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Subgingival dental plaque is the main etiological agent for initiating inflammatory changes in the periodontal tissue and the cell component of bacteria, which exist in the dental plaque and recruit and activate hyper-responsive polymorphonuclear leukocytes (PMNs), which are innate immune cells that may play both defensive and destructive roles in periodontitis (Nicu and Loos, 2016) and accelerate oxidative stress biomarkers ( A