ABSTRACT
Hereditary hyperplastic gingivitis is a progressive growth of gingival tissues in foxes resulting in dental encapsulation. It is an autosomal recessive condition displaying a gender-biased penetrance, with an association with superior fur quality. This disease has been primarily described in European farmed foxes. Here we document its emergence in Canada.
Gingivite hyperplasique héréditaire chez le renard argenté d'élevage d'Amérique du Nord(Vulpes vulpes). La gingivite hyperplasique héréditaire est une croissance progressive des tissus gingivaux chez les renards qui produit une encapsulation dentaire. Il s'agit d'une affection récessive autosomique qui manifeste une pénétration privilégiant un sexe et qui présente une association avec une qualité de fourrure supérieure. Cette maladie a été principalement décrite chez les renards d'élevage européen. Nous documentons ici son émergence au Canada.(Traduit par Isabelle Vallières).
Subject(s)
Foxes , Genetic Predisposition to Disease , Gingivitis/veterinary , Hyperplasia/veterinary , Animals , Gingivitis/genetics , Gingivitis/pathology , Hyperplasia/genetics , Hyperplasia/pathologyABSTRACT
Hereditary hyperplastic gingivitis (HHG) is an autosomal recessive condition found predominantly in farmed silver foxes, first documented in Europe in the 1940s. Hereditary gingival fibromatosis (HGF) is an analogous condition occurring in humans. HGF has a heterogeneous aetiology with emphasis placed on the autosomal dominant forms of inheritance for which there are three known loci: HGF1, HGF2, and HGF3. Among these, only one causative mutation has been determined, in the Son of sevenless homolog 1 (SOS1) gene. The goal of this study was to explore potential molecular or cellular mechanisms underlying HHG by analysis of global gene expression patterns from Affymetrix Canine 2.0 microarrays cross-referenced against candidate genes within the human loci. We conclude that the SOS1 gene involved in HGF1 is not significantly up-regulated in HHG. However, the structurally and functionally similar SOS2 gene is up-regulated in affected foxes, and we propose this as a candidate gene for HHG. At HGF2 we identify RASA1 (rat sarcoma viral p21 protein activator 1) as a candidate gene for HHG, as it is up-regulated in affected foxes and is involved in MAPK signalling. From comparison to the genes within the HGF3 locus, we find evidence for a role of androgens in HHG phenotype severity by differential up-regulation of SRD5A2 in HHG-affected foxes. We hypothesize that the putative mutation occurs upstream of RAS in the extracellular signal-regulated kinase component of MAPK signalling.
