Itch and nerve fibers with special reference to atopic dermatitis: Therapeutic implications

Abstract Nerve density in the epidermis is partly involved in itch sensitization in pruritic skin diseases, such as atopic dermatitis ( AD ). Epidermal innervation is thought to be regulated by the balance between nerve elongation factors (e.g. nerve growth factor) and nerve repulsion factors (e.g. semaphorin 3 A ). Semaphorin 3 A ( S ema3 A ) has been shown to inhibit nerve growth factor ( NGF )‐induced sprouting of sensory nerves, and epidermal S ema3 A levels are lower in AD patients, concomitant with an increase in epidermal nerve density. In addition, treatment with anti‐ NGF , S ema3 A replacement, and several existing treatments, such as ultraviolet‐based therapies, normalized the hyperinnervation in AD , resulting in suppression of itching. This review expands knowledge regarding potential therapeutic strategies for ameliorating intractable pruritus in AD .