38 Enamel dysplasia
The permanent teeth appeared normal when they erupted. However, within a few months sections of enamel seemed to flake off and the teeth started to discolour. The dog had received professional periodontal therapy (scaling and polishing) twice with no obvious improvement. The dog was well mannered until 4 years old, when she started avoiding having her face touched and grew progressively more wary and aggressive. It was now impossible to examine the face at all. There were no problems with a full general examination and aggressive behaviour was only manifest when approaching the head.
Figure 38.2 Selected radiographs. All teeth (except the incisors and canines) were affected by periapical disease. Note the distinct periapical radiolucencies. The inflammation and necrosis of the pulp of these teeth have spread to involve inflammation and destruction of the periapical bone.
Enamel dysplasia (hypoplasia) may be defined as an incomplete or defective formation of the organic enamel matrix of teeth. The result is defective (soft, porous) enamel. It can be caused by local, systemic or hereditary factors. Depending on the cause, the condition can affect one or only a few teeth (localized form), or all teeth in the dentition (generalized form). It is essential to remember that enamel dysplasia results only if the defect occurs during the formative stage of enamel development, i.e. during amelogenesis. Thus, the defect occurs before the tooth erupts into the oral cavity. Crown formation lasts from the 42nd day of gestation through to the 15th day postpartum for the primary teeth, and from the second week through to the third month postpartum for the permanent teeth of dogs and cats. Depending on the time of the insult, enamel dysplasia will affect primary and/or permanent teeth. Only those areas of enamel undergoing active formation during the period of the insult will be affected. This is seen clinically as bands of dysplastic enamel encircling the crown, with areas of normal enamel elsewhere on the tooth.
Teeth with enamel dysplasia may appear normal at the time of eruption, but they soon become discoloured as the defective (porous) enamel soaks up pigments (from food, soil, etc.). In more severely affected teeth, the defective enamel may flake off with use. In very severe cases, the enamel is visibly deficient, discoloured in patches or partly missing already at the time of eruption.
As already mentioned, enamel dysplasia may be caused by local, systemic or hereditary factors. Local factors include trauma to the developing crown, e.g. a blow to the face or an infection. Usually, only one or a few teeth are affected. Systemic factors include nutritional deficiencies, febrile disorders, hypocalcaemia and excessive intake of fluoride during the period of enamel formation. Usually, most teeth are affected. Historically, enamel dysplasia in dogs occurred due to distemper infection. This is rare today, as most dogs are vaccinated against distemper. Hereditary types of enamel dysplasia have been described in humans, but the incidence of this in cats and dogs is unknown.
Poorly protected or exposed dentine is painful. Affected teeth become less sensitive with increasing age of the animal, since secondary dentine is laid down continuously by the pulp. Another consideration is that dysplastic enamel harbours dental plaque.
In severe cases of generalized enamel hypoplasia, where the dentine is effectively exposed to the oral environment, chronic pulp disease and potentially periapical disease may occur due to pulpal irritation via the poorly protected or exposed dentine tubules.