Overall, clinical studies demonstrated that daily moisturisation increased skin hydration and decreased trans-epidermal water loss (TEWL) in both children and adults, resulting in skin barrier improvements.1
Why is epidermal barrier protection important?
Healthy skin is characterised by invisible desquamation, smooth texture, elasticity, and the ability to respond to shearing forces without rigidity and micro-fissuring. The epidermis, which is constructed of multiple sub-layers such as the stratum corneum (often referred to as the skin’s brick wall), stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale, acts as the body’s first line of defence (barrier) against the external environment and is therefore essential in the maintenance of healthy skin.2,3
The skin barrier is responsible for the maintenance of water content and balance (permeability), prevention and responses to invasion by microbial organisms and antigens (antimicrobial and immune response barrier), reduction of the effects of ultraviolet (UV) light exposure (photoprotection), and mitigation of the effects of oxidative stresses.2,3
In AD, a compromised or dysfunctional skin barrier has been shown to provoke increased TEWL, which result in excessive cutaneous dehydration, allowing allergens, microbes, and irritants to penetrate the skin. This causes a proinflammatory reaction typically seen in patients with AD. The extent of barrier dysfunction strongly correlates with the degree of inflammation within AD lesions.3
Brick and mortar
The stratum corneum is made up of two components: the corneocytes and the extracellular lipid matrix. Each of these plays a different role. The corneocytes, which are the terminally differentiated keratinocytes, provide mechanical reinforcement, protect underlying mitotically active cells from UV damage, regulate cytokine-mediated initiation of inflammation, and maintain hydration (bricks).4
Abnormal desquamation leads to clumping of corneocytes, which presents visibly as scaling and flaking, loss of elasticity and increased rigidity. Increased rigidity leads to micro-and macro-fissuring, while epidermal proliferation can lead to hyperkeratosis.2
The extracellular lipid matrix, which comprises about 20% of the volume of the stratum corneum and is composed of ceramides (40%–50%), cholesterols (25%), and free fatty acids (10%–15%), regulates permeability, initiates corneocyte desquamation, has antimicrobial peptide activity, and excludes toxins, and allows for selective chemical absorption (mortar).3,4
An equimolar ratio of ceramides, cholesterols and fatty acids are needed for normal skin barrier repair. Further acceleration of barrier repair occurs as the ratio of any of these ingredients is increased up to three-fold.5
The importance of the acid mantle
A dysfunctional skin barrier can be attributed to several factors. In AD dysfunction is the result of for example altered enzymatic activity and altered pH of the skin. The acid mantle is characterised by a pH value of 4-6, as a result of amino acids, fatty acids, sebum secreted by the sebaceous gland, and lactate excreted from sweat. All of these compounds are acidic and when present together on the human skin, become a barrier that prevents bacterial colonisation.3,6
A number of factors, including both endogenous (eg age, genetic predisposition, ethnicity) and exogenous elements (eg detergents, cosmetics, soaps) affect skin pH.6
Protecting skin barrier integrity
Guidelines recommend the consistent and liberal use of emollients/moisturisers and barrier repair formulations for the prevention and maintenance of the epidermal skin barrier in patients with AD. Their use may even reduce the need for topical corticosteroids. Emollients also add a protective layer that helps aid corneocyte water retention and inhibits irritant entry.7
Barrier repair formulations - usually made available as prescription products - contain the fundamental ingredients of a conventional moisturiser along with specific physiologic ingredients (eg ceramides, essential fatty acids) and formulation design characteristics that directly target barrier repair (eg replenishment of the stratum corneum intercellular lipid membrane).2
Emollients work to moisturise the skin by increasing the amount of water held in the stratum corneum. Specifically, depending on the constituents of the emollients, they work either by occlusion, trapping moisture into the skin (which slows the evaporation of water), or in an active way by drawing moisture into the stratum corneum from the dermis. As the emollient penetrates the stratum corneum, it mimics the natural lipids that are so vital to the barrier function.7
Research evidence suggests that emollients accelerate the regeneration of skin barrier function following disruption, with the most lipid-rich emollients restoring the skin barrier more rapidly.7
What do guidelines recommend?
