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Year : 2011  |  Volume : 14  |  Issue : 2  |  Page : 228-231

Hepatitis C virus infection in patients with oral lichen planus

1 Department of Oral Medicine and Radiology, Career Post Graduate Institute of Dental Sciences and Hospital, Sitapur Road, Lucknow, UP, India
2 Sree Sai Dental College and Research Institute, Chapuram, Sreekakulam, AP, India

Date of Acceptance20-Feb-2011
Date of Web Publication19-Aug-2011

Correspondence Address:
A Konidena
Department of Oral Medicine and Radiology, Career Post Graduate Institute of Dental Sciences and Hospital, Sitapur Road, Lucknow - 226 020, UP
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1119-3077.84025

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Background: Lichen planus (LP) is a chronic mucocutaneous disease of uncertain etiology. Recent reports suggest that LP is an extrahepatic manifestation of Hepatitis C infection.
Objective: To determine the association of Hepatitis C virus (HCV) infection with oral LP and to study the tests of liver function in patients with oral LP.
Study Design : A cross-sectional case-control study was carried out on 25 patients with oral LP and an equal number of controls. The study was conducted in the outpatient department of a dental college for a period of six months between January and June 2008. The sera of the patients and controls were tested for HCV ribonucleic acid (RNA) using reverse transcription primed-polymerase chain reaction and liver function tests (bilirubin, transaminases, and alkaline phosphatase).
Results: Of the 25 patients with LP, three (12%) had HCV infection. None of the controls had HCV RNA positivity ( P = 0.2347). Oral LP patients had higher serum bilirubin and transaminases when compared with controls ( P < 0.05). However, there was no significant difference in alkaline phosphatase. HCV-positive and -negative patients did not differ significantly in liver function tests.
Conclusions: An increased prevalence of HCV infection was seen in oral LP patients. Our findings support a possible etiological association between these two diseases.

Keywords: Hepatitis C virus infection, liver disease, oral lichen planus

How to cite this article:
Konidena A, Pavani B V. Hepatitis C virus infection in patients with oral lichen planus. Niger J Clin Pract 2011;14:228-31

How to cite this URL:
Konidena A, Pavani B V. Hepatitis C virus infection in patients with oral lichen planus. Niger J Clin Pract [serial online] 2011 [cited 2021 Jun 23];14:228-31. Available from:

   Introduction Top

Lichen planus (LP) is a chronic mucocutaneous disease of uncertain etiology. Stress, anxiety, genetic predisposition, and altered cell-mediated immune response have been considered as possible etiological factors. [1] LP was earlier considered to be associated with systemic diseases like diabetes mellitus, hypertension, myasthenia gravis, ulcerative colitis, and systemic lupus erythematosus, but a consistent association has not been demonstrated. [2],[3] An increased association of LP with chronic liver disease (CLD) was found in the past. [4],[5] Recent reports suggest an association between hepatitis C virus (HCV)-related CLD and oral lichen planus (OLP). [6],[7] HCV is a hepatotropic, single-stranded ribonucleic acid (RNA) virus and has been associated with extrahepatic manifestations and autoimmune diseases, like LP, polyarteritis nodosa, and erythema nodosum. [8] The prevalence of HCV infection among general population in various states of India ranges between 0.1 and 7.9%. [9] Previous published studies from our country showed no correlation between HCV infection and OLP. [10],[11] Hence, we conducted this study to determine the association of OLP and its clinical types with HCV infection.

   Materials and Methods Top

This study was conducted in the outpatient department of a dental college for a period of six months between January and June 2008. A total of 25 consecutive, newly diagnosed OLP patients were selected as study population. OLP patients receiving treatment were excluded from the study. OLP was diagnosed based on clinical features and histopathological findings of overlying keratinization, lymphocytic infiltration into underlying connective tissue, and liquefaction degeneration of basal cell layer. The patients were divided into the following clinical types: [12]


Erosion or ulceration covered with fibrous plaque or pseudoexudate.


