INTRODUCTION
Facial hyperpigmentation, characterized by the excessive production of melanin in the skin, is a prevalent dermatological concern affecting individuals of various ethnic backgrounds. Among the various forms of facial hyperpigmentation, melasma stands out as a distinct and challenging condition. This multifactorial disorder is characterized by symmetrically distributed, brownish facial hyperpigmentation, often affecting sun-exposed areas, particularly the forehead, cheeks, and upper lip.
The epidemiology of facial hyperpigmentation, including melasma, exhibits a notable predilection for women, with estimates suggesting a prevalence of up to 10% to 50% among females and a considerably lower prevalence among males. Furthermore, there is a higher incidence in individuals with darker skin phototypes, emphasizing the role of ethnicity in melasma development.1
The pathogenesis of facial hyperpigmentation, particularly melasma, is intricate and involves the interplay of genetic, hormonal, and environmental factors.2,3 Genetic predisposition is evident in familial cases, emphasizing the hereditary component of melasma. Hormonal factors, including pregnancy, oral contraceptive use, and hormonal replacement therapy, contribute to the dysregulation of melanogenesis and are mediated by the upregulation of melanocyte-stimulating hormone (MSH) and estrogen receptors, which contributes to the gender disparity observed in melasma. Chronic exposure to UV radiation exacerbates melanin production by stimulating melanocyte activity and promoting the release of proinflammatory mediators. Additionally, inflammatory pathways, such as increased expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1), further contribute to melanin hyperproduction, linking inflammation to the pathogenesis of melasma.
Effective management of facial hyperpigmentation, especially melasma, involves a comprehensive approach targeting various aspects of its pathogenesis. Sun protection, including the regular use of broad-spectrum sunscreen with a high sun protection factor (SPF), is fundamental in preventing UV-induced exacerbation. Topical agents, such as hydroquinone, retinoids, and corticosteroids, are commonly employed to inhibit melanin synthesis and promote skin turnover. Procedural interventions, including chemical peels, laser therapy, and intense pulsed light (IPL), offer additional modalities for pigment reduction by
The epidemiology of facial hyperpigmentation, including melasma, exhibits a notable predilection for women, with estimates suggesting a prevalence of up to 10% to 50% among females and a considerably lower prevalence among males. Furthermore, there is a higher incidence in individuals with darker skin phototypes, emphasizing the role of ethnicity in melasma development.1
The pathogenesis of facial hyperpigmentation, particularly melasma, is intricate and involves the interplay of genetic, hormonal, and environmental factors.2,3 Genetic predisposition is evident in familial cases, emphasizing the hereditary component of melasma. Hormonal factors, including pregnancy, oral contraceptive use, and hormonal replacement therapy, contribute to the dysregulation of melanogenesis and are mediated by the upregulation of melanocyte-stimulating hormone (MSH) and estrogen receptors, which contributes to the gender disparity observed in melasma. Chronic exposure to UV radiation exacerbates melanin production by stimulating melanocyte activity and promoting the release of proinflammatory mediators. Additionally, inflammatory pathways, such as increased expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1), further contribute to melanin hyperproduction, linking inflammation to the pathogenesis of melasma.
Effective management of facial hyperpigmentation, especially melasma, involves a comprehensive approach targeting various aspects of its pathogenesis. Sun protection, including the regular use of broad-spectrum sunscreen with a high sun protection factor (SPF), is fundamental in preventing UV-induced exacerbation. Topical agents, such as hydroquinone, retinoids, and corticosteroids, are commonly employed to inhibit melanin synthesis and promote skin turnover. Procedural interventions, including chemical peels, laser therapy, and intense pulsed light (IPL), offer additional modalities for pigment reduction by
