Chronic venous disease (CVD) is defined as any morphological and functional abnormalities of long duration manifested either by symptoms and/or signs indicating the need for investigation and/or care. The pathophysiological mechanism of CVD can be characterized by reflux, obstruction, or a combination of both, which leads to increased venous pressure. Compression therapy remains the gold standard of the conservative treatment of CVD in all stages. The possible forms of compression therapy are elastic stocking, non-elastic and elastic bandages, and intermittent pneumatic compression. Compression bandages have been proven to improve the healing of venous ulcers, in comparison with standard care without compression therapy. In the last years, inflammation has been shown to play an important role in the pathophysiology of CVD. The influence of the altered shear stress on the endothelial cells (EC) causes EC to release inflammatory molecules, chemokines, vasoactive agents, express selectins, and prothrombotic precursors such as ICAM-1, MCP-1, MIP 1β, VCAM, L-selectin, E-selectin, IL-1β, IL-4, IL-6, IL-8, IL-12p40, IL-13, G-CSF, GM-CSF, IFN-γ, TNF-α, MIP-1α. Several studies were performed to investigate the influence of compression therapy on the level of various inflammatory biomarkers in patients with CVD. In these studies level of the most inflammatory molecules, such as IL-1β, IL-6, IL-8, IL-12p40, G-CSF, GM-CSF, IFN-γ, TNF-α, VEGF, MMP 3, 8, 9 and TIMP-1 decreased after the therapy.