Evidence of Barrier Deficiency in Rosacea and the Importance of Integrating OTC Skincare Products into Treatment Regimens

April 2021 | Volume 20 | Issue 4 | Original Article | 384 | Copyright © April 2021


Published online March 16, 2021

Hilary Baldwin MDa, Andrew F. Alexis MD MPHb, Anneke Andriessen PhDc, Diane S. Berson MD FAADd, Patricia Farris MD FAADe, Julie Harper MDf, Edward Lain MD FAADg, Shari Marchbein MDh, Linda Stein Gold MDi, Jerry Tan FRCPCj

aAcne Treatment & Research Center, Brooklyn, NY
bIcahn School of Medicine at Mount Sinai, New York, NY
cRadboud UMC Nijmegen, Andriessen Consultants, Malden, The Netherlands
dCornell University Weill Medical College, Weill Cornell Medical Center, Dermatology, New York, NY
eTulane University School of Medicine, New Orleans, LA; Sanova Dermatology, Metairie, LA
fThe Dermatology and Skin Care Center of Birmingham, Birmingham, AL
gSanova Dermatology, Austin TX; Austin Institute for Clinical Research, Austin, TX
hNYU School of Medicine, New York, NY
iHenry Ford Health System, Detroit, MI
jRoyal College of Physicians and Surgeons of Canada; Schulich School of Medicine and Dentistry, Department of Medicine, Western University, Windsor, ON, Canada; Windsor Clinical Research Inc; The Healthy Image Centre, Windsor, ON, Canada

therapeutic approaches need to consider all aspects of a patient's presenting features as there is no single medication that addresses them all.1,2,6

Patients often report disease flares triggered by environmental factors and food/drink consumption. Various stimuli that promote vasodilation, such as sun exposure, hot or spicy food, drinks, alcohol, physical exercise, high-temperature environments, or abrupt changes of temperature, may trigger disease flares.1,2 Vasodilators (eg, antihypertensives) or angiogenic drugs (eg, topical corticosteroids) may also induce rosacea exacerbation.1,2

Frequent and repeated flushing may cumulatively lead to progressive damage of the endothelium, angiogenesis, and inflammatory changes in the dermis.9 Studies evaluating barrier dysfunction in rosacea demonstrated that inflammation could cause or prolong flares and worsen symptoms.9,10

This article explores the role of skin barrier impairment in rosacea and the effect of over the counter (OTC) skincare products in improving barrier function and disease symptomatology.

MATERIALS AND METHODS

A panel comprised of nine dermatologists from the US and Canada (the authors) convened a webinar meeting on October 10, 2020. The online conference replaced a face to face meeting that was canceled due to the COVID-19 pandemic.

Topics for discussion included: What is the evidence that rosacea is a barrier defect disorder? What role does quality skincare play in the therapeutic algorithm? Are there particular ingredients that skincare products designed for rosacea patients should contain? Are there ingredients that should be avoided?

Prior to the meeting, panel members completed a survey on OTC skincare products recommended for rosacea patients in their practice. The survey examined which OTC products were recommended for rosacea monotherapy, an adjunct to prescription medications, and maintenance therapy.

The results of the survey were summarized, presented, and discussed during the online meeting. The outcome of these discussions, coupled with the panel's expert opinion and experience, is shown in the current review.

Clinical guidelines, algorithms, and evidence-based recommendations describing current practice for rosacea were culled from the literature through August 2020. Literature in the English language from 2015 to July 2020 was selected for clinical relevance, addressing aspects of rosacea related to skin barrier impairment and management using OTC skincare.

Rosacea Pathophysiology and the Role of the Stratum Corneum Permeability Barrier
Rosacea pathophysiology
The pathophysiology of rosacea has yet to be fully elucidated. The current model implicates two main physiologic components: an upregulated and dysregulated innate immune system and neurovascular dysregulation, both of which are triggered by genetic and exogenous factors. Consequently, this results in the activation of inflammatory cascades culminating in chronic inflammation and acute and chronic changes in the facial vasculature.1,11-14 Innate immune dysfunction in rosacea promotes photosensitivity and vascular adhesion molecule expression.14 Additionally, impairment of the skin barrier may play a role in disease occurrence and severity. However, it is unclear if this is causative for rosacea or if it results from the existence of diseased rosacea skin.12,15

Skin barrier composition and function
The skin barrier consists of enucleated protein-rich corneocytes with highly organized intercellular lipids interspersed around and between them. The organization of these two components has often been compared to a brick-and-mortar wall. But this static view does not consider the dynamic nature of the highly organized remodeling that occurs as the stratum corneum is created. Corneocytes are the building blocks of the epidermal barrier. A water-resistant layer of lipid lamellae encases the corneocytes (cornified lipid envelope), preventing water loss and controlling barrier permeability.15,16 Together, these two components serve as a nearly impenetrable interface between the body and the outside world.15,16

The intact barrier prevents excess water loss and serves to thwart the ingress of toxins and microorganisms. Harsh chemicals, surfactants, exfoliants, and aggressive cleansers – especially those with a high pH – can damage the skin barrier. Disease processes such as atopic dermatitis (AD), psoriasis, and acne may cause a barrier deficiency due to their inflammatory nature.16,17 Conversely, exogenously created barrier dysfunction (including dysbiosis of the cutaneous microbiota) may cause or exacerbate the disease state.

The role of skin lipids in the healthy skin barrier
The skin lipids play a particularly significant role in barrier function. They are produced in the lamellar bodies of the stratum granulosum during keratinocyte differentiation.The intercellular lamellar lipid membrane is primarily composed of roughly equimolar concentrations of ceramides, cholesterol, and free fatty acids, which play a vital role in the physiological maintenance of SC hydration.20,21 The physiologic SC lipids comprise approximately twenty percent of the volume of the SC and are composed of ceramides (CERs) (40–50%), cholesterols (25%), and free fatty acids (10–15%).18-22 The lipids' composition and organization are crucial to allow the formation