[Academic Presentation] Rosacea and the Skin Barrier

Impaired skin barrier function plays a significant role in the clinical manifestations of facial dryness and sensitivity observed in patients with rosacea. The alterations in skin barrier function vary across different subtypes of rosacea. The most common subtypes are erythematotelangiectatic rosacea and papulopustular rosacea. Erythematotelangiectatic rosacea is characterized by transient flushing or persistent erythema on the cheeks, often accompanied by facial skin sensitivity, whereas papulopustular rosacea predominantly presents with facial papules and pustules. Measurements of skin barrier function in these two subtypes reveal a marked reduction in stratum corneum water content, an increase in transepidermal water loss (TEWL), and a rise in skin surface pH, while sebum levels remain relatively unchanged; however, the composition of sebum undergoes notable shifts. These abnormalities are also evident in non‑lesional skin but are more pronounced at lesional sites, suggesting that skin barrier dysfunction may be present even before the appearance of typical clinical lesions in rosacea patients, and that such disturbances may worsen as the disease progresses.

1.1 Changes in the Moisture Content of the Stratum Corneum

The water content of the stratum corneum is an important indicator of skin barrier function and can also be used to assess the degree of skin dryness. In patients with rosacea, the skin is prone to developing sensitive symptoms—such as dryness and pruritus—in response to external stimuli, with dryness being the most common. Studies have shown that 66.7% of rosacea patients exhibit symptoms of skin dryness, accompanied by a significant reduction in stratum corneum water content. Another study reported that papules… Compared with healthy controls, patients with pustular rosacea exhibit a significant reduction in the water content of the stratum corneum on the forehead, cheeks, and other areas.

1.2 Changes in Sebum Secretion

Lipids on the skin surface can be classified, based on their origin and composition, into sebaceous gland lipids and intercellular lipids. Sebaceous gland lipids are secreted directly from the sebaceous glands onto the skin surface, whereas intercellular lipids are primarily distributed between keratinocytes as cells grow and metabolize; ultimately, they are released to the skin surface upon the desquamation of the stratum corneum. As a key structural component of the skin barrier, lipids play an indispensable role in maintaining its function. Sebum not only helps prevent the loss of water and electrolytes but also acts as a barrier against harmful substances, exhibits antimicrobial activity, and contributes significantly to the maintenance of skin pH. Interestingly, one study compared sebum levels at seven facial sites in 35 patients with papulopustular rosacea and 34 healthy controls, concluding that there was no significant difference in epidermal sebum content between these two groups. However, a separate study by Ní Raghallaigh et al. examining sebum composition found that the fatty acid profile of sebum in the skin barrier of patients with papulopustular rosacea had changed. This research measured and compared the fatty acid content of facial sebum in 25 patients with papulopustular rosacea and 24 healthy controls, revealing that the concentration of myristic acid was markedly elevated in the facial sebum of rosacea patients, while long-chain saturated fatty acids were reduced, indicating a shift in the lipid composition.

1.3 Changes in Transepidermal Water Loss

TEWL reflects the amount of water evaporating from the skin’s surface and is therefore an important indicator for assessing skin barrier function. TEWL indicates the extent of water loss through the stratum corneum, thereby reflecting the skin’s water‑permeability barrier. The higher the TEWL value, the greater the water loss through the skin and the poorer the barrier function of the stratum corneum. Dirshka et al., by measuring… The transepidermal water loss (TEWL) measured on the faces of 75 patients with rosacea and 125 healthy controls indicated that TEWL was significantly elevated around the nose, on the cheeks, and on the nasal region in patients with rosacea.

1.4 Changes in Skin pH Value

The skin surface pH not only reflects the body’s biological activities at the epidermal level but also influences the biological functions of both the epidermis and even the dermis, serving as an important indicator for assessing skin barrier function. Under normal conditions, the skin surface pH is slightly acidic, with slight variations across different regions of the epidermis. Studies have shown that the skin surface pH… The value increases as skin dryness intensifies, and the higher the skin’s pH, the weaker its barrier function against water permeation. Studies by Wu Yan et al. have shown that patients with rosacea exhibit an elevated skin surface pH compared to that of healthy controls. Furthermore, research by Ní Raghallaigh et al. on changes in skin barrier function in papulopustular rosacea also indicates an increased skin surface pH in the facial skin of individuals with this condition.

