The interplay between chemical species transport and transformation and the pathogenesis of integumentary diseases underscores the importance of these mechanisms in the systemic response to skin disorders. In psoriasis, aberrant T-cell trafficking and altered skin microenvironment favors an environment conducive to chronic inflammation. Thus, hyperproliferative keratinocytes and heightened inflammation disrupt normal diffusion and biochemical homeostasis, leading to the characteristic plaques . As a result, the impaired blood flow within the dermis can hinder the delivery of immune cells, cytokines, and other signaling molecules needed to address the underlying pathology. Disruption in biophysical and biomechanical stability occurs as alterations in skin barrier function affect hydration and elasticity, leading to exacerbated disease symptoms .