost with what appears to be an innocuous injury. It is at this stage, however, that the unseen pathology is developing, which can make salvage of these teeth impossible, resulting in the need for tooth extraction. 

The pathology of pulp exposure

As is common with many oral pathologies, traumatic damage can be seen as a battle between the oral bacterial flora and the host’s immune response, which works to prevent those bacteria from reaching the underlying structures. Therefore, in the initial stages of tooth trauma, when the pulp is first exposed and oral bacteria are allowed access, the pulp will mount an inflammatory response in order to combat this invasion.

This inflammatory response releases inflammatory cytokines which along with bacterial endotoxins will stimulate a pain response from the tooth. In humans, this commonly manifests itself as an increased sensitivity to hot and cold stimulation, a test commonly used to assess pulp vitality and inflammation in human patients.

This is a response that is very difficult to quantify in our animal patients. At this stage, the only diagnostic test for disease is by assessing the fracture surface with a sharp explorer, which will identify the exposed pulp chamber.

This situation of bacterial infection and the inflammatory response from the tooth can be sustained for some time, although eventually the pulp becomes necrotic owing to the continuous bacterial invasion. Bacteria at this stage will digest the pulp tissue and establish colonies within the pulp and dentinal tubules.

Pulp sensitivity per se is lost as the tissue is digested; however, the bacteria will now start to release endotoxins and other waste products which will exit the tooth through the canals of the apical delta. These products will now stimulate an inflammatory response within the periapical tissues. 

At this stage, the only diagnostic test for assessing disease will still be the use of a sharp explorer as no radiographic evidence of periapical bone loss will be seen. The patient is, however, likely to now be feeling a dull ache associated with periapical inflammation; inflammation in the periapical tissue owing to leakage of material from the necrotic pulp stimulates the release of prostaglandins and leukotrienes.

The release of these functions to recruit osteoclasts into the periapical tissues which will result in bone loss in the periapical region. The function of this is to provide a buffer zone around the tooth apex, to prevent bacteria present within the root canal from penetrating the surrounding bone. This is a periapical granuloma.

Eventually, osteoclast/odontoclast activity can cause radicular resorption allowing bacteria to now directly escape from the root canal and into the periapical space, and this pathology can now be called a (tooth root) abscess.

At this stage, once periapical bone resorption has occurred in a suitable plain, it may now be seen radiographically as a periapical lucency. Another radiographic feature that can now often be seen is a disparity between the pulp dimensions between the contralateral teeth.

Dentine is produced throughout life, resulting in a continuously narrowing root canal and pulp chamber. Once a pulp has become necrotic, dentine production will cease and so the necrotic pulp will appear wider on a radiograph in comparison to the contralateral tooth.

Periapical pathology can progress from here in a number of ways. If the root canal is not impacted, the exudate may drain through here, so the periapical lesions may hardly increase in size.

If the root canal is blocked, then the volume of inflammatory exudate will increase, and this will either result in an increase in size in the periapical lesion, the development of a sinus tract, or the invasion and destruction of the periodontal ligament, known as an endo-perio lesion.

How it develops will depend on the characteristics of the bone surrounding the periapical tissues. Each of these sequelae can affect the prognosis of the tooth if preservation with root canal treatment is chosen.

Sinus tract formation in our animal patients can often be the first external sign of developing pathology associated with the necrotic pulp. As the inflammation penetrates the cortical bone and contacts the surrounding soft tissues, a soft tissue inflammatory response can be seen. This is characterised by facial swelling over the tract and is very commonly seen with pulp necrosis of the maxillary 4th premolar tooth which presents as an infra-ocular swelling.

Eventually the tract will form an opening at the mucosal surface and the release of exudate in human patients is often associated with a marked reduction in pain associated with pressure of the increasing volume of exudate.

The open sinus tract may now be seen as an opening or sometimes blistered lesion on the mucosal surface or skin depending on the course of the tract.

This open sinus tract represents a significant change in the prognosis for the tooth, as bacteria can now also enter the tract to form a biofilm around the root apex. These are bacteria which can now not be affected by irrigation of the canal with disinfectants, which will decrease the likelihood of success with root canal treatment.

When inflammation and exudate enter the periodontal ligament space, again the likelihood of success with root canal treatment will decrease.

Endo-perio lesions are associated with a significant loss of attachment of the tooth which will often be an indication for the extraction of that tooth.

