RESUMEN
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.