Creative Touch Permanent Makeup and Aesthetics

Psoriasis is a chronic immune-mediated inflammatory skin condition driven by a T-cell/cytokine cascade centred on the IL-23/Th17 axis, producing hyperproliferation of keratinocytes, epidermal thickening, and the characteristic scaly plaque morphology. It affects approximately 2–3% of the UK population and carries a systemic inflammatory burden that extends beyond the skin – increasing the risk of psoriatic arthritis, cardiovascular disease, and metabolic syndrome through shared inflammatory pathway spillover. Its barrier dysfunction – including filaggrin and loricrin suppression – is acquired through TNF-α and IL-17 signalling rather than constitutive genetic defect in most patients, distinguishing it mechanistically from atopic dermatitis. The Koebner phenomenon, by which skin trauma initiates new lesions, is explained by type 1 interferon signalling from injured keratinocytes that activates the adaptive immune cascade. Aesthetics intervention has a limited but defined role in psoriasis management, and understanding where that boundary lies is clinically important.

Psoriasis is a chronic, immune-mediated inflammatory skin condition affecting approximately 2–3% of the UK population, characterised by well-demarcated, erythematous, scaly plaques most commonly found on the extensor surfaces (elbows, knees, scalp, and lower back), though any skin area may be affected. It is a systemic disease whose most visible manifestations are cutaneous – the same inflammatory pathways driving plaque formation in the skin operate in joints (psoriatic arthritis, affecting approximately 30% of psoriasis patients), blood vessels, and metabolic tissue. Understanding psoriasis as a systemic inflammatory condition with prominent skin expression – rather than a skin condition that sometimes involves joints – is the framing most consistent with its immunology and most useful for clinical management decisions. ^[6]

What Psoriasis Is (and Isn’t)

Psoriasis is not a barrier condition that becomes inflamed, and it is not an allergic or hypersensitivity condition. It is a T-cell-mediated autoimmune inflammatory disease in which the skin is the primary target tissue of a dysregulated immune response. The hyperproliferation of keratinocytes – which reduces the normal 28-day epidermal turnover to as little as 3–4 days in active plaques – is not the disease itself but the visible consequence of cytokine signalling that is driving abnormal keratinocyte behaviour. This distinction matters: treatments that address only the keratinocyte proliferation without modulating the immune driver (moisturisers, keratolytics) manage symptoms but do not alter the underlying process.

Two comparisons are routinely confusing for clients and worth stating explicitly. First, psoriasis is not eczema, despite both presenting with inflamed, scaling skin. Eczema (atopic dermatitis) is dominated by Th2 cytokine activity ( IL-4, IL-13) that suppresses barrier proteins and drives itch; psoriasis is dominated by Th17 cytokine activity (IL-17, IL-22, TNF-α) that drives keratinocyte hyperproliferation and neutrophil infiltration with comparatively little itch. The two conditions are not merely different presentations of the same inflammatory type – they are immunologically opposing, and treatments effective for one can trigger the other: dupilumab (anti-IL-4/IL-13, used for atopic dermatitis) has been documented to trigger psoriasiform reactions in some patients by suppressing Th2 responses and allowing Th17 rebound. ^[7] Second, psoriasis is not primarily a stress-sensitive or allergically triggered condition – triggers (infections, medications, physical trauma, stress) work through specific immune mechanisms rather than through general sensitisation.

How Psoriasis Starts: The Innate Immune Trigger

The initiation of psoriasis – how the first lesion forms in a genetically susceptible individual – involves an innate immune event that precedes the T-cell cascade. Plasmacytoid dendritic cells (pDCs), a rare innate immune cell subset, accumulate in the skin of psoriasis-susceptible individuals and become activated – possibly by self-DNA/RNA complexes released from stressed or damaged keratinocytes – to produce large quantities of IFN-α (type 1 interferon). This IFN-α production by pDCs has been shown in xenograft models to be essential for initiating the downstream T-cell activation cascade; blocking IFN-α signalling prevented the development of psoriatic lesions. ^[5]