Symmetrical, fine, white striae (Wickham's Striae).


Diffuse red lesion; and


Presence of two or more types in the same patient.

A total of 25 age- and sex-matched healthy controls were selected from the friends and relatives attending the hospital outpatient department along with the patients. All participants (study subjects and controls) were asked a detailed history including drug intake like thiazides, beta blockers, chloroquine, etc. A detailed clinical examination was carried out to identify the lesions of LP and other associated hepatic/systemic diseases such as liver cirrhosis, diabetes mellitus, systemic lupus erythematosus, and ulcerative colitis. They also had their blood samples taken for the detection of HCV RNA, serum total bilirubin, alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). Serum total bilirubin was estimated by Van den Bergh reaction, [13] transaminases by colorimetric method, [14] and ALP by King Angstrom method, respectively. [15] The normal range of the laboratory assays were serum bilirubin (3.42-17 μmol/l), AST (0-50 IU/l), ALT (0-60 IU/l), and ALP (0.7-1.9 μkat/l). Detection of HCV RNA was conducted by reverse transcription primed - polymerase chain reaction (RT-PCR) method after RNA isolation by Guanidine isothiocyanate-acid phenol method. [16] HCV antibody was not tested in study participants. All participants gave informed consent and the study protocol was approved by the institutional ethics committee.

The continuous data were presented as mean with standard deviation. Chi-square test and Student's t test was used for statistical analysis to compare between the groups. A significance level of less than 0.05 was considered significant.

   Results Top

There were 15 females and 10 males in the study group with their age ranging between 9 to 65 years. The average age in men and women was 33.1 years and 47.1 years, respectively. The commonest type of OLP was the reticular form, although the erosive form was exclusively seen in two patients. Mixed pattern was seen in 11 patients and the details are shown in [Table 1]. Cutaneous involvement was found in only two patients, with the skin lesions preceding the oral lesions by 8 to 12 months.
Table 1: Demographic data and clinical types of study population

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Three of 25 (12%) patients with OLP tested positive for HCV infection and none of the controls were positive (P = 0.2347). All three HCV-positive patients had reticular lesions and one patient had a mixed pattern including erosive component. Two of three HCV-positive patients with OLP had elevated transaminases, as seen in [Table 2].
Table 2: Details of HCV-positive patients

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Serum bilirubin was elevated in three of 25 (12%), ALT in two (8%), AST in four (16%), and ALP in two (8%) patients with OLP. Serum bilirubin, ALT, and AST showed a significant rise in patients with OLP when compared with controls, but ALP did not differ significantly, as shown in [Table 3]. The mean values of serum bilirubin and ALT of HCV-positive patients were comparable with HCV-negative patients, though mean AST levels of HCV-positive patients was lower [Table 4].
Table 3: Liver function test results in patients and controls

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Table 4: Liver function test results in HCV-positive and -negative patients

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When correlated with the clinical type, the mean values of serum bilirubin and transaminases were lower and ALP was higher in the erosive group (data not shown since there were only two patients with exclusive erosive LP). Patients with atrophic LP had the highest mean transaminase values but not that of ALP. However, when subjected to statistical analysis, the correlation between clinical types and liver function test alterations was not significant.

   Discussion Top

From our study, 12% of patients with OLP were positive for HCV infection. None of the controls had HCV infection. Bagan et al. found that 14.9% of patients with OLP had antibodies to HCV in a study population of 187 patients. [17] Several authors have reported an increased prevalence of CLD in patients with LP and association with Hepatitis C. [4],[5],[6],[7] However, studies from our country and other parts of South Asia did not find an association of LP with HCV infection. [18],[19] Our findings showed an association between patients with OLP and HCV infection, which could be due to differences in genetic, environmental, geographic, or other host factors as described earlier. [20] In our study, we tested for the presence of HCV infection by doing RT-PCR, whereas most of the previous studies used antibodies to HCV as a diagnostic marker of HCV infection. [10],[11] Some studies have detected the presence of positive and negative strands of HCV in the normal as well as lesional mucosa by RT-PCR and in situ hybridization. [21],[22] However, in a study by Femiano and Scully, HCV RNA could not be demonstrated in the lesional or normal mucosa in 25 HCV-positive Italian patients. [23]

