INTRODUCTION
Facial eczema presents a challenging entity in patients with atopic dermatitis (AD).1 Facial eczema differs from body eczema in both management and severity. Facial eczema has unique challenges to treatment due to adverse effects of potent topical corticosteroid steroid (TCS). Furthermore, recent reports regarding "dupilumab facial redness" or drug-associated face and neck dermatitis (DAFND) highlight the distinctions in facial vs body eczema.2 While many agree that management and presentation of facial vs body eczema differ,3 little research has explored why these differences might exist. Herein, we propose the biological and environmental differences contribute to variations in presentation and management of facial and body eczema.
DISCUSSION
Biological Differences Between Facial and Body Atopic Dermatitis
Microbiome
The microflora directly interacts with the epidermal barrier and cutaneous immune system, supporting immune development, homeostasis, and skin barrier maintenance. Alterations in the skin microbiota, including increases in Staphylococcus species, is a hallmark feature of AD.4 On the forehead, patients with AD have a significant increase in Staphylococcus species (36%) compared with healthy controls (11%), and in patients with moderate-to-severe forehead AD, the Staphylococcus ratios reached more than 70%.5 Furthermore, research demonstrates an inverse relationship between the diversity of the cutaneous microbiome and AD severity.6
Microbial imbalance, specifically increased S. aureus and decreased commensal skin bacteria, results in deficient skin barrier function and inflammation.7 S. aureus enhances inflammation via its Toll-like receptor ligands, which cause interleukin (IL)-4 mediated suppression of IL-10, ultimately supporting the development of AD.8 Compared with other commensal bacteria, S. aureus is prone to adhere to injured skin regions, such as the excoriated skin seen in AD.9 Studies comparing the microbiome of lesional skin vs non-lesional skin demonstrate an increase in S. aureus as well as a decrease in microbiome diversity. Subsequent treatment with topical ozone therapy restores microbiome diversity and decreases severity of inflammatory papules and edema.10
Reduced quantities of Propionibacterium acnes (P. acnes) and Lawsonella clevelandensis in lesions is also a feature of AD. The levels of S. aureus and P. acnes are inversely correlated, due to the fermentation product of P. acnes, propionic acid, inhibiting
Microbiome
The microflora directly interacts with the epidermal barrier and cutaneous immune system, supporting immune development, homeostasis, and skin barrier maintenance. Alterations in the skin microbiota, including increases in Staphylococcus species, is a hallmark feature of AD.4 On the forehead, patients with AD have a significant increase in Staphylococcus species (36%) compared with healthy controls (11%), and in patients with moderate-to-severe forehead AD, the Staphylococcus ratios reached more than 70%.5 Furthermore, research demonstrates an inverse relationship between the diversity of the cutaneous microbiome and AD severity.6
Microbial imbalance, specifically increased S. aureus and decreased commensal skin bacteria, results in deficient skin barrier function and inflammation.7 S. aureus enhances inflammation via its Toll-like receptor ligands, which cause interleukin (IL)-4 mediated suppression of IL-10, ultimately supporting the development of AD.8 Compared with other commensal bacteria, S. aureus is prone to adhere to injured skin regions, such as the excoriated skin seen in AD.9 Studies comparing the microbiome of lesional skin vs non-lesional skin demonstrate an increase in S. aureus as well as a decrease in microbiome diversity. Subsequent treatment with topical ozone therapy restores microbiome diversity and decreases severity of inflammatory papules and edema.10
Reduced quantities of Propionibacterium acnes (P. acnes) and Lawsonella clevelandensis in lesions is also a feature of AD. The levels of S. aureus and P. acnes are inversely correlated, due to the fermentation product of P. acnes, propionic acid, inhibiting
