ABSTRACT
BACKGROUND: Transfer of melanosomes from melanocytes to the neighboring keratinocytes is a critical step in normal pigmentation. However, the mechanism of melanosome transfer and the regulation of pigmentation by the keratinocyte-melanocyte interactions are not well understood. It has recently been identified that keratinocytes use Foxn1 (transcription factor) to recruit melanocytes and induce their own pigmentation. OBJECTIVE: The purpose of this study was to assess the expression of Foxn1 in hypopigmentary disorders (vitiligo, pityriasis alba (P. alba) and postinflammatory hypopigmentation (PIHo)) and hyperpigmentary disorders (melasma, caf?-au-lait macule (CALM) and postinflammatory hyperpigmentation (PIHer)). METHODS: Immunohistochemical staining was performed on the formalin-fixed, paraffin-embedded tissue sections of hypopigmentary and hyperpigmentary disorders using anti-Foxn1 antibody with an avidin-biotin peroxidase complex procedure. The intraepidermal melanin pigments were examined in all the lesions by Fontana-Masson staining. RESULTS: We found a significantly lower Foxn1 expression (p<0.05) and less intraepidermal melanin pigments (p< 0.01) in the hypopigmentary disorders as compared to that of the hyperpigmentary disorders. In the hypopigmentary disorders such as vitiligo, P. alba and PIHo, the expression of Foxn1 was decreased in the order named. In thehyperpigmentary disorders such as CALM, PIHer and melasma, the expression of Foxn1 was increased in the order named. CONCLUSION: The intraepidermal Foxn1 expression and melanin pigments in PIHer, PIHo and melasma showed a positive correlation, but there was no statistically significant. Our findings suggest that the expression of Foxn1 might be associated with the pathogenesis of three pigment disorders (PIHo, PIHer, melasma). We consider that inflammatory mediators might interact with the intraepidermal Foxn1 expression in PIHo, PIHer and melasma, resulting in an abnormality of the mechanism of melanosome transfer. Further studies are warranted to elucidate the role of the Foxn1 expression in the pathogenesis of pigment disorders.