In our study, 44% of patients showed alteration in liver function tests, whereas previous studies reported alterations in 7 to 60% patients. [5],[24] Patients with reticular form of OLP mostly had elevated transaminases in our study. Several authors found a statistically significant association between erosive LP and liver function abnormality. [25],[26] This observed discrepancy could be explained as reticular form was the predominant type of LP in our study. HCV infection was seen to be associated more commonly with both erosive and reticular forms. [25],[26],[27] The mean values of bilirubin and ALT of HCV-positive patients were comparable with HCV-negative patients with OLP, though the mean AST levels of HCV-positive patients were lower. This may be due to the frequent fluctuations in biochemical abnormalities in HCV-infected patients.

There are various theories to explain the association between LP and HCV infection. First, alteration in epidermal antigenicity induced by HCV infection leading to proliferation of keratinocytes and second, cytopathic replication of HCV eliciting an autoimmune process. [18] Mega et al. [28] noted a deeper lymphocytic infiltration in the lamina propria and a significant rise in CD-8 cells in cases of HCV-associated LP than idiopathic LP, thereby suggesting that probably HCV acts through the modulation of the quality of the immunologic response.

Our study, though suggest a possible association between OLP and HCV infection, is limited by the small sample size. It also showed elevated transaminases in patients with OLP. Further studies involving larger number of patients are required to validate this association. We recommend routine screening of patients with LP with liver function tests to detect symptomless hepatopathies.

