Lichen planus is an autoimmune disease that affects the skin and mucous membranes, including the ear canals, resulting in conductive deafness and esophageal involvement that leads to strictures and dysphagia.3,4 It has a slight female predominance (1.4:1) and affects 1% to 2% of adults.5 In most patients, it is self-limiting and follows a benign course. The mucosal variant of LP may involve the oral and genital mucosa and is characterized by sores and erosions. Scarring results in fibrous bands in the buccal mucosa, leading to a reduced vestibular sulcus and limitation of the oral aperture.6 In our series, 7 of 9 women had VVG syndrome, which is a severe subtype of LP characterized by erosions or desquamation of vulval, vaginal, and gingival mucosa, with predilection for scarring and stricture formation.6,7 The pathogenesis of LP is unclear, but it is believed to be caused by specific and nonspecific immunological mechanisms. Specific mechanisms probably include antigen presentation by basal keratinocytes and antigen-specific T cells that are cytotoxic to keratinocytes, whereas nonspecific mechanisms include activation of matrix metalloproteinases and mast cells.8 A potential association with the HLA-DQB1*0201 allele has been described in patients with VVG, suggesting a genetic predisposition; however, a strong association with autoimmune disorders in this variant of LP may in part explain the increased frequency of this allele.6 Five of 7 patients herein with VVG LP tested positive for the HLA- DQB1*0201 allele, whereas the 2 patients without VVG LP were negative for this allele. Given the strong association between erosive mucocutaneous LP, particularly of the VVG syndrome subtype, and multisite scarring sequelae, it is not unexpected that ocular inflammation may lead to subconjunctival fibrosis and lacrimal duct stenosis.