Is beauty truly skin deep? – an overview to importance of maintaining good skin barrier

The skin - for most of our young adult life we struggle against its rebellious breakouts, its stubborn oiliness, and blackheads. Why should we love our skin when it seems to hate us in return?

Impaired Skin Barrier and Sensitive Skin

The skin – for most of our young adult life we struggle against its rebellious breakouts, its stubborn oiliness, and blackheads. Why should we love our skin when it seems to hate us in return? The skin is vital for our survival, let alone for our vanity, without the skin we would be exposed to every germ and bacteria floating around and would die instantly – a good enough reason to start with as to why we should be concerned with the health of our skin. On a slightly lighter note, healthy skin usually means healthy body; the state of the skin is a great indication of the internal state of affairs of the body. The skin also plays an important role in aesthetics. You can buy the best makeup, creams or fillers, no matter what you do, if your skin doesn’t look good, you don’t feel you look good. So how can we take care of this vital asset? To start with, it would be good to know what the skin is actually comprised of and how it works.

The skin acts as an essential barrier against ultraviolet radiation, infiltration of toxic chemicals, maintains surveillance of immune system and hydration of the body. The skin consists of two main layers – the epidermis and the dermis.

The epidermis is where keratin, melanin and filaggrin reside. Langerhans cells are also present which play important role in maintaining skin immune system. Stratum corneum (SC) is the outermost layer of the epidermis providing the barrier function of the skin. The SC is comparable to a ‘bricks and mortar’ arrangement in which keratin filled corneocytes act as ‘bricks’.  Surrounding the bricks are lipid-rich phase ‘mortar’ consisting of ceramide, fatty acid and cholesterol. Ceramide is an important component of the lipid bilayer which helps to reduce transepidermal water loss of the skin. Adequate hydration of SC is vital for optimum skin function. Production of Natural moisturising factor (NMF) in SC plays an essential part in retaining SC’s water-binding capacity. Production of NMF is a multistep process within SC.  Its main components are free amino acids, pyrrolidone carboxylic acid, and lactate and filaggrin degradation products.   NMF absorbs water from its surroundings and retains it, thereby increasing SC hydration. In situations of low humidity, production of NMF is upregulated to retain hydration of SC.  NMF also causes pH of SC to be slightly acidic and guards it from over-degradation.

The dermis consists of collagen, elastin, and glycosaminoglycans (GAG’s), which form the extracellular matrix. The dermis also comprises of blood vessels, nerves, lymphatics and sebaceous glands. Collagen is responsible for skin’s strength/structure and elastin provides elasticity. GAGs are made up of 4 groups: HSGAG and CSGAG, keratin sulphate types, hyaluronic acid. Hyaluronic acid is the most important constituent which helps to keep dermis volume and turgor.  GAGs also allow collagen to retain water as well as helping epidermis to be moisturised. Sebaceous glands in the dermis produce acid mantle film which covers the skin. This slightly acidic layer acts a barrier to bacteria, viruses and other harmful contaminants that might permeate the skin. Its pH ranges from 4.5-6.5.

Skin is a large immune organ and can trigger multiple complex pathways enabling protection against hostile environmental substances. There are 2 types immune response that skin hosts – innate and adaptive. Innate immune response is rapid. Keratinocytes and Langerhans cells in the epidermis are major players in innate immune response. Pattern recognition receptors cause activation of innate cells when skin becomes exposed to hostile substance. Activated innate cells produce factors such as reactive free radicals and antimicrobial. Additionally, activated innate cells produce cytokines and other inflammatory mediators that can trigger adaptive immune pathway.

The adaptive immune response is slower than innate immune response. The adaptive immune system can activate either humoral immunity involving B cells or cell-mediated immunity involving T cells.  It is also involved in immune memory, which allows prolonged immune protection to the body.

Extrinsic and intrinsic factors can impair skin barrier. Such examples for intrinsic factors are natural ageing and multiple skin conditions (e.g. atopic dermatitis).

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 plentiful, less solvent and thinner.
  • There is the more production of faulty elastin in the aged skin with slower elastin degradation.
  • There is greater number of GAGs in the aged skin, but they are present on the on the superficial dermis rather than being well distributed throughout dermis. Hence, their water binding abilities are reduced.
  • Ageing skin is less acidic than younger skin due to the decrease in metabolic and enzymatic reactions.

Skin barrier defect is one of the main elements in the pathogenesis of atopic dermatitis. In particular, filaggrin mutations strongly predispose to its development. Note that multiple components of NMF derive from filaggrin. In atopic dermatitis, there is also alteration in intercellular lipid composition and organisation in SC which results in weakening of skin barrier. There is also a reduction in ceramide leading to more transepidermal water loss as well as modification in the immune system in the skin.

Common extrinsic factors that 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.