The Koebner phenomenon – the well-known clinical observation that psoriatic lesions develop at sites of physical skin trauma (scratching, injury, tattoos, surgical wounds) – is explained by this same type 1 interferon mechanism. Physical injury to keratinocytes releases self-double-stranded RNA (dsRNA), which activates MAVS and TLR3 pattern recognition receptors on keratinocytes, triggering IFN-β production. Keratinocyte-derived IFN-β promotes maturation of classical dendritic cells, which then activate T-cells – completing the bridge from physical trauma to autoimmune cascade. ^[9] This mechanism has a direct clinical implication: procedures that cause cutaneous trauma – microneedling, laser, dermabrasion – can induce Koebner responses in psoriasis patients, and aesthetics treatment planning must account for this risk before any skin-disrupting intervention.

The IL-23/Th17 Axis: The Core Inflammatory Driver

Once the innate immune trigger is established, psoriasis pathogenesis is driven by the IL-23/Th17 cytokine axis – the central mechanism on which essentially all modern biological treatments for psoriasis act. ^[3]

IL-23 is produced primarily by activated myeloid dendritic cells and macrophages in the dermis. It drives the differentiation and survival of Th17 cells – a CD4+ T-cell subset – and promotes their production of IL-17A, IL-17F, and IL-22. These cytokines act on keratinocytes to produce the defining features of psoriatic plaques:

• IL-17A and IL-17F stimulate keratinocyte proliferation, reduce keratinocyte differentiation (producing the hyperproliferative, parakeratotic epidermis of psoriatic plaques), and induce production of antimicrobial peptides (including LL-37, also involved in rosacea pathogenesis) and further pro-inflammatory cytokines that sustain and amplify the cascade ^[1]
• IL-22 drives epidermal thickening (acanthosis) by promoting keratinocyte proliferation and inhibiting terminal differentiation; its selective action on keratinocytes makes it a major driver of the hyperplastic epidermis characteristic of plaque psoriasis
• TNF-α, produced by multiple cell types in psoriatic lesions, amplifies the inflammatory signal and – critically for barrier function – directly suppresses filaggrin and loricrin expression through a c-Jun N-terminal kinase (JNK) pathway ^[4]

The self-amplifying character of this axis is as important as its individual components. IL-17 from Th17 cells stimulates keratinocytes to produce IL-36 and TNF-α, which promote further IL-23 production from dendritic cells, sustaining Th17 activation – a positive feedback loop structurally similar to the KLK5/LL-37 loop in rosacea, operating through entirely different molecular actors.

Barrier Dysfunction: Acquired, Not Constitutional

Psoriatic skin demonstrates reduced filaggrin and loricrin expression, elevated TEWL, and structurally abnormal corneocytes – a barrier defect phenotypically similar to that seen in atopic dermatitis but with a critically different aetiology. In atopic dermatitis, barrier compromise is frequently constitutive – driven by FLG gene mutations present from birth – and the barrier defect precedes and facilitates immune activation. In psoriasis, FLG gene mutations are found in fewer than 5% of patients; the remaining 80%+ who show filaggrin deficiency in lesional skin have acquired it through TNF-α-mediated c-Jun pathway suppression. ^[4] The filaggrin loss in psoriasis is a downstream consequence of the inflammatory process rather than a driver of it.

This distinction has both mechanistic and therapeutic implications. It means that restoring barrier proteins in psoriasis requires resolving the inflammatory cytokine environment that is suppressing them – topical barrier support can reduce symptom burden and improve skin comfort, but it does not address the mechanism producing the deficit. It also means that the NMF depletion and structural barrier weakness of psoriatic skin is real and clinically significant, making psoriatic skin reactive to many standard skincare ingredients – fragrance, alcohol, high-pH cleansers – even in periods of relative disease quiescence.

The relationship between psoriasis and atopic dermatitis barrier pathology is further complicated by the existence of a shared inflammatory pathway: barrier disruption (from any cause) can activate Th2 responses, and chronic Th2 activity can eventually shift toward Th17 dominance – meaning that patients with primary atopic dermatitis can develop psoriasiform features, and patients with primary psoriasis can develop atopic overlap in barrier-disrupted areas. ^[2] These are not different diseases running concurrently; they are expressions of the dynamic relationship between the Th2 and Th17 pathways across a shared immune landscape.

