Dermal pathology, cellular biology, and inflammation in chronic venous disease

Abstract

The pathophysiology of venous dermal pathology in chronic venous disease (CVD) is reflective of a complex interplay that involves sustained venous hypertension, inflammation, cytokine and matrix metalloproteinase (MMP) activation, and altered cellular function. Endothelial expression of specific adhesion molecules recruits leukocytes, and diapedesis of these cells into the dermal microvasculature promotes an inflammatory response with activation of cytokines and proteinases. Altered cell function enhances a state of vulnerability in the surrounding tissues initiating specific changes associated with venous disease. Ultimately, the persistent inflammatory-proteinase activity leads to advanced chronic venous insufficiency (CVI) and ulcer formation.