Neutrophils at the Crossroads of Oral Microbiome Dysbiosis and Periodontal Disease

Abstract

Neutrophils are the most abundant circulating leukocytes and essential components of innate immunity. Through mechanisms such as phagocytosis, reactive oxygen species (ROS) production, degranulation, and neutrophil extracellular trap (NET) formation, they play a crucial role in host defense. However, dysregulated neutrophil responses are linked to chronic inflammatory conditions, including periodontitis. This review summarizes current evidence on neutrophil biology in periodontal health and disease, focusing on functional mechanisms, recruitment pathways, the influence of dysbiosis, and their potential as biomarkers and therapeutic targets. Neutrophils display a dual role in periodontal tissues: while protecting against microbial invasion, their excessive or impaired activity contributes to tissue destruction. Altered chemotaxis, defective phagocytosis, and uncontrolled NET release perpetuate inflammation and alveolar bone loss. Neutrophil-derived enzymes, including myeloperoxidase, elastase, and matrix metalloproteinases, emerge as promising biomarkers for early diagnosis. In parallel, therapeutic strategies targeting oxidative stress, NET regulation, or neutrophil hyperactivity are being explored to preserve periodontal tissues. Neutrophils are central players in periodontal pathophysiology. Understanding their regulation and interaction with the oral microbiome may enable the development of novel diagnostic and therapeutic approaches, ultimately improving periodontal disease management.