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Background: Lichen planus (LP) is an idiopathic, chronic, relapsing, inflammatory, autoimmune dermatological disease. The etiopathogenesis of LP is still unclear. Autophagy is a strictly regulated lysosomal degradation pathway that is crucial for maintaining intracellular homeostasis and normal development. The dysregulation of autophagy-associated genes was recognized to increase the susceptibility to multiple diseases, including inflammation, autoimmune disorders and cancer. Aims: Our study aimed to detect the expression of autophagy-related gene 9 b (ATG9B) in LP patients compared to normal control persons to investigate the possible role of autophagy in pathogenesis of this disease. Methods: This case–control study included 30 LP patients and 30 age-, gender-matched healthy controls. Four millimeters punch skin biopsies were obtained from LP lesions and from the controls and they were kept in lysis solution for the stability of the studied parameters and were kept frozen at –80°C till analysis of ATG9B using real-time polymerase chain reaction. Results : The level of ATG9B in lesional skin of LP was significantly decreased compared to normal control persons (P < 0.01); also, there was a non-significant relation between ATG9B level and age, sex, duration and family history among LP patients. Limitations: Limited number of patients included in our study (30 patients). Conclusion: Autophagy may play a role in the pathogenesis of cutaneous LP.

Background: Lichen planus (LP) is a mucocutaneous disease that is relatively common between adult populations. LP can present as skin and oral lesions. Objective: The present study aimed to detect the expression of SOCS3 in lichen planus of diseased patients as compared to normal control persons. Patients and methods: This study was a case control study included 30 Lichen planus patients as cases chosen from outpatients attending Dermatology Department at Beni-Suef University Hospital and 30 normal as controls calculated by sample size calculator formula.Results: In our study, LP cases and control were compared using SOCS3; to determine the cut-off value, we performed a ROC analysis. SOCS3 has perfect value for discrimination between LP cases and controls with an area under the ROC curve of 1.0 (95% CI = 0.940 to 1.000, P-value <0.0001).Best cut-off is a value of 1.5 (sensitivity = 100%, specificity = 1.0, J-index = 1.0). Conclusion: Our results were unique in studying the role of SOCS3 in skin form of LP. SOCS3 has perfect value for discrimination between LP cases and controls.

There is controversy about the role of auto anti-bodies against desmoglein 3 (Dsg 3) in the pathogenesis of lichen planus (LP). The goal of this study is to detect desmoglein-3 auto-antibodies in lichen planus patients comparted to normal control persons via investigating its potential role in the pathogenesis of this disease. A case control study for detection of Desmoglein-3 autoantibodies in serum of 40 lichen planus patients and 40 healthy controls using enzyme-linked immunosorbent assay (ELISA) technique.The patients and healthy controls were recruited from Dermatology outpatient clinic at Beni-Suef University hospital. The measurement of anti Dsg3 antibodies in LP patients was significantly higher as compared to normal control persons. The mean scores were 1361.37 ± 300.5 in oral LP & 2118.70 ± 584.37 in cutaneous LP vs. 66.98 ±70.95 in controls (pvalue < 0.001). Desmoglein-3 auto-antibodies in LP may have a role in the pathogenesis of the disease. Further investigations are needed for detection of Dsg 3 auto-antibodies in LP skin biopsy or blood samples by other methods such as Immunofluorescence.