Impact of ultraviolet radiation and exposome on rosacea: Key role of photoprotection in optimizing treatment.

BACKGROUND

Pathophysiology of rosacea is not completely understood and involves a complex interaction among genetics, ultraviolet (UV) light, microorganisms, impaired skin barrier, neuronal and vascular dysfunction, and immune system disruption.

AIMS

To describe the etiology of rosacea with an emphasis on the role of UV radiation and exposome, and to review the importance of non-pharmacologic strategies focusing on photoprotection.

METHODS

We conducted a narrative review of the literature. We performed literature searches with PubMed from January 1990 to November 2020 using the keywords "rosacea", "pathogenesis", "ultraviolet radiation", "exposome", "photoprotection", "sunscreens" and "non-pharmacologic agents". The search was limited to English, Spanish, and French language articles.

RESULTS

Several environmental factors such as UV light, diverse microorganisms, air pollution, tobacco smoking, nutrition, and psychological stress showed to trigger or worsen rosacea. UV radiation was reported to induce pro-inflammatory, pro-angiogenic, and pro-fibrotic responses. We found 6 original articles about the impact of sunscreens on rosacea. The use of sunscreens containing ingredients with emollient, anti-inflammatory, and/or vasoregulatory properties was shown to significantly improve symptomatology.

CONCLUSION

UV radiation and the exposome play a key role in the development of rosacea. UV light is implicated in all significant aspects of rosacea: skin inflammation, neoangiogenesis, telangiectasia, and fibrosis, and may even initiate rosacea. While the use of sunscreens is widely recommended, the literature on the impact of photoprotection in rosacea is scarce. Adequately formulated sunscreens could not only provide the required level of photoprotection, but may also help to mitigate the barrier dysfunction, neutralize facial redness (tinted sunscreens), and decrease inflammation and vascular dysfunction.