The release of the pro-inflammatory cytokine IL-1β from an epithelial cell is dependent on two separate signals. The first signal comes from the binding of a pathogen associated molecular pattern to a pathogen recognition receptor, which then promotes the production of the immature form of IL-1β. The second signal will come from a danger signal in the form of extracellular ATP, which will lead to the assembly of an inflammasome, activation and caspase-1 and secretion of the mature IL-1β. This thesis evaluates whether the mechanism by which extracellular ATP activates the inflammasome is in a P2X7 dependent manner. The characterizing of this mechanism is to be done for the first time in gingival epithelial cells (GECs), the first host cells a periodontal pathogen like Porphyromonas gingivalis would encounter. We have shown that GECs express a functional P2X7 receptor, but the mechanism by which we get activated caspase-1 is still uncertain. In this study, we compared reactive oxygen species (ROS) production levels between cells treated with just ATP and cells pretreated with a P2X7 antagonist. The cells treated with the antagonist before the ATP showed significantly lower levels of ROS production suggesting that ATP stimulated ROS production is P2X7 dependent. ROS production has been shown to promote the assembly of the inflammasome, leading to caspase-1 activation. Thus, we also want to show that caspase-1 activation by ATP stimulation is P2X7 dependent. Our results on that front are still inconclusive. After this project, we still need to investigate the effects of infection by P. gingvalis and its NDK deficient mutant on ROS production and caspase-1 activation.