Apical Elongation of Molar Teeth in Captive Microtus Voles.

Molar apical elongation (MAE) was the leading cause for euthanasia or death in a captive breeding colony of endangered Amargosa voles ( Microtus californicus scirpensis). Clinical signs included ocular discharge, abnormal mastication, dyspnea, abnormal mentation, weight loss, and death. Although the severity varied, all molars in all quadrants were affected. When severe, the overgrown molar reserve crown and apex protruded into the nasal meatuses, the orbit, the calvarial vault and through the ventral margin of the mandible. Overall prevalence in the colony was 63% (92/146 voles) and increased to 77% in aged voles (>1 year). Mean age of onset was 5.3 months (1.7-11.2 months). Progression to extreme severity occurred over 1 to 3 months. Mean survival was 10.9 months (7.1-21.7 months). Histologically, the lesion was characterized by odontogenic hyperplasia and dysplasia. MAE was also documented in museum specimens of 2 other M. californicus subspecies ( M. californicus californicus, M. californicus vallicola) and 3 other Microtus species ( M. montanus, M. pennsylvanicus, M. socialis). In the M. californicus californicus collection, overall prevalence was 35.1% (129/368 skulls) and increased to 77.3% in aged voles (>1 year). A probable genetic influence was identified in the museum collection of M. californicus californicus. The etiopathogenesis of MAE is likely multifactorial, due to (1) inherent continuous odontogenic proliferation, (2) inadequate occlusal attrition, and (3) possible heritable disease susceptibility. In captivity, dietary or other management of occlusal attrition to prevent or delay MAE is a fundamental concern.

Odontogenic dysplasia in the molar teeth of Steppe lemmings (Lagurus lagurus).

In a colony of Steppe lemmings (Lagurus lagurus), of the rodent sub-family Arvicolinae, 8.6% of animals exhibited dysplastic growth of the molar teeth. Clinical findings included nodular swellings of the mandible, hypersalivation, malocclusion and emaciation. To investigate the underlying cause, two control and 10 affected animals, aged between 6 and 18 months, were examined using radiography and computed tomography and at post mortem examination. Bilaterally symmetrical masses were identified in the molar regions of the left and right mandible and maxillae. Histologically, the masses were characterised by dysplastic odontogenic epithelium, dentin, cementum, enamel and dental pulp formation that resembled odontogenic dysplasia. This tumour-like proliferative lesion has been reported in the continuously-growing incisor teeth of ageing rodents and lagomorphs but this is the first description of the clinico-pathological features of such odontogenic dysplasia of the molar teeth of Steppe lemmings.

Multifocal odontoblastic dysplasia in a dog.

A two-year-old Boerboel dog presented for a discolored left maxillary canine tooth. Dental radiographs revealed abnormally mineralized pulp within the discolored tooth. Similar radiographic findings were also seen in both maxillary third incisor teeth and in the remaining canine teeth to varying degrees. The discolored tooth was treated by surgical extraction and histopathology revealed abnormal dentin deposition within the canal indicative of dentin dysplasia. Although not previously documented in the dog, the pulpal changes in multiple teeth of the dog reported here were similar to those described for odontoblastic dysplasia in humans. This case report includes a review of developmental abnormalities of dentin in humans and pulpal response to inflammation and injury.

Odontodysplasia in a horse.

Weight loss, poor growth and dysphagia occurred in a young stallion with some teeth missing, and soft, discolored and/or deformed deciduous incisors, premolars and molars. At necropsy, permanent teeth sites were filled with yellow, gelatinous material. Clinical signs suggested fluorosis but laboratory findings did not confirm the diagnosis.