Filaggrin
Filaggrin and its breakdown products are essential to epidermal homeostasis, and mutations in filaggrin are associated with AD.20-22 The breakdown products of filaggrin protein include the components of natural moisturizing factor (NMF), which helps maintain adequate skin hydration.23 Decreased NMF levels are associated with increased AD severity and early-onset AD with marked elevations of total IgE levels.24-25 Cheeks have the lowest levels of NMF within the first year of life, which correlates with the fact that the cheeks are frequently the initial site of infantile AD.26 Products that replenish NMF levels through topical application of moisturizers containing NMF successfully treat xerotic skin, and there is evidence that NMF components could be incorporated into the treatment of AD.23 Ultraviolet (UV) radiation impairs filaggrin breakdown to NMF, which is significant since the face tends to be exposed to UV radiation more than the body, thus contributing to further differences in facial vs body eczema.27
Filaggrin mutations also increase transepidermal water loss (TEWL).23 TEWL is much higher in the facial skin than in the forearm/upper arm, and high levels of TEWL are associated with acutely inflamed, eczematous facial lesions of AD.28 The high TEWL on the face can contribute to the reasons that facial eczema may be more severe.
Environmental Exposures Between Facial and Body Skin
Environmental exposures, such as pollutants, cosmetic products, soaps, and hygiene products, are associated with AD development and exacerbation. Facial skin, unlike most other body sites, is continually exposed to environmental stress and this is a contributor to the differences seen between face and body eczema.26
Aeroallergens/Pollutants
Airborne etiologies such as pollens, fungal spores, sawdust, dust mites, pets, and cockroaches contribute to AD exacerbations on air-exposed skin, including the head and neck. These exposures can cause both type I and type IV hypersensitivity reactions, and elevated IgE following sensitization.29 Tobacco smoke is an aeroallergen more specific to the face and known to contribute to AD flares.30 Airborne etiologies are often refractory to standard AD treatments.
Ultraviolet Radiation
Ultraviolet (UV) radiation can have deleterious effects on the skin, leading to macroscopic damage and decreasing the intercellular strength, strain, and cohesion of the stratum corneum.31 UV radiation impairs filaggrin breakdown to its NMF components.24,27 Increased daily sun exposure has been associated with poorly controlled AD.32 Despite these deleterious effects of UV radiation on the skin, it can also have protective effects through facilitation of the conversion of trans-urocanic acid, another filaggrin breakdown product, into the cis-urocanic isoform, which has immunosuppressive effects.33 Overall, UV radiation has been shown to have beneficial effects in those with AD, with most patients having complete resolution of AD during periods of increased sunlight exposure.34 Inverse associations have been found between childhood AD and number of sunny hours per climactic region.35 Phototherapy is often a secondline treatment for AD due to its immunosuppressive effects and antibacterial activity, suppressing superantigen production by S. aureus, which can prevent S. aureus and P. orbiculare infections that are common in patients with AD.33,36 UVB in particular stimulates synthesis of pre-vitamin D in the skin, and some studies show that oral vitamin D supplementation improved AD severity.33,37 The lifetime accumulation of UV radiation may be one reason why adults are less likely to have facial eczema compared with infants.
Cosmetic Products
Personal cosmetics often contain irritants and allergens, which can result in allergic contact dermatitis.38 Use of facial cosmetic products alters the skin’s chemical environment and microflora. Staphylococcus epidermidis and Cutibacterium acnes are normally commensal organisms that help fight cutaneous pathogenic bacteria. However, these commensal microbes, upon exposure to changes in skin temperature and pH, become opportunistic pathogens, which develop virulence factors contributing to the onset or worsening of acne and AD.39 Additionally, synthetics commonly used in cosmetics alter the natural state of the skin, thereby impacting not only the biodiversity of the skin but also the role of individual microbes on the host’s cutaneous immune system.40 Moisturizers with lipid components provide nutrients for the growth of lipophilic bacteria, including Staphylococcus and Propionibacterium species, which positively influence AD development.41 Cosmetic products are more frequently applied to the face than the body, increasing the incidence of facial AD.
