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Impaired skin barrier and acid mantle function leading to sensitive skin issues

Human skin serves as an essential barrier against ultraviolet radiation, penetration of toxic compounds, surveillance of immune system and hydration of the body. The skin comprises of primary two layers - the epidermis and the

Impaired Skin Barrier and Sensitive Skin

Human skin serves as an essential barrier against ultraviolet radiation, penetration of toxic compounds, surveillance of immune system and hydration of the body. The skin comprises of primary two layers – the epidermis and the dermis.The epidermis is where keratin, melanin and filaggrin are present. Langerhans cells are also present which regulate immune surveillance. Stratum corneum ( SC) is the outermost layer of the epidermis providing the barrier function of the skin. The SC is analogous to a ‘bricks and mortar’ structure in which keratin filled corneocytes act as ‘bricks’.  Surrounding the bricks are lipid rich phase consisting of ceramide, fatty acid and cholesterol which makes up the ‘mortar’. Ceramide is a crucial component of the lipid bilayer in SC, and this helps to reduce transepidermal water loss. Proper hydration of SC is essential for optimum skin function. Natural moisturising factor ( NMF) production in SC is important in maintaining SC’s water binding capacity. Its main components are free amino acids, pyrrolidone carboxylic acid, lactate and filaggrin degradation products.  Production of NMF is a multistep process within SC. NMF absorbs water from surroundings and retains it, increasing SC hydration. In situations of low humidity, production of NMF is increased to maintain hydration of SC. NMF causes pH of SC to be slightly acidic and protects it from over-degradation.

The dermis consists of collagen, elastin, glycosaminoglycans (GAG’s) which form the extracellular matrix. Dermis also contains blood vessels, nerves, lymphatics and sebaceous glands. Collagen is responsible for skin’s strength/structure and elastin provides elasticity of the skin. GAGs. GAGs consist of 4 groups: HSGAG and CSGAG, keratan sulphate types, hyaluronic acid. Hyaluronic acid is the most important component which helps to maintain dermis volume and skin turgor.  GAGs also contribute to retain moisture and allows collagen to retain water. They also enable epidermis to be hydrated. Sebaceous gland produces acid mantle film which covers the skin. This slightly acidic layer acts a barrier to bacteria, viruses and other potential contaminants that might infiltrate the skin. Its pH ranges from 4.5-6.5.

Extrinsic and intrinsic factors can impair skin barrier. Examples of intrinsic factors are intrinsic ageing and many skin conditions (e.g. atopic dermatitis). We will go through how aging and atopic dermatitis cause changes in skin barrier in more depth. With age, multiple changes occur in the skin, both at the level of the epidermis and at dermis:

  • Hyperkeratosis of SC
  • Thinning of epidermis and dermis
  • Reduced number of melanocytes and Langerhans cells.
  • Collagen becomes less abundant, less soluble and thinner in the intrinsically aged skin. In photoaging, it is more soluble but thickened and fragmented.
  • There is the greater production of defective elastin in the aged skin, and elastin degradation is slower with the accumulation of elastoic material.
  • There is a more significant number of GAGs in the aged skin, but they are present on the elastoic material on the superficial dermis, hence are not able to bind to water well when distributed throughout the dermis.
  • Ageing skin is less acidic than older skin due to the reduction in metabolic and enzymatic reactions.

Skin barrier impairment is thought to be the primary factor in the pathogenesis of atopic dermatitis leading to increased transepidermal water loss. Filaggrin mutations strongly predispose to development of atopic eczema. Filaggrin is primary source of several components of NMF. There is also change in intercellular lipid composition and arrangement in SC which reduce skin barrier in atopic eczema. There is less ceramide in atopic eczema leading to greater transepidermal water loss.  Furthermore, in atopic dermatitis, there is an alteration in the immune system. It is a powerful, superantigen-driven vicious cycle involving T- helper type 2 dominated immune response, downregulation of antimicrobial peptides, S. aureus overgrowth and production of immunoactivation toxins with superantigenic properties. This interacts with an antigen –specific vicious circle involving IgE production and binding to high – affinity IgE receptors expressed on skin dendritic cells, followed by IgE- mediated, facilitated antigen presentation. An interaction of dysfunctional innate and adaptive immune responses in atopic dermatitis lesions may cause severe disease flares.

