Subset of CD8+ and FOXP3 + T cells in lichen planus associated with chronic hepatitis C infection.

OBJECTIVE: To verify whether there are differences between populations of CD8 + and FoxP3 + T cells in lesions of oral lichen planus associated with hepatitis C virus chronic infection (OLP-HCV) and lesions of idiopathic oral lichen planus (OLP-I). MATERIALS AND METHODS: A case-control study was performed using a convenience sample of 11 paraffin-embedded tissue blocks of OLP-HCV and 19 of OLP-I. Histological sections stained with haematoxylin and eosin were used to classify the intensity of inflammatory infiltrate. Immunohistochemistry was used to identify CD8 + and FoxP3 + T cells. The count of positive cells was compared between the two groups and correlated to clinical and demographic data (p < 0.05). RESULTS: There were no statistically significant differences in the distribution of CD8 + and FoxP3 + T cells regarding the inflammatory infiltrate in lesions of OLP-HCV and OLP-I. Atrophic/erosive lesions showed a higher relationship between counts of CD8/FoxP3 T cells per mm2 (p = 0.018) and counts of CD8 + T cells per mm2 (p = 0.034) in OLP-HCV group compared to OLP-I group. CONCLUSION: Overall, no difference was found between cell populations in the lesions of OLP-HCV and OLP-I. However, atrophic/erosive lesions of OLP-HCV had a higher amount of CD8 + T cells and lower FoxP3 expression.

Distinct expression profile of HCMV encoded miRNAs in plasma from oral lichen planus patients.

BACKGROUND: Oral lichen planus (OLP) is a T cell-mediated autoimmune disease. The aetiology and molecular mechanisms of OLP remain unclear. Human cytomegalovirus (HCMV) infection is a causal factor in the development of various diseases, but the clinical relevance of HCMV in OLP has not been thoroughly investigated. METHODS: In the present study, we firstly examined twenty-three HCMV-encoded microRNA (miRNA) expression profiles in plasma from training set that including 21 OLP patients and 18 healthy controls using RT-qPCR technology. Dysregulated miRNAs were subsequently confirmed in another larger cohort refereed as validation set consisting of 40 OLP patients and 33 healthy controls. HCMV DNA in peripheral blood leukocytes (PBLs) was also measured in an additional cohort of 13 OLP patients and 12 control subjects. Furthermore, bioinformatics analyses, luciferase reporter assay and western blotting were also performed to predict and verify the direct potential targets of HCMV-encoded miRNAs. RESULTS: The RT-qPCR results showed that the plasma levels of five HCMV-encoded miRNAs including hcmv-miR-UL112-3p, hcmv-miR-UL22a-5p, hcmv-miR-UL148d, hcmv-miR-UL36-5p and hcmv-miR-UL59 were significantly increased in OLP patients in both training and validation sets. HCMV DNA in PBLs was also significantly higher in OLP patients than in control subjects. Additionally, by using a combination of luciferase reporter assay and western blotting, we demonstrated that cytomegalovirus UL16-binding protein 1, a molecule that mediates the killing of virus-infected cells by natural killer cells, is a direct target of hcmv-miR-UL59. CONCLUSIONS: Our results demonstrate a distinct expression pattern of HCMV-encoded miRNAs in OLP patients, which may provide insight into the relationship between HCMV infection and OLP, and warrants additional study in the diagnosis and aetiology of OLP.

No detection of Merkel cell polyomavirus in oral lichen planus: Results of a preliminary study in a French cohort of patients.

Oral lichen planus (OLP) is a chronic inflammatory disease considered as a CD8+ T lymphocyte-mediated autoimmune reaction, which may be triggered by undetermined virus. Recent reports have described the detection of Merkel cell polyomavirus (MCPyV) DNA in oral samples from healthy patients and in patients with different forms of oral cancers. We therefore investigated in a prospective way whether MCPyV was detectable in oral lesions of patients with active OLP. Our preliminary results do not support the hypothesis that OLP may be triggered by MCPyV infection. Further studies are needed to evaluate the involvement of other human polyomaviruses in OLP pathogenesis.

