Persistent dysfunction of the epidermalmelanin unit - resulting in recurring pigmentation in the skin with melasma - derives from a disarray of the melanogenesis. Its regulatory components and their interactions are not well known.123
Due to the incomplete understanding of its pathogenesis, treatments of melasma aim, essentially, at blocking solar radiation (through strategies that reduce the biosynthesis, transport and transfer of melanin), and reducing the amount of epidermal melanin, instead of aiming at the causal dysfunction of the disease. Thus, long-term therapies are necessary, since recurrence rates are high. However, this matter is beyond the scope of this study.54,57,124-126
In general, prognosis of melasma is favorable. There is a reduction in its prevalence, in the intensity of lesions with age, and the attenuation of pigmentation with treatment.
It is intriguing that a more intense melanogenic response behavior occurs in melasma lesions than in adjacent healthy areas, since both are subjected to similar photo-exposure schemes. This suggests a postsomatic genetic mosaicism behavior of the pigmentary system, whose genomic substrate is not yet fully understood.
Controlled epidemiological studies may support hypotheses for research on pathophysiology, therapeutic strategies, as well as promote primary prevention in risk groups.