Oxidative stress in chronic periodontitis

Abstract

It is well documented that the primary etiological agent of periodontal disease is a polymicrobial complex, predominantly gram-negative anaerobic or facultative bacteria within the subgingival biofilm. These bacteria trigger the release of numbers of cytokines, leading to elevated numbers and activity of polymorphonucleocytes (PMNs). As a result of stimulation by bacterial antigens, PMNs produce the reactive oxygen species (ROS) superoxide via the respiratory burst as part of the host response to infection. The human body does contain an array of antioxidant defence mechanisms to remove harmful ROS as soon as they are formed and to prevent their deleterious effects. This review focuses predominantly on the role of ROS and antioxidant defence systems in the pathobiology of periodontitis, with a view to identify specific therapeutic targets for future host-modulating therapies.