Chronic skin diseases accompanied by itching, as well as inflammation, can result from dysfunction of the stratum corneum of the skin. Dr. Karl Thornfeldt discusses the importance of restoring and optimizing the skin's protective barrier, and presents the results of his research into a series of products to combat inflammation and optimize the function of the skin's protective barrier.
The main mysteries for me as a dermatologist were two skin diseases – polymorphic photodermatosis and asteatosis dermatitis. Both of these diseases appeared out of nowhere and disappeared every year at a certain time. Our understanding of the function and structure of the skin was insufficient to explain this phenomenon.
Polymorphic photodermatosis is also known as sun allergy. This disease manifests itself on the skin in the form of red bumps or rashes or foci of dermatitis on any part of the body that is not protected from sun exposure. As a rule, signs of polymorphic photodermatosis begin to appear in the spring. This disease is most common among allergy sufferers and people with sensitive skin. Despite our treatment, in most patients with polymorphic photodermatosis, the signs of the disease disappeared in early August.
Asteatosis dermatitis (or winter itching) usually begins on the shins during the winter holidays and then spreads to the feet, hands and torso. After months of fighting this disease, asteatous dermatitis, as a rule, also suddenly disappears in mid-April. Moreover, our successes in treating chronic inflammatory skin diseases such as psoriasis and dermatitis have been modest, but we have not succeeded in preventing their recurrence.
Corny layer – protective skin barrier
Polymorphic photodermatosis receded as the stratum corneum thickened (reaction to solar radiation, characteristic of the summer period). Elimination of asteatosis dermatitis is associated with softening and thickening of the stratum corneum during an increase in humidity and air temperature.
It became clear that in both cases, chronic inflammation decreased as the stratum corneum strengthened and thickened. Accordingly, inflammation and dermatitis accompanied by itching also appear as the function of the stratum corneum deteriorates. The skin's protective barrier is most vulnerable in places where sebum is the least secreted (for example, on the legs), as well as in people with atopy.
This is how a partial answer was received to the question of the treatment of chronic inflammatory diseases accompanied by the appearance of scales on the skin, as well as maintaining their remission. Standard corticosteroid treatment was effective in reducing inflammation, but further thinned and destroyed the skin's protective barrier, allowing contaminants, radiation, microbes, and chemicals to enter the skin.
Also, corticosteroids stimulated the growth of such pro-inflammatory microbes – after cessation of corticosteroid treatment, chronic inflammation returned. This can also explain the reaction of Koebner – the appearance of diseases such as psoriasis as a result of trauma.
Therefore, dysfunction of the skin's protective barrier is usually associated with chronic inflammation, which is a key factor in many skin diseases.
And so the question began to interest us: if we can optimize the structure and function of the skin, can we more successfully treat the disease and prevent their recurrence? And can such morphological changes affect the aging process and even skin cancer?
Destruction of the protective barrier of the skin: main factors and consequences
It was found that exposure to environmental factors led to the destruction of the protective barrier of the skin, inhibiting its recovery, as a result of which inflammatory processes led to damage to existing skin structures.
Among the factors causing the destruction of the protective barrier of the skin are:
- pollution;
- sunbeams;
- smoking;
- poor nutrition;
- x-rays;
- warmth;
- too high or low humidity;
- high testosterone levels;
- low estrogen;
- severe emotional and physical stress;
- lipid-lowering agents;
- insufficient consumption of healthy fats;
- excessive consumption of unhealthy fats and sugars;
- exposure to heavy metals.
A number of substances used in medicines against skin diseases, including propylene glycol, lactic acid, retinoic acid, as well as formaldehyde, quaternium-15 and sodium lauryl sulfate, not only contributed to the destruction of the skin's protective barrier, but also activated inflammation through the release of tumor necrosis factor alpha.
Further studies have shown that skin diseases characterized by chronic inflammation were accompanied by a deterioration in the function of the protective barrier of the skin, as well as visible aging and sensitivity of the skin, dermatosis, including atopic, seborrheic, chronic contact and asteatotic, ichthyosis, hairy keratosis , rosacea, polymorphic photodermatitis, some types of psoriasis, and precancerous actinic keratosis.
