In the 2022 article by Contento et al entitled “Why Does Facial Eczema Differ from Body Eczema?,” the authors highlight biological and environmental factors underlying key aspects of facial eczema as a unique entity.1
Background and Study Results
While facial and body eczema may be clinically distinct in their presentations, there has been limited exploration of the mechanisms behind these differences. Contento et al describe how the microbiome of the face differs significantly from that of the body. Patients with facial atopic dermatitis (AD) have increased colonization by Staphylococcus species and reduced microbial diversity, a pattern that correlates with more severe AD. At the same time, the higher density of sebaceous and sweat glands on the face creates conditions favorable to Malassezia growth, which can aggravate AD, although excess sebum may also limit S. aureus proliferation by promoting commensal bacteria such as Cutibacterium acnes.
Filaggrin, a protein essential for skin barrier function, further contributes to differences. Facial skin has reduced filaggrin and its breakdown products, such as natural moisturizing factor (NMF), leading to higher water loss and a weaker barrier. This may explain why facial AD develops earlier, is often more severe, and can be worsened by environmental exposures. The face is uniquely and continuously exposed to aeroallergens, ultraviolet radiation, cosmetics, and even food particles in saliva, all of which can provoke hypersensitivity reactions and worsen inflammation.
Management strategies also diverge between facial and body eczema. Potent topical corticosteroids are commonly used on the body but are generally avoided on the face due to potential side effects. This therapeutic limitation often results in poorer disease control on the face. Instead, non-steroidal topical agents are favored for the face, where they have demonstrated both efficacy and safety.
Comments/Clinical Implications
This review emphasizes that facial and body eczema differ due to biological structure and environmental exposures. Contento et al underscore the need for a tailored management of facial eczema due to greater barrier fragility, increased environmental exposures, and the need to avoid potent topical steroids. Clinicians should also be aware of more recently described drug-related conditions in this area. Drug-associated face and neck dermatitis (DAFND) has emerged as a diagnosis linked to dupilumab therapy, with at least 20 cases reported in the scientific literature.2
Facial involvement in AD is particularly distressing and presents additional therapeutic challenges.3 Thus, understanding the unique drivers of facial and body eczema may guide the development of more effective and location-specific AD treatments in the future.
1. Contento M, Maher J, Cline A, Rose S. Why does facial eczema differ from body eczema? J Drugs Dermatol. 2022;21(10):1119-1123. https://doi.org/10.36849/jdd.6354
2. Jaros J, Hendricks AJ, Shi VY, Lio PA. A practical approach to recalcitrant face and neck dermatitis in atopic dermatitis. Dermatitis. 2020;31(3):169-177. https://doi.org/10.1097/DER.0000000000000590
3. Maarouf M, Saberian C, Lio PA, Shi VY. Head-and-neck dermatitis: diagnostic difficulties and management pearls. Pediatr Dermatol. 2018;35(6):748-753. https://doi.org/10.1111/pde.13642
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