In 2011, a review by Escalas-Taberner et al.2 listed the main definitions of the term sensitive skin in the literature and described the condition as a complex syndrome with a high component of subjectivity on the part of the patient. In 2013, the explanation of the etiology of sensitive skin was expanded to include environmental factors.4,5

The authors of subsequent publications have noted the lack of consensus on the meaning of the term and the challenge presented by any effort to research this syndrome.6,7 The most recent definition—and the first to achieve consensus—was published in a position paper drawn up by a group of European experts at the International Forum for the Study of Itch in 2017.8 The group used the Delphi method to reach a very specific definition of sensitive skin as follows: “A syndrome defined by the occurrence of unpleasant sensations (stinging, burning, pain, pruritus, and tingling sensations) in response to stimuli that normally should not provoke such sensations.These unpleasant sensations cannot be explained by lesions attributable to any skin disease. The skin can appear normal or be accompanied by erythema. Sensitive skin can affect all body locations, especially the face”.

Moreover, it has been considered necessary to distinguish between sensitive skin syndrome and selective sensitivities to specific products. This led to a proposed amendment to the terminology (Misery, 2017 #202), with the suggested new term being reactive skin. Although this new term is more accurate if we take into account what is known about the etiology and pathogenesis of the condition, the use of the term sensitive skin is still more widespread.

Several studies have posited a connection between sensitive skin and a disruption of epidermal barrier function, which is thought to give rise to a feeling of discomfort in the skin (Draelos, 1997; Effendy, 1995; Goffin, 1996; Roussaki-Schulze, 2005; Saint-Martory, 2008). In terms of epidermal barrier function, sensitive skin can be classified into 3 types9:

• 1.

  Type I: low barrier function

• 2.

  Type II: normal barrier function with inflammatory changes

• 3.

  Type III: normal barrier function without inflammation but with reactivity problems

In all 3 groups, it has been observed that concentrations of nerve growth factor in the epidermis are higher than the levels observed in non-sensitive skin. Furthermore, in both type II and type IIIpatients, sensitivity to electrical stimuli is high.

In terms of the factors that cause a reaction in sensitive skin, the condition can be classified as follows10:

• 1.

  High sensitivity: reactive to a wide variety of both endogenous and exogenous factors and associated with acute or chronic symptoms and a strong psychological component

• 2.

  Environmental sensitivity: fair, dry, and fine skin that has a tendency to blush and is reactive to primary environmental factors

• 3.

  Cosmetic sensitivity: skin that exhibits transient reactivity to specific cosmetic products.

Finally, we propose a classification of the syndrome according to the presence or absence of associated skin diseases.

• 1.

  Primary sensitive skin, in which the affected person has no associated underlying disease.

• 2.

  Secondary sensitive skin, in which the patient has a skin condition, such as seborrheic, atopic, or contact dermatitis, rosacea, or acne.

The prevalence of sensitive skin syndrome in Europe is high, approximately 39%, and the condition appears to affect women more than men.11 The only reference to the prevalence of sensitive skin in Spain comes from a study published by Misery et al. in 2009.11 In that study, data were collected by telephone and through on-line surveys of representative samples of people aged 15 years or older in various European countries. The findings indicate that 11.6 million people in Spain could be affected by sensitive skin syndrome.

The data collected also showed a higher prevalence of the syndrome in women and no correlation with factors such as age, rural or urban setting, and socioprofessional category. Although these data provide an initial insight into the epidemiology of sensitive skin in Spain, further studies based on clinical diagnosis are needed to provide more consistent information on the prevalence of this syndrome.

The mechanisms underlying sensitive skin syndrome continue to be studied and debated in the literature. Current evidence indicates that individuals with sensitive skin have one of the following cutaneous alterations: increased nerve fiber density, increased immune response, or low epidermal barrier function. All of these alterations contribute to the activation of a response to several factors. These factors may be environmental (pollution, radiation, UV exposure, weather), lifestyle-related (diet, use of cosmetics, alcohol consumption), or endogenous (psychological factors and emotional stress). In the following section, we will discuss the biological mechanisms activated by these different factors.

There are several mechanisms through which the cutaneous nervous system may contribute to sensitive skin syndrome. One mechanism that could contribute to the condition is hyperreactivity of the cutaneous nerve endings. A lower density of intraepidermal nerve fibers, especially those of the peptidergic amyelinic C-fiber type, has been reported in patients with sensitive skin.12 This alteration would help to explain the neurogenic inflammation some people experience,12 irrespective of the presence of barrier function alterations. Transient receptor potential [TRP) channels expressed on the membrane of group C nerve fibers would appear to play a central role.13 While the evidence remains inconclusive, it appears likely that TRP channels play a central role in the perception and pathophysiology of sensitive skin as they can be activated by the many stimuli—physical, chemical, and thermal—that trigger sensitive skin.14–16 Vanilloid receptor 1 (TRPV1) appears to play a particularly important role, since it mediates the response to many of these factors.16–20

The activation of TRPV1 channels in reactive skin triggers the cutaneous release of substance P and other neuropeptides and subsequently the release of proinflammatory cytokines, such as interleukin (IL) 2, tumor necrosis factor α, interferon γ, IL-23, and IL-31. This, in turn, enhances the immune response by recruiting more immune cells to the skin.6 All of these factors are related to the itching and burning sensations characteristic of sensitive skin syndrome.

