Pressure ulcers (PrUs)* are chronic wounds caused by a combination of factors, such as repetitive ischemia perfusion injury, bacterial colonization of the wound bed, local tissue hypoxia, or an altered cellular and systemic stress response. The objectives of this study were to analyze fragments of devitalized tissue of Stages III and IV PrUs and compare them with healthy tissue to evaluate the expression of the genes involved in wound inflammation. Samples of healthy skin from patients undergoing plastic surgery (n = 3) were collected, as well as from patients with devitalized tissue from Stages III and IV PrUs (n = 3) by means of sharp debridement. Gene expression analysis identified 5 up-regulated genes and 6 down-regulated genes in the devitalized tissue. Fibroblast cultures treated with devitalized tissue extract showed less attraction and cellular growth compared with the control group. Western blotting analysis showed a tendency of 3 particular genes to decrease in cell cultures treated with devitalized tissue extract. This study demonstrates that all of these mediators stimulate and promote inflammation in the wound bed and that a better understanding of the mechanisms of chronic wound development could lead to novel therapeutic strategies.