The pathogenesis of rosacea is multifactorial, including:
- Genetic Susceptibility: Single nucleotide polymorphisms related to the class II major histocompatibility complex.
- Altered Microbiome: Bacterial overgrowth in the small intestine, Helicobacter pylori infection, and increased density of Demodex folliculorum and Staphylococcus epidermidis.
- Immune Dysregulation: Excessive inflammation, vasodilation, lymphatic dilatation, and angiogenesis due to dysregulated immune responses.
- Neurocutaneous Mechanisms: Triggers such as UV radiation, temperature changes, exercise, spicy foods, alcohol, psychological stress, air pollution, and tobacco smoking.
- Impaired Skin Barrier: Features of skin barrier impairment allow bacterial colonization and inflammation.
Innate and Adaptive Immunity: Increased expression and activity of toll-like receptor 2, cathelicidins, kallikrein 5, and mast cells, alongside dominant T-helper (Th)1/Th17 gene expression, contributing to inflammation.