patients suffering from long-standing diabetes, end-products of advanced glycoxidation and lipoxidation of structural molecules accumulate in the extracellular matrix of the skin (and other tissues). These change the biological behaviour of involved cells. If elimination of these metabolites is slowed because of impaired renal function, visible skin changes occur. Binding of water resulting in sub-epidermal oedema results in mechanical vulnerability: thin-roofed accumulations of local oedema will easily rupture under friction or pressure in that area. Leakage of fluid and lymph from the resulting erosions is unpleasant and necessitates frequent dressing changes, as well as permitting invasion by micro-organisms and allergens. Inflammation Inflammation of the skin is characterised by the migration of neutrophils, macrophages and lymphocytes, followed by a proliferation of endothelial cells and fibroblasts. In inflammatory skin diseases infiltration of the skin is by inflammatory cells from the surrounding tissues or via diapedesis from blood vessels. Secreted proteins influence different enzymatic functions at the cellular and extracellular levels. Proteolysis of cell surface and extracellular matrix molecules is intrinsically linked to cell function. The inflammatory reaction can impact heavily on the epidermis and underlying dermis, profoundly disturbing their cellular turnover, maturation and function, and the synthesis of the skin-barrier elements. Both acute and chronic eczema result in vesicular lesions (see Figure 13 ), leading to erosions that become easily colonised or even infected. In desquamative inflammatory dermatoses, such as seborrheic dermatitis, psoriasis and eczema, skin barrier function is less effective. Figure 13 - Eczematous skin Expression of -defensin-2 is upregulated by