Abstract
Recent studies have indicated that vitiligo areas contain inactive or dormant melanocytes. Melanin synthesis is related to tyrosinase presence and indicative of active metabolic state. The aim of this study was to compare repigmentation, epidermal melanocyte distribution and tyrosinase mRNA detection through reverse transcriptase polymerase chain reaction, in tissue samples of vitiligo, before and after curettage, with or without subsequent autologous skin graft using a new method. Prospective, in the Department of Dermatology, Faculdade de Medicina do ABC, Santo André. Two vitiligo areas were curetted. One subsequently received grafted normal sacral autologous skin, whereas the other had no further treatment. The curetted areas were examined after 30 days, to evaluate the degree of repigmentation. The melanocyte percentages and tyrosinase mRNA presence in normal skin and vitiligo areas, before and after curettage and grafting, were compared. Complete repigmentation was seen in all grafted areas, whereas non-grafted curetted vitiligo presented partial repigmentation. The melanocyte percentage in grafted areas was greater than in non-treated vitiligo skin (p = 0.01) and skin with curettage alone (p = 0.015). Tyrosinase mRNA was negative in 93.75% of non-treated vitiligo areas. After treatment (curettage alone or curettage and grafting), all lesions became positive for tyrosinase mRNA. Metabolically inactive or dormant melanocytes are probably present within vitiligo areas, and may be activated by exogenous or endogenous stimuli.
Highlights
Vitiligo, a cutaneous achromia, is poorly understood and is related to three hypothetical pathogenetic mechanisms: autotoxicity,[1] neurological[2] and immunological.[3,4] the end result of the disease is epidermal depigmentation, the presence or absence of remaining melanocytes within vitiligo areas, and the possible melanocyte metabolic arrest are still controversial.[5,6] Characterization of the melanocyte metabolic status is an essential matter
Skin grafts prepared as explained above have resulted in homogeneous pigmentation, and have proven to be a valuable tool for longstanding localized vitiligo
Statistical analysis has shown that this finding is probably due to the addition of melanocytes, which reach the same levels as in the donor tissue
Summary
A cutaneous achromia, is poorly understood and is related to three hypothetical pathogenetic mechanisms: autotoxicity (excessive endogenous production of phenol radicals, derived from dopaquinone oxidation into melanin products),[1] neurological (damage of end-terminal portions of autonomic nerves)[2] and immunological (anti-tyrosinase and TRP-2 autoantibodies, as well as through activation of cellular immunity).[3,4] the end result of the disease is epidermal depigmentation, the presence or absence of remaining melanocytes within vitiligo areas, and the possible melanocyte metabolic arrest are still controversial.[5,6] Characterization of the melanocyte metabolic status is an essential matter. The dopa reaction for tyrosinase was the gold standard for determining melanocyte activity, just as the detection of melanosomes via electron microscopy was a condition for characterizing cells as melanocytes These techniques are, unable to distinguish immature or metabolically inactive melanocytes. Germinative buds of the initial anagen phase of new hair growth express tyrosinase mRNA, which can be detected by means of the reverse transcriptase polymerase chain reaction (RT-PCR), whereas telogen phase hair follicles do not This indicates that melanocytes may alternate cycles of activity with metabolic rest.[8] Tyrosinase mRNA via RT-PCR has recently been used to detect melanoma micrometastasis.[9] This technique has rarely been used to study melanocyte activity and melanogenesis, or to evaluate curettage and/or melanocyte skin graft for vitiligo
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