Exploring the Multifactorial Pathophysiology of Vitiligo: Genetic, Immunological, and Oxidative Stress Interactions

Vitiligo is a prevalent pigmentary disorder. Numerous studies conducted over many years and across various countries have attempted to elucidate the pathophysiology of vitiligo, yet it remains incompletely understood. This review article presents recent research supporting the most widely accepted theories regarding this disfiguring illness. Emphasis is placed on the genetic predisposition theory, the neurological theory proposed in the 1950s, and other significant theories including the autoimmune hypothesis, the reactive oxygen species model, zinc-α2-glycoprotein deficiency, viral infection, intrinsic theory, and biochemical, molecular, and cellular mechanisms that lead to the loss of functional melanocytes in vitiligo. The formation and maintenance of disease are predisposed by the discovery of several genes implicated in these processes. However, the integration of hypotheses related to the pathogenesis of vitiligo is challenged by the interaction between vitiligo and psychological stress, comorbidities, environmental variables, and the characteristics that characterize individual vulnerability to the disease. The condition's complexity arises from multiple interacting factors. Further research is needed to understand these interactions better and improve vitiligo treatment.