Rosacea is a chronic condition that has no definitive cause. It is characterized by periods of exacerbation (symptoms) and remission (temporary alleviation of symptoms). Only 4% of those affected by Rosacea originate from Africa, Asia, or Latin America. The condition predominantly affects women, particularly those in northern and western Europe. All undesirable states that negatively impact the appearance of the skin result in a significant deterioration of the quality of life. Various forms of this ailment can be distinguished, each presenting with distinct symptoms.
Rosacea: pathophysiological mechanisms and predisposing factors in disease development
The pathogenesis of rosacea remains a multifaceted interplay of immunological dysregulation, aberrant angiogenic signaling, ultraviolet (UV) radiation exposure, and potential microbial contributions—including the implicated role of *Helicobacter pylori*. Clinical manifestations such as persistent erythema arise from excessive cutaneous blood flow within the microvasculature. Research demonstrates that individuals diagnosed with rosacea exhibit elevated levels of pro-angiogenic mediators, most notably vascular endothelial growth factor (VEGF), whose synthesis is further upregulated by UV exposure. Beyond this, UV radiation triggers the activation of matrix metalloproteinases, initiating a cascade of pro-inflammatory responses that exacerbate disease severity. Consequently, daily application of broad-spectrum sunscreen represents a critical preventive measure. From a microbiological perspective, heightened colonization of sebaceous glands by the mite *Demodex folliculorum*—alongside its associated bacterium *Bacillus oleronius*—correlates with amplified inflammatory lesions. Targeted antibiotic therapies, designed to eradicate these microorganisms, have shown promising efficacy in alleviating symptomatic burden.
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