Psoriasis as a Systemic Disease

The systemic inflammatory burden of psoriasis is not incidental to its skin manifestation – it is produced by the same IL-17/TNF-α/IL-23 cytokine milieu that drives plaque formation, which spills over into systemic circulation and affects multiple organ systems. ^[8]

Psoriatic arthritis affects approximately 30% of people with psoriasis, involving the same Th17 axis at synovial tissue, producing erosive joint disease that can progress significantly if unrecognised. Clients presenting with joint pain, swollen digits (dactylitis), or spinal stiffness alongside psoriatic skin disease require rheumatological assessment, not only dermatological management.

Cardiovascular and metabolic comorbidity are substantially elevated in psoriasis – the risk is proportional to disease severity, with severe psoriasis conferring cardiovascular risk comparable to type 2 diabetes in some population studies. The mechanism is direct: the same Th1/Th17 inflammatory cytokines (TNF-α, IL-17, IL-1β) that drive plaque formation also promote endothelial dysfunction, promote foam cell formation in arterial walls, and sustain a pro-atherogenic inflammatory state. ^[6] Obesity, metabolic syndrome, and non-alcoholic fatty liver disease are all significantly more prevalent in psoriasis patients, partly through shared inflammatory mechanisms and partly through disease burden and lifestyle factors.

This systemic dimension is why psoriasis management is appropriately considered a medical rather than cosmetic matter in moderate-to-severe presentations – controlling skin disease through effective medical treatment reduces the systemic inflammatory burden and its downstream cardiovascular consequences, not just the plaque area.

Clinical Context: Aesthetics Role and Limits

The aesthetics role in psoriasis is clearly bounded, and being explicit about those bounds is more useful to clients – and more honest – than suggesting aesthetics treatments address the disease itself.

What falls outside aesthetics scope: Active plaque psoriasis, psoriatic arthritis, and moderate-to-severe disease require medical management – topical corticosteroids, vitamin D analogues, methotrexate, ciclosporin, or biological treatments targeting IL-23 (ustekinumab, risankizumab), IL-17 (secukinumab, ixekizumab), or TNF-α (adalimumab, etanercept). These represent the primary intervention tier; aesthetics treatments cannot substitute for disease-modifying therapy.

The Koebner risk is the most important clinical consideration for aesthetics practitioners. Any procedure causing epidermal disruption – microneedling, ablative laser, dermabrasion, chemical peels at concentrations that compromise barrier integrity – carries the risk of inducing new psoriatic lesions at the treatment site in susceptible individuals. This risk applies even in patients whose psoriasis is well-controlled; the IFN-β/dendritic cell cascade can be triggered by skin injury regardless of systemic disease activity. Clients with active or recently active psoriasis should not receive skin-disrupting aesthetic treatments without explicit medical clearance, and the Koebner risk should be disclosed in consultation.

Where aesthetics adds value is primarily in the skin health support layer: barrier-supportive skincare guidance, reduction of inflammatory triggers in the treatment environment, and – for clients with well-controlled psoriasis in remission – treatments that do not disrupt the barrier and that support skin comfort. Cold atmospheric plasma warrants specific mention: its mechanism of suppressing pro-inflammatory cytokine environments and reducing NF-κB-mediated inflammatory signalling is relevant to the psoriatic inflammatory context. Whilst the specific evidence base for CAP in psoriasis is less developed than for atopic dermatitis, the mechanistic rationale for using it as an environment-stabilising rather than tissue-disrupting intervention is sound – and it avoids the Koebner risk entirely.

Clinical Pearl Psoriasis clients often arrive having been told their skin is “just sensitive” or advised to manage it with moisturiser. A client with well-demarcated, silvery-scaled plaques on extensor surfaces who has not received a formal diagnosis should be directed to their GP before proceeding with any aesthetic treatment. The Koebner risk, the systemic comorbidity profile, and the availability of highly effective medical treatments make early diagnosis and appropriate medical management genuinely important – not a reflexive “see your doctor” deflection.