Proposed pathological mechanisms

Several theories have been proposed to explain the functional inhibition and melanocyte destruction in vitiligo: the autocytotoxic hypothesis, the neural hypothesis and the autoimmune hypothesis. In the autocytotoxic hypothesis, toxic melanin intermediates are produced in excess or imbalance, causing autocytotoxicity. The neural hypothesis is based on a proposed adrenergic/cholinergic imbalance in some vitiligo patients, and was promoted as a cause for segmental vitiligo. Schallreuter and Wood have proposed a variant of this hypothesis, that vitiligo is a disease of the entire epidermis in which heightened adrenergic responses lead to biochemical imbalances which inhibit melanization, but do not necessarily destroy melanocytes. They have demonstrated a number of biochemical abnormalities which induce decreases in antioxidant defenses and increases in tetrahydrobiopterin, which are proposed to inhibit melanization or to bleach melanin. The autoimmune hypothesis is based on the association of vitiligo with numerous autoimmune syndromes. Melanocyte-spe-cific autoantibodies have been consistently found in modern studies of vitiligo, and these antibodies have been proven to induce cytotoxic damage of melanocytes.

Melanocytes are abnormally susceptible to immunologic cytotoxicity and to cytotoxicity induced by reactive oxygen species, in part because of defective antioxidant defenses. Abnormalities observed in cultured melanocytes from the margins of vitiligo lesions have led to the proposal that there are intrinsic melanocyte defects in vitiligo. It is accepted that multiple factors may influence melanocyte destruction in vitiligo, leading to a common endpoint of melanocyte inhibition, then cytotoxic destruction. However, immunologic damage to melanocytes in vitiligo is still the most convincing mechanism of melanocyte damage, supported by extensive immunopathology and immunocytotox-icity experiments.

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