Role of moisturizers and cleansers in managing pediatric eczema

Epidermal Barrier dysfunction in AD

In AD, the skin barrier is compromised due to both primary factors, like FLG gene mutations, and secondary factors, such as the itch-scratch cycle or cytokine-driven reductions in structural proteins and lipids (e.g., due to interleukin [IL]-4, IL-13, and IL-33).^[6] These changes occur even in seemingly unaffected skin and include higher skin pH, lower water retention, increased irritability, and greater permeability to irritants and pathogens.

At the molecular level, patients show reduced levels of skin structural and tight junction proteins, altered lipid organization, protease imbalance, and abnormal microbiota. Barrier disruption also leads to inflammation through the release of damage signals called alarmins (e.g., IL-1b, IL-25, IL-33, and thymic stromal lymphopoietin [TSLP]), which further promote immune responses and allergen sensitization.^[7] This cycle can be initiated by genetic factors (e.g., FLG deficiency) or immune dysregulation, as seen in immunodeficiencies such as DOCK8 or Wiskott–Aldrich syndrome, where inflammation (e.g., IL-31 overexpression) intensifies itch and barrier damage.^[8]

Cutaneous inflammation in AD

AD lesions are marked by an infiltration of immune cells, especially CD4+ T cells, which drive inflammation, along with increased dendritic cells such as Langerhans cells – likely due to heightened antigen presentation. These Langerhans cells, more active in lesional skin, extend dendrites through tight junctions to capture antigens – unlike in healthy or non-lesional skin.

Non-lesional skin, though appearing normal, shows mild immune changes such as spongiosis and T-cell infiltration, similar to lesional skin. Both lesional and non-lesional areas show decreased expression of epidermal barrier genes and increased expression of T helper (TH) cell-related genes.

In lesional skin, gene expression changes are more pronounced, especially those related to keratinocytes and TH2 (IL-4, IL-10, and IL-13) and TH22 (IL-22) cytokines. TH1 and TH17 cytokines may also be upregulated in chronic AD, particularly in children and individuals of Asian descent. AD progression appears to involve a gradual increase in TH2, TH17, and TH22 cytokines.^[9] Barrier disruption releases alarmins that activate dendritic cells and initiate TH2 responses. While specific T-cell clones targeting these antigens have been identified in lesions, their overall presence is low. T-cell receptor sequencing reveals a highly diverse T-cell population in both lesional and non-lesional skin.^[10]

Neuroimmune interactions in itch

Itch is triggered by pruritogens like histamine and transmitted by cutaneous sensory nerves (C fibers and Aq fibers) to the spinal cord. In AD, skin shows increased nerve density and branching, likely due to an imbalance between nerve growth factors (NGF) (e.g., IL-31 and NGF) and repulsion factors (e.g., semaphorin 3A).^[11] Artemin, produced by keratinocytes and fibroblasts (and induced by pollutants through the aryl hydrocarbon receptor), contributes to abnormal nerve growth and sensitivity. While histamine, acting through H1R, H4R, and transient receptor potential vanilloid 1, is a well-known pruritogen, other factors are more relevant in AD. These include ET-1, TSLP, and type 2 cytokines (IL-4, IL-13, and IL-31), which signal through TRPA1, IL-4Ra/Janus kinase 1, and IL-31Ra. TSLP and cytokines directly activate sensory neurons. This explains why treatments like dupilumab (anti-IL-4Ra) relieve both inflammation and itch, and why IL-31 blockade (e.g., with nemolizumab) reduces itch but has limited impact on other AD symptoms.^[12]

The role of the microbiota

AD is characterized by marked dysbiosis of the skin microbiota, although it remains unclear whether these changes cause AD or result from epidermal barrier defects and TH2-skewed immunity. Staphylococcus aureus colonization is substantially increased in AD patients: Reported prevalence ranges from ~30% to 100% (depending on patient age, disease severity, and sampling methods) versus ~20% in healthy controls. A meta-analysis of 95 culture-based studies found S. aureus on 70% of lesional and 39% of non-lesional skin sites in AD patients, and polymerase chain reaction-based studies confirm that S. aureus abundance correlates with disease severity.^[13] Commensal skin microbes normally suppress S. aureus, and epidemiological studies indicate that early colonization by other Staphylococcus species (detected at ~2 days of age) may protect against later development of AD.^[14] S. aureus produces numerous virulence factors implicated in both superficial and invasive infection; many of these factors exacerbate AD by acting on keratinocytes and immune cells in vitro and in vivo (for example, in human skin biopsies and murine models). In addition to S. aureus, other microbes such as Malassezia yeasts (formerly Pityrosporum spp.) likely contribute significantly to AD pathogenesis, for example, by directly inducing skin inflammation.^[15]

Now, we will discuss the various types of moisturizers and cleansers in detail, along with their evidence and recommendations in pediatric eczema.

