International Journal of Research and Reports in Dentistry

Periodontitis is a chronic, microbially associated inflammatory disease in which host-derived mediators, rather than bacteria alone, drive the destruction of tooth-supporting tissues. Neutrophil extracellular traps, chromatin scaffolds decorated with granule proteins that are expelled by activated neutrophils, have been proposed as a central effector arm of that destruction and, more recently, as a therapeutic target. This critical narrative review evaluates the strength, coherence and translational readiness of the evidence linking these structures to periodontal pathology. Literature was identified through structured searching of eight scholarly databases and indexes, supplemented by backward and forward citation tracking, and appraised for design adequacy, measurement validity, biological plausibility and reproducibility. Three principal conclusions emerge. First, the observation that trap-associated material accumulates in inflamed periodontal tissues, crevicular fluid and saliva is consistent across independent groups and detection platforms, and can be regarded as well supported. Second, the causal contribution of these structures to attachment and bone loss rests almost entirely on rodent models and pharmacological or genetic manipulation of trap release, which reduce complex phenotypes to single readouts; human causal evidence remains absent. Third, the field is constrained by a measurement problem that is rarely acknowledged: surrogate markers such as cell-free DNA, myeloperoxidase–DNA complexes and citrullinated histone H3 are neither specific nor interchangeable, which plausibly explains several apparent contradictions in the literature, including disagreement over whether release capacity is elevated, unchanged or impaired in affected individuals. Emerging therapeutic strategies, including nuclease delivery, peptidylarginine deiminase inhibition, redox modulation and engineered local delivery systems, show consistent efficacy in experimental periodontitis but have not been examined in controlled human trials, and their safety implications for oral antimicrobial defence are largely unexplored. Progress will depend less on additional descriptive comparisons than on standardised, validated quantification, longitudinal designs anchored to clinical endpoints, and interventional studies capable of separating pathogenic from protective trap functions.