Oral lichen planus: an update on its pathogenesis.

Oral lichen planus (OLP) is a common T cell-mediated mucocutaneous disease of unknown etiology. A great number of factors have been suggested as relevant to the etiology of this disease. In this article, the authors assemble recent knowledge about the pathogenesis of OLP, discuss some proposed hypotheses, and compare OLP with oral lichenoid lesions.

Increased number of Langerhans cells in oral lichen planus and oral lichenoid lesions.

OBJECTIVE: The aim of this study was to quantify the presence of Langerhans cells (LC) in oral lichen planus (OLP) and oral lichenoid lesions (OLL), comparing them with normal epithelium. STUDY DESIGN: Thirty-six patients with biopsy-proven OLP or OLL were selected for the study, as well as 23 control subjects free of inflammatory conditions. Immunohistochemical reactions were performed using the streptavidin-biotin peroxidase complex method with CD1a and CD83 primary antibodies. Densities were compared between groups and correlated with microscopic findings. RESULTS: Patients with lichenoid conditions (OLP + OLL) presented higher densities of CD1a(+) cells than the control subjects (P = .03). Higher densities of CD1a were associated with a thinner layer of inflammatory cells (P = .02). CONCLUSIONS: This study indicates that OLP and OLL are characterized by the recruitment of LC, which may play a significant role on its pathogenesis.

Lichen planus and lichenoid drug-induced eruption: a histological and immunohistochemical study.

INTRODUCTION: Lichenoid drug eruption (LDE) shares similar features with lichen planus (LP), that could reflect the same pathogenesis. In LP, an autoimmune attack is accepted and cytotoxic T-lymphocytes (CD8+) predominate, especially in late lesions. Apoptosis of keratinocytes may be mediated by CD8+ T and NK cells in two distinct ways: by the release of cytotoxic molecules such as perforin and granzyme B or by the Fas/FasL system. The immunological mechanisms involved in LDE are not yet fully established. OBJECTIVES: Investigate immunohistological features in LP and LDE to add clues to better understand their pathogenesis. MATERIAL AND METHODS: Twenty-two patients fulfilled all clinical, laboratory, histopathological, and follow-up features of lichen planus (n = 16) and lichenoid drug eruption (n = 6). Classic histological features favoring LP or LDE were evaluated by two observers. HAM56, MAC387, UCHL-1, OPD4, CD8, Granzyme B, Perforin, and ICAM-1 antibodies were used to decorate the immune infiltrate. Results were analyzed through Pearson correlation, Student's t-test, and linear discriminant analysis. RESULTS: A higher number of necrotic keratinocytes as well as plasma cells and eosinophils within inflammatory cells were associated with LDE diagnosis. Only in LDE, a correlation was found between the number of T and CD8+ cells and between the number of granzyme B+ cells and apoptotic keratinocytes. CONCLUSION: Our findings suggest a more important role of CD8+ granzyme B-containing cells in LDE group, being its synthesis associated with more intense apoptosis. So, LP and LDE may have a somewhat distinct pathogenesis.

Antigen mimicry followed by epitope spreading: A pathogenetic trigger for the clinical morphology of lichen planus and its transition to Graham Lassueur Piccardi Little Syndrome and keratosis lichenoides chronica - Medical hypotheses or reality? / Mimetismo antigênico seguido de espalhamento de epítopos: agente desencadeador patogênico da morfologia clínica do líquen plano e de sua transição para a Síndrome de Graham-Little-Piccardi-Lassueur e para a ceratose líquenóide crônica - Hipótese médica ou realidade?

