Focus on Vitiligo: A Generalized Skin Disorder

Abstract

Vitiligo is an acquired pigmentation disorder due to a disappearance of functioning melanocytes from the epidermis and clinically characterized by achromic patches, often spreading over time. It is still not fully understood how melanocytes disappear in vivo, inducing these peculiar lesions. There are three major hypotheses for the pathogenesis of the disease: the autoimmune hypothesis considers that the disappearance of melanocytes is due to an autoimmune effector mechanism, the neural hypothesis suggests that an accumulation of neurochemical substances is able to damage epidermal melanocytes, and the metabolic hypothesis indicates that an increased sensitivity of melanocytes to oxidative stress is the crucial factor of the disease. Besides these well accepted hypotheses there are also some new interpretations based on a defective adhesion of melanocytic cells, an imbalance in the epidermal production of cytokines and an altered expression of melanocyte receptors. All these theories seem to be based on convincing evidence, indicating that they may contribute in variable proportions to the disease. There is also reasonable evidence at present that vitiligo potentially involves the whole integument, suggesting that it is a generalized skin disorder probably including different cell types during the active phase of the disease. It appears that the different theories may integrate with each other, supporting the concept that in vitiligo there is a final common step, i.e. a loss of pigment in the epidermis as well as different, possibly interacting, pathways leading up to this conclusive result.