Creative Touch Permanent Makeup and Aesthetics

All three dermatitis subtypes share a common mechanistic foundation – barrier disruption, elevated TEWL, and a self-reinforcing cycle of permeability and immune activation – but differ in aetiology and immune pathway. Atopic dermatitis is driven by filaggrin deficiency and Th2/ IL-4/ IL-13 immune polarisation that further suppresses filaggrin in a self-perpetuating cycle; dupilumab (IL-4Rα antagonist) restores filaggrin expression by neutralising this signal. Contact dermatitis divides into irritant (non-immunological, cytotoxic barrier disruption) and allergic (type IV delayed hypersensitivity, allergen-specific CD4+ T-cell response, diagnosed by patch testing). Seborrhoeic dermatitis involves Malassezia-driven immunometabolic disruption with Th17/Th22 polarisation at sebaceous-rich sites. All three represent treatment contraindications or modifiers at active sites; barrier restoration is a management component in each.

The mechanistic thread connecting all three dermatitis types is barrier disruption preceding or perpetuating inflammation. When the stratum corneum is compromised – whether by genetic protein deficiency, allergen exposure, microbial dysbiosis, or sustained irritant contact – TEWL rises, permeability to immune-activating stimuli increases, and the cutaneous innate immune system responds with cytokine production that further degrades barrier proteins. This creates the bidirectional cycle described in the TEWL entity: barrier failure drives immune activation, and immune activation drives further barrier failure. The clinical expression of this cycle differs across the three conditions – the immune pathways engaged, the triggers involved, and the tissue distribution of lesions vary considerably – but the underlying logic is shared, and barrier restoration is a component of management in all three.

Atopic Dermatitis

Atopic dermatitis (AD) is a chronic relapsing inflammatory skin condition affecting approximately 15–20% of children and 2–10% of adults in high-income countries, characterised by intense pruritus, eczematous lesions, and a profoundly compromised skin barrier. It is the most common inflammatory skin disease and the most extensively researched in terms of barrier biology – the condition through which much of the mechanistic understanding of filaggrin, TEWL, and the barrier-immune bidirectional cycle was established.

Pathogenesis: the inside-out and outside-in debate

AD has two initiating pathways that interact rather than compete. The inside-out pathway begins with genetic loss-of-function mutations in the filaggrin gene (FLG) – present in approximately 30% of European AD patients – which produce absent or reduced filaggrin protein, thinning the natural moisturising factor (NMF) pool, disrupting corneocyte scaffold integrity, and elevating TEWL. The permeable barrier allows environmental allergens, irritants, and microbial products to penetrate the epidermis, where they encounter dendritic cells that drive CD4+ T-cell differentiation toward the Th2 phenotype. ^[8]

The outside-in pathway begins with Th2 immune activation – driven by epidermal alarmins TSLP, IL-25, and IL-33 released by keratinocytes in response to physical or chemical disruption – which activates innate lymphoid cells type 2 (ILC2s) and Th2 cells to produce IL-4 and IL-13. These cytokines then directly suppress filaggrin expression in keratinocytes: IL-4 and IL-13 reduce filaggrin gene expression to 25% of baseline levels in keratinocytes, establishing the immune response as itself a driver of the barrier defect rather than simply its consequence. ^[3] IL-22, produced by Th22 and Th17 cells in the chronic phase, additionally suppresses filaggrin and drives epidermal thickening. ^[7]

The result is a cycle that sustains itself without continuous external trigger: barrier failure → allergen penetration → Th2 activation → IL-4/IL-13 production → filaggrin suppression → further barrier failure. This explains both the chronicity of AD and why barrier restoration – not inflammation suppression alone – is essential to sustained disease control. Dupilumab, which antagonises the shared IL-4/IL-13 receptor (IL-4Rα), has been shown to increase filaggrin expression in lesional AD skin, demonstrating that neutralising the Th2 cytokine signal is sufficient to partially restore barrier protein synthesis. ^[2]

AD in aesthetics practice

Active AD is a contraindication for procedures involving epidermal disruption at or adjacent to lesional skin – including microneedling, chemical peels, laser resurfacing, and energy-based treatments. The elevated TEWL and compromised tight junction integrity of AD skin increases infection risk post-procedure, reduces predictability of healing, and heightens sensitisation risk to topically applied post-treatment products. Notably, uninvolved AD skin – clinically clear skin in an AD patient – also shows measurably elevated TEWL relative to healthy controls, meaning the contraindication extends beyond visible lesions to the broader cutaneous context. ^[5] Clients with well-controlled AD in remission with a sustained stable barrier are better candidates than those with active or recently active disease.

Contact Dermatitis

Contact dermatitis is an inflammatory skin response to direct skin contact with an exogenous substance, presenting as localised erythema, oedema, vesiculation, and pruritus at the site of exposure. It accounts for approximately 80% of occupational skin disease and is the most common cause of a client presenting with a reaction to a cosmetic or skincare product. The fundamental clinical distinction is between its two mechanistic subtypes, which share the same surface appearance but require entirely different management approaches.

