Neutrophils are essential for antimicrobial defense and tissue maintenance at mucosal barriers. However, dysregulated neutrophil responses, particularly excessive release of neutrophil extracellular traps (NETs), contribute to various diseases. This review discusses neutrophil functions, including NET formation, in the context of periodontitis, a common inflammatory disease affecting oral tissues. Neutrophils play a critical role in periodontitis by eliminating pathogens and maintaining tissue integrity. Deficiencies in neutrophils or excessive NETs are implicated in different forms of periodontitis. Neutrophils originate in the bone marrow, mature, and differentiate into various cell types, including neutrophils. They perform functions such as phagocytosis, degranulation, and NET release, which are crucial for antimicrobial defense. NETs, first described by Brinkmann in 2004, are strand-like webs of decondensed chromatin containing histones and granule proteins, which trap and neutralize pathogens. NET formation is triggered by various stimuli, including pathogens, cytokines, and host-derived components. The process involves chromatin decondensation, nuclear rupture, and NET release. NETs can have both antimicrobial and inflammatory roles, contributing to periodontitis pathology. Neutrophil accumulation and NET formation are evident in common and genetic forms of periodontitis. Neutrophils also play homeostatic roles in oral immunity, and their dysfunction is linked to severe periodontitis. NETs are involved in the pathogenesis of various inflammatory conditions, including sepsis, atherosclerosis, and autoimmune diseases. Extracellular histones, components of NETs, contribute to inflammation and tissue damage. In periodontitis, NET formation is triggered by oral microbes and can lead to periodontal destruction. Fibrin accumulation in oral tissues facilitates neutrophil retention and activation, contributing to periodontitis. NETs and extracellular histones mediate periodontal pathology by triggering inflammation and bone destruction. Inhibiting NET formation or extracellular histones reduces periodontitis severity. This review highlights the complex roles of neutrophils and NETs in oral health and disease, emphasizing their importance in periodontitis pathogenesis.Neutrophils are essential for antimicrobial defense and tissue maintenance at mucosal barriers. However, dysregulated neutrophil responses, particularly excessive release of neutrophil extracellular traps (NETs), contribute to various diseases. This review discusses neutrophil functions, including NET formation, in the context of periodontitis, a common inflammatory disease affecting oral tissues. Neutrophils play a critical role in periodontitis by eliminating pathogens and maintaining tissue integrity. Deficiencies in neutrophils or excessive NETs are implicated in different forms of periodontitis. Neutrophils originate in the bone marrow, mature, and differentiate into various cell types, including neutrophils. They perform functions such as phagocytosis, degranulation, and NET release, which are crucial for antimicrobial defense. NETs, first described by Brinkmann in 2004, are strand-like webs of decondensed chromatin containing histones and granule proteins, which trap and neutralize pathogens. NET formation is triggered by various stimuli, including pathogens, cytokines, and host-derived components. The process involves chromatin decondensation, nuclear rupture, and NET release. NETs can have both antimicrobial and inflammatory roles, contributing to periodontitis pathology. Neutrophil accumulation and NET formation are evident in common and genetic forms of periodontitis. Neutrophils also play homeostatic roles in oral immunity, and their dysfunction is linked to severe periodontitis. NETs are involved in the pathogenesis of various inflammatory conditions, including sepsis, atherosclerosis, and autoimmune diseases. Extracellular histones, components of NETs, contribute to inflammation and tissue damage. In periodontitis, NET formation is triggered by oral microbes and can lead to periodontal destruction. Fibrin accumulation in oral tissues facilitates neutrophil retention and activation, contributing to periodontitis. NETs and extracellular histones mediate periodontal pathology by triggering inflammation and bone destruction. Inhibiting NET formation or extracellular histones reduces periodontitis severity. This review highlights the complex roles of neutrophils and NETs in oral health and disease, emphasizing their importance in periodontitis pathogenesis.