Moisturising to address the defective barrier is an important therapeutic concept in AD, state the authors of the 2020 American Academy of Dermatology AD guideline.8
Prescription emollients are designed to target specific defects in skin barrier function observed in AD. They include preparations having distinct ratios of lipids that mimic endogenous compositions and creams containing palmitoylethanolamide, glycyrrhetinic acid, or other hydro lipids. They are generally recommended for two or three times daily use depending on the specific agent.8
A number of clinical trials have shown that emollients lessen symptoms and signs of AD, including pruritus, erythema, fissuring, and lichenification. These agents can therefore reduce inflammation and AD severity. In addition, their use decreases the amount of prescription anti-inflammatory treatments required for disease control, as demonstrated in random.8
The choice of agent depends on individual preference. The ideal agent should be safe, effective, inexpensive, and free of additives, fragrances, perfumes, and other potentially sensitising agents.8
The British Dermatological Nursing Group recommends:7
- Mild AD: Simple emollients without added excipients are usually sufficient to manage symptoms and keep the disease under control.
- Moderate to severe disease: Emollients with added active ingredients eg humectants may be helpful.
Maximising outcomes for patients with AD
Healthcare providers can maximise patient outcomes by:1
1. Stressing the benefits of daily emollient therapy to their patients, particularly highlighting flare prevention. Evidence has consistently shown that the daily application of a therapeutic moisturiser improves the skin barrier and reduces the number and frequency of flares. These outcomes can result in greater quality of life and potential cost benefits by reducing the number of lost days at work. For neonates, those at high risk of developing AD can delay or even avoid AD by proactive treatment with a therapeutic moisturiser (primary prevention)
2. Recommending clinically proven therapeutic moisturisers to patients is key to a successful therapeutic outcome. Instructions should stress that moisturisers should be applied liberally and daily — ideally twice. Recommendations should be based on formula composition and the strength of clinical data supporting the formulation
3. Clinical demonstrations should include both objective measures of skin hydration and TEWL and validated clinical scales to assess symptom improvement. Product selection should also consider patients’ experience and preference, as therapeutic efficacy can be provided in aesthetically pleasing, lighter formulations that can improve compliance
4. Topical corticosteroids are generally recommended as the next step in the treatment of AD, particularly for the targeted treatment of flares. Topical steroid formulations may include penetration enhancers designed to enhance the delivery of active steroids to its target, which may weaken the barrier. Consequently, maintaining daily moisturisation is important when topical steroids are added to the treatment regimen.
As has been highlighted above, emollients should be considered a key therapeutic agent in the management of dry skin diseases such as AD. It would seem from clinical practice that they are also important for promoting skin health and preventing skin breakdown.7
1. Herbert AA, Rippke F, Weber TM and Nicol NH. Efficacy of Nonprescription Moisturizers for Atopic Dermatitis: An Updated Review of Clinical Evidence. American Journal of Clinical Dermatology, 2020.
2. Del Rosso J, Zeichner J, Alexis A, et al. Understanding the Epidermal Barrier in Healthy and Compromised Skin: Clinically Relevant Information for the Dermatology Practitioner Proceedings of an Expert Panel Roundtable Meeting. Journal of Clinical and Aesthetic Dermatology, 2016.
3. Alizadehfar R. Skin Barrier Repair in the Management of Atopic Dermatitis. Skin Therapy Letter.com, 2016.
4. Murphrey MB, Miao JH and Zito PM. Histology, Stratum Corneum. StratPearls (Internet), 2021. https://www.ncbi.nlm.nih.gov/books/NBK513299/
5. Mao-Qiang M, Feingold KR, Thornfeldt CR and Elias PM. Optimization of Physiological Lipid Mixtures for Barrier Repair. J Invest Dermatol, 1996.
6. Ali SM and Yosipov G. Skin pH: From Basic Science to Basic Skin Care. Acta Derm Venereol, 2013.
7. Penzer R. Best practice in emollient therapy a statement for healthcare professionals. https://bdng.org.uk/wp-content/uploads/2017/02/EmollientBPG.pdf
8. Eichenfield LF, Tom WL, Berger TG. Guidelines of care for the management of atopic dermatitis Section 2. Management and treatment of atopic dermatitis with topical therapies. Journal of the American Academy of Dermatology, 2020.