Background:
Although the cause of lichen planus is not completely clear, there is strong evidence suggesting that the underlying pathologic mechanism is immunologic.
Objective:
The aim of this study was to show the effect of apoptotic markers in the etiopathogenesis of lichen planus.
Subjects and Methods:
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.
Results:
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).
Conclusion:
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.
Keywords: Lichen planus, TNF-α, IFN-γ, FAS/APO1