That is why the main effective treatment and prevention of such diseases is to optimize the function of the protective barrier of the skin and prevent destructive chronic inflammation.
Destruction of the protective barrier of the skin and chronic inflammation
Chronic inflammation is activated in the epidermis and dermis by constant or regular destruction of the skin's protective barrier. In this case, there are two types of developments.
- Endogenous protective inflammatory pathways are activated by the release of biological response modifiers contained in granules located in corneocytes deep in the stratum corneum. Once released, these cells expel granules that break down as the stratum corneum breaks down.
- Pro-inflammatory substances and microorganisms penetrate more and to a greater depth, which enhances the inflammatory effect.
We have found that when the stratum corneum of the skin is damaged, regardless of the cause, five pathways for the spread of inflammation are opened. Among them:
- release of cytokines such as interleukins and tumor necrosis factor alpha;
- growth factors such as transforming growth factor beta;
- histamine;
- nuclear receptors such as the hepatic X receptor and the peroxisome proliferator-activated receptor.
All of the above ways contribute to an increase in the amount of matrix metalloproteniasis (MMP) – an enzyme that destroys skin structures, leading to the appearance of micro-scars that develop into wrinkles and dysplasia, which in turn develop into skin cancer and lead to an increase in its sensitivity.
Bacterial and fungal infections, which are exacerbated when the protective barrier of the skin is damaged, also contribute to increased inflammation by activating receptors.
Among the other two ways of spreading inflammation in the skin, not associated with the destruction of the protective barrier of the skin, it is worth noting the glycation reaction and increased synthesis of arachidonic acid – groups of pro-inflammatory molecules.
Acute inflammation is characterized by neutrophilic leukocyte infiltration, proliferation, and chemotaxis, which is essential for defense and initiation of recovery. Chronic inflammation develops 10-12 days after skin injury.
On the other hand, chronic inflammation is characterized by lymphocytic infiltration and an increase in matrix metalloproteinase (MMP). Under conditions of frequent, regular or prolonged damage, the accumulation of excessive amounts of matrix metalloproteinase leads to serious damage to collagen and elastin fibers, as well as to the basic substance – glycosaminoglycans.
Therefore, recovery from such damage and its further prevention through the use of therapeutic ingredients aimed at combating chronic inflammation, along with strengthening the protective barrier of the skin, is necessary.
Restoring the protective barrier of the skin – researched ingredients
Five pathways are involved in the restoration of the protective barrier of the skin, which lead to an increase in the proliferation of keranocytes, and then to an improvement in differentiation into corneocytes – protein "bricks" that make up the protective barrier of the skin, – with rejuvenation of the lipid layer located between these cells.
The normal functioning of the stratum corneum of the skin requires essential physiological lipids, cholesterol, ceramides and free fatty acids in a certain molar ratio to maximize recovery and optimize the function of the skin's protective barrier.
The study showed that chemically and physically stable results could not be achieved using the then known synthetic ingredients. Therefore, we directed the study to the study of plant extracts.
Such herbs contain stable but biologically active molecules that perform various biological functions for the plant. Years later, we were able to develop a skin barrier repair formula based on safflower, mountain rose, avocado and flax extracts, which provided an optimal ratio of barrier lipids and their precursors.
This product accelerated the repair of the skin's protective barrier, which was four times more effective than any commercially available moisturizing product used by dermatologists.
In addition, we were able to create an anti-inflammatory formula based on extracts of date, meadowfoam, apple, flax and avocado, which were more effective than grape, olive, teas and soy, respectively. This product was 2.5 times more effective at suppressing chronic inflammation than 1% hydrocortisone.
Skin barrier repair ingredients were combined with anti-inflammatory ingredients and tested for safety – the products have demonstrated efficacy and safety at the level of the means used for the procedures. This was evidenced by repeated skin allergy tests, which showed no irritation and no reaction to allergens when using this formula.
A double-blind, prospective, controlled clinical trial, the results of which were evaluated by third-party experts, was the main determination of the effectiveness of the product. The study involved a sufficient number of human subjects to determine statistically significant values.
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