Lichen planus (LP) is an inflammatory mucocutaneous disease, showing a wide variety of clinical subtypes. The classic presentation of LP involves the appearance of polygonal, flat-topped, violaceous papules and plaques with reticulated white lines, termed “Wickham's striae”. Cutaneous lesions tend to be extremely pruritic, and this symptom does not subside after common antipruritic treatment. Moreover, based on our previous pilot study, it could be stated, that itch is the most unpleasant and bothersome symptom of LP for majority of patients suffering from this disease. However, the underlying mechanisms of itch in lichen planus remain still unknown. In addition, there is no study on mediators of this sensation, but taking into account pathogenesis of LP there are some possible mediators implicated to transmit or modulate itch. In pathogenesis of LP important are such mechanisms as apoptosis, autoimmune reaction, and role of stress. With these pathways some, previously described in other diseases, itch mediators such as cytokines, proteases, and opioid system are connected. Whether these mechanisms are involved in pruritus accompanying LP requires further investigation. Limited knowledge of pruritus origin in lichen planus is responsible for the lack of the effective antipruritic treatments. Here, we describe possible mechanisms participating the pathogenesis of pruritus in lichen planus. 1. Introduction Lichen planus (LP) is a chronic inflammatory disease involving both the skin and mucous membranes. This is relatively rare disease, occurring in about 0.5% of general population, with the similar incidence in males and females; the disease rarely develops in children [1]. LP shows a wide variety of clinical manifestations, and numerous subtypes of LP have been described, showing variable lesion configuration and morphology, that is, eruptive LP, inverse LP, mucosal LP, lichen planopilaris, hypertrophic LP, bullous LP, actinic LP, annular atrophic LP, erosive LP, pigmented LP, perforating LP, invisible LP, and others. However, all types of LP have similar histology showing band-like lymphohistiocytic infiltrate at the dermoepidermal junction with vacuolar degeneration of the basal layer of epidermis. Necrotic keratinocytes (civatte bodies or cytoid bodies) are extruded into the papillary dermis. Irregular acanthosis may result in a saw-toothed appearance of dermoepidermal junction. Hyperorthokeratosis may also be seen but is rather considered as a feature of lichenoid drug eruption [2]. The classic clinical manifestation of LP involves the presence of
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