ABSTRACT

Although the cause of lichen planus is not completely clear, there is strong evidence suggesting that the underlying pathologic mechanism is immunologic.

The aim of this study was to show the effect of apoptotic markers in the etiopathogenesis of lichen planus.

Twenty-one patients diagnosed with lichen planus clinically and histopathologically were included in the study. The control group included 12 healthy subjects. TNF- α, IFN-γ and Fas/APO levels in tissue and serum were measured using ELISA kits.

No significant difference was found between the patient and control groups with regard to serum TNF-α and Fas antigen levels, but IFN-γ level was significantly lower in the patient group than in the control group (p=0.003). No significant difference was found between tissues with lesion and control tissues in terms of TNF-α and IFN-γ (p=0.178, p=0.190), but Fas antigen was statistically significantly higher in the patient group than the control group (p=0.001). No difference was found between non-lesional tissues in the patient group and control tissues with regard to TNF-α, Fas antigen and IFN-γ levels (p=0.575, p=0.238, p=0.085). No significant difference was found between the tissues with and without lesions in the patient group with respect to TNF-α values (p=0.448), but Fas antigen was established to be statistically significantly higher in the tissues with lesion than those without (p=0.000) while IFN-γ was significantly higher in the tissues without lesion (p=0.014).

In lichen planus, while IFN-γ tissue levels were low and Fas antigen tissue levels were high, serum TNF-α levels were found to be low. These parameters support the pathogenesis of the disease and the results of previous studies.