Background: Vitiligo is a disease in which destruction of skin melanocytes results in hypopigmented or depigmented skin patches, The loss of melanin is in the skin but partly also in mucous membranes, various mechanisms have been implicated to explain melanocyte destruction, including genetic predisposition, environmental triggers (such as friction), metabolic alteration and altered inflammatory and immune responses. It is classified into 3 types, that is, non-segmental, segmental, and undetermined/unclassified vitiligo, the uniform classification of vitiligo is very important in predicting its clinical course and prognosis and communication among researchers. Generally, vitiligo can be diagnosed depending on clinical features. While biopsy is usually not required, it may be useful in individual cases for differential diagnosis. vitiligo is a multifactorial disorder characterized by the loss of functional melanocyte, multiple mechanisms have been proposed for melanocyte destruction in vitiligo. These include genetic, autoimmune responses, oxidative stress, generation of inflammatory mediators and melanocyte detachment mechanisms, none of these proposed theories are in themselves sufficient to explain the different vitiligo phenotypes; and the overall contribution of each of these processes is still under debate, although there is now consensus on the autoimmune nature of vitiligo. The Vitiligo Area Severity Index (VASI) and Vitiligo European Task Force (VETF) were considered as responsive and reliable tools to assess the extent of depigmentation in patients with vitiligo. The diagnosis of vitiligo is generally straightforward, made clinically based upon the finding of acquired, amelanotic, nonscaly, chalky-white macules with distinct margins in a typical distribution: periorificial, lips and tips of distal extremities, penis, segmental and areas of friction.