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Phospholipase A2 : activation via IL1-α, TNFα or UV Stimulation of the nerve response is a determining step in the phenomenon of sensitive skin. The skin included many nerve structures like nervous corpuscles and nerve fibers, in particular teh C fibers present in the epidermis up to the stratum granulosum. They allow control of all skin functions by the central nervous system. Stimulaton of the nerve fibers by a variety of stimuli (environmental or chemical) generates a nervous influx to the central nervous system, indducing subjective symptoms like itching, burning, stinging, prickling, tingling or discomfort and even pain. Stimultaneously, nerve ending activation provokes locally the release of neuromediators like CGRP, which then activates the release of cytokines, inducing a vasodilatation and an inflammatory process. Thermal and pain sensation in humans depend on the impulse produced in distinctive cutaneous receptors and conveyed to the central nervous system by the thinnest myelinated (Aδ) and unmyelinated (C) nerve fibers. Thermal and pain sensation in humans depend on the impulse produced in distinctive cutaneous receptors and conveyed to the central nervous system by the thinnest myelinated (Aδ) and unmyelinated (C) nerve fibers. TRPV1 stimulators : low pH ( 5.9) noxious heat ( 42?C) the cannabinoid/ endovanilloid anandamide arachidonic acid metabolites: e.g. leukotriene B4, prostaglandins nerve Growth Factor , bradykinin capsaicin, piperine (red - black pepper) allicin (garlic) eugenol, ethanol, campher polyamines nicotine PAR2 agonists increase cAMP = PKA = TRPV1 activation Sensitive skin is not restricted to the face but rather it is also present at other localizations, mainly the hands and often the sclap and feet. Sensitive skin is decreasing with age as facial sensitive epidermal nerve density is also decreasing while skin ages predict an increased susceptibility to irritants * Let’s start with where sensitive skin comes from accor
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