Lack of evidence of hepatitis in patients with oral lichen planus in China: A case control study.

BACKGROUND: China has been one of the countries with high prevalence of chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) liver disease. And lichen planus is an extrahepatic manifestation of patients with chronic HCV infection. This case-control study was conducted to investigate the relationship between oral lichen planus (OLP) and HBV/HCV infection in China. MATERIAL AND METHODS: A total of 776 patients, including 150 patients with OLP (Group OLP), 429 inpatients from the Trauma Ward of Oral and Maxillofacial Surgery Department (Group A), 110 patients with other oral mucosal diseases, but without a reported association with HCV infection (Group B) and 87 patients with oral lichenoid lesion (Group OLL), were compared with their seroprevalence of anti-HCV antibody (HCVAb), hepatitis B surface antigen (HBsAg) and the parameters of liver functions. Moreover, the clinical characteristics of OLP were also observed, such as gender, age, chief complaint, course of the disease, clinical type, sites involved and so on. RESULTS: The positive rates of HCVAb and HBsAg in OLP patients were 0.7% and 4%, respectively. Neither HCVAb nor HBsAg was associated with OLP as demonstrated by both the univariate and the multivariate analyses. The clinical features and liver functions of OLP patients with negative or positive HBsAg were nearly the same. CONCLUSIONS: Our findings verify that there is no association between OLP and hepatitis and there is no need to run a screening test for HCV or HBV in OLP patients in China.

[Determination of human papillomavirus in oral leukoplakia,oral lichen planus and oral squamous cell carcinoma].

OBJECTIVE: To investigate the possibility for human papillomavirus (HPV) infection to be a predictable signal for the carcinogenesis of oral mucosa by comparing the prevalences of HPV in each stage of oral mucosal carcinogenesis and to compare the sensitivity differences of the two methods in detecting HPV infection in oral cavity. METHODS: The hybrid capture (HC-II) was used to detect infection of HPV in 255 samples taken from 12 cases of healthy oral mucosa, 211 cases of patients with pathological diagnosis and 32 cases of patients with clinical diagnosis. The diagnosed cases included 8 cases of benign lesions of the oral mucosa, precancerous lesions [74 cases of oral leukoplakia (OLK) with hyperplasia and 42 cases of OLK with oral epithelial dysplasia (OED)], 91 cases of precancerous condition [oral lichen planus (OLP)] and 28 cases of oral squamous cell carcinoma (OSCC). And in situ hybridization (ISH) was used to detect infection of HPV in 33 cases of OSCC and 76 cases of OLK, including 30 cases of hyperplasia, 15 cases of mild OED, 15 cases of moderate OED and 16 cases of severe OED. RESULTS: The prevalence of HPV in OLP samples was higher (12.12%, 8/66) than that of OLK (2.59%, 3/116) (χ(2)=4.666, P=0.031) and OSCC(7.14%, 2/28, χ(2)=0.513, P=0.474). The prevalence of HPV in OSCC (7.14%, 2/28) was higher than that of OLK (2.59%, 3/116), and no significant difference was found. There was only one case of smoke spot and statistical analysis was not carried out. ISH was used to detect type 16/18 and type 31/33 HPV DNA in 109 cases of oral mucosal lesions in paraffin sections and only one case of OSCC was HPV positive. Thirty-seven cases were detected by HC-II and ISH methods at the same time. The same negative results by the two methods were found in 94.6% samples (35/37). In the other two samples, one was OSCC with early infiltration and the other was OLK with hyperplasia, The HC-II results were positive while the ISH results were negative. The patients with OLP and HPV testing results were followed up and the average follow-up period was (36.2 ± 10.5) months. It was found that three of them had a malignant transformation, and the malignant transformation rate of HPV positive patients was 12.50% (1/8), which was higher than that of HPV negative patients (3.45%, 2/58), and the difference was not statistically significant, P=0.249. CONCLUSION: HC-II assay was more sensitive in detecting HPV infection of oral mucosal lesions than ISH. The results of this study showed that there was insufficient evidence for taking HPV infection as a predictor of OLK carcinogenesis. Patients suffering from OLP were in a precancerous condition. The prevalence of HPV in OLP patients of this study was higher than that in OLK and OSCC patients, suggesting that for some reason, OLP patients were susceptible to HPV. HPV testing can be considered as routine in patients with OLP, and HC-II assay was recommended. And patients with OLP and HPV positive should be followed up regularly.

