Several studies have explored the origin and development mechanism of oral lichen planus (OLP) with limited attention to the role of bacteria in the progression of this common oral disease. Here we utilized MiSeq sequencing of 16S rRNA gene amplicons to identify complex oral microbiota associated with OLP from saliva samples of two subtypes (reticular and erosive) of OLP patients and healthy controls. Our analyses indicated that the overall structure of the salivary microbiome was not significantly affected by disease status. However, we did observe evident variations in abundance for several taxonomic groups in OLP. Porphyromonas and Solobacterium showed significantly higher relative abundances, whereas Haemophilus, Corynebacterium, Cellulosimicrobium and Campylobacter showed lower abundances in OLP patients, as compared with healthy controls. In addition, we explored specific microbial cooccurrence patterns in OLP, and revealed significantly fewer linkers of Streptococcus comprising species in erosive OLP. Furthermore, the disease severity and immune dysregulation were also genusassociated, including with Porphyromonas that correlated to disease scores and salivary levels of interleukin (IL)-17 and IL-23. Overall, this study provides a general description of oral microbiome in OLP, and it will be useful for further investigation of their potential roles in the initiation and immune modulation of OLP.Lichen planus is a common chronic mucocutaneous inflammatory disease affecting skin, oral, genital mucosa, scalp and nails. The prevalence of oral lichen planus (OLP) ranges from 0.1-4% in the general population, and females between 30 and 60 are more vulnerable to this disease 1 . Lesion manifestations can often persist for years alternating between periods of quiescence and exacerbation 2 . Intraorally, OLP presents as white striations, papules, plaques, mucosal atrophy, erosions or blisters, mainly affecting the buccal mucosa, tongue, gingiva and lips 3 . Among those clinical phenotypes, the reticular form is the most prevalent lesion characterized by the presence of Wickham striae and usually asymptomatic. Whereas the erosive type, although less frequent, always causes different degrees of discomfort and soreness, it may need ongoing concern due to its malignant potential 4 . Despite of numerous literatures appraising the OLP origin and development mechanism, its aetiology remains uncertain, and the pathogenesis of this disease still needs more investigations. Several internal and external factors have been implicated, such as immunodeficiencies and microbial infection 5 . Several lines of evidences have suggested that immune dysregulation and complex cytokine network played important roles in the exacerbation and perpetuation of OLP 6,7 . For instance, a high proportion of the novel CD4 + T helper cells subset-Th17 cells were detected in OLP lesions 8 . And interleukin (IL)-17 and IL-23, the newly discovered Th17-associated cytokines, were found to be important proinflammatory factors involved in OLP 9,10 . In...