Bullous pemphigoid (BP) is an autoimmune skin disease characterized by the binding of autoantibodies directed against two hemidesmosal proteins of the dermal–epidermal junction, namely BP180 and BP230 (1–6). The disease typically presents in the elderly with a generalized pruritic blistering eruption (7–9), which results from an inflammatory associated disruption of the dermal–epidermal junction induced by the binding of autoantibodies onto their targets. Clinical criteria for typical skin eruption of BP include the absence of associated external mucous membrane (almost exclusively oral) involvement, the absence of skin atrophy, and the absence of head and neck predominant involvement (10). However, clinical presentation of BP can be polymorphic, notably during the early, pre-bullous stage of the disease or in atypical variants, in which full-blown bullous lesions may be absent (11, 12). Beside, blisters and erosions arising on mucosal membranes, mainly within the oral cavity, may be observed in up to 20% of BP patients (6, 11–13), without identified pathophysiologic mechanism(s) associated with their development.