Humectants

Humectants are hygroscopic compounds that draw moisture from both the dermis and, in humid conditions, the environment. Many also act as emollients. The skin’s natural moisturizing factor – composed of lactic acid, pyrrolidone carboxylic acid, and amino acids – plays a key role in stratum corneum (SC) hydration.^[19] Urea reduces transepidermal water loss (TEWL) and irritation; at low concentrations (~10%), it hydrates, while at higher levels (20–30%), it becomes keratolytic. Alpha hydroxy acids like lactic acid boost ceramide synthesis, strengthening the skin barrier. However, humectants can also increase TEWL by pulling water to the surface, so they are often combined with occlusives to prevent moisture loss.^[20]

Examples include glycerin, alpha hydroxyl acids (glycolic acid and lactic acid), sodium pyrrolidine, carboxylic acid, propylene and butylene glycol, hyaluronic acid, urea, panthenol, aluminum and sodium lactate, gelatin, sorbitol, and honey.

Emollients

Emollients, primarily composed of lipids and oils, help hydrate the skin and improve its softness, flexibility, and smoothness. They enhance the skin’s lubricity, boosting user satisfaction. The SC contains multilamellar intracellular lipids – mainly ceramides and neutral lipids – which form protective barrier layers.^[21] Due to the high cost of natural and synthetic ceramides, pseudo-ceramides are often used as alternatives.^[22] Lipophilic compounds such as cholesterol and ceramides are commonly included in topical creams, often within liposomes, to improve skin texture. Nano-encapsulated tri-ceramides further enhance skin hydration.^[23] Essential fatty acids – such as stearic, linoleic, oleic, and lauric acids – naturally found in oils such as palm, coconut, and wool fat, support skin barrier function and influence cellular processes. Emollients can be further classified into dry, fatty, astringent, and protective emollients. Examples include cholesterol, squalene, fatty acids, fatty alcohols, and pseudoceramides.

Occlusives

Occlusives are substances that form a hydrophobic barrier on the skin to prevent TEWL, especially effective on slightly damp skin. These mainly include oils that integrate into the skin’s lipid matrix.^[20] Key occlusives include mineral oil (liquid paraffin) and petrolatum, both petroleum-derived hydrocarbons refined for stability and long shelf life. Petrolatum, though greasy, is highly effective – resisting water loss 170 times better than olive oil and reducing TEWL by over 98% at just 5% concentration. Other occlusives such as lanolin, mineral oil, and silicones offer moderate protection (20–30%). Downsides include greasiness, odor, and potential for allergic reactions.^[24]

Examples include petrolatum, paraffin, mineral oil, caprylic triglyceride, squalene, lanolin acid, stearic acid, cetyl alcohol, stearyl alcohol, lanolin lecithin, propylene glycol, cholesterol, beeswax, lanolin, and stearyl stearate.

Different formulations are available depending on skin type and extent of xerosis including creams which are thick and rich (oil-in-water or water-in-oil) and suited for dry to very dry skin, lotions which are lighter in texture than creams (higher water content) and can be used for normal to slightly dry or oily skin, and gels which are lightweight, water-based and are often oil-free, these are suited for oily and acne-prone skin, which are very thick and greasy (high occlusive content) so suited for severely dry, cracked, or damaged skin.

Barrier function improvement

A study by Simpson et al. found that twice-daily application of emollients in high-risk neonates significantly delayed or prevented the onset of AD.^[17]

National institute for health and care excellence (NICE) guidelines (UK)

• Recommends liberal and frequent use of emollients for all children with atopic eczema

• Emphasizes the importance of regular moisturization even when the skin appears normal.

European Task Force on AD

• Recognizes emollients as cornerstone maintenance therapy in pediatric AD.

World allergy organization

• Supports early use of emollients to prevent eczema and possibly atopic march progression.

Application guidelines

• Apply moisturizers immediately after bathing to lock in moisture (“soak and seal” method).

• Use liberally and frequently, ideally 2–3 times daily.

• Choose fragrance-free, dye-free, and hypoallergenic products.

Guideline recommendations for use of cleansers in AD

American Academy of Dermatology guidelines (2014)^[25] recommend non-soap cleansers with neutral to low pH. Furthermore, it advises against harsh soaps, which can disrupt the skin barrier and worsen eczema. Short, lukewarm baths or showers using gentle cleansers followed by moisturizers are preferred.

NICE guidelines (UK)

Recommends using emollient wash products instead of soap for washing. Emollients should be continued during flare and remission periods.^[41]

European dermatology forum guidelines (2018)

Suggests the use of syndets (synthetic detergents), which are less irritating than soaps.

Supports the inclusion of mild cleansers in daily care to reduce microbial colonization and irritation.^[42]