Creative Touch Permanent Makeup and Aesthetics

Lips occupy a structural position between skin and mucosa that leaves them uniquely exposed. The vermilion – the visible red zone – is covered by a keratinised epithelium, but the corneocytes it produces are parakeratotic: they retain their nuclei rather than completing full terminal differentiation, producing a stratum corneum that is thinner, less structured, and measurably weaker as a barrier than the epidermis elsewhere. TEWL through the vermilion is almost three times higher than through the cheek – itself already a relatively high- TEWL site – with a surface hydration state approximately one-third of the cheek by high-frequency conductance measurement. ^[3] The lip stratum corneum contains ceramides, cholesterol, and fatty acids in the same classes as facial skin, but in lower absolute quantities – a thinner lipid matrix that is more permeable and less resistant to moisture loss under environmental stress. ^[5]

The sebaceous gland issue is widely cited but warrants precision: the vermilion is essentially devoid of sebaceous glands in the majority of people, with Fordyce spots – ectopic sebaceous glands – present in some individuals but not contributing to meaningful surface lipid production in the way that facial sebaceous glands do. The practical consequence is that lips have no endogenous lipid replenishment mechanism for the barrier layer – they are dependent on external lipid supply or on migration of moisture from the inner labial mucosa and the rich submucosal capillary network, which provides some baseline hydration but cannot compensate for the barrier deficit under sustained dryness conditions.

Barrier Failure Mechanisms

Lip barrier failure follows the same three-pathway model as facial barrier disruption: ceramide depletion, disruption of the lipid lamellar architecture, and failure of corneocyte scaffold integrity. In lips, however, the threshold for each is lower because the baseline barrier is weaker. Environmental triggers – cold air (which reduces ambient humidity and increases evaporative loss), forced-air heating (which compounds indoor dryness), UV radiation (which the vermilion lacks melanin to resist), and wind – each independently accelerate TEWL at a tissue whose reserve capacity is limited. Habitual lip-licking compounds the effect: salivary enzymes, particularly amylase and lipase, degrade the residual surface lipids of the vermilion, and the evaporation of the salivary water film leaves the surface drier than before contact – a net negative exchange that many patients engage in reflexively in response to the dryness it creates.

Contact irritant exposure is disproportionately impactful at the vermilion because of the thinner barrier: ingredients that are tolerated at normal facial skin concentrations – fragrance compounds, preservatives, sodium lauryl sulphate, menthol, cinnamon oil – may produce irritant or sensitisation reactions at the lip that present as persistent dryness, erythema, or fissuring without the patient identifying the causative product. The differential between simple environmental chapping and contact irritant cheilitis is clinically important and is covered in the Cheilitis section below.

Systemic and Nutritional Causes

Persistent lip dryness or recurrent chapping that does not respond adequately to topical care often has a systemic upstream cause. The nutritional deficiencies most directly associated with lip barrier compromise are:

• Riboflavin (B2) and pyridoxine (B6): Both are involved in epithelial cell turnover and energy metabolism; deficiency produces characteristic lip dryness, angular fissuring, and the magenta discolouration of the tongue – a clinical triad that may appear in restrictive dieters, vegans with inadequate fortification, and clients on GLP-1 medications with reduced dietary variety
• Iron: Iron-deficiency anaemia is a well-documented cause of angular cheilitis; iron is required for epithelial proliferation and wound healing, and deficiency impairs both the repair of existing fissures and the maintenance of the commissural mucosa
• Zinc: Zinc deficiency compromises barrier lipid synthesis and immune regulation in skin, producing lip dryness alongside broader cutaneous and immunological signs
• Vitamin C: Required for hydroxylation of proline and lysine in collagen synthesis; deficiency impairs the structural integrity of the submucosal connective tissue that underlies the vermilion and supports its vascular supply

Systemic diseases with lip manifestations include iron-deficiency anaemia, coeliac disease (which produces multiple B-vitamin and mineral deficiencies through malabsorption), Crohn’s disease (which may present with granulomatous lip swelling – Miescher-Melkersson-Rosenthal syndrome), hypothyroidism, and Sjögren’s syndrome (through secondary xerostomia). Retinoids – both topical tretinoin at perioral application and systemic isotretinoin – produce cheilitis as a consistent, dose-dependent side effect through their effects on sebaceous gland function and barrier lipid synthesis. ^[1]

Cheilitis: Classification and Clinical Distinction

Cheilitis is the clinical term for lip inflammation, encompassing a range of presentations that share the surface appearance of dryness, erythema, and fissuring but have distinct aetiologies requiring different management approaches. The key classification framework distinguishes mainly reversible from mainly irreversible forms: ^[4]

Reversible cheilitis

• Cheilitis simplex – common environmental chapping from dryness, cold, UV, and barrier depletion; responds to topical barrier restoration
• Angular cheilitis – inflammatory fissuring at the labial commissures, most commonly due to Candida albicans and/or Staphylococcus aureus polymicrobial infection, often precipitated by saliva pooling, iron or B-vitamin deficiency, denture wearing, or immunosuppression; requires antifungal/antibacterial treatment, not just moisturiser ^[2]
• Contact cheilitis – allergic (type IV delayed hypersensitivity, requires patch testing to identify allergen) or irritant (direct epithelial damage from identified exposure); common allergens include fragrance components, colophony, preservatives, and nickel; most implicated products are lip cosmetics, toothpaste, and mouthwash ^[2]
• Drug-induced cheilitis – isotretinoin, lithium, and topical retinoids; resolves on dose reduction or cessation
• Exfoliative cheilitis – chronic superficial peeling of the lip, often associated with habitual lip picking, factitial behaviour, or contact irritant exposure; may be treatment-resistant due to behavioural perpetuation

Mainly irreversible / requiring specialist assessment:

• Actinic cheilitis – sun-induced dysplasia of the lower lip vermilion, presenting as persistent whitish plaque, blurring of the vermilion border, or persistent ulceration; requires biopsy to exclude squamous cell carcinoma in situ and is a premalignant condition in fair-skinned individuals with chronic UV exposure
• Granulomatous cheilitis – persistent non-tender lip swelling with granulomatous inflammation on biopsy; may be a manifestation of Crohn’s disease or Melkersson-Rosenthal syndrome
• Glandular cheilitis – inflammatory hypertrophy of minor salivary glands, predominantly lower lip; may require surgical treatment

The clinical rule of thumb is that any lip lesion persisting beyond two weeks of adequate topical care, any lesion with induration, persistent ulceration, or rapid change, and any case of unilateral angular fissuring in a patient with no obvious predisposing factors warrants medical evaluation before aesthetic treatment. Angular cheilitis in particular is frequently misidentified as simple dryness in aesthetics consultations and managed topically when the underlying polymicrobial infection requires targeted treatment.