Pathophysiology of atopic dermatitis

A complex range of factors influence the development and onset of atopic dermatitis, but what is the underlying mechanism that drives skin barrier dysfunction and inflammation? Discover how breakdown of the skin barrier can lead to allergen penetration and immune system activation.


In the past, atopic dermatitis was thought to be primarily a consequence of immune dysfunction in susceptible children. However, recent advances point towards a complex pathophysiology with genetic, barrier function, immunity and environmental factors acting together and synergistically to drive barrier dysfunction, inflammation and disease progression (McPherson, 2016). 

Two theories have been proposed for the pathophysiology of atopic dermatitis. The inside-out model proposes that an allergic response triggers inflammation that disrupts the skin barrier enabling further allergen and microbe exposure. The outside-in hypothesis, however, suggests that skin barrier dysfunction initiates the process of atopic dermatitis, with immune dysregulation occurring subsequently (Avena-Woods, 2017).

Theories of atopic dermatitis pathogenesis.

Figure 6: Theories of atopic dermatitis pathogenesis (Barton & Sidbury, 2015).

While some suggest that these models are unlikely to be exclusive and probably both play a role (Avena-Woods, 2017), others suggest that skin barrier dysfunction, or the outside-in model, is the initiating step (Kim & Leung, 2018).