Literature data analysis, providing an exact explanation of the lichen planus pathogenesis, as well as its transition into other rare forms such as Keratosis lichenoides chronica or Graham Lassueur Piccardi Little Syndrome are scant, or totally missing. The chronological course of the disease, known in the literature as lichen planus, varies. Some patients develop Lichen planus or lichen nitidus and there is no logical explanation why. It is also not clear why single patients initially develop ulcerative lesions in the area of the mucosa and only in a few of them these lesions affect the skin. Antigen Mimicry and Epitope Spreading could be the possible pathogenic inductor in cases of lichenoid dermatoses, as well as the cause for their transition into ulcerative, exanthematous or other rare forms. The Epitope Spreading is probably not the leading pathogenetic factor in lichen planus but a phenomenon which occurs later. This manuscript analyzes some basic pathogenic aspects and presents some possible medical hypotheses regarding the heterogenic clinical picture and pathogenesis of lichen planus and lichenoid like pathologies of the skin which, in the near future should be analyzed in details in order to clarify several dilemmas the clinical dermatologist has to face.

Análises das informações disponíveis na literatura que forneçam uma explicação precisa sobre a patogênese do Líquen Plano, assim como sobre sua transição para outras formas raras da doença, como Ceratose Liquenóide Crônica ou Síndrome de Graham-Little-Piccardi- Lassueur , são raras ou inexistentes. O curso cronológico da doença, conhecida na literatura como Líquen Plano, varia. Alguns pacientes desenvolvem Líquen Plano ou Líquen Nítido e não ha uma explicação lógica do por quê. Também não está claro por que alguns pacientes inicialmente desenvolvem lesões ulcerativas na área da mucosa e em apenas alguns deles essas lesões afetam a pele. Mimetismo Antigênico ou Espalhamento de Epítopos poderiam ser fatores patogênicos indutores em casos de Dermatoses Liquenóides, e também fatores responsáveis pela transição para a forma ulcerativa, exantematosa ou outras formas raras da doença. Espalhamento de Epítopos provavelmente não é o principal fator patogênico envolvido no Líquen Plano, mas um fenômeno de ocorrência posterior.Esse manuscrito analisa alguns aspectos patogênicos básicos e apresenta algumas hipóteses médicas sobre o quadro clínico heterogênico e a patogênese do Líquen Plano e de patologias da pele do tipo liquenóide. Essas patologias devem, em um futuro próximo, ser analisadas minuciosamente a fim de esclarecer vários dilemas que o dermatologista clínico tem de enfrentar.

Antigen mimicry followed by epitope spreading: a pathogenetic trigger for the clinical morphology of lichen planus and its transition to Graham Lassueur Piccardi Little Syndrome and keratosis lichenoides chronica - Medical hypotheses or reality?

Literature data analysis, providing an exact explanation of the lichen planus pathogenesis, as well as its transition into other rare forms such as Keratosis lichenoides chronica or Graham Lassueur Piccardi Little Syndrome are scant, or totally missing. The chronological course of the disease, known in the literature as lichen planus, varies. Some patients develop Lichen planus or lichen nitidus and there is no logical explanation why. It is also not clear why single patients initially develop ulcerative lesions in the area of the mucosa and only in a few of them these lesions affect the skin. Antigen Mimicry and Epitope Spreading could be the possible pathogenic inductor in cases of lichenoid dermatoses, as well as the cause for their transition into ulcerative, exanthematous or other rare forms. The Epitope Spreading is probably not the leading pathogenetic factor in lichen planus but a phenomenon which occurs later. This manuscript analyzes some basic pathogenic aspects and presents some possible medical hypotheses regarding the heterogenic clinical picture and pathogenesis of lichen planus and lichenoid like pathologies of the skin which, in the near future should be analyzed in details in order to clarify several dilemmas the clinical dermatologist has to face.

Successful treatment of oral lesions of chronic lichenoid graft-vs.-host disease by the addition of low-level laser therapy to systemic immunosuppression.

We report a case of severe oral stomatitis caused by lichenoid chronic graft-vs.-host disease in which low-level laser therapy applied to the oral mucosa, in addition to standard systemic immunosuppressive treatment, resulted in quick healing and symptomatic relief.