Role of human papilloma virus-16 in the pathogenesis of oral lichen planus--an immunohistochemical study.

BACKGROUND: Oral lichen planus (OLP) is a common chronic inflammatory immune-mediated disease with an aetiopathogenesis associated with cell-mediated immunological dysfunction. It is possible that oral mucosal viral infections, including human papilloma virus-16 (HPV-16) infection, may have a causative role in OLP pathogenesis. AIM: To assess the prevalence of HPV-16 in histopathologically diagnosed specimens of OLP and to evaluate whether any clinical features (such as the localisation of specimens) or the age or gender of patients, are correlated with the presence of this virus. MATERIALS AND METHODS: This study was conducted on 30 specimens with a histopathological diagnosis of OLP, using the immunohistochemical marker HPV-16. Thirty normal oral mucosa specimens were also included as controls. Brown nuclear staining was accepted as positive for the HPV-16 antibody. The results were analysed using Fisher's exact test. P values<0.05 were considered to be significant. RESULTS: Significant correlation (P=0.0001) was observed between HPV-16 infection and samples with OLP. No statistical conclusions could be drawn regarding age, gender, localisation and HPV-16 positivity. CONCLUSION: Our study showed that HPV-16 may play a role in the pathogenesis of OLP. Taking into account the oncogenic potential of HPV-16, patients with OLP should be screened for the presence of this virus.

Candidiasis and other oral mucosal lesions during and after interferon therapy for HCV-related chronic liver diseases.

BACKGROUND: Oral lichen planus (OLP) is seen frequently in patients with hepatitis C virus (HCV) infection. The aim of this study was to evaluate the occurrence of oral candidiasis, other mucosal lesions, and xerostomia during interferon (IFN) therapy for HCV infection. METHODS: Of 124 patients with HCV-infected liver diseases treated with IFN therapy in our hospital, 14 (mean age 56.00 ± 12.94 years) who attended to receive administration of IFN once a week were identified and examined for Candida infection and other oral lesions and for the measurement of salivary flow. Serological assays also were carried out. RESULTS: Cultures of Candida from the tongue surfaces were positive in 7 (50.0%) of the 14 patients with HCV infection at least once during IFN therapy. C. albicans was the most common species isolated. The incidence of Candida during treatment with IFN did not increase above that before treatment. Additional oral mucosal lesions were observed in 50.0% (7/14) of patients: OLP in three (21.4%), angular cheilitis in three (21.4%) and recurrent aphthous stomatitis in one (7.1%). OLP occurred in one patient before treatment with IFN, in one during treatment and in one at the end of treatment. 85.7% of the oral lesions were treated with topical steroids. We compared the characteristics of the 7 patients in whom Candida was detected at least once during IFN therapy (group 1) and the 7 patients in whom Candida was not detected during IFN therapy (group 2). The prevalence of oral mucosal lesions (P=0.0075) and incidence of external use of steroids (P=0.0308) in group 1 were significantly higher than in group 2. The average body weight of group 1 decreased significantly compared to group 2 (P=0.0088). Salivary flow decreased in all subjects throughout the course of IFN treatment and returned at 6th months after the end of treatment. In group 1, the level of albumin at the beginning of the 6th month of IFN administration was lower than in group 2 (P=0.0550). According to multivariate analysis, one factor, the presence of oral mucosal lesions, was associated with the detection of Candida. The adjusted odds ratio for the factor was 36.00 (95% confidence interval 2.68-1485.94). CONCLUSION: We should pay more attention to oral candidiasis as well as other oral mucosal lesions, in patients with weight loss during IFN treatment.

