Sensitive skin syndrome

The overall prevalence of SENSITIVE SKIN SYNDROME is about the same in different countries:
USA – 44.6%
Europe – 38.4%
China – 36%

Sensitive skin syndrome (SSS)

is now defined as less resistance or greater reactivity of the skin in response to normal external and/or internal stimuli, which cannot be considered as ordinary irritants (irritants).
A syndrome is a set of symptoms!!!
These are mostly subjective sensations (burning, tingling, tightness, itching, paresthesias, heat)
In 50% of patients, subjective symptoms are accompanied by weakly expressed objective symptoms of skin inflammation (hyperemia, in severe cases – edema of the papillae of the dermis)
SSS can be characterized as hyperreactive skin to normal external and internal influences.

Localisation of SSS

The most sensitive areas are the nasolabial fold, followed by the chin, forehead and upper lip. Less often, hyperreactivity of the skin is observed on the hands, the upper part of the head, the upper half of the chest, and the genitals

Factors contributing to the formation of SSS

Gender (women report SSS more often than men)
According to research, the prevalence of SSS among women is about 51%, among men – 38%.
This is due to the greater thickness of the epidermis in men and less influence of hormonal factors that lead to increased skin reactivity.

Age – Sensitive skin syndrome is most often observed at the age of 18-50 and decreases with age
Sensitive skin syndrome most often occurs at the age of 21-25 years – 47%.
It then declines and occurs in 20.8% of cases at the age of 51-55
This factor is associated with a decrease in the density of the nerve structures of the skin during the ageing process.

Stress aggravates malfunctions of the neuroreceptor apparatus of the skin.

increasing the sensitivity of receptors to neurotransmitters (substance P)
increased secretion of nerve growth factor (NGF – nerve growth factor)

Genetic and constitutional factors – genetically determined tendency to vagotonia (activity of the parasympathetic nervous system)
reactivity of skin vessels
violation of the skin barrier (thinning, decrease in hydration of the stratum corneum)
high transepidermal water loss
decrease in the content of sphingolipids

Exogenous factors (cold, wind, temperature change, UV radiation, dry air)

The B-spectrum of ultraviolet radiation can stimulate the synthesis of vascular endothelial growth factor (VEGF), which is primarily produced by keratinocytes in the skin. Additionally, it can lead to an upregulation of pro-inflammatory cytokines, contributing to an inflammatory response.

Food irritants (alcohol, spices, caffeinated products) that increase vascular reactivity.

Dermatological diseases (atopic, allergic contact dermatitis, rosacea, psoriasis)

Pathogenesis of Sensitive skin syndrome

3 main interconnected mechanisms:

violation of barrier properties
violation of the neuroreceptor apparatus of the skin
persistent inflammation caused by dermatological diseases

Disruption of barrier functions according to Sensitive skin syndrome

Balance of highly specialised intercellular lipids: ceramides, glycosylceramides, phospholipids, cholesterol, fatty acids, sphingoid bases, etc.

the main barrier preventing transepidermal moisture loss
intercellular cementing substance that ensures the strength of the adhesion of horny scales
form a water-lipid mantle on the surface of the skin, containing in its composition lipids of the stratum corneum, sebum, secret of sweat glands

All this provides the barrier functions of the skin!!!

Malfunction of the neuroreceptor apparatus of the skin in SSS

Represented by numerous afferent and efferent fibers + encapsulated nerve endings.

Afferent fibers, responsible for receiving impulses from the outside, are connected to encapsulated nerve endings

(lamellar corpuscles of Father-Pacini, end bulbs of Krause, tactile corpuscles of Ruffini, tactile corpuscles of Meissner, genital corpuscles of Dogel, etc.), which are located in the dermis and are mechanoreceptors.

Afferent fibers are also connected to free endings (noci- and thermoreceptors) present in the epidermis and dermis.

Nerve impulse transmission is carried out with the help of neurotransmitters, which in the skin are represented by substance P and a peptide, the synthesis of which is encoded by the calcitonin gene (CGRP – calcitonin gene-related peptide)

substance P causes vasodilatation and degranulation of mast cells
increased release of neurotransmitters is observed during psycho-emotional stress, pathological processes in the skin and causes the activation of the production of pro-inflammatory cytokines
increased inflammatory response
NGF – a peptide sensitises sensitive receptors to various thermal, mechanical and chemical stimuli, which contributes to the induction of itching and other subjective sensations.

Increased sensitivity of various skin structures to the release of neurotransmitters in the case of SS, as well as in the case of rosacea, acne, atopic dermatitis and a number of other dermatoses.

Persistent inflammation in Sensitive skin syndrome

Persistent inflammation caused by dermatological diseases

Rosacea
Atopic dermatitis
Allergic contact dermatitis
Psoriasis

Phase 1 – damage to the cellular structures of the epidermis and dermis
Phase 2 – activation of trigger mechanisms with abnormally increased production of inflammatory cytokines by keratinocytes
Phase 3 – stimulation of cellular activity of the epidermis (hyperproliferation of keratinocytes) under the influence of cytokines, factors of epidermal lymphocytic origin.

Sensitive Skin Syndrome = ROSACEA diagnosis

Stage 1 – erythematous
Stage 2 – papulopustular
Stage 3 – phymatous
Stage 4 – ophthalmosis

Keratinocytes and Langerhans cells increase the production of pro-inflammatory cytokines – tumor necrosis factor α, interleukin-1, responsible for vascular reactivity in transient erythema

In persistent erythema, hyperexpression of VERG (glycoprotein) by keratinocytes is noted. VERG interacts with receptors on the surface of endotheliocytes of blood vessels – increases the formation of new vessels. VERG increases vascular permeability 50 thousand times stronger than histamine. In addition, VERG stimulates the synthesis of enzymes – collagenases or matrix metalloproteinases, capable of destroying the fibrous structures of the dermis, making room for the growth of newly formed blood vessels.

Persistent inflammation in SSS

Reduction of local immune response (antibacterial peptides)
Violation of the microbiome
Predominance of conditionally pathogenic microflora – S. Aureus (synthesis of peptidases that destroy the normal functioning of keratinocytes)

Sensitive skin syndrome
= Atopic dermatitis
= Contact allergic dermatitis
= Psoriasis

Immune-inflammatory reactions
Eosinophilia
Increase in immunoglobulins E
Violation of keratinocyte proliferation
Transepidermal moisture loss

The main methods for Sensitive skin syndrome

Topical therapy (emollients, calcineurin inhibitors, antihistamine receptor blockers, glucocorticoids)

Systemic therapy (desensitization – membrane stabilizers, antihistamines, detoxification – sorbents, restoration of microflora – pro-/prebiotics)

Tasks of a dermatocosmetologist in Sensitive skin syndrome

Exclusion of triggers!!!
Restoration of barrier function – fatty acid balance
Restoration of the microbiome – probiotics
Moisturising the skin – saturation of the skin’s natural moisturising factor
Selection of daily home care

SENSITIVE SKIN SYNDROME

A comprehensive program for the correction of sensitive skin syndrome,
4-6 procedures, interval: 5-7 days

Clinical picture:

Hyperemia is transient/persistent
Delineation of the skin pattern
Flaking
+Complaints of skin tightness, burning, itching, paresthesias

Course program:

Nourishing care with a corneotherapeutic effect
Device-based care with a booster to reduce the reactivity of sensitive skin/moisturising booster
Moisturising care with a muscle-relaxing effect
Enzyme peeling: express care / Peel-Expert Light