Abstract
Oral Lichen Planus (OLP) is an oral inflammatory condition, mediated by host immune system reaction, presenting basal membrane damages with inflammatory lesions in the mouth and/or skin. In this study, the role of functional polymorphisms in the MBL2 gene, encoding for Mannose-Binding Protein C (MBP-C), a member of the innate immune response and an acute-phase protein able to activate the complement cascade, was investigated to assess a possible association with OLP susceptibility in Italian patients. Two variations at the promoter region (called H/L and X/Y) and three at the first exon (at codon 52, 54, and 57) of the MBL2 gene were analyzed in 69 OLP patients and 244 healthy controls from northeastern Italy. Considering the polymorphisms singularly, the MBL2 X allele and C/T genotype of the D allele (correlated with low MBP-C expression) were associated with susceptibility to develop OLP. Moreover, when taking into account MBL2 combined genotypes, more OLP patients were deficient MBP-C producers than not deficient, who were more represented among healthy controls. MBL2 combined genotypes, responsible for deficient MBP-C production, are associated with an increased risk of developing OLP.
Highlights
Oral Lichen Planus (OLP) is a chronic inflammatory disease with unknown etiology that affects the oral mucosa (Wang and van der Waal, 2015)
We considered the clinical characteristics of the OLP patients: more than 80% were affected by typical bilateral hyperkeratotic reticulated white striae in the buccal mucosa
Taking into account the polymorphisms singularly, the X allele was more frequent in OLP patients compared to healthy controls (p=0.04; OR=1.58; 95%CI=0.98-2.49) (Table 1)
Summary
Oral Lichen Planus (OLP) is a chronic inflammatory disease with unknown etiology that affects the oral mucosa (Wang and van der Waal, 2015). The current hypothesis about OLP etiology and pathogenesis proposes that a T-cell mediated process causes tissue lesions, increasing local cytokines production and altering the expression of adhesion molecules (De Rossi and Ciarrocca, 2014). OLP pathogenesis involves a series of complex non-specific antigens as well as specific mechanisms, and considering the latter, it has been suggested that basal keratinocyte apoptosis is triggered by CD4- and CD8-activated lymphocytes and inflammatory cytokines (Sugerman et al, 2002; Roopashree et al, 2010). OLP is characterized by damaged basal membrane areas forming colloid bodies, resulting in inflammatory eruptive lesions with reddish-purple spots in the mouth and/or skin. A cure for OLP is not available and the only treatment is for symptoms relief (De Rossi and Ciarrocca, 2014)
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