An Insight into the Pathogenesis of Oral Lichen Planus: A Genomic and Proteomic Case-Control Study

Oral lichen planus (OLP) is a refractory mucosal disease. Its pathogenesis is thought to involve immunologic and genetic alterations. As previous literature pointed out to the significance of interferon-gamma (INF-γ) gene polymorphisms in the pathogenesis of OLP, the present study was performed on a total of 60 OLP patients and 20 unrelated individuals not suffering from any mucosal lesions, to test the role of one of the polymorphisms previously identified among some populations and investigate its link to increased INF-γ production and disease severity. IFN-γ polymorphism at position 5644 (A/T) was identified using Sequence Specific Primers-Polymerase Chain Reaction (SSP-PCR). Also, whole unstimulated saliva samples were collected from all the included individuals in order to determine IFN-γ level in saliva utilizing the ELISA technique. The results revealed no statistically significant difference in T allele distribution among different types of OLP, neither when all patients were considered as a whole nor when they were considered as separate groups. However, there was highly significant increase in the frequency of TT genotype among OLP patients compared to controls. Conversely, there was an increase in AT genotype in controls. Patients carrying TT homozygous genotype were found to have about 9 times more risk of developing OLP, while those with AT heterozygous genotype had low risk of developing the disease. When cases with reticular pattern were considered alone, the risk was found to increase to 12. The results also showed that the control group had the lowest level of salivary IFN-γ, whereas all types of OLP showed highly significant increase in its level. The highest values were registered by the atrophic and erosive groups. When genotypes were considered, TT individuals registered significantly increased salivary IFN-γ levels than other genotypes. It seems that the tested INF-γ gene polymorphism contributes to the predisposition to OLP where the genetic variation affects the gene expression and may contribute to the disease chronicity.