Background. Oral lichen planus (OLP) is a common chronic inflammatory immune-mediated disease, with an etiopathogenesis associated with cell-mediated immunological dysfunction. Viral infection has been hypothesized as a predisposing factor in the pathogenesis of this disease. Viruses may alter host cell function by inducing the abnormal expression of cellular proteins leading to disease development. However, reports on the relationship between human papillomavirus (HPV) and OLP are inconclusive. Objective. To explore the association between HPV and OLP in Thai patients. Materials and Methods. DNA was extracted from thirty-seven fresh-frozen tissue biopsy specimens from OLP lesions, and polymerase chain reaction assay for the L1 and E1 genes covering 32 types of high- and low-risk HPV was performed. Results. HPV DNA was detected in one tissue biopsy from an atrophic-type OLP lesion. All control samples were negative. Genomic sequencing of the E1 gene PCR product demonstrated that the HPV-type 16 found in the lesion is closely related to the East Asian type. Conclusion. Our data indicate a low prevalence of HPV infection in OLP lesions in Thai patients. 1. Introduction Oral lichen planus (OLP) is a chronic inflammatory disease in which the immunopathogenesis involves cell-mediated immune dysregulation [1]. OLP affects 0.5–2.2% of the global population. However, prevalence varies according to geographic location [2]. This disease is commonly seen in Thai patients [3], with presentations ranging from symptom-free to a burning sensation or severe pain interfering with phonation, mastication, and deglutition [1]. OLP is classified as a potentially malignant disorder (PMD) of the oral mucosa with a transforming rate of 0–6.25% [1, 4]. Histologically, lesions are characterized by hyperkeratosis, basal layer liquefaction of the oral epithelium-connective tissue interface, and a dense infiltration of a band of lymphocytes [5, 6]. Unidentified antigen presented to lymphocytic cells may play a role in this disease. Previous studies suggest that OLP is a T-cell-mediated inflammatory disease in which autocytotoxic CD8+T cells trigger apoptosis in oral epithelial cells [1]. Exogenous agents may also alter keratinocyte antigen expression. The response of these specific CD8+T cells is similar to what occurs during a viral infection where a virus can act as a cytoplasmic antigen or induce the expression of host cell proteins, resulting in an altered host cell protein profile [7]. Therefore, it is of interest to investigate the possibility of viral involvement in the
References
[1]
G. Lodi, C. Scully, M. Carrozzo, M. Griffiths, P. B. Sugerman, and K. Thongprasom, “Current controversies in oral lichen planus: report of an international consensus meeting—part 1: viral infections and etiopathogenesis,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 100, no. 1, pp. 40–51, 2005.
[2]
B. E. McCartan and C. M. Healy, “The reported prevalence of oral lichen planus: a review and critique,” Journal of Oral Pathology and Medicine, vol. 37, no. 8, pp. 447–453, 2008.
[3]
K. Thongprasom, P. Youngnak-Piboonratanakit, S. Pongsiriwet, T. Laothumthut, P. Kanjanabud, and L. Rutchakitprakarn, “A multicenter study of oral lichen planus in Thai patients,” Journal of Investigative and Clinical Dentistry, vol. 1, no. 1, pp. 29–36, 2010.
[4]
M. Gorsky and J. B. Epstein, “Oral lichen planus: malignant transformation and human papilloma virus: a review of potential clinical implications,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 111, no. 4, pp. 461–464, 2011.
[5]
M. H. Thornhill, “Immune mechanisms in oral lichen planus,” Acta Odontologica Scandinavica, vol. 59, no. 3, pp. 174–177, 2001.
[6]
I. Al-Hashimi, M. Schifter, P. B. Lockhart et al., “Oral lichen planus and oral lichenoid lesions: diagnostic and therapeutic considerations,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 103, pp. S25.e1–S25.e12, 2007.
[7]
A. K. Abbas and A. H. Lichtman, “Immunity to microbes,” in Cellular and Molecular Immunology, chapter 15, pp. 345–366, WB Saunders, Philadelphia, Pa, USA, 5th edition, 2004.
[8]
J. Rautava and S. Syrj？nen, “Human papillomavirus infections in the oral mucosa,” Journal of the American Dental Association, vol. 14, pp. 905–914, 2011.
[9]
S. M. Syrj？nen, G. Lodi, I. von Bültzingsl？wen et al., “Human papillomaviruses in oral carcinoma and oral potentially malignant disorders: a systematic review,” Oral Diseases, vol. 17, supplement 1, pp. 58–72, 2011.
