Introduction

Oral lichen planus is a chronic inflammatory  dermal and mucosal disease (1). The prevalence of lichen planus is between 0.1% and 2.2% (2). Some of the contributing co-factors are high blood pressure, diabetes, hepatitis C, blow and increase in drug and metal allergy (1). Recently, a considerable attention has been given to the influence of viruses on neoplasms and premalignant lesions. Human malignancies which appear to be directly related to viral infections have been estimated to be approximately 10% to 20% (2). The investigations have shown that CD8 (+) T cells are activated in lichen planus and substitute keratinocytes. On the other hand, CD8 (+) cytotoxic T cells induce apoptosis in virally infected cells. Therefore, viral infections in oral mucosa may play an important role in oral lichen planus (3).  Oral lichen planus has been reported along with other systemic diseases such as ulcerative colitis, diabetes mellitus, candidiasis, syphilis, AIDS, amoebiasis, acute dermatomyositis, herpes simplex virus type 2, chronic bladder infection and various liver diseases (4-6). The association between erosive OLP and liver cirrhosis has been reported by Rebora et al. (7) in 1978. Since then, this relation has been demonstrated by a number of authors (8-15), however, pathogenesis of LP is still unclear (16). The association of primary biliary cirrhosis and chronic active hepatitis with lichen planus has been mentioned by many studies (12,17-19). According to these studies, the highest prevalence of hepatitis B has been observed in Italy and Spain.

Daramola OO et al. found a higher prevalence of HBsAg in patients with lichen planus when compared with patients with other cutaneous dermatoses or with apparently normal individuals (20). The association of hepatitis B with lichen planus was reported in a research done by Ayala et al. to be 4.7%(21), in the study of a group of dermatologists as 4.8% (22), in the study of Korkij et al. as 4.2%(13) and in Robera et al. research as 11.3%. According to the study by Bagan et al. from 187 oral lichen planus patients, 40 individuals (21.39%) showed an abnormally elevated liver enzymes as well as hepatitis; Hepatitis C was detected in 28 patients (15%) and the rest had hepatitis B(23). In a research by Del Almo et al. (14) in Spain, of 65 oral lichen planus patients, 22 (33.8%) demonstrated clinical symptoms of chronic liver diseases. High prevalence of active chronic hepatitis has also been observed among the lichen planus patients in USA, Sweden and England (15,24,25). Garg et al. in Nepal (26) and Ibrahim et al. in Egypt (27), showed the prevalence of HBsAg to be the same as the control group. According to the research by Banihashemi and Daneshmandrakhi, in Zahedan (south east of Iran), the prevalence of HBsAg positive cases among lichen planus patients was significantly higher compared with the general population (28). Hepatitis B is one of the major public health problems in Iran. According to a study carried out by  Meshkat et al. 1% of population in the city of Mashhad were HBsAg positive, (29). As previous studies have shown a relationship between hepatitis B and OLP, and since the prevalence of HBsAg is greatly influenced by the geographical location, we aimed to distinguish the relationship between OLP and hepatitis B in Mashhad, northeast of Iran.

Materials and Methods

This study was approved by the Ethic Committee of Mashhad University of Medical Science. 134 patients with OLP who referred to the Oral Medicine Department of Mashhad Dental School were participated in the research. All cases were clinically diagnosed in the Oral Medicine Department of Mashhad Dental School. Standard histopathological evaluation and investigation of the biopsy specimens were performed by direct immunofluorescence for suspected cases. Diagnostic criteria, as explained by WHO in 1978, were the basis for clinical and histopathological diagnosis. Patients likely to have developed oral lichenoid reaction, in response to drugs and dental restorative materials, were excluded from this study. The control group consisted of 134 patients that were clinically examined by two dentists to ensure the absence of OLP. Furthermore, patients with suspicious lesions were excluded. Medical histories of study groups were evaluated and all available data on viral hepatitis, risk factors for liver diseases e.g. episodes of jaundice, liver dysfunction, blood transfusion, previous surgery,  smoking habits, intravenous drug abuse, alcohol consumption and other risks of HBsAg infection such as family history of liver disorders were recorded. After signing the consent form, a 5 mL blood sample was obtained from each participant in order to measure levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and bilirubin in serum by standard biochemical methods.
Third-generation enzyme-linked immunosorbent assay (ELISA) was used to perform HBsAg tests.
Chi-square test, Student's t test and nonparametric tests were used for statistical analysis to compare the groups. A significance level of less than 0.05 was considered significant.

Results

Demographic information of OLP patients and the control group is listed in table 1 (30). The average age of patients was 51.60 ± 12.03 and that of the controls was 45.61 ± 17.51. The prominent type of OLP lesions was reticular (31.3 %), which is usually observed in buccal mucosa (76.9%). In addition, liver function tests (LFT) were abnormal in 24.6% of patients and 31.34% of the control group (30). Prevalence of HBsAg in patients with lichen planus was 6.71% which is significantly higher than that of the control group (1.49%) (P=0.03).

Table 1. Demographic Data of the study groups (adapted from 30).