Prevalence of herpes simplex, Epstein Barr and human papilloma viruses in oral lichen planus.

OBJECTIVES: The aim of the present study was to assess the prevalence of Herpes Simplex virus, Epstein Barr virus and Human Papilloma virus -16 in oral lichen planus cases and to evaluate whether any clinical variant, histopathological or demographic feature correlates with these viruses. STUDY DESIGN: The study was conducted on 65 cases. Viruses were detected immunohistochemically. We evaluated the histopathological and demographic features and statistically analysed correlation of these features with Herpes Simplex virus, Epstein Barr virus and Human Papilloma virus-16 positivity. RESULTS: Herpes Simplex virus was positive in six (9%) cases and this was not statistically significant. The number of Epstein Barr virus positive cases was 23 (35%) and it was statistically significant. Human Papilloma virus positivity in 14 cases (21%) was statistically significant. Except basal cell degeneration in Herpes Simplex virus positive cases, we did not observe any significant correlation between virus positivity and demographic or histopathological features. However an increased risk of Epstein Barr virus and Human Papilloma virus infection was noted in oral lichen planus cases. CONCLUSIONS: Taking into account the oncogenic potential of both viruses, oral lichen planus cases should be detected for the presence of these viruses.

Hepatitis C virus infection in patients with oral lichen planus.

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.

New markers of oxidative stress in lichen planus and the influence of hepatitis C virus infection - a pilot study.

Introduction. Lichen planus (LP) is a mucocutaneous T-cell mediated disorder of unknown etiology. There is growing evidence that oxidative stress is an important player in the pathogenesis of LP. Therefore, we have investigated oxidative stress markers in LP and the influence of hepatitis C virus (HCV) infection, a frequently associated condition, on oxidative stress in LP patients. Method. We have determined the serum levels of 4- hydroxynonenal (4-HNE) and symmetric dimethylarginine (SDMA), as markers of oxidative stress, and total antioxidant capacity (TAC), as a marker of the antioxidant defence, in 4 groups: group A - HCV positive patients with LP (n=12), group B - HCV positive patients without LP (n=12), group C - HCV negative patients with LP (n=31) and group D - control group (n=26). Results. In LP patients, we have identified an increased level of lipid peroxidation (4-HNE - group A - 8.41±1.11 µg/mL, group B - 7.97±2.17 µg/mL, group C - 7.81±1.96 µg/mL and group D - 6.15±1.17 µg/mL) and alterations in arginine methylation (SDMA - group A - 1.10±0.24 µmol/L, group B - 1.03±0.16 µmol/L, group C - 0.84±0.19 µmol/L and group D - 0.50±0.06 µmol/L) associated with a diminished antioxidant defence (TAC - group A - 234.50±49.96, µmol/L group B - 255.83±41.41 µmol/L, group C - 269.83±43.33 µmol/L and group D - 316.46 ±29.33 µmol/L), processes augmented by the association with HCV infection. Conclusion. There is an imbalance between oxidants and antioxidants in patients with LP, an imbalance that is augmented by the presence of HCV infection. SDMA could be regarded as a novel biomarker of oxidative stress among these patients. To the best of our knowledge this is the first study to investigate the influence of HCV infection on oxidative stress in LP patients.

High Prevalence of Human Papillomavirus Type 18 in Oral Potentially Malignant Disorders in Thailand.