The etiology of rosacea is complex; it is currently widely regarded as a chronic inflammatory condition driven by genetic predisposition and triggered by multiple factors, with dysregulation of innate immunity and vascular tone as the central pathogenic mechanisms. Numerous studies have demonstrated that various steps in the pathogenesis of rosacea are associated with impaired skin barrier function.

2.1 Inflammatory Response and the Skin Barrier

Activation of the innate immune response in patients with rosacea plays a crucial role in the development of inflammation, primarily manifesting as heightened reactivity to external environmental stimuli. Skin antimicrobial peptides (AMPs), in particular, Cathelicidin antimicrobial peptide (CAMP) is highly expressed, and LL‑37 fragments are upregulated, thereby promoting angiogenesis and the initiation and progression of inflammation. Studies have shown that epidermal barrier function also modulates cutaneous innate immunity, such as the expression of epidermal antimicrobial peptides. Consequently, on the one hand, inflammation can alter the skin barrier in patients with rosacea, rendering the face more susceptible to environmental factors and leading to symptoms of barrier dysfunction, including flushing and stinging; on the other hand, skin barrier integrity can influence the onset and development of rosaceous inflammation. Furthermore, research indicates that following disruption of the skin barrier, dermal mast cell infiltration markedly increases, and mast cells serve as key mediators of rosacea‑related inflammation. In particular, mounting evidence in recent years demonstrates a complex and intimate crosstalk between mast cells and sensory nerves, while abnormalities in sensory and autonomic neural regulation are closely linked to heightened responsiveness to external stimuli and the early pathogenesis of rosacea.

2.2 Neural and Vascular Changes and the Skin Barrier

Patients with rosacea exhibit markedly heightened reactivity to both endogenous and exogenous environmental stimuli; sun exposure, high temperatures, and emotional stress can all trigger episodic flushing or erythema. These responses are closely linked to vascular dysregulation and abnormal neurovascular control in rosacea. Ultraviolet radiation and temperature fluctuations can activate sensory nerves, and the activation of the cutaneous sensory nervous system is intimately associated with the onset and progression of early‑stage rosacea.

Blood vessels, lymphatics, and the skin are all involved in development, homeostasis, and wound repair. Recent studies have demonstrated a close association between vascular and lymphatic structures and rosacea. Schwab et al. reported that in erythematotelangiectatic rosacea and papulopustular rosacea, the hallmark features include dilation and enlargement of blood vessels and lymphatics, increased vascular permeability, and elevated blood flow; whereas in some cases of hypertrophic rosacea, there is evidence of angiogenesis and lymphangiogenesis. Moreover, vasodilation and increased blood flow contribute to heightened transepidermal water loss and stimulate the proliferation and differentiation of keratinocytes.

The roles of the cutaneous nervous system in regulating inflammation, immunity, and vascular homeostasis have been well established. Recently, research on the neurovascular regulatory mechanisms underlying rosacea has focused on ion channels, with particular attention paid to the capsaicin receptor (TRPV1). Investigators have found that TRPV1 is highly upregulated in patients with rosacea. Triggers of rosacea—such as heat, alcohol, and chemical irritants—can all activate TRPV1, leading to the release of key neuroinflammatory and nociceptive mediators, including substance P and calcitonin gene‑related peptide. This activation disrupts neurovascular regulation, contributing to the onset and progression of rosacea. Denda reported that treatment with TRPV1 inhibitors accelerates skin barrier repair, suggesting a close link between activated TRPV1 in epidermal keratinocytes and impairment of the skin barrier. Moreover, TRPV1 exhibits high expression in epidermal keratinocytes as well as in nerve fibers within both the epidermis and dermis. Jun-Won Yun et al. further demonstrated, through mouse experiments, that blocking TRPV1 activation can expedite the restoration of the skin barrier.