Food Allergens and Irritants
Almost a third of children with moderate-to-severe eczema also suffer from contact allergies to food.42 Contact reactions from food-related allergens and irritants can exacerbate head and neck dermatitis. For example, while young children are teething/ drooling and initiating solid foods into their diets, saliva mixed with food particles can aggravate AD and trigger irritant and type IV hypersensitivity reactions on the face.29,43 Thus, application of a perioral and cheek barrier protectant as well as rinsing the child’s cheeks and mouth with water, can prevent antigen entry through broken skin and minimize AD flaring.29
Management
Facial and body eczema differ in management. Topical steroids increase microbiome diversity and decrease S. aureus levels
Filaggrin and its breakdown products are essential to epidermal homeostasis, and mutations in filaggrin are associated with AD.20-22 The breakdown products of filaggrin protein include the components of natural moisturizing factor (NMF), which helps maintain adequate skin hydration.23 Decreased NMF levels are associated with increased AD severity and early-onset AD with marked elevations of total IgE levels.24-25 Cheeks have the lowest levels of NMF within the first year of life, which correlates with the fact that the cheeks are frequently the initial site of infantile AD.26 Products that replenish NMF levels through topical application of moisturizers containing NMF successfully treat xerotic skin, and there is evidence that NMF components could be incorporated into the treatment of AD.23 Ultraviolet (UV) radiation impairs filaggrin breakdown to NMF, which is significant since the face tends to be exposed to UV radiation more than the body, thus contributing to further differences in facial vs body eczema.27
Filaggrin mutations also increase transepidermal water loss (TEWL).23 TEWL is much higher in the facial skin than in the forearm/upper arm, and high levels of TEWL are associated with acutely inflamed, eczematous facial lesions of AD.28 The high TEWL on the face can contribute to the reasons that facial eczema may be more severe.
Environmental Exposures Between Facial and Body Skin
Environmental exposures, such as pollutants, cosmetic products, soaps, and hygiene products, are associated with AD development and exacerbation. Facial skin, unlike most other body sites, is continually exposed to environmental stress and this is a contributor to the differences seen between face and body eczema.26
Aeroallergens/Pollutants
Airborne etiologies such as pollens, fungal spores, sawdust, dust mites, pets, and cockroaches contribute to AD exacerbations on air-exposed skin, including the head and neck. These exposures can cause both type I and type IV hypersensitivity reactions, and elevated IgE following sensitization.29 Tobacco smoke is an aeroallergen more specific to the face and known to contribute to AD flares.30 Airborne etiologies are often refractory to standard AD treatments.
Ultraviolet Radiation
Ultraviolet (UV) radiation can have deleterious effects on the skin, leading to macroscopic damage and decreasing the intercellular strength, strain, and cohesion of the stratum corneum.31 UV radiation impairs filaggrin breakdown to its NMF components.24,27 Increased daily sun exposure has been associated with poorly controlled AD.32 Despite these deleterious effects of UV radiation on the skin, it can also have protective effects through facilitation of the conversion of trans-urocanic acid, another filaggrin breakdown product, into the cis-urocanic isoform, which has immunosuppressive effects.33 Overall, UV radiation has been shown to have beneficial effects in those with AD, with most patients having complete resolution of AD during periods of increased sunlight exposure.34 Inverse associations have been found between childhood AD and number of sunny hours per climactic region.35 Phototherapy is often a secondline treatment for AD due to its immunosuppressive effects and antibacterial activity, suppressing superantigen production by S. aureus, which can prevent S. aureus and P. orbiculare infections that are common in patients with AD.33,36 UVB in particular stimulates synthesis of pre-vitamin D in the skin, and some studies show that oral vitamin D supplementation improved AD severity.33,37 The lifetime accumulation of UV radiation may be one reason why adults are less likely to have facial eczema compared with infants.
Cosmetic Products
Personal cosmetics often contain irritants and allergens, which can result in allergic contact dermatitis.38 Use of facial cosmetic products alters the skin’s chemical environment and microflora. Staphylococcus epidermidis and Cutibacterium acnes are normally commensal organisms that help fight cutaneous pathogenic bacteria. However, these commensal microbes, upon exposure to changes in skin temperature and pH, become opportunistic pathogens, which develop virulence factors contributing to the onset or worsening of acne and AD.39 Additionally, synthetics commonly used in cosmetics alter the natural state of the skin, thereby impacting not only the biodiversity of the skin but also the role of individual microbes on the host’s cutaneous immune system.40 Moisturizers with lipid components provide nutrients for the growth of lipophilic bacteria, including Staphylococcus and Propionibacterium species, which positively influence AD development.41 Cosmetic products are more frequently applied to the face than the body, increasing the incidence of facial AD.
Food Allergens and Irritants
Almost a third of children with moderate-to-severe eczema also suffer from contact allergies to food.42 Contact reactions from food-related allergens and irritants can exacerbate head and neck dermatitis. For example, while young children are teething/ drooling and initiating solid foods into their diets, saliva mixed with food particles can aggravate AD and trigger irritant and type IV hypersensitivity reactions on the face.29,43 Thus, application of a perioral and cheek barrier protectant as well as rinsing the child’s cheeks and mouth with water, can prevent antigen entry through broken skin and minimize AD flaring.29
Management
Facial and body eczema differ in management. Topical steroids increase microbiome diversity and decrease S. aureus levels
