“…In both AgP and CP, PMNs appear to be functionally activated and exhibit increased production of reactive oxygen species (ROS), free radicals (FRs), and proteolytic enzymes 8–13 as local bacteriostatic mechanisms 14 . During normal conditions, these molecules ensure an efficient defense against microorganisms; in the presence of persistent inflammation, they also may produce adverse effects on periodontal tissue structures through a mechanism known as oxidative stress, 15 , 16 which involves multiple pathways such as lipid peroxidation, DNA damage, oxidation of important enzymes, protein damage, and the release of proinflammatory cytokines, 17 thus leading to progressive collagen and bone loss.…”