The integrity of the epidermal barrier is essential to the maintenance of the skin's structure and functions. Disruption of this barrier, resulting in a thinner and more permeable stratum corneum,10,13,21 has been proposed as a trigger mechanism for the symptoms associated with sensitive skin. A weak epidermal barrier facilitates the penetration of irritants and allergens10 and is associated with poor protection of nerve endings and increased transepidermal water loss.22,23 The integrity of the epidermal barrier is highly dependent on lipid composition. In fact, it is known that sensitive skin results in changes in levels of neutral lipids, sphingolipids, and ceramides.24,25

Today, it is also known that barrier function also depends largely on the community of microorganisms that inhabit the skin, known as the skin microbiome. While sensitive skin, unlike dermatitis, is not associated with any imbalance or dysbiosis,6 the microbiome is a new field of study and numerous questions remain unanswered.

As sensitive skin is a condition with a highly subjective component, diagnosis must be based, fundamentally, on the interpretation of the symptoms reported by the patient and an assessment of the patient's medical history (personal and family), daily habits, and use of cosmetics. Among other aspects, it is important to manage the symptoms reported and investigate other possible causes. Since these patients often do not present any objective physical signs of disease, questionnaires are a useful diagnostic tool in this setting.26

Table 1 lists a series of questions that will help the specialist to reach a correct diagnosis of sensitive skin syndrome. This set of questions can be divided into 3 blocks: the patient's own perception of the sensitivity, irritation, and reactivity of their skin (block I, questions 1-4), the skin's reaction to cosmetic products (block II, questions 5-7), and to environmental factors (block III, questions 8-13). The patient who gives a positive answer to at least 2 questions from block I, 3 questions from block II, or 3 questions from block III is considered to have sensitive skin.

In addition to the questionnaire proposed in Table 1, we also recommend the use of the 10-item questionnaire validated by Misery et al.27 On that scale, a score between 20 and 60 points (or more) identifies individuals with sensitive skin.

Although, as indicated above, questionnaires are still the most reliable method for diagnosing sensitive skin, the results of a number of physical tests can help the specialist make a correct diagnosis. A list of these tests, together with their advantages and disadvantages, is shown in Table 2.

Appropriate cleaning and treatment regimens are essential for the care of sensitive skin because the use of inappropriate products could exacerbate symptoms. It is therefore important for these patients to use products with a pH in the physiological range (5.5-6.0) and avoid products that have a high pH or contain harsh surfactants that could damage the skin or mucous membranes. Skin cleansers should be fragrance-free and contain only mild amphoteric or anionic surfactants. Appropriate products may also contain hydrating elements of proven biocompatibility, such as glycerin, hyaluronic acid, in addition to relipidization components, such as vegetable oils or ceramides. Patients with sensitive skin should use a gentle cleansing routine, avoid scrubbing the skin with mechanical devices or exfoliating products. It is recommended that they should dry drying their skin by gently dabbing it with paper tissues (never cotton pads).10

These patients should use cosmetic products that have been shown to improve skin barrier function, with minimal concentrations of preservatives and no surfactants.29 Some authors recommend the use of products with simple formulas containing very few ingredients to avoid as far as possible common sensitizing agents, sensory stimulants, and cutaneous vasodilators and to minimize the content of irritants, such as benzoic acid, cinnamic acid, sodium lauryl sulfate, bronopol, lactic acid, propylene glycol, urea, and sorbic acid.10,30–32

It is also recommended that these patients should maintain their skin highly hydrated to reduce their susceptibility to irritation and to restore the integrity of the stratum corneum.33 Their regimen should include passive moisturizers (vegetable oils, silicones) to reduce transepidermal water loss and balance the skin's acid mantle, active moisturizing or hydrating products that retain water in the stratum corneum (glycerol, hyaluronic acid, filaggrin derivatives, all natural moisturizing factors), and finally relipidizing agents (vegetable oils, ceramides, and pseudoceramides).25,34,35 The formulation of the products used is also important: products containing active ingredients that are non-occlusive and favor a lightweight texture will facilitate the application of the product, reducing the need to rub or massage the skin.36,37

Certain substances can be used to relieve the symptoms of sensitive skin. For instance, the efficacy of TRPV1 antagonists has been demonstrated.38 Specifically, pimecrolimus, a calcineurin inhibitor that acts on TRPV1, was shown to improve the symptoms of sensitive skin in a study of Chinese women.39 Efficacy has also been achieved with neurosensine, a molecule derived from a neurosensorial dipeptide naturally present in the skin. Neurosensine stimulates the production of endorphins and enkephalins in keratinocytes and contributes to the creation of a barrier that protects group C nerve fibers, thereby reducing stimulation of the nociceptive signaling pathways, including the TRPV1 and proinflammatory mediators (substance P). In a clinical study, a product containing neurosensine inhibited neurogenic inflammation, helping to reduce the most specific symptoms of sensitive skin, including burning, heat, itching, and stinging sensations.40

Another active ingredient of interest for the treatment of sensitive skin is nicotinamide, which helps to restore barrier function by increasing the synthesis of epidermal lipids and ceramides. This improvement in barrier function helps to reduce water loss. Nicotinamide also reduces the release of proinflammatory mediators and regulates the release of histamine, thereby reducing inflammation and itching. It has also been observed to have probiotic properties.41,42