Publication date: January 2017
Source:Archives of Oral Biology, Volume 73
Author(s): Vania Polesello, Luisa Zupin, Roberto Di Lenarda, Matteo Biasotto, Gabriele Pozzato, Giulia Ottaviani, Margherita Gobbo, Sergio Crovella, Ludovica Segat
ObjectivesThe aetiology of Oral Lichen Planus (OLP), a chronic inflammatory disease of oral mucosa, is not yet well understood. Since innate immunity may be hypothesized as involved in the susceptibility to OLP, we studied human beta defensin 1 (hBD-1) an antimicrobial peptide constitutively expressed in the saliva, looking at functional genetic variants possibly able to diminish hBD-1 production an consequently conferring major susceptibility to OLP.DesignWe analysed three DEFB1 polymorphisms at 5′ UTR, −52G>A (rs1799946), −44C>G (rs1800972), −20G>A (rs11362) and two DEFB1 polymorphisms at 3′UTR, c*5G>A (rs1047031), c*87A>G (rs1800971), with the aim of correlating these genetic variants and hBD-1 salivary level in a group of OLP patients and in healthy subjects. We also evaluated hBD-1 salivary concentrations, using ELISA, in OLP and healthy controls.ResultsWe compared hBD-1 concentrations in OLP and healthy subjects: hBD-1 concentration was significantly higher in OLP patients respect to control.When considering the correlation between DEFB1 polymorphisms genotypes and hBD-1 expression levels, significant results were obtained for SNPs −52G>A (p=0.03 both in OLP patients and healthy individuals) and −44C>G (p=0.02 in OLP patients).ConclusionshBD-1 production was different between OLP and healthy subjects (not age-matched with OLP). DEFB1 gene polymorphisms, −52G>A and −44C>G, correlated with hBD-1 salivary concentrations.
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