Common extrinsic factors that can affect skin barriers are UV rays, irritants, allergens, harsh cleansers, soaps and high heat/steam. Even water can affect skin barrier after a single wash. We will go through how cleansing can affect skin barrier in more detail.

Surfactants are active ingredients in cleaning products. Anionic surfactants are present in cleansers due to their high –foaming properties.  However, they are alkaline and irritating to the skin.

Carboxylate –based soaps ( pH – 10) and their use transiently increases the alkalinity of skin post wash. PH of topically used products, even independent of surfactant has been shown to affect SC. Swelling of SC and increased rigidity of SC lipids is noted with topical products at pH 10.  Note that most enzymatic process in skin function within relatively narrow pH window- hence, even brief increase in skin pH may disrupt biochemical processes of desquamation, lipid synthesis and NMF production. Also,  surfactants in cleansers can directly bind and damage SC proteins as well as disrupt SC lipids. Furthermore, cleansing can result in leaching of NMF components from the skin, decreasing skin’s ability to hold moisture and contributing to post-wash dryness.

To maintain good skin barrier, we need to minimise exposure to extrinsic damage and have good effective skin care. Use of ultra – mild cleansers can help to reduce damage to both proteins and lipids in the skin during washing. For instance, directly esterified fatty isethionate ( DEFI ) cleaners protect SC lipids from extraction during cleansing due to the presence of skin identical fatty acids within surfactant system. Also, DEFI based cleansers can penetrate SC and replace lipid layer within SC as soon as they are lost.

Emollients are used to prevent trans-epidermal water loss. They do not provide moisture, but emollients can be used to deliver humectants ( e.g. glycerol) to hydrate SC. Formulations for emollients vary:

Ointments – oil based – more occlusive and more effective at reducing trans-epidermal water loss

Gels – provide water based delivery system whereby insoluble drug is mixed with gelling agents to aid absorption Creams and lotions are water based. Note water based products need preservatives to prevent bacterial contamination and growth. Hence, water based products may cause allergic contact dermatitis.

While emollients are useful to some degree, they only transiently ameliorate damage already done to the skin. However, some special topical agents can help to enhance skin barrier in targeted ways. Use of topical retinoic acid leads to compaction of stratum corneum, epidermal hyperplasia, correction of atypia, dispersion of melanin granules and increase in dermal collagen synthesis and angiogenesis. Peptides and proteins also have the ability to enhance collagen production. Niacinamide boots barrier function by increasing production of ceramide in SC.


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  2. Janssens. M et Al. Lipid to protein ratio plays an important role in the skin barrier function in patients with atopic eczema. British Journal of dermatology ( 2014) 170, pp1248-1255
  3. Ananthapadamnabhan K.P et al. A global perspective on caring for healthy stratum corneum by mitigating the effects of daily cleansing: report from an expert dermatology symposium. British journal of dermatology ( 2013) 168, pp1-9
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I am graduated from the University of Bristol in 2010 with Bachelor of Medicine and Surgery and Bachelor of Science in Biochemistry. I am a member of Royal College of Physicians as well as being the member of Royal College of General Practitioners. I am also registered with the General Medical Council. I work as a General Practitioner and has keen interest in teaching. I have obtained Royal College of Physicians education accreditation and has been examiner and clinical tutor for St George's Medical University, London I have ardent interest in aesthetics – in particular skin rejuvenation and non-surgical aesthetic procedures. I have spent 1 year in prestigious Yonsei University Hospital in South Korea learning about dermatology and aesthetics. I have obtained Post Graduate Diploma with merit in clinical dermatology at Queen Mary University of London. I am passionate about helping people achieve youthful and naturally enhanced appearance.