Peripheral blood neutrophil extracellular trap production and degradation in chronic periodontitis. (27th October 2016)

• Record Type: Journal Article
• Authors: White, Phillipa; Sakellari, Dimitra; Roberts, Helen; Risafi, Idyli; Ling, Martin; Cooper, Paul; Milward, Mike; Chapple, Iain
• Is Part Of: Journal of clinical periodontology. Volume 43:Number 12(2016:Dec.)
• Page Start: 1041
• Page End: 1049
• Publication Date: 2016-