A Critical Appraisal of Vitiligo Etiologic Theories. Is Melanocyte Loss a Melanocytorrhagy?

Abstract

Common generalized vitiligo is an acquired depigmenting disorder characterized by a chronic and progressive loss of melanocytes from the epidermis and follicular reservoir. However, the mechanism of melanocyte disappearance has never been clearly understood, and the intervention of cellular and humoral autoimmune phenomena as primary events remains unproven. In this review, is discussed the data supporting the major theories of vitiligo, namely melanocyte destruction (autoimmune, neural and impaired redox status) and melanocyte inhibition or defective adhesion. Based on recent morphologic findings in vivo supporting a chronic detachment and transepidermal loss of melanocytes in common generalized vitiligo, a new theory is suggested proposing melanocytorrhagy as the primary defect underlying melanocyte loss, integrating most of the possible triggering/precipitating/ enhancing effects of other known factors.

Anisaldehyde, a Melanogenesis Potentiator

“…According to the conclusion described, the aryl aldehydes, benzaldehyde and anisaldehyde, are nonsensitizing in the murine LLNA (Patlewicz et al, 2001). Despite this advantage, biological impact of anisaldehyde in melanogenesis is still largely unknown, but it is a potential candidate for the treatment of a dermatological disease such as vitiligo (Gauthier et al, 2003). On the other hand, if the adverse effect of anisaldehyde is also producible in human melanocytes, it would be useful in a different sense since melanins play a crucial role in the absorption of free radicals generated within the cytoplasm and in shielding the host from various types of ionizing radicals, including ultraviolet (UV) irradiation.…”

Vitiligo and other hypopigmentation disorders in children and adolescents

“…Th e emergence of segmental vitiligo can be best explained by the neurogenic theory according to which the nerve endings release the neurochemical mediators that inhibit melanogenesis or have toxic eff ects on melanocytes, destroying them. Microscopic examination and ultrastructural investigations in people with segmental vitiligo showed damage to axons and disrupted neuropeptide balance in vitiligo lesions (27,28). As possible provoking factors for the occurrence of vitiligo the following are cited: stress, sun burns, recurrent skin injuries.…”

“…Th e melanocytes of active vitiligo reveal an increase in oxidants and antioxidant enzyme defi cit, with resultant oxidative damage to melanocytes (3,26,27). Th e emergence of segmental vitiligo can be best explained by the neurogenic theory according to which the nerve endings release the neurochemical mediators that inhibit melanogenesis or have toxic eff ects on melanocytes, destroying them.…”

Bowman lecture on the role of inflammation in degenerative disease of the eye

“…Of interest is the marked evidence of melanocyte rounding: this is well recognised as sign of melanocyte activation and stress that occurs in such conditions as vitiligo. 88 Most recently, the phenotype of the macrophages associated with drusen in human choroid associated with geographic atrophy has been reported as CD68 þ macrophages, while those associated with wet AMD also express iNOS, that is, appear to be express a more proinflammatory phenotype. 89 The pathogenic process of AMD: wet vs dry disease While drusen are considered to be pathognomic of AMD, the major and somewhat neglected aspect of the disease is that the primary pathology is RPE cell death.…”