Background: Acne pathophysiology includes a complex interaction among inflammatory mediators, hyperseborrhea, alteration of keratinization and follicular colonization by Propionibacterium acnes.Aims: To describe the impact of the exposome on acne and how photoprotection can improve outcomes.Methods: A narrative review of the literature was carried out; searches with Google Scholar and Pubmed from January 1992 to November 2022 were performed. The keywords used were “acne,” “sunscreens,” “photoprotection,” “cosmetics,” “cosmeceuticals,” “pathogenesis,” “etiology,” “exposome,” “sunlight,” “stress,” “lack of sleep,” “diet,” “postinflammatory hyperpigmentation,” “pollution,” “exposome,” “ultraviolet radiation,” and “visible light.”Results: Environmental factors such as solar radiation, air pollution, tobacco consumption, psychological stress, diverse microorganisms, nutrition, among others, can trigger or worsen acne. Solar radiation can temporarily improve lesions. However, it can induce proinflammatory and profibrotic responses, and produce post‐inflammatory hyperpigmentation and/or post‐inflammatory erythema. While photoprotection is widely recommended to acne patients, only four relevant studies were found. Sunscreens can significantly improve symptomatology or enhance treatment and can prevent post‐inflammatory hyperpigmentation. Furthermore, they can provide camouflage and improve quality of life. Based on acne pathogenesis, optimal sunscreens should have emollient, antioxidant and sebum controlling properties.Conclusions: The exposome and solar radiation can trigger or worsen acne. UV light can induce post‐inflammatory hyperpigmentation/erythema, and can initiate flares. The use of specifically formulated sunscreens could enhance adherence to topical or systemic therapy, camouflage lesions (tinted sunscreens), decrease inflammation, and reduce the incidence of post‐inflammatory hyperpigmentation/erythema.

Background Lichen planus is a common inflammatory autoimmune condition of unknown etiology that commonly affects the skin and mucous membranes. Isolated ocular lichen planus is an extremely rare presentation that most commonly involves the eyelids, conjunctiva, and cornea, leading to severe scarring, and is clinically indistinguishable from other causes of cicatricial conjunctivitis. Observations A 79-year-old man complained of a chronic keratoconjunctivitis refractory to multiple topical treatments. Slit-lamp examination revealed diffuse bilateral conjunctival hyperemia, subepithelial fibrosis, and symblepharon, with a marked shortening of the lower conjunctival fornix. There were no other skin or mucosal lesions. Hematoxylin-eosin staining revealed acanthosis, focal thickening of the basement membrane, and a dense subepithelial mononuclear infiltrate. Direct immunofluorescence demonstrated a linear shaggy fibrinogen deposition along the basement membrane, suggestive of lichen planus. Ultrastructural examination revealed a marked widening of the epithelium–lamina propria interphase, with prominent fragmentation, reduplication, and reticulation of the lamina densa of the basement membrane. The patient was successfully treated with systemic immunosuppressive agents. Conclusions Isolated conjunctival lichen planus is an exceptional and severe cause of cicatricial conjunctivitis. Distinguishing this unusual presentation from other inflammatory diseases with conjunctival involvement is crucial to initiate an appropriate therapy early to avoid irreversible damage of the visual function.