Rosacea is a chronic skin condition primarily affecting the face, characterized by redness, pimples, swelling, and visible small blood vessels. It is a common condition, often with flare-ups and periods of remission. While the exact causes of rosacea are not fully understood, it is believed to result from a complex interplay of various factors.
The Role of Genetics
Rosacea frequently appears to run in families, suggesting an inherited component, and studies have identified specific genetic markers that may increase an individual’s susceptibility. For instance, certain genes within the Human Leukocyte Antigen (HLA) complex, such as HLA-DRB103:01, HLA-DQB102:01, and HLA-DQA105:01, have been associated with rosacea. These HLA genes are involved in the immune system’s ability to distinguish the body’s own proteins from foreign invaders, and variations can lead to abnormal inflammation. Other genetic factors, including a specific single nucleotide polymorphism (SNP) located between the HLA-DRA and BTNL2 genes, and genes related to glutathione S-transferases, have also been implicated, potentially affecting oxidative stress responses and inflammatory pathways. A genetic predisposition means an increased likelihood, not a certainty, of developing the condition.
Immune System Overactivity
An overactive or dysregulated innate immune system plays a significant role in the progression of rosacea. This involves the abnormal processing and overexpression of antimicrobial peptides, particularly cathelicidin. In individuals with rosacea, cathelicidin levels are elevated in the facial skin compared to normal skin; furthermore, the forms of cathelicidin present in rosacea patients are often different due to post-translational processing abnormalities, specifically an increase in stratum corneum tryptic enzyme (SCTE), also known as kallikrein 5. This leads to more active cathelicidin peptides, which have vasoactive and proinflammatory properties, contributing to the redness, inflammation, and visible blood vessels characteristic of rosacea. These peptides can also stimulate the production of proinflammatory cytokines and activate mast cells, further driving the inflammatory cascade.
Blood Vessel and Nerve Involvement
Physiological abnormalities in blood vessels and nerves also contribute to the visible symptoms of rosacea. Increased reactivity or fragility of blood vessels in the skin can lead to frequent flushing, persistent redness, and the development of visible blood vessels, known as telangiectasias. The condition involves neurovascular dysregulation, where the nerves controlling blood flow in the skin become hypersensitive. An imbalance in neuropeptides, small protein-like molecules used by nerve cells for communication, can disrupt normal signaling and result in exaggerated flushing responses. External factors that stimulate the sensory nervous system, such as temperature changes, emotional stress, or certain foods, can trigger vasodilation and inflammatory responses, making these physiological issues evident.
Microbes and Environmental Triggers
External factors can interact with internal predispositions to exacerbate rosacea symptoms. The skin microbiome, particularly the Demodex folliculorum mite, is thought to play a role. While these mites are normal inhabitants of human skin, their increased numbers in individuals with rosacea or an abnormal immune response to them, potentially involving bacteria, such as Bacillus oleronius, they carry, may contribute to inflammation. Beyond microbes, various environmental factors act as common triggers for rosacea flare-ups, including exposure to ultraviolet radiation, extreme temperatures, certain foods and drinks (like spicy foods or alcohol), and psychological stress; these triggers do not cause the underlying condition but rather provoke or intensify the symptoms in individuals already prone to rosacea due to their genetic makeup, immune system function, and vascular characteristics.