Aetiology

The underlying cause is not fully understood. Factors that affect the inflammatory/immune response or cause vascular dysfunction seem to be important. The most important climatic exposure is sunlight, which affects both of these.[10][11]

There is also evidence that the skin barrier is impaired in people with rosacea.[11][12]

A twin study found the genetic contribution to rosacea was 46%.[13]

Factors or triggers that may precipitate onset include:[1][13][14][15][16]

  • Sun/ultraviolet exposure

  • Hot, cold, or windy weather

  • Humidity, indoor heating, hot baths, hot beverages

  • Heavy exercise

  • Alcohol consumption

  • Spicy foods

  • Emotional stress

  • Some skincare and toiletry products (e.g., those that contain menthol, camphor, or sodium lauryl sulfate)

  • Some medicines

  • Medical conditions that cause hot flushes

  • Some fruits and vegetables, or certain dairy products.

There appears to be an exaggerated vasodilatory response to increased temperature, and redness can be easily exacerbated by hot drinks and hot baths or showers.[10]

General inflammation may be induced by medicines (e.g., amiodarone; nasal corticosteroids; and, paradoxically, topical corticosteroids), spicy foods, or micro-organisms (e.g., Helicobacter pylori, demodex mite).[17][18][19]

Pathophysiology

Gaps remain in scientific knowledge underlying the pathophysiology of rosacea.[20] Pathways that lead to the development of rosacea are not well understood.

Abnormalities in immune response

Symptoms may be caused or exacerbated by dysregulation of innate immune responses.[10][21]

  • Cathelicidin LL-37 has been reported to induce skin inflammation through activation of the NLRP3 inflammasome in vitro and in mice.[22][23] Mast cell numbers are increased in the dermis of patients with rosacea, and have been shown in a mouse model to be key mediators of cathelicidin-initiated skin inflammation.[24]

  • Increased expression of Toll-like receptor 2 (TLR2) has been observed in the epidermis of patients with rosacea, but not in other inflammatory skin disorders such as atopic dermatitis or psoriasis.[23][25]

The adaptive immune system may also play a role in rosacea.[26] One study showed activation of the T-helper (Th) 1/Th17 pathway in patients with rosacea.[27]

Inflammatory reactions to micro-organisms

Micro-organisms associated with the development of rosacea include Helicobacter pylori, Demodex folliculorum, Staphylococcus epidermidis, and Chlamydia pneumoniae; however, studies have been inconclusive.[19][28][29][30]

Vascular dysfunction

Flushing episodes are very common in people with rosacea, suggesting that vascular hyper-reactivity and increased blood flow may contribute to the pathogenesis.[10] Studies have demonstrated a measurable increase in blood flow in skin lesions.[31][32]

Ultraviolet exposure

Exposure to ultraviolet (UV) light can lead to inflammation, neoangiogenesis, telangiectasia, and fibrosis.[11] UV radiation may be the cause of abnormalities in immune response via multiple mechanisms (e.g., activation of Toll-like receptor 2 [TLR-2]; production of reactive oxygen species; and the release of cathelicidin LL-37 due to keratinocyte damage).[33][34]

Genetics

A cohort study of fraternal twins concluded that the genetic contribution to rosacea was 46%.[13] A genome-wide association study identified two significant single nucleotide polymorphisms (rs763035 and rs111314066) and three human leukocyte antigen (HLA) alleles (HLA-DRB1*, HLA-DQB1*, and HLA-DQA1*), consistent with the importance of the inflammatory response in the pathogenesis of rosacea.[35] One case-control study found that the +405C/G polymorphism of the vascular endothelial growth factor (VEGF) gene increased the risk of rosacea.[36]

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