Potential Role of Allergens and Other Exogenous Triggers in Lichen Sclerosus: Etiological Drivers or Disease Modifiers?

Lichen sclerosus (LS) is a chronic immune-mediated and fibrosing mucocutaneous disorder with a multifactorial pathogenesis. Although autoimmune mechanisms and genetic susceptibility are well recognized, the contribution of exogenous triggers and contact allergens remains debated. This narrative review critically evaluates whether irritants, allergens, mechanical trauma, microbial dysbiosis, and infectious agents should be interpreted as primary etiological factors or as secondary disease modifiers in LS. A literature search was conducted in PubMed, Scopus, and Web of Science from database inception to June 2026, focusing on studies addressing epithelial barrier dysfunction, Koebnerization, contact dermatitis, patch testing, microbiome alterations, infectious triggers, immune pathways, and clinical management. Current evidence suggests that barrier dysfunction and cutaneous fragility may create a permissive microenvironment in which mechanical stress, irritants, contact allergens, repeated topical exposure, and microbial alterations can amplify inflammation and symptoms. Patch-testing studies support the clinical relevance of allergic contact dermatitis in selected patients with persistent or treatment-refractory symptoms, but do not establish contact allergy as a primary cause of LS. Similarly, microbiome and infectious data remain associative rather than causal. Overall, exogenous factors in LS are neither a complete myth nor a primary explanation for the disease; their relevance lies mainly in disease modulation and personalized management in selected patients.