Periodontal disease is a chronic and progressive inflammatory disease in which the hard and soft tissues that support the teeth are damaged. It is caused by the interaction between harmful bacteria and the body's immune responses, and most periodontal tissues are damaged by the body's abnormal response to these microorganisms and their products. When bacteria enter the body, immune cells (neutrophils) produce reactive oxygen species (ROS) in a process called the "respiratory burst". These ROS damage cells, causing tissue destruction through a variety of mechanisms, including DNA damage, fat oxidation and protein damage. Studies have shown that neutrophils from individuals with periodontal disease produce more ROS than neutrophils from healthy individuals. High amounts of ROS lead to oxidative damage to gum tissue, periodontal ligament and alveolar bone. Oxidative stress occurs when antioxidants in the body are insufficient or when high levels of ROS are present. Therefore, disruption of the balance between oxidant and antioxidant activities is considered an important cause of oxidative damage in periodontal tissues. Parameters such as total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) are used to determine oxidative stress. Furthermore, some enzymes such as arylesterase (ARE), heme oxygenase (HO) and nuclear factor erythroid 2-related factor 2 (NRF-2) are involved in defense mechanisms against oxidative stress. Many recent studies have shown a strong association between oxidative stress and periodontal disease.
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serum and saliva TAS (mmol Trolox Eq/L) levels
Timeframe: 6 months
serum and saliva TOS (µmol H₂O₂ Eq/L) levels
Timeframe: 6 months
serum and saliva OSI levels
Timeframe: 6 months
serum and saliva ARE (U/L) levels
Timeframe: 6 months
serum and saliva NRF-2 (ng/ml) levels
Timeframe: 6 months
serum and saliva HO-1(ng/ml) levels
Timeframe: 6 months