OBJECTIVES: The main objectives of this study were to investigate the detection rate of high-risk human papillomavirus types 16 and 18 (high-risk HPV16/18) in oral potentially malignant disorders (OPMDs) including oral leukoplakia (OL) and oral lichen planus (OLP) in a Thai population and their associations with demographic, risk habits, and clinicopathologic features. METHODS: Paraffin-embedded formalin-fixed specimens from 101 OL and 59 OLP patients with patients' demographic, risk habits, and clinicopathologic data were collected. Conventional qualitative polymerase chain reaction was used to detect high-risk HPV16/18 DNA. Associations between high-risk HPV type 16/18 and demographic, clinicopathologic, risk factors (tobacco and alcohol uses) of OPMDs were analysed by Chi-square or Fisher's exact test. The results with p value less than 0.05 were considered statistically significant. RESULTS: HPV16/18 DNA was found in both OL and OLP groups with the detection rate of 19.8% and 18.6%, respectively. Approximately 90% of high-risk HPV were HPV18 subtype. Additionally, in OL group, high-risk HPV was found more frequently in patients with moderate/severe dysplasia than that in mild dysplasia. Interestingly, in OLP group, high-risk HPV was only detected in atrophic/ulcerative subtypes. None of risk factors was associated with high-risk HPV. CONCLUSIONS: Approximately 19% of OPMDs were HPV16/18-positive. HPV18 DNA was predominantly detected in both OL and OLP patients (90%). Additionally, the detection rate of high-risk HPV was higher in more severe dysplastic cases of OL and more clinically severe cases of OLP.

Prevalence of Merkel Cell Polyomavirus (MCPyV) in the Oral Cavity Biopsies in Northern Iran.

OBJECTIVE: Infection with human tumor viruses is one of the hypothesized causes of cancer. The current investigation aimed to explore the presence and quantitative analysis of a new human tumor virus, Merkel cell polyomavirus (MCPyV) in tissue samples of 114 patients with oral cavity lesions including oral squamous cell carcinoma (OSCC), oral lichen planus (OLP), Dysplasia and oral irritation fibroma (OIF) in Northern Iran. METHODS: From 114 formalin fixed paraffin embedded samples; 35 with SCC, 29 with OLP, 14 with dysplasia and 36 with OIF were cut, deparaffinized and DNA was extracted. Quantitative detection of MCPyV large T antigen was performed by absolute quantitative Real-Time PCR. RESULT: MCPyV DNA was detected in 30.6% (n: 11/36) of IF, 24.1% (n; 7/29) of OLP, 21.4% (n:3/14) of dysplasia and 20% (n;7/35) of OSCC samples. The mean MCPyV DNA copy number was 2.32×10-2 ± 3.97 ×10-2, 2.02×10-2 (SD=3.13×10-2), 2.69×10-4 (SD=2.51×10-4), and 2.56×10-4 (SD=6.73×10-4) per cell in OSCC, dysplasia and both of OLP and OIF samples, respectively (P=0.76). CONCLUSION: This study provides the first data from Iran regarding the presence of MCPyV genome in oral cavity lesions and oral cancer. These results also emphasize that MCPyV has an active role in the occurrence of oral lesions and progression to cancer. Further studies should be carried out to clarify the role of MCPyV in oral cavity lesions.

Progressive increase of human papillomavirus carriage rates in potentially malignant and malignant oral disorders with increasing malignant potential.

INTRODUCTION: We investigated the potential role of human papillomaviruses (HPVs) in potentially malignant oral disorders, oral leukoplakia (OL) and oral lichen planus (OLP), and in oral squamous cell cancer (OSCC) in an Eastern Hungarian population with a high incidence of OSCC. METHODS: Excised tumor samples (65 OSCC patients) and exfoliated cells from potentially malignant lesions (from 44 and 119 patients with OL and OLP, respectively) as well as from healthy controls (72 individuals) were analysed. OLPs were classified based on clinical appearance, 61 patients had erosive-atrophic lesions (associated with higher malignancy risk, EA-OLP) and 58 had non-erosive non-atrophic lesions (with lower risk of becoming malignant, non-EA-OLP), respectively. Exfoliated cells collected from apparently healthy mucosa accompanied each lesion sample. HPV was detected by MY/GP polymerase chain reaction (PCR) and genotyped by restriction analysis of amplimers. Copy numbers in lesions were determined using real-time PCR. Prevalence rates, copy number distributions, and association with risk factors and diseases were analysed using chi-square test, t-test, and logistic regression, respectively. RESULTS: We detected HPVs significantly more frequently in lesions than in controls (P < or = 0.001 in all comparisons). HPV prevalence increased gradually with increasing severity of lesions (32.8, 40.9, and 47.7% in OLP, OL, and OSCC, respectively). Copy number distribution patterns roughly corresponded to prevalence rates, but OLP and OL were comparable. HPV prevalence differed significantly between EA-OLP and non-EA-OLP groups (42.6 vs. 22.4%); EA-OLP group showed a prevalence similar to that found in OL. CONCLUSION: HPVs may be involved in the development or progression of not only OSCC but also of potentially malignant oral lesions.

