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.
Highlights
Periodontitis is a prevalent inflammatory disease, influencing at least 10% of people worldwide (Richards, 2014)
It has been confirmed that periodontitis is associated with a hyperactivity of peripheral blood neutrophils, which are supposed to be the predominant source of reactive oxygen species (ROS)
Numerous studies suggested that periodontitis could contribute to both local and systemic oxidative stress
Summary
Periodontitis is a prevalent inflammatory disease, influencing at least 10% of people worldwide (Richards, 2014). It can result in the destruction of teeth supporting tissue and ends up with a loss of teeth. Current concept suggests that this inflammatory disease is initiated by bacterial infection and subsequently progressed by aberrant host response, which mainly contributes to periodontal tissue destruction (Bartold and Van Dyke, 2013). ROS are described as oxygen free radicals and other non-radical oxygen derivatives involved in oxygen radical production (Lushchak, 2014). They are involved in normal cellular metabolism and continuously generated by the cells in most tissues. ROS production is drastically increased mainly due to cells of innate immune system, e.g., neutrophils and macrophages during
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