Neutrophil Dynamics in Periodontal Disease

Neutrophils are the principal innate immune cells patrolling the gingival crevice, where they orchestrate rapid responses to microbial incursions. In health, these cells migrate with precision to sites of bacterial challenge, efficiently phagocytosing pathogens and releasing antimicrobial mediators while preserving tissue integrity. Periodontal disease arises when this balance is disturbed by a dysbiotic biofilm, leading to persistent neutrophil recruitment, exaggerated degranulation and uncontrolled formation of neutrophil extracellular traps (NETs). The sustained presence of activated neutrophils drives collateral damage to the periodontal ligament and alveolar bone, culminating in tissue destruction and tooth support loss. Moreover, altered neutrophil survival and impaired chemotactic accuracy prolong the inflammatory milieu, reinforcing a feed‐forward loop of host‐driven pathology. Beyond local effects, aberrant neutrophil activation in the gingiva contributes to systemic inflammation and has been implicated in cardiovascular comorbidities. Contemporary research seeks not only to elucidate the molecular pathways that govern neutrophil activation and NETosis in the periodontal pocket but also to identify strategies for restoring neutrophil homeostasis without compromising antimicrobial defence. Advances in understanding the immunometabolic reprogramming of neutrophils under hyperglycaemic or inflammatory conditions further highlight the potential for targeted therapies that modulate neutrophil function to arrest disease progression and reduce systemic risk.

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Neutrophil Dynamics in Periodontal Disease publication trend

The graph below shows the total number of articles in neutrophil dynamics in periodontal disease across all publications each year (not limited to Nature Index journals).

Technical terms

Neutrophil extracellular traps (NETs): Meshworks of DNA and granule proteins expelled by activated neutrophils to immobilise pathogens, whose overaccumulation can damage host tissues.

Chemotaxis: The guided movement of neutrophils along chemical gradients towards sites of infection or inflammation.

Dysbiosis: An imbalance in the composition of the oral microbiome that favours pathogenic species over commensals.

Immunometabolic reprogramming: Metabolic adjustments within neutrophils that alter their activation, survival and effector functions under inflammatory or hyperglycaemic conditions.

References

1. Hyperglycemia‐Enhanced Neutrophil Extracellular Traps Drive Mucosal Immunopathology at the Oral Barrier. Advanced Science (2024).
2. Local Drug Delivery Systems as Novel Approach for Controlling NETosis in Periodontitis. Pharmaceutics (2024).
3. Neutrophils’ Contribution to Periodontitis and Periodontitis-Associated Cardiovascular Diseases. International Journal of Molecular Sciences (2023).
4. Oral Neutrophil Transcriptome Changes Result in a Pro-Survival Phenotype in Periodontal Diseases. PLOS ONE (2013).
5. Impaired neutrophil directional chemotactic accuracy in chronic periodontitis patients. Journal Of Clinical Periodontology (2015).
6. Neutrophil Functions in Periodontal Homeostasis. Journal of Immunology Research (2016).
7. Neutrophil Extracellular Traps in Periodontitis. Cells (2020).