Tooth fractures and treatment options in dogs and cats

David Clarke, BVSc, Diplomate AVDC, Fellow AVD, MANZCVS
Registered Specialist, Veterinary Dentistry and Oral Surgery, Dental Care for Pets, www.vdec.com.au
Telisha Noller, BSc, DVM

Structure of the teeth and tooth supporting apparatus

The adult tooth is comprised of two sections: the crown positioned above the gum margin and the root positioned below the gum margin (Figure 1). The crown is covered by enamel which is formed by ameloblasts prior to tooth eruption. After eruption the ameloblasts die and therefore the enamel has no regenerative properties. Enamel thickness varies from 0.1 – 1mm in cats and dogs (Crossley 1995). The root is covered by cementum, which is formed by cementoblasts. Cementoblasts retain the capacity to produce cementum throughout the tooth’s lifespan. The central portion of the tooth, termed the pulp canal, is a hollow chamber occupied by dental pulp. Dental pulp contains nerves, blood and lymphatic vessels, connective tissue and odontoblasts. Odontoblasts, which line the pulp canal and remain alive throughout the tooth’s lifespan, produce dentine. Dentine produced during tooth development is termed ‘primary dentine’, whilst dentine produced after root formation is termed ‘secondary dentine’ or ‘tertiary dentine’. Secondary dentine is the normal physiological production of dentine resulting in narrowing of the pulp canal and thickening of the tooth wall. Tertiary dentine is produced as an attempt to protect and repair the tooth and prevent pulp exposure when a tooth suffers external wear (abrasion or attrition). The periodontal ligament attaches to the cementum and anchors the tooth onto the surrounding bone.

The pulp communicates with the periodontal ligament at the apical tip of the tooth root. The apical opening in immature adult teeth is open and large. It closes into an apical delta at approximately 11 months of age through a process of apexogenesis (Verstraete 2011, Nanci 2008, Pashley and Liewehr 2006, Evans and de Lahunta 2013, Wilson 1999).

Common Causes of Tooth Fracture

Fractures are a common problem in dogs and cats presented to veterinary clinics worldwide. Fractured teeth have been found in 27% of client-owned dogs (Golden et al 1982) and nearly 10% of cats (Harvey et al 1994) and are often an incidental finding on routine physical examination during vaccination or other visit to the clinic. In dogs presented as referral clients to our practice, the most common teeth fractured are all canine teeth and maxillary 4th premolar teeth. In cats, it is the maxillary canine teeth that are commonly fractured.

A significant number of dogs and cats have access to hard objects, including raw natural bones, antlers, hooves, and nylon bones resulting in injuries caused during chewing; they may also be involved in high impact trauma such as car accidents, sporting injuries, i.e. golf stick/ball, baseball bat; or low impact trauma such as falls resulting in tooth fractures (WSAVA Dental Guidelines 2018). The British Veterinary Dental Association Position Statement has reported that “Many veterinary dentists are reporting that they are seeing fractured teeth as a direct result of chewing on antler bars. In particular, the maxillary fourth premolar tooth” (BVDA website).

A study in foxhounds fed raw carcasses, including raw bones, showed that they had a high prevalence of tooth fractures (Robinson and Gorrel 1997). The skulls of 29 African wild dogs eating a “natural diet”, mostly wild antelope, also showed evidence of teeth wearing (83%) and fractured teeth (48%) (Steenkamp and Gorrel 1999). Nineteen free-ranging maned wolves in Brazil on oral examination revealed 34 teeth with crown fracture in twelve animals (Furtado et al 2007).
Classification of Tooth Fractures

Classification of fractures may be done using the system of traumatic dentoalveolar injuries (Soukup et al 2015) which is based on the amount of tooth structure exposed, i.e. enamel / dentine, crown / root, as well as whether the pulp tissues are exposed. Superficial fractures may result in loss of enamel and/or dentine with no pulp exposure, termed ‘uncomplicated’, whereas more extensive tooth loss may expose the pulp, termed ‘complicated’.

The most common classifications seen in practice are: (See images below)

  • Enamel damage or infraction (Figures 2 and 3):
  • An incomplete fracture (crack) of the enamel without any loss of any tooth substance
  • Enamel loss with no exposure of dentine (Figures 4 and 5): Fracture confined to the enamel
  • Enamel and dentine exposure without pulp exposure (Figures 6 and 7)
  • Crown and root involvement without pulp exposure (Figures 8 and 9)
  • Root fracture without crown damage or pulp exposure (Figures 10 and 11)
  • Pulp exposure isolated to the crown (Figure 12 and 13)
  • Pulp exposure involving both crown and root (Figure 14 and 15)
  • Images (where indicated) are the copyright AVDC, used with permission

Clinical Presentation

When the pulp is exposed and left untreated, the resulting disease will progress over months to years from pulpitis and pulp necrosis to osteomyelitis and sepsis. Clinically, a non-vital maxillary canine or premolar tooth may result in a draining sinus tract adjacent to the medial canthus of the eye or lateral bridge of the nose. A non-vital mandibular canine tooth may produce a sinus tract on the ventral or lateral surface of the mandible. It is also possible for pulpitis or necrosis to occur as a result of an uncomplicated tooth fracture, especially when the fracture is close to the pulp canal, as the exposure of the dentinal tubules can allow communication between the oral cavity and the pulp.