[10]
A. Marini, M. Wagenmann, E. Ting, and U. R. Hengge, “Squamous cell cancer and human papillomavirus infection in oral lichen planus: case report and literature review,” Dermatologic Surgery, vol. 33, no. 6, pp. 756–760, 2007.
[11]
H. zur Hausen, “Papillomaviruses and cancer: from basic studies to clinical application,” Nature Reviews Cancer, vol. 2, no. 5, pp. 342–350, 2002.
[12]
S. Syrj？nen and K. Syrj？nen, “HPV infections of the oralmucosa,” in Papillomavirus Infections in Human Pathology, K. Syrj？nen and S. Syrj？nen, Eds., chapter 17, pp. 379–412, John Wiley & Sons, New York, NY, USA, 2000.
[13]
M. Jontell, S. Watts, M. Wallstrom, L. Levin, and K. Sloberg, “Human papilloma virus in erosive oral lichen planus,” Journal of Oral Pathology and Medicine, vol. 19, no. 6, pp. 273–277, 1990.
[14]
G. Campisi, L. Giovannelli, P. Aricò et al., “HPV DNA in clinically different variants of oral leukoplakia and lichen planus,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 98, no. 6, pp. 705–711, 2004.
[15]
L. Giovannelli, G. Campisi, G. Colella et al., “Brushing of oral mucosa for diagnosis of HPV infection in patients with potentially malignant and malignant oral lesions,” Molecular Diagnosis and Therapy, vol. 10, no. 1, pp. 49–55, 2006.
[16]
V. E. Furrer, M. B. Benitez, M. Furnes, H. E. Lanfranchi, and N. M. Modesti, “Biopsy versus superficial scraping: Detection of human papillomavirus 6, 11, 16, and 18 in potentially malignant and malignant oral lesions,” Journal of Oral Pathology and Medicine, vol. 35, no. 6, pp. 338–344, 2006.
[17]
D. J. Adelstein, J. A. Ridge, M. L. Gillison et al., “Head and neck squamous cell cancer and the human papillomavirus: summary of a national cancer institute state of the science meeting, November 9-10, 2008, Washington, D.C.,” Head & Neck, vol. 31, no. 11, pp. 1393–1422, 2009.
[18]
K. Szarka, I. Tar, E. Fehér et al., “Progressive increase of human papillomavirus carriage rates in potentially malignant and malignant oral disorders with increasing malignant potential,” Oral Microbiology and Immunology, vol. 24, no. 4, pp. 314–318, 2009.
[19]
T. Yamada, M. M. Manos, J. Peto et al., “Human papillomavirus type 16 sequence variation in cervical cancers: a worldwide perspective,” Journal of Virology, vol. 71, no. 3, pp. 2463–2472, 1997.
[20]
F. Stubenrauch and L. A. Laimins, “Human papillomavirus life cycle: active and latent phases,” Seminars in Cancer Biology, vol. 9, no. 6, pp. 379–386, 1999.
[21]
W. Lurchachaiwong, P. Junyangdikul, S. Payungporn et al., “Human papillomavirus genotypes among infected Thai women with different cytological findings by analysis of E1 genes,” New Microbiologica, vol. 34, no. 2, pp. 147–156, 2011.
[22]
S. P. Khovidhunkit, W. Buajeeb, S. Sanguansin, S. Poomsawat, and W. Weerapradist, “Detection of human papillomavirus in oral squamous cell carcinoma, leukoplakia and lichen planus in Thai patients,” Asian Pacific Journal of Cancer Prevention, vol. 9, no. 4, pp. 771–775, 2008.
[23]
N. J. Maitland, T. Bromidge, M. F. Cox, I. J. Crane, S. S. Prime, and C. Scully, “Detection of human papillomavirus genes in human oral tissue biopsies and cultures by polymerase chain reaction,” The British Journal of Cancer, vol. 59, no. 5, pp. 698–703, 1989.
[24]
M. Cox, N. Maitland, and C. Scully, “Human herpes simplex-1 and papillomavirus type 16 homologous DNA sequences in normal, potentially malignant and malignant oral mucosa,” European Journal of Cancer Part B: Oral Oncology, vol. 29, no. 3, pp. 215–219, 1993.
[25]
M. A. González-Moles, A. Rodríguez-Archilla, I. Ruiz Avila, F. Esteban, S. González-Moles, and M. Bravo, “Presence of HPV 16 sequences in oral lichen planus lesions.,” Bulletin du Groupement International pour la Recherche Scientifique en Stomatologie & Odontologie, vol. 40, no. 2-3, pp. 92–97, 1998.
[26]
L. Sand, J. Jalouli, P. A. Larsson, and J. M. Hirsch, “Human papilloma viruses in oral lesions,” Anticancer Research, vol. 20, no. 2 B, pp. 1183–1188, 2000.
[27]
J. K. Kellokoski, S. M. Syrj？nen, F. Chang, M. Yliskoski, and K. J. Syrj？nen, “Southern blot hybridization and PCR in detection of oral human papillomavirus (HPV) infections in women with genital HPV infections,” Journal of Oral Pathology and Medicine, vol. 21, no. 10, pp. 459–464, 1992.
[28]
C. Ostwald, P. Muller, M. Barten et al., “Human papillomavirus DNA in oral squamous cell carcinomas and normal mucosa,” Journal of Oral Pathology and Medicine, vol. 23, no. 5, pp. 220–225, 1994.
[29]
S. K. Young and K. W. Min, “In situ DNA hybridization analysis of oral papillomas, leukoplakias, and carcinomas for human papillomavirus,” Oral Surgery Oral Medicine and Oral Pathology, vol. 71, no. 6, pp. 726–729, 1991.
[30]
C. S. Miller, D. K. White, and D. D. Royse, “In situ hybridization analysis of human papillomavirus in orofacial lesions using a consensus biotinylated probe,” The American Journal of Dermatopathology, vol. 15, no. 3, pp. 256–259, 1993.
[31]
A. R. Kreimer, G. M. Clifford, P. Boyle, and S. Franceschi, “Human papillomavirus types in head and neck squamous cell carcinomas worldwide: a systemic review,” Cancer Epidemiology Biomarkers and Prevention, vol. 14, no. 2, pp. 467–475, 2005.
[32]
A. R. Kreimer, R. K. Bhatia, A. L. Messeguer, P. González, R. Herrero, and A. R. Giuliano, “Oral human papillomavirus in healthy individuals: a systematic review of the literature,” Sexually Transmitted Diseases, vol. 37, no. 6, pp. 386–391, 2010.
[33]
R. Mattila, J. Rautava, and S. Syrj？nen, “Human papillomavirus in oral atrophic lichen planus lesions,” Oral Oncology, vol. 48, no. 10, pp. 980–984, 2012.
[34]
H. Nielsen, B. Norrild, P. Vedtofte, F. Pr？torius, J. Reibel, and P. Holmstrup, “Human papillomavirus in oral premalignant lesions,” European Journal of Cancer B, vol. 32, no. 4, pp. 264–270, 1996.
[35]
J. L. Brandsma and A. L. Abramson, “Association of papillomavirus with cancers of the head and neck,” Archives of Otolaryngology—Head and Neck Surgery, vol. 115, no. 5, pp. 621–625, 1989.
[36]
M. L. Gillison, W. M. Koch, R. B. Capone et al., “Evidence for a causal association between human papillomavirus and a subset of head and neck cancers,” Journal of the National Cancer Institute, vol. 92, no. 9, pp. 709–720, 2000.
[37]
I. Cornet, T. Gheit, M. R. Iannacone et al., “HPV16 genetic variation and the development of cervical cancer worldwide,” The British Journal of Cancer, vol. 108, no. 1, pp. 240–244, 2013.
[38]
R. Kirnbauer, J. Taub, H. Greenstone et al., “Efficient self-assembly of human papillomavirus type 16 L1 and L1-L2 into virus-like particles,” Journal of Virology, vol. 67, no. 12, pp. 6929–6936, 1993.
[39]
L. F. Xi, G. W. Demers, L. A. Koutsky et al., “Analysis of human papillomavirus type 16 variants indicates establishment of persistent infection,” Journal of Infectious Diseases, vol. 172, no. 3, pp. 747–755, 1995.
[40]
P. Londesborough, H. O. Linda, G. Terry, J. Cuzick, C. Wheeler, and A. Singer, “Human papillomavirus genotype as a predictor of persistence and development of high-grade lesions in women with minor cervical abnormalities,” International Journal of Cancer, vol. 69, no. 5, pp. 364–368, 1996.
[41]
M. C. St？ppler, K. Ching, H. St？ppler, K. Clancy, R. Schlegel, and J. Icenogle, “Natural variants of the human papillomavirus type 16 E6 protein differ in their abilities to alter keratinocyte differentiation and to induce p53 degradation,” Journal of Virology, vol. 70, no. 10, pp. 6987–6993, 1996.
