Hyperglycemia induces skin dysfunctions and disturbs keratinocyte homeostasis with increased layers of the stratum corneum. In addition hyperglycemia disturbs skin barrier function. The epidermal cell number is significantly reduced, epidermal differentiation is disturbed, and the proliferation/differentiation process of keratinocytes in the diabetic patient is disrupted.
Skin physiologically has the outside-in barrier that blocks the invasion of harmful substances and pathogenic microorganisms from the outside into the epidermis. Another skin function is the inside-out skin barrier, through which water evaporation from epidermis is adequately regulated in order to maintain biological body fluid homeostasis. The term xerosis is used to describe dryness in the epidermal layers of the skin.
Xerosis, abnormaly dry skin, is an example where barrier functions are impaired. The skin commonly observed in diabetic patients is characterized by dryness, scaling, flaking and persistent itching. Risk factors for xerosis include friction, low humidity, and use of soap. The plantar area of the foot is particularly susceptible, due to its reliance on sweat secretions to remain hydrated.
The treatment for dry skin is the repeated use of moisturizers to hydrate the skin. Their use is based on evidence of the importance of maintaining the skin’s water content. Although the skin on the plantar surface of the foot is very thick, it is highly visco-elastic and copes with high levels of frictional, compressive and shear stresses applied to it by being supple and well hydrated. Problems arise when the skin becomes dry and loses its elastic properties. Fissures can occur which are often painful and can act as portals for infection.