Epstein-Barr virus prevalence in oral squamous cell cancer and in potentially malignant oral disorders in an eastern Hungarian population.

We tested 65, 44, and 116 patients with oral squamous cell cancer (OSCC), oral leukoplakia (OL), and oral lichen planus (OLP) against 68 age-matched controls for the presence of Epstein-Barr virus (EBV). Apparently healthy mucosa was simultaneously sampled and examined in all patients. Paraffin-embedded tissue sections of all EBV-positive patients with OSCC were examined for latent membrane protein-1 (LMP-1) expression (demonstrable in most EBV-associated malignancies) using immunohistochemistry. The prevalence of EBV in the controls and in OSCC, OL, and OLP lesions was 19.1%, 73.8%, 29.5%, and 46.6%, respectively, and 66.2%, 22.7%, and 31.9% in the healthy mucosa of patients, respectively. The prevalence of EBV in OSCC patients was significantly higher than in controls or in respective samples of the other two patient groups both in the lesion and in the healthy mucosa. Comparisons including only patients with EBV-negative lesions yielded similar results. Lesions of patients with OLP, but not of patients with OL, differed significantly from controls in EBV prevalence. In OSCC, LMP-1 expression was not detected, and EBV carriage was not significantly associated with any risk factors and did not influence the outcome. Although a high prevalence of EBV was found in OSCC, comparable carriage rates on healthy mucosa of patients indicated that an aetiological role of EBV is unlikely.

Human papillomavirus in premalignant oral lesions: No evidence of association in a Spanish cohort.

BACKGROUND: Human papillomavirus (HPV) is the cause of a fraction of head and neck squamous cell carcinoma. Although this relation is well-known, it is still not clear the role of HPV in premalignant oral lesions such as oral lichen planus (OLP) and dysplasia. We aimed to evaluate the HPV-DNA prevalence and type distribution in a set of oral biopsies obtained from patients diagnosed with OLP and dysplasia, as well as the role of HPV in these lesions. METHODS: A retrospective cohort of all premalignant oral lesions consecutively diagnosed from March 30th 1995 to May 21st 2014 at Hospital of Bellvitge and Odontological University Hospital of Bellvitge was identified and classified in four groups: OLP (groups 1 and 2) and dysplasias (groups 3 and 4) that progressed or not to invasive cancer during follow-up. A random selection targeting 25 cases was aimed to be performed for each group. All selected cases were subjected to pathological evaluation, DNA quality control and HPV-DNA detection. HPV-DNA positive samples were further subject to p16INK4a analysis. RESULTS: A total of 83 cases yielded a valid HPV-DNA result. From those, 7 and 34 cases were OLP that progressed or not to invasive cancer during follow-up, whereas 24 and 18 cases were displasias that progressed or not to invasive cancer during follow-up, respectively. HPV-DNA was detected in 4 samples (3 dysplastic lesions and 1 OLP). Two samples were HPV16 positive (2%), 1 sample HPV18 positive (1%) and 1 sample (1%) was HPV indeterminate. Two out of four HPV-DNA positive cases had high p16INK4a expression and none of the HPV positive cases progressed to invasive cancer during long-term follow-up. CONCLUSIONS: We found a low HPV-DNA attributable fraction in premalignant lesions of the oral cavity, suggesting that HPV is unlikely to play a significant role in oral carcinogenesis in our setting.