UV rays cause inflammation and increased production of pro-inflammatory cytokines such as IL-1, IL-6, and IL-8 in skin. These cytokines cause inflammation and activation of keratinocytes, macrophages, and other immune cells that produce reactive oxygen species. These reactive oxygen species trigger the production of activator protein-1 and the creation of destructive enzymes such as collagenases that leads to aging.

Surfactants are active ingredients commonly found 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 briefly raise the alkalinity of skin post wash. The pH of topical products, even independent of surfactant has been shown to affect SC. Topical products at pH of >10 results in engorgement of SC and increased stiffness of SC lipids.  Note that majority of enzymatic process in skin work within small pH window- hence, even transient rise in skin pH may disturb biochemical processes of desquamation, lipid synthesis and NMF production. Furthermore, surfactants in cleansers can directly bind and damage SC proteins and lipids. Also, cleansing can result in leaching of NMF components from the skin, reducing skin’s function to retain moisture with subsequent post-wash dryness.

To maintain good skin barrier, we need to minimise exposure to extrinsic damage and have effective skin care.

Using multiple over the counter cosmetics (make-up, skin and body care, hair dyes…etc.) daily poses increase risk of having reaction to these products. 80% of all contact dermatitis is due to cosmetics. Other reactions such as allergic dermatitis and contact dermatitis can also occur which can impair skin barrier. Common causes of cosmetic allergy are fragrances, preservatives (e.g. parabens, formaldehyde) and paraphenylenediamine found in hair dyes. Hence, patients should aim to minimise the number of cosmetics used and should be educated in reading list of ingredients in all cosmetics and avoid those which contain potential allergens. Patients should be encouraged to look for products that are hypoallergenic, fragrance-free and non-comedogenic.

Use of ultra–mild cleansers can help to lessen the harm to proteins and lipids during cleansing. For instance, directly esterified fatty isethionate (DEFI) cleaners can protect SC lipids from leaking due to the presence of skin identical fatty acids within its surfactant system. DEFI based cleansers can also penetrate SC and replace lipid layer as soon as they are lost during cleansing.

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

  • Ointments are oil based hence more occlusive and effective at reducing trans-epidermal water loss
  • Gels provide water-based delivery system whereby insoluble substance is mixed with gelling agents to help with absorption
  • Creams and lotions are water-based. Water-based products require preservatives to avoid bacterial contamination and growth. Hence, water-based products may cause allergic contact dermatitis.

While emollients are useful to some degree, they only transiently ameliorate harm already done to the skin. However, some special topical agents can help to enhance skin barrier in targeted ways. Alpha-hydroxyl acids (e.g. glycolic acid and lactic acid) enable SC exfoliation allowing SC to be more compact and flexible allowing better penetration of cosmeceuticals. In higher concentrations, it may also affect the dermis stimulating collagen and hyaluronic acid. They also act as humectants improving hydration of skin. Use of topical vitamin A (retinol, retinal, retinal palmitate or retinoic acid) helps to enhance ageing skin. This is via compaction of stratum corneum, epidermal hyperplasia, correction of atypia, dispersion of melanin granules and increase in dermal collagen synthesis and angiogenesis. Topical vitamin C (L- ascorbic acid) is a potent antioxidant and helps to protect from free radicals created from UV rays.  It also acts as an anti-inflammatory, stimulates collagen production and can help with hyperpigmentation issues.  Peptides and proteins also have the ability to enhance collagen production. Niacinamide is biologically active amide of vitamin B. It helps to improve barrier function by increasing production of ceramide in SC. It also has anti-inflammatory and antioxidant properties.

By understanding and appreciating just how important and sensitive the skin is, we should be able to better approach our skin with adequate and appropriate care to keep the barrier strong and the skin healthy.

References
  1. Wollenberg A et Al. Immunological and molecular targets of atopic dermatitis treatment. British Journal of dermatology ( 2014) 170, pp 7-11
  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
  4. Waller. J et al. Age and skin structure and function.Skin research and technology. 2006.12, pp145-154
  5. Cosmetic dermatology and non- invasive treatments. PG dip clinical dermatology Queen Mary university of London online learning environment 2015
  6. How to recognise and investigate skin disease. PG dip clinical dermatology Queen Mary university of London online learning environment 2015
  7. Baumann, Leslie. Cosmetic dermatology. New York. McGraw- Hill Professional Publishing, 2009. Print
  8. Dermnetnz.org. ( 2012). Cosmetics allergy. DermNet New Zealand. [online] Available at: https://www.dermnetnz.org/topcis/cosmetics-allergy/[accessed 18 Sep. 2017]

I graduated from Bristol in 2010 and completed my core medical training in kent, sussex and surrey deanery to obtain Membership of Royal College of Physicians (MRCP). I obtained post graduate diploma with merit in dermatology at Queen Mary's University. I am currently working as GP registrar and is undergoing fellowship in aesthetics medicine. I am registered with the General Medical Council.

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