   References Top

1.Anuradha Ch, Reddy BV, Nandan SR, Kumar SR. Oral lichen planus: A review. N Y State Dent J 2008;74:66-8.  Back to cited text no. 1
2.Eisen D. The clinical features, malignant potential, systemic associations of oral lichen planus: A study of 723 patients. J Am Acad Dermatol 2002;46:207-14.  Back to cited text no. 2
3.Mollaoglu N. Oral lichen planus: A review. Br J Oral Maxillofac Surg 2000;38:370-7.  Back to cited text no. 3
4.Robert AS, La Deane F, Keyoumars S, Richmond. The association of mucocutaneous lichen planus and chronic liver disease. Oral Surg Oral Med Oral Pathol 1989;68:406-10.  Back to cited text no. 4
5.Scully C, Potts AJ, Hamburger J, Wiesenfeld D, McKee JI, Elkom M. Lichen planus and liver disease: How strong is the association. J Oral Pathol 1985;14:224-6.  Back to cited text no. 5
6.Tonsi A, Samdani AJ. Association of lichen planus with hepatitis C virus infection. Ann Saud Med 2005;25:243-6.  Back to cited text no. 6
7.Lodi G, Giuliani M, Majorana A, Sardella A, Bez C, Demarosi F et al. Lichen planus and hepatitis C virus: A multicentre study of patients with oral lesions and a systematic review. Br J Dermatol 2004;15:1172-81.  Back to cited text no. 7
8.Bonkovsky HL, Mehta S. Hepatitis C: A review and update. J Am Acad Dermatol 2001;44:159-82.  Back to cited text no. 8
9.Mukhopadhya A. Hepatitis C in India. J Biosci 2008;33:465-73.  Back to cited text no. 9
10.Udayashankar C, Nath A, D'Souza M. Hepatitis C Virus serology in patients with lichen planus. Int J Dermatol 2009;7:2.  Back to cited text no. 10
11.Das A, Das J, Majumdar G, Bhattacharya N, Neogi DK, Saha B. No association between seropositivity for hepatitis C virus and lichen planus: A case control study. Indian J Dermatol Venereal Leprol 2006;72:198-200.  Back to cited text no. 11
12.Thorn JJ, Holmstrup P, Rindum J, Pindborg J. Course of various clinical forms of oral lichen planus: A prospective follow-up study of 611 patients. J Oral Pathol Med 1988;17:213-8.  Back to cited text no. 12
13.Gray CH, Whidborne J. Studies of the Van den Bergh reaction. J Biochem 1946;40:81-8.  Back to cited text no. 13
14.Singh MM, Singh G. An accurate colorimetric technique for serum glutamic oxaloacetate transaminase. Ann Biochem Exp Med 1962;22:309-12.  Back to cited text no. 14
15.King EJ, Abul-Fadl MA, Walker PG. King-Armstrong phosphatase estimation by the determination of liberated phosphate. J Clin Pathol 1951;4:85-91.  Back to cited text no. 15
16.Tuttle RM, Waselenko JK, Yosseffi P, Weigand N, Martin RK. Preservation of nucleic acids for polymerase chain reaction after prolonged storage at room temperature. Diagn Mol Pathol 1998;7:302-9.  Back to cited text no. 16
17.Bagan JV, Aguirre JM, del Olmo JA, Milian A, Penarrocha M, Rodrigo JM. Oral lichen planus and chronic liver disease: A clinical and morphometric study of oral lesions in relation to transaminase elevation. Oral Surg Oral Med Oral Pathol 1994;78:337-42.  Back to cited text no. 17
18.Prabhu S, Pavithran K, Sobhanadevi G. Lichen planus and hepatitis c virus (HCV): Is there an association? A serological study of 65 cases. Indian J Dermatol Venereol Leprol 2002;68:273-4.  Back to cited text no. 18
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19.Ali AA, Suresh CS. Oral lichen planus in relation to transaminase levels and hepatitis C virus. J Oral Pathol Med 2007;36:604-8.  Back to cited text no. 19
20.Al Robaee AA, Al Zolibani AA. Oral lichen planus and hepatitis C virus: Is there real association? Acta Dermatoven 2006;15:15-9.  Back to cited text no. 20
21.Arrieta JJ, Rodriguez-Inigo E, Casqueiro M. Detection of hepatitis C virus replication by in situ hybridization in epithelial cells of anti-hepatitis C virus-positive patients with and without oral lichen planus. Hepatology 2000;32:97-103.  Back to cited text no. 21
22.Nagao Y, Sata M, Noguchi S. Detection of hepatitis C virus RNA in oral lichen planus and oral cancer tissues. J Oral Pathol Med 2000;29:259-66.  Back to cited text no. 22
23.Femiano F, Scully C. Functions of cytokines in relation oral lichen planus-hepatitis C. Med Oral Patol Oral Cir Bucal 2005;10: E40-4.  Back to cited text no. 23
24.Gandolfo S, Gallo V, Carbone M, Zulian P, Carrozzo M. Oral lichen planus in liver pathology: The prevalence of liver damage in a case load of 96 patients with oral lichen planus. Minerva Stomatol 1992;41:203-7.  Back to cited text no. 24
25.Gandolfo S, Carbone M, Carozzo M, Gallo V. Oral lichen planus and hepatitis C virus infection: Is there a relationship: A report of 10 cases. J Oral Pathol Med 1994;23:119-22.  Back to cited text no. 25
26.Dupond AS, Lacour JP, Lafont C, Ortonne JP. Prevalence of hepatitis C virus in oral erosive lichen. Ann Dermatol Venereol 1998;125:676-8.  Back to cited text no. 26
27.Mignogna MD, Lo Muziol L, Lo Russo L, Fedele S, Ruoppo E, Bucci E. Oral lichen planus: Different clinical features in HCV-positive and HCV-negative patients. Int J Dermatol 2000;39:134-9.  Back to cited text no. 27
28.Mega H, Jiang WW, Takagi M. Immunohistochemical study of oral lichen planus associated with hepatitis C virus infection, oral lichenoid contact sensitivity reaction and idiopathic oral lichen planus. Oral Dis 2001;7:296-305.  Back to cited text no. 28


  [Table 1], [Table 2], [Table 3], [Table 4]

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