2.3 Microbial Changes and the Skin Barrier

The relationship between microbial infection and the pathogenesis of rosacea has long been a subject of considerable debate. Some researchers argue that microbial infections play a significant role in the development of rosacea, while others contend that such infections are not directly linked to its onset. Investigators have identified several microorganisms potentially involved in rosacea, including Demodex folliculorum, Cutibacterium acnes, Staphylococcus epidermidis, and Helicobacter pylori. Zhao et al., through an analysis of relevant studies, concluded that Demodex folliculorum exhibits a statistically significant association with rosacea, suggesting that infection with this mite is an important risk factor for the condition. Evidence indicates that patients with rosacea harbor a markedly higher density of Demodex folliculorum per unit area compared to healthy individuals, particularly in the papulopustular subtype. As for Cutibacterium acnes (PA), Jahns, in a study involving 82 cases of rosacea and 25 cases… Studies conducted in healthy individuals have found no significant association between PA and the pathogenesis of rosacea. However, other research indicates that PA can activate Toll‑like receptor 2 (TLR2), and activation of Toll‑like receptors represents an important molecular pathway in the pathogenic mechanisms of rosacea. A survey by El Khalawany et al. demonstrated that the detection rate of Helicobacter pylori (HP) is significantly higher in patients with rosacea than in healthy controls. Nevertheless, there is currently no definitive evidence to suggest that Staphylococcus epidermidis is a causative factor in rosacea.

The skin surface microbiota is an essential component of the skin barrier, and microbial homeostasis serves as a robust protective shield for the skin. Alterations in the abundance of individual microbial species or imbalances in the overall microbial community can both disrupt the skin barrier. Studies have shown that an acidic environment can inhibit the growth of bacteria, yeasts, and other pathogenic microorganisms. Consequently, when the skin barrier is compromised, the skin pH rises, fostering the proliferation of surface microbes or disturbing their ecological balance, which may lead to skin infections or inflammation and further exacerbate barrier dysfunction.

Rosacea often manifests as skin sensitivity on the face, and clinical studies have demonstrated that medical skincare products with barrier‑repairing properties can effectively alleviate symptoms such as dryness, stinging, and burning in patients with rosacea, while also reducing episodic flushing—making them a cornerstone of rosacea management. Research indicates that topical medical skincare products can progressively improve key skin barrier parameters, including transepidermal water loss (TEWL), stratum corneum hydration, and cutaneous sebum levels, and markedly ameliorate clinical signs like dryness and pruritus.

According to the literature, tranexamic acid, as a protease inhibitor, can effectively restore impaired skin barrier function. Sun Nan et al. conducted a self‑controlled topical application study involving 30 patients with rosacea and demonstrated that tranexamic acid improves the skin barrier in rosacea by inhibiting the activity of serine proteases in the stratum corneum and downregulating the expression of the antimicrobial peptide LL‑37.

Through comparative clinical efficacy studies, the author found that radiofrequency rejuvenation can enhance the skin’s moisturizing capacity, thereby helping to restore the skin barrier. In the short term, radiofrequency treatment increases the stratum corneum water content at lesional sites in patients with rosacea, reduces transepidermal water loss (TEWL), and rapidly alleviates clinical symptoms such as dryness, pruritus, and episodic flushing.

Rosacea is a complex dermatological condition characterized by cutaneous inflammation and neurovascular alterations. Its onset and clinical manifestations are closely linked to external irritants, while also being intimately associated with and mutually influenced by impaired skin barrier function. Most patients with rosacea exhibit compromised skin barrier integrity, and such impairment can both precipitate and exacerbate the disease. Restoring skin barrier function can markedly alleviate clinical symptoms in affected individuals. Investigating the role of skin barrier dysfunction in the pathogenesis and progression of rosacea can provide additional evidence and innovative approaches for long-term, effective management.