Oxidative Stress and Antioxidant System in Periodontitis

Abstract

Periodontitis is a common inflammatory disease, which is initiated by bacterial infection and subsequently progressed by aberrant host response. It can result in the destruction of teeth supporting tissues and have an influence on systemic health. When periodontitis occurs, reactive oxygen species, which are overproduced mostly by hyperactive neutrophils, could not be balanced by antioxidant defense system and cause tissues damage. This is characterized by increased metabolites of lipid peroxidation, DNA damage and protein damage. Local and systemic activities of antioxidants can also be influenced by periodontitis. Total antioxidant capacity, total oxidant status and oxidative stress index have been used to evaluate the oxidative stress associated with periodontitis. Studies have confirmed that inflammatory response in periodontitis is associated with an increased local and systemic oxidative stress and compromised antioxidant capacity. Our review focuses on increased oxidative stress in periodontal disease, specifically, on the relationship between the local and systemic biomarkers of oxidative stress and periodontitis and their association with the pathogenesis of periodontitis. Also, the relationship between periodontitis and systemic inflammation, and the effects of periodontal therapy on oxidative stress parameters will be discussed.

Keywords: antioxidants; neutrophils; oxidative stress; periodontitis; reactive oxygen species.

Figure 1

Reactive oxygen species production in periodontal disease. Upon internalization of pathogens, neutrophils produce ${\text{O}}_2^{-}$ via the metabolic pathway called “respiratory burst” by NADPH-oxidase. ${\text{O}}_2^{-}$ can be converted to hydrogen peroxide (H₂O₂) by superoxide dismutase or spontaneous dismutation. H₂O₂ can be further converted to different derivatives, such as hypochlorous acid (HOCl), hydroxyl radical (^•OH) and singlet oxygen (¹O₂).