Features of immune status in patients with various clinical forms of oral lichen planus

Abstract

Oral mucosal lesions hold one of the lead places in the structure of dental diseases. Oral lichen planus (OLP) considered as a multifactorial disease is of top priority among dermatoses of oral mucosa and red lip border. Diverse putative concepts behind developing lichen planus pathogenesis are discussed including immunoallergic, viral, genetic and membrane-destructive theories. However, an immune theory is thought to play a crucial role in developing lichen planus. Despite documented induction of immune mechanisms, complex interaction between pathological process and normal defense response as well as stirred interest to it, multiple aspects of immunological conflict in lichen planus remain unclear. Few data describing altered immune parameters depending on clinical picture of lichen planus are currently available that suggested to perform the study aimed at examining immune status in patients with various forms of oral lichen planus. There were enrolled 286 oral lichen planus patients (248 females and 38 males), aged 2784 years. Based on clinical picture, all OLP patients were divided into 6 groups: a typical type, exudative-congestive, erosive-ulcerous, hyperkeratotic, atypical, bullous type. An immune status in peripheral blood samples was evaluated by analyzing innate defense mechanisms as well as humoral and cellular immunity. Multiple altered immune parameters characterized by impaired phagocytic capture and metabolic activity, disimmunoglobulinemia, altered ratio of major immunocompetent cell types and subsets were documented during the study. Moreover, OLP patients with typical, hyperkeratotic, exudative hyperemic, atypical and erosive ulcerous forms were found to have increased amount of CD4+ helper T cells associated with a self-sustained immune response due to suppressed elimination of pathogenic agents consequently resulting in developing autoimmune process. While analyzing immune status in OLP patients, it allowed to find a relationship between dysphagocytosis signs, impaired humoral and cellular immunity as well as various clinical forms of the disease. Thus, it suggests imbalanced mechanisms responsible for pathogen elimination might play a role in OLP pathogenesis, including infectious agents being involved in its development.