Melasma: The need for tailored photoprotection to improve clinical outcomes

Abstract

Background/purpose: Melasma is a frequent photoexacerbated hyperpigmentary disorder, which can significantly impact on the quality of life. We sought to review the pathogenesis of melasma, and the role of photoprotection in the prevention and treatment of this disorder.

Methods: We conducted a narrative review of the literature. We performed literature searches with PubMed from January 1990 to December 2021 using the keywords "melasma," "pathogenesis," "ultraviolet radiation," "visible light," "photoprotection," and "sunscreens."

Results: The physiopathology of melasma includes a complex interaction between genetics, sex hormones, and sun exposure. Visible light, in particular high-energy visible light (HEVL), and long-wave UVA (UVA1) play a key role in melasma pathophysiology, and recent research suggests that melasma shares many features with photoaging disorders. Melasma disproportionately affects dark-skinned individuals. Some 30% to 50% of South Americans and Asians, among other ethnicities, can present with melasma. Dark-skinned patients take fewer photoprotective measures. Also, the majority of melasma patients do not adequately follow photoprotection recommendations, including the application of sunscreen. Intensive use of a broad-spectrum sunscreen can prevent melasma in high-risk individuals, can lessen melasma severity (associated or not with depigmenting agents), and can reduce relapses.

Conclusions: Due to the physiopathology of melasma, sunscreens should be broad-spectrum with high sun protection factor, and provide high protection against UVA1 and VL. Sunscreens should be cosmetically acceptable and leave no white residue. Tinted sunscreens are an excellent choice, as pigments can protect from HEVL and UVA1, and may provide camouflage, but they must offer colors that match the skin tone of each patient.

Keywords: dark skin; ethnic skin; melasma; photoprotection; skin of color; sunscreens.

FIGURE 1

Diagram summarizing pathologic changes and mechanisms in melasma. Melanocytes are producing and distributing melanin to surrounding keratinocytes. UVB‐induced DNA damage of keratinocytes activates P53, binding to the POMC promoter and finally leads to the secretion of α‐MSH by keratinocytes. Chronic exposure to UVA and VL alters the dermal component. VL induces skin pigmentation through the activation of Opsin 3, a photoreceptor, which mediates the expression and activity of the rate‐limiting enzyme tyrosinase in melanocytes. Basal membrane alteration promotes the descent of melanocytes to the dermis (pendulous melanocytes). Keratinocytes produce cytokines and hormones, especially after UVB exposure. Fibroblasts secrete factors that influence melanogenesis and melanocyte proliferation. The increased vascularization plays a key role, especially with endothelial cells that produce ET1, which is a potent activator of melanogenesis. Abbreviations: DCT dopachrome tautomerase; DKK1, Dickkopf 1; DNA, Deoxyribonucleic Acid; ET1, Endothelin 1; HGF, hepatocyte growth factor; KC, Keratinocytes; p53, Tumor protein p53; PGE2, prostaglandin‐E2; POMC, Proopiomelanocortin; SCF, stem cell factor; sFRP2, Frizzled‐related protein 2; SPF, Sun Protection Factor; TYR/P COMPLEX, tyrosinase‐related protein complex; TYRP1, tyrosinase‐related protein 1; UVA, Ultraviolet A; UVB, Ultraviolet B; UVC, Ultraviolet C; WIF1, Wnt inhibitory factor 1; α‐MSH, α‐Melanocyte‐stimulating hormone