Oral human papilloma virus infection: an overview of clinical-laboratory diagnosis and treatment.

OBJECTIVE: The aim of this review is to describe the "hot points" of current clinical governance for oral HPV comprising the use of new diagnostic molecular procedures, namely, Pyrosequencing and Next Generation Sequencing. MATERIALS AND METHODS: The data on oral HPV was collected through two levels of research. First for all, we used the canonical medical search engines, PubMed, and Medline, followed by the study of current commercial tools for HPV diagnosis, particularly within commercial companies involved in the molecular procedures for HPV detecting and genotyping. RESULTS: Different medical procedures are now described and used throughout the world in HPV diagnosis and treatment. However, the laboratory methods are often validated and used for genital infections, and, in these cases, data are missing in the literature as regards the clinical approach for oral lesions. CONCLUSIONS: Dental care units are often the front line for a clinical evaluation of a possible HPV lesion in the oral cavity, which means that correct clinical governance could avoid a viral neoplastic progression of this disease with great advantages for the patient. In this case, the problem is due to the difficulty in lesion recognition but also and more especially the absence of correct laboratory diagnosis and subsequent treatment in the clinical course.

Skew in T cell receptor usage with polyclonal expansion in lesions of oral lichen planus without hepatitis C virus infection.

Oral lichen planus (OLP) is a refractory disorder of the oral mucosa. Its predominant symptoms are pain and haphalgesia that impair the quality of life of patients. OLP develops via a T cell-mediated immune process. Here, we examined the characteristics of the infiltrating T cells in terms of the T cell receptor (TCR) repertoires, T cell clonality, T cell phenotypes and cytokine production profiles. TCR repertoire analyses and CDR3 size spectratyping were performed using peripheral blood mononuclear cells (PBMCs) and tissue specimens of OLP biopsies from 12 patients. The cytokine expression profiles and T cell phenotypes were measured by real-time quantitative polymerase chain reaction. We observed that there were skewed TCR repertoires in the tissue samples (TCRVA8-1, VA22-1, VB2-1, VB3-1 and VB5-1) and PBMCs (TCRVA8-1, VB2-1, VB3-1 and VB5-1) from OLP patients. Furthermore, the CDR3 distributions in the skewed TCR subfamilies exhibited polyclonal patterns. We observed increases in CD4(+) T lymphocytes, interleukin (IL)-5, tumour necrosis factor (TNF)-alpha and human leucocyte antigen D-related in the OLP tissue specimens. Taken together, the present results suggest that T cells bearing these TCRs are involved in the pathogenesis of OLP, and that IL-5 and TNF-alpha may participate in its inflammatory process.

Oral diseases associated with hepatitis C virus infection. Part 2: lichen planus and other diseases.

Some of the most frequent extrahepatic manifestations of hepatitis C virus (HCV) infection involve the oral region predominantly or exclusively. Part 2 of this review discusses the current evidences regarding the association of lichen planus (LP) and other diseases frequently involving the oral cavity with HCV. Epidemiological data suggest that LP may be significantly associated with HCV infections especially in southern Europe and Japan but not in northern Europe. These geographical differences are possibly influenced by immunogenetic factors, the duration of the HCV infection and the design of the published studies. Because of the fact that most of the studies published are retrospective, it is impossible to establish whether the HCV exposure occurred earlier to or after the onset of disease and more prospective studies are clearly warranted. As the virus may replicate in the skin and oral mucosa and HCV-specific T lymphocytes can be found in the oral mucosa of patients with chronic hepatitis C and LP, HCV may be implicated in the pathogenesis of LP. However, little attention has been paid to the variable effect of therapy with interferon-alpha (IFN-alpha), with or without ribavirin for LP. Conversely, it is unlikely that other oral diseases such as oral carcinoma, pemphigus and Behcet disease are triggered by HCV.