Periodontitis is a general term for diseases characterised by inflammatory destruction of
tooth-supporting tissues, gradual destruction of the marginal periodontal ligament and resorption
of alveolar bone. Early-onset periodontitis is due to disturbed neutrophil extracellular trap (NET)
formation and clearance. Indeed, mutations that inactivate the cysteine proteases cathepsin C result
in the massive periodontal damage seen in patients with deficient NET formation. In contrast,
exaggerated NET formation due to polymorphonuclear neutrophil (PMN) hyper-responsiveness
drives the pathology of late-onset periodontitis by damaging and ulcerating the gingival epithelium
and retarding epithelial healing. Despite the gingival regeneration, periodontitis progression ends
with almost complete loss of the periodontal ligament and subsequent tooth loss. Thus, NETs help to
maintain periodontal health, and their dysregulation, either insufficiency or surplus, causes heavy
periodontal pathology and edentulism
