Elodontoma in Captive Southern Red-Backed Voles (Myodes gapperi)

Fernández, Julia Rodríguez-Ramos; Pinkerton, Marie E.; Heisey, Dennis M.; Drees, Randi; Schneider, Jay R.; Stickney, Lacey; Hofmeister, Erik K.; Guzmán, David Sánchez-Migallón

doi:10.1638/2009-0244.1

Cited by 3 publications

(8 citation statements)

References 15 publications

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“…Pseudo-odontoma was considered appropriate for some of the dysplastic changes, particularly the abnormal matrigenesis, observed at the molar apices but not for the masses of markedly disrupted, haphazardly organized and proliferative odontogenic epithelium. Despite these challenges, the gross and histopathologic features here are very similar to those described in rat-like and squirrel-like rodents, 1,2,13,22 rabbits, 17 and other voles 29 though less proliferative and destructive than those described in guinea pigs and degus. 2,4,16,19,23 Observations in CSF-1-deficient, 14 Snx10-deficient and bisphosphonate-treated (personal observations, D. Imai) osteopetrotic rodents have confirmed that microtraumatic disruption and fragmentation of odontogenic epithelium by bone can produce isolated and disorganized islands of proliferative odontogenic epithelium that can subsequently proliferate into odontoma-like masses.…”

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confidence: 69%

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confidence: 99%

mentioning

confidence: 99%

“…2,6,11 Elongation of the apices of elodont teeth, whether incisor or molar teeth, is well recognized as an acquired dental disease in rabbits and a variety of pet rodents 2 and has been previously described in other arvicoline rodents. 11,12,15,18,29,30 The proposed pathophysiologic mechanisms vary from being a heritable trait 14,15,18 to an acquired disease process 1,2,14 to a multifactorial combination of both. 11,12,29 Because of the inherent implications to management of an endangered species, a detailed investigation into MAE was pursued in this captive breeding colony of Amargosa voles and in museum specimens of other Microtus voles.…”

mentioning

confidence: 99%

“…11,12,15,18,29,30 The proposed pathophysiologic mechanisms vary from being a heritable trait 14,15,18 to an acquired disease process 1,2,14 to a multifactorial combination of both. 11,12,29 Because of the inherent implications to management of an endangered species, a detailed investigation into MAE was pursued in this captive breeding colony of Amargosa voles and in museum specimens of other Microtus voles. The purpose of this study was to morphologically and epidemiologically characterize MAE in this captive breeding colony of Amargosa voles, to ascertain whether MAE is unique to Amargosa voles and to investigate potential causes of MAE, such as a heritable trait, that would influence colony management.…”

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confidence: 99%

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Apical Elongation of Molar Teeth in Captive Microtus Voles

et al. 2018

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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.

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