Abstract
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.
Highlights
Lichen planus (LP) is a chronic inflammatory disease involving both the skin and mucous membranes
Some previous studies suggested that interleukin 31 (IL31) and its receptor components IL-31RA and OSMR could be a key cytokine pathway involved in itching which accompanies a number of inflammatory skin conditions, mostly atopic dermatitis [11,12,13]
It was reported that TNF-α, a proinflammatory cytokine which plays an important role in the pathogenesis of LP and is elevated in the skin of patients with LP, may stimulate IL-31 expression, a phenomenon that might be responsible for escalation of itch sensation in LP [14, 15]
Summary
Lichen planus (LP) is a chronic inflammatory disease involving both the skin and mucous membranes. Itch or pruritus is a cutaneous sensation different from pain It is evoked by pruritogenic stimuli activating distinct subgroups of dedicated primary afferent C-fibers, including both histamine-sensitive and histamine-insensitive nonnociceptive polymodal nerve fibers, nociceptive polymodal fibers are involved to some extend [5,6,7]. Keratinocytes, leukocytes, mast cells, fibroblasts, endothelial cells, and cutaneous nerves may produce several endogenous pruritogens, including histamine, kinins, proteases, neurotrophins, some opioids, and cytokines [8] Many of these mediators and modulators released at the periphery can directly activate the itch-sensitive C-fibers by specific receptors on the nerve endings or they can act indirectly by inducing the release of pruritogenic mediators and modulators from other cells [9]. The exact pathogenesis of LP is still not fully elucidated, here we would like to discuss some of possible pruritic mediators and mechanisms which may be involved in pruritus present in LP
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