Pulp exposure and necrosis is also a feature of dental caries. Although much less common than traumatic damage, and with a vastly lower incidence than caries in the human population, caries are also seen in dogs. They tend to affect the flat occlusal surfaces of teeth and are caused by acid production by bacteria fermenting sugar on these flat surfaces.

The acid will then erode enamel and dentine and ultimately lead to the exposure of the underlying pulp. Once exposed, the pulp will progress through the same pathological process as traumatically injured teeth, resulting in pulp necrosis and periapical pathology.

Treatment of pulp exposure

From the description of the pathological processes following pulp exposure, one can see that the pathology is entirely governed by the bacterial infection of the pulp. Treatment, therefore, is focused on the elimination of bacteria from the pulp.

This can be done in one of two ways: either extraction of the tooth which will remove the infected pulp, or root canal treatment.

Extraction

Extraction for the smaller teeth is often the more straightforward procedure and will always eliminate bacteria from the pulp. When extracting teeth affected by periapical pathology, it is essential to remove that periapical pathology in order for the extraction site to heal efficiently.

Periapical pathology is a combination of chronic inflammatory tissue and sometimes bacteria. Neither of these present within an alveolus are conducive for the formation of an aseptic blood clot within the alveolus and the subsequent infiltration of bone. These tissues therefore need to be removed at the time of extraction.

Radiography is essential in order to assess the extent of the periapical pathology prior to extraction so that the alveolus can be cleared of all debris. If there is no pathology present radiographically, then there is no need to disturb the blot clot forming following extraction. But, if periapical pathology is identified, then this can be scooped out using a periosteal elevator or spoon curette. The alveolus can then be flushed to reduce local contamination with bacteria.

Radiography is also essential to ensure the complete root has been removed. The pathology associated with traumatic damage is bacterial infection of the pulp; therefore, if any pulp (or potentially periapical pathology) is left, then the disease process can continue and is unaffected by the removal of the coronal portion of the root.

A post-extraction radiograph will confirm successful removal and will provide a medico-legal record of this successful treatment. 

Root canal treatment

Root canal treatment has two aims: firstly, the elimination of sufficient bacteria within the root canal to prevent further stimulation of the periapical tissue, and secondly to prevent the re-infection of the root canal.

To this end, root canal treatment involves the preparation of access channels in the tooth to allow the successful irrigation of the root canal with disinfectant solutions.

Once the root canal is suitably disinfected and any remaining pulp tissue has been removed, then the root canal is filled with a material which will set, and the access preparations are sealed which will prevent future bacterial infection.

Root canal treatment in dogs and cats has a very high success rate, a feature the author attributes to the relatively simple canal anatomy when compared with the root canals of human teeth. 

Conclusions

Endodontic disease is of huge significance in veterinary practice, but it is often left untreated owing to the limited external signs of disease. Careful examination and dental radiography will, however, demonstrate to veterinary clinicians how significant that pathology can be and the absolute need for treatment.

References and further reading

Andreasen, J. O. and Andreasen, F.M. (1992) Essentials of Traumatic Injuries to the Teeth: Munksguard, Copenhagen. Duke, A. (1998) Forces involved in upper fourth premolar fracture in dogs. Proceedings 12th Annual Veterinary Dental Forum: 175.

Golden, A. L., Stoller, N. and Harvey, C. E. (1982) A survey of oral and dental diseases in dogs anaesthetized at a veterinary hospital. Journal of the American Animal Hospital Association 18: 891-899.

Gorrel, C. and Robinson, J. (1995) Endodontics in Small Carnivores. In: Crossley, D. A. and Penman, S. (eds.) BSAVA Manual of Small Animal Dentistry (2nd edition) pp168-181: BSAVA.

Hale, F. A. (2001) Localized intrinsic staining of teeth due to pulpitis and pulp necrosis in dogs. Journal of Veterinary Dentistry 18 (1): 14-20. 

Harvey, C. E. and Emily, P. (1993) Chapter 6 – Endodontics. In: Small Animal Dentistry pp156-212: Moseby, St Louis. 

Kuntsi-Vaatovaara, H., Verstraete, F. J. M. and Kass, P. H. (2002) Results of root canal treatment in dogs: 127 cases (1995-2000). Journal of the American Veterinary Medical Association 220: 775-780. 

Soukup, J. W., Mulherin, B. L. and Snyder, C. J. (2013) Prevalence and nature of dentoalveolar injuries among patients with maxillofacial fractures. Journal of Small Animal Practice 54: 9-14.