Irritant contact dermatitis

Irritant contact dermatitis (ICD) is a non-immunological response – it requires no prior sensitisation and can occur on first exposure in any individual given sufficient concentration and duration of contact. The mechanism is direct cytotoxic disruption of the stratum corneum lipid matrix and corneocyte integrity, followed by release of pro-inflammatory cytokines (IL-1α, TNF-α, IL-8) from damaged keratinocytes that recruit neutrophils and macrophages to the exposure site. ^[4] Strong irritants – sodium lauryl sulphate, acids, alkalis, solvents – produce acute ICD; weak irritants – fragrance, preservatives, surfactants at low concentration – produce cumulative ICD through repeated subthreshold exposures that collectively deplete the barrier faster than it regenerates. Cumulative ICD is the most common pattern in aesthetics product reactions and may be misattributed to allergy.

Allergic contact dermatitis

Allergic contact dermatitis (ACD) is a type IV (delayed-type) hypersensitivity reaction requiring prior sensitisation. On first exposure, an allergen penetrates the epidermis and is processed by Langerhans cells, which migrate to regional lymph nodes and prime allergen-specific CD4+ T-cells. This sensitisation phase produces no visible reaction. On re-exposure, primed T-cells recognise the allergen-Langerhans cell complex in the skin and mount an immune response – cytokine release, keratinocyte activation, inflammatory cell recruitment – that typically peaks 48–96 hours after contact, the characteristic delayed timeline that distinguishes ACD from ICD. ^[4]

The most common allergens in aesthetics-relevant products are fragrance mix I and II, methylisothiazolinone (MI) and methylchloroisothiazolinone (MCI) preservatives, colophony, nickel (from instrument contact), and certain acrylates in nail and adhesive products. Patch testing – applying diluted allergens to the skin under occlusion for 48 hours and reading at 96 hours – is the gold-standard method for identifying the specific allergen; it detects type IV allergy only and does not diagnose ICD.

Contact dermatitis in aesthetics practice

Contact reactions to post-treatment products – particularly fragrance components, preservatives, and occlusive agents applied to a freshly disrupted barrier – are more likely and more severe than the same products applied to intact skin, because the compromised post-procedure barrier provides lower resistance to allergen and irritant penetration and a more reactive immune environment. Product selection in the post-procedure period should prioritise minimal ingredient lists, absence of fragrance and known sensitisers, and formulations that have been tested for skin compatibility. A client presenting with a reaction that recurs with a specific product should be referred for patch testing before the reaction is managed empirically.

Seborrhoeic Dermatitis

Seborrhoeic dermatitis (SD) is a chronic inflammatory condition producing erythema, greasy yellowish scaling, and variable pruritus at sebaceous gland-rich sites: the scalp, central face (nasolabial folds, glabella, eyebrows), external ear canal, and less commonly the central chest and flexural areas. It affects 3–5% of the general adult population and up to 83% of individuals with HIV – the latter frequency implicating immune competence as a significant modifier of disease expression. The spectrum of SD encompasses dandruff (pityriasis capitis) at the milder end through to confluent facial erythema and scaling at the more severe.

Pathogenesis: Malassezia, barrier disruption, and immune dysregulation

SD pathogenesis has historically been framed around Malassezia spp. – lipophilic yeasts that colonise sebaceous sites and metabolise sebum triglycerides into free fatty acids, some of which (particularly oleic acid) are pro-inflammatory and barrier-disrupting when present in excess. The partial clinical response to antifungal treatments supports a Malassezia contribution. However, emerging evidence from genome-wide association studies and novel anti-inflammatory therapeutics has prompted a reframing of SD as primarily an immune dysregulation and barrier dysfunction condition in which Malassezia acts as a metabolic and immunologic catalyst rather than a straightforward pathogenic cause – consistent with the observation that Malassezia colonisation density does not consistently correlate with disease severity across patients. ^[1]

The current model involves Malassezia lipid hydrolysis products altering the sebaceous microenvironment and activating Th17/Th22 immune polarisation, which drives IL-17 and IL-22 production, keratinocyte activation, and the characteristic epidermal dysregulation – with barrier disruption both predisposing to Malassezia proliferation and being perpetuated by the resulting inflammation. ^[6] The Th17 immune pathway distinguishes SD from AD (predominantly Th2) and from psoriasis (Th17-dominant but with distinct genetic and histological features) – a pathway distinction that is clinically relevant when the three conditions present with overlapping facial erythema and scaling in the differential diagnosis.

Differential diagnosis relevance

SD overlaps clinically with rosacea (facial erythema and sebaceous distribution), psoriasis (scalp scaling, facial plaques), and perioral dermatitis (perioral and perinasal erythematous papules). The distinction matters in aesthetics practice because rosacea and SD may both present as facial redness and flaking in a treatment consultation, and the management – including what topical products, procedures, and referral pathways are appropriate – differs. SD on the face responds to antifungal agents; rosacea does not. Procedures that increase sebaceous activity or alter the facial microbiome may exacerbate SD; the same procedures may be indicated or contraindicated in rosacea depending on subtype.

SD in aesthetics practice

Active facial SD is a relative contraindication for ablative or disruptive procedures at affected sites – the combination of Malassezia colonisation, compromised barrier, and active inflammation creates elevated post-procedure infection risk and unpredictable healing. Mild, well-controlled SD in remission is a less significant modifier. Clients with chronic scalp SD presenting for PRP hair treatment require clinical assessment to distinguish SD-related shedding (which may contribute to or mimic diffuse hair loss) from primary androgenetic alopecia or telogen effluvium, as the treatment approach and expected outcome differ.