Diagnosis

Every endodontic examination requires tooth exploration and radiographs to confirm or rule out pulp exposure, internal root resorption and to assess the health of the periapical area. When the pulp is not exposed a dental explorer probe drawn across the tooth should feel hard and mineralised. If the fracture is acute and extends into the pulp canal, the pulp will appear pink and may haemorrhage when probed (Figures 13 and 15). Pulp exposure is quite often painful and the patient may hyper-salivate, show anorexia, behavioural changes or resist conscious oral examination. Once the pulp is necrotic, it may appear grey / black and there is usually no haemorrhage or pain on probing.

Treatment Options

Treatment is directly related to the type and degree of damage, the duration of any pulp exposure, as well as the presence or absence of endodontic infection. All teeth with any type of damage should be radiographically examined for signs of non-vitality or infection. If there is evidence of this on radiology, root canal therapy or extraction is necessary.

  • When the defect is confined to the enamel (Figure 5), without dentine or pulp exposure and without radiographic signs of infection, smoothing any sharp edges and restoration is recommended. The tooth should be checked and radiographed after six months to rule out internal resorption and pulp necrosis, which would be observed as decreased pulp canal narrowing, due to no dentine production, compared to the contra-lateral tooth.
  • When dentine is exposed without pulp exposure (Figures 7 and 9) or radiographic signs of infection, smoothing any sharp edges and restoration are recommended. Treatment of dentine exposure is necessary to reduce sensitivity, to seal the dentinal tubules to prevent ingress of bacteria into the pulp canal, to smooth the tooth and to decrease plaque and calculus accumulation. The tooth should be checked and radiographed after six months to rule out internal resorption, pulp necrosis or periapical pathology. Pulpal necrosis would be observed as decreased pulp canal narrowing, due to no dentine production. Periapical pathology, such as a granuloma or abscess is observed as a periapical lucency.
  • Teeth with pulp exposure (Figure 13 and 15) of less than 48hrs may be treated by direct pulp capping or extraction (Clarke 2001). Teeth treated by capping should be radiographed after four months to confirm success, which is observed by formation of a dentinal bridge covering the pulp canal, narrowing of the pulp canal and no signs of the periapical lucency.
    Teeth with pulp exposure (Figure 13 and 15) of longer than 48hrs or radiographic signs of pulpal necrosis/tooth infection requires treatment by extraction or root canal therapy to prevent periapical abscess and osteomyelitis formation which may lead to systemic complications. Teeth treated by root canal treatment should be radiographed after 12 months to confirm success which is observed by resolution of the periapical lucency.
  • Chronic wear results in the production of tertiary or sclerotic dentine so the tooth pulp continues to be protected by a dentinal layer. These teeth require no therapy, as long as they are radiographically healthy. When the tooth is undergoing endodontic disease, they should be extracted or have a root canal procedure performed.

 

 

References

Crossley DA (1995) Tooth enamel thickness in the mature dentition of domestic dogs and cats–preliminary study. J Vet Dent 12(3): 111-113
Verstraete FJM (2011) Small animal dentistry syllabus VSR413 – Winter 2011. Department of surgical and radiological sciences, School of veterinary medicine, University of California-Davis, Davis. 4-14, 22-31
Nanci A (2008) Ten Cate’s oral histology. Development, structure and function. 7th edn. Mosby Elsevier, St. Louis. pp 1-15, 141-318
Pashley DH and Liewehr FR (2006) Structure and functions of the dentin-pulp complex. In: Pathways of the pulp. 9th edn. Eds S. Cohen and K.M. Hargreaves. Mosby Elsevier, St. Louis. pp.460-513
Evans HE and de Lahunta A (2013) Miller’s anatomy of the dog. 4th edn. Elsevier Saunders, St. Louis
Wilson G (1999) Timing of apical closure of the maxillary canine and mandibular first molar teeth in cats. J Vet Dent 16(1):19-21
Golden AL, Stoller N, Harvey CE (1982) A survey of oral and dental diseases in dogs anaethetised at a veterinary hospital. Am Anim Hosp Assoc 18:891-9
Harvey CE, Shofer FS and Laster L (1994). Association of age and body weight with periodontal disease in North American dogs. J Vet Dent 11:94-105
WSAVA Dental Guidelines. http://www.wsava.org/Guidelines/Global-Dental-Guidelines, launched WSAVA Copenhagen 2017
http://www.bvda.co.uk/position-statements
Robinson JGA and Gorrel C (1997) The oral status of a pack of foxhounds fed a “natural” diet. In: Proceedings. World Veterinary Dental Congress, Birmingham, UK
Steenkamp G and Gorrell C (1999) Oral and dental conditions in adult African wild dog skulls: a preliminary result. J Vet Dent 16(2):913-918
Furtado MM, Kashivakura CK and Ferro C (2007) Prevalence of crown trauma in free-ranging maned wolves (Chrysocyon brachyurus) in central Brazil. J Vet Dent 24(4):231-4
Soukup JW, Hetzel S and Paul A (2015) Classification and Epidemiology of Traumatic Dentoalveolar Injuries in Dogs and Cats: 959 Injuries in 660 Patient Visits (2004-2012). J Vet Dent 32(1):6-14
AVDC website. www.avdc.org
Clarke DE (2001) Vital pulp therapy for complicated crown fracture of permanent canine teeth in dogs: a three-year retrospective study. J Vet Dent 18(3): 117-121

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