Oral Medicine
Current controversies in oral lichen planus: Report of an international consensus meeting. Part 1. Viral infections and etiopathogenesis

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Despite recent advances in understanding the immunopathogenesis of oral lichen planus (LP), the initial triggers of lesion formation and the essential pathogenic pathways are unknown. It is therefore not surprising that the clinical management of oral LP poses considerable difficulties to the dermatologist and the oral physician. A consensus meeting was held in France in March 2003 to discuss the most controversial aspects of oral LP. Part 1 of the meeting report focuses on (1) the relationship between oral LP and viral infection with special emphasis on hepatitis C virus (HCV), and (2) oral LP pathogenesis, in particular the immune mechanisms resulting in lymphocyte infiltration and keratinocyte apoptosis. Part 2 focuses on patient management and therapeutic approaches and includes discussion on malignant transformation of oral LP.

Section snippets

Oral lichen planus and viruses

The wide range of factors that may precipitate the cell-mediated reaction resulting in oral LP lesions is discussed elsewhere.1 Among the exogenous factors, several infective agents including some viruses and Helicobacter pylori3, 4 have recently been linked with oral LP but sometimes on the basis of equivocal data. The present paper is focused on viral agents.

Immunopathogenesis of oral LP

A large body of evidence supports a role for immune dysregulation in the pathogenesis of oral LP, specifically involving the cellular arm of the immune system. The inflammatory infiltrate consists primarily of T cells and macrophages. Plasma cells are rarely seen and immune deposits are not characteristic.

Oral LP and graft versus host disease

Graft-versus-host disease (GVHD) is a common serious complication following allogeneic hematopoietic stem cell transplantation (HSCT), and is a major cause of HSCT-related mortality.147 Acute GVHD occurs within the first 100 days of transplantation and comprises dermatitis, enteritis, and hepatitis with immunosuppression and cachexia. Chronic GVHD develops after day 100 and comprises an autoimmune-like syndrome comparable to ulcerative colitis, primary biliary cirrhosis, Sjögren's syndrome,

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    This work was partially supported by the Ministero dell'Università e della Ricerca Scientifica e Technologica (ex quota 60%), the Italian Ministry of Public Instruction, and the Department of Biomedical Sciences and Human Oncology, University of Turin, and by Grant mm06153729 from the Italian Ministero dell'Istruzione dell'Università e della Ricerca. Philip Sugerman is supported by an Industry Research Fellowship from the National Health and Medical Research Council of Australia.

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