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Kim Thien Le, Jordana Schachter, Michael G Quigley; The role of melanin in protecting the skin and the retina from light damage: A comparative biological framework for Age-Related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2014;55(13):627.
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Light damage is implicated in the pathophysiology of Age-Related Macular Degeneration (AMD). Population studies have shown a lower incidence of AMD in black patients compared to Caucasians. Of note, dark skin in contrast to fair skin is less prone to light damage which is attributed to the difference in melanin content. The purpose of this study is to compare the role of melanin in protecting the skin and the retina from light damage.
A literature review was performed using PubMed to identify articles comparing racial differences in the skin, retina, choroid, response to light damage and development of AMD. Supplemental information was obtained from dermatology, ophthalmology and histopathology textbooks. Relevant full-texts were qualitatively analyzed to determine whether an analogy could be drawn between light damage to the vasculature of the skin and the retina and choroid.
Melanin acts as a photo-screen by scattering UV light. Melanin also scavenges light-induced free radicals. Melanocytes are located superficial to dermal blood vessels and superficial to and among choroidal vessels. Eumelanin, which is more photoprotective than pheomelanin, is present in higher quantities in dark skin and in dark eyes. Overall melanin content is also substantially higher in the basal epidermis of black skin compared to white skin. While melanin in the RPE is similar between races, choroidal melanin in the black population is significantly greater than in the white population. In response to acute UV exposure, dermal blood vessels undergo vasodilation via an inflammatory linked immune response. This response can be quantified as the minimal erythema dose, which is 33 times higher in black skin than white skin. Chronic sun damage causes a reduction in the size and number of dermal vessels, which is also more pronounced in light skin. Similarly, in AMD there is a reduction in choroidal blood flow, presumably caused by oxidative damage to choroid endothelial cells. This begs the question as to the role of decreased choroidal circulation in the genesis and evolution of AMD.
Melanin plays a role in protecting dermal and choroidal blood vessels from light damage. AMD could be a choroidal vascular damage process from cumulative light exposure.
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