Reactive Oxygen Species and Human Inflammatory Periodontal Diseases

Abstract

Reactive oxygen species (ROS) have emerged as important signaling molecules in the regulation of various cellular processes. They can be generated by the mitochondrial electron transport chain in mitochondria and activation of polymorphonuclear leukocytes (PMN) during inflammatory conditions. Excessive generation of ROS may result in attack of and damage to most intracellular and extracellular components in a living organism. Moreover, ROS can directly induce and/or regulate apoptotic and necrotic cell death. Periodontal pathologies are inflammatory and degenerative diseases. Several forms of periodontal diseases are associated with activated PMN. Damage of tissues in inflammatory periodontal pathologies can be mediated by ROS resulting from the physiological activity of PMN during the phagocytosis of periodontopathic bacteria.

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

“…The deleterious effects of increased oxidative stress are termed oxidative damage and generally occur after exposure to a relatively high concentration of reactive oxygen species (ROS) and/or a decrease in the antioxidant (AO) defense system against ROS. Free radicals and related species have well-defined roles in the inflammatory process (Canakci et al 2005). ROS and ROS-derived radical formations can cause extensive damage to proteins, lipids, and DNA molecules and have been implicated as a major contributor in over 100 disorders and, more recently, periodontitis (Canakci et al 2005).…”

“…Free radicals and related species have well-defined roles in the inflammatory process (Canakci et al 2005). ROS and ROS-derived radical formations can cause extensive damage to proteins, lipids, and DNA molecules and have been implicated as a major contributor in over 100 disorders and, more recently, periodontitis (Canakci et al 2005).…”

“…A study carried out by Moseley et al (Moseley et al 1997) demonstrates that PMNs produce a range of antimicrobial factors, including ROS, during the phagocytosis of periodontopathic bacteria. ROS have recently been reviewed in the pathogenesis of periodontitis (Canakci et al 2005). It has been suggested that as a result of stimulation by bacterial antigens, PMNs produce and release a large quantity of ROS, culminating in heightened oxidative damage to gingival tissue, periodontal ligament, and alveolar bone (Sculley and Langley-Evans 2002).…”

“…It has been suggested that as a result of stimulation by bacterial antigens, PMNs produce and release a large quantity of ROS, culminating in heightened oxidative damage to gingival tissue, periodontal ligament, and alveolar bone (Sculley and Langley-Evans 2002). ROS are active in the depolymerization of extracellular matrix components, lipid peroxidation, oxidation of enzymes such as anti-proteases, induction of pro-inflammatory cytokines, and DNA damage (Canakci et al 2005;Ozmeric 2005).…”

Gingipain-dependent interactions with the host are important for survival of Porphyromonas gingivalis

“…During active infection including tissue invasion, toxic reactive oxygen metabolites (e.g. superoxides, hydrogen peroxide and hydroxyl radicals) are mostly generated by polymorphonuclear leukocytes and macrophages (27,29). In order to survive in the inflammatory environment of the periodontal pocket, the bacterium must not only obtain nutrients for growth, but also overcome oxidative stress and subvert the immune defense system.…”