Causes of Vitiligo
Vitiligo causes are related to both genetic and nongenetic factors. Although several theories have been proposed, the precise cause remains unknown.
Vitiligo is caused by a reduction, elimination, or absence of functional melanocytes. Melanin is the pigment in the body that colors skin and hair. It is produced in cells called melanocytes. Melanocytes are located in the upper skin and in the hair follicles. Areas of skin with patches of vitiligo have no or very few melanocytes. The melanocytes are either damaged or destroyed in the body. When melanin cannot be made, the pigment of the skin is lost.
The mechanism(s) of action for the depletion of melanocytes in vitiliginous skin are not well understood. In some cases, it appears to be an auto-immune system disorder, as immune system supressants have been shown to reduce the spread of vitiligo and allows repigmentation in some individuals. In other cases, it has been suggested that substances toxic to melanocytes are present in, or are introduced (from the environment) into, vitiligo skin and that certain people are genetically more susceptible to those substances than others. Genetic research has identified several regions of the human genome that may contribute to the condition, but none have been identified as definite markers. Recent research indicates that several systems contribute to the actual presentation of vitiligo, as opposed to a single pathway. Research involving the many pathways and possibilities that lead to vitiligo is ongoing.
Many people report that their vitiligo first appeared following a traumatic or stressful event, such as an accident, job loss, death of a family member, severe sunburn, or serious illness. The Koebner effect is frequently reported in clinical literature as instigating onset or aggravation of vitiligo regions. The Koebner effect describes a physical external stimulus affecting the disease state. While the connection between stress and onset of vitiligo is uncertain, scientists have identified markers that might indicate stressful events can trigger an autoimmune reaction such as vitiligo. In this manner, a field of dermatology termed “psychodermatology” has arisen which addresses a patient’s emotions and their mind-body interaction as it relates to their disorder.
Additional research has suggested deficiencies in certain vitamins and minerals including vitamins B12 and C, copper and zinc may contribute to vitiligo presentation. Clinical studies on vitamin and mineral deficiency are inconclusive, but suggest improvements may be had with supplementation. Other studies suggest antioxidant supplementation can improve patient’s vitiligo, though again these studies are inconclusive.
Current hypotheses on the mechanisms by which melanocytes are depleted include:
Autoimmune hypothesis: Originating from the observation that vitiligo is associated with some autoimmune diseases and that some forms of vitiligo respond to immune system suppressants. Both cellular and humoral factors responsible for autoimmune damage to melanocytes have been demonstrated. Although anti-melanocyte autoantibodies have been demonstrated in vitiligo, their role as a pathogen remains uncertain.
Autocytotoxic (or self-destruct) hypothesis: Suggests that some toxic molecules produced during the biosynthesis of melanin are responsible for melanocyte damage in susceptible individuals.
Neural hypothesis: Suggests that norepinephrine (which is toxic to melanocytes) is released from nerve endings killing melanocytes. In addition, norepinephrine induces an enzyme (MAO), which favors the formation of toxic levels of hydrogen peroxide in the vicinity of melanocytes, thereby injuring them.
Although vitiligo is asymptomatic and does not cause any physical discomfort or disability, it may be associated with devastating psychological and social consequences, greatly impacting a patient's Quality of Life (QoL). Since a person's appearance is a major determinant of his/her personality traits, vitiligo can have major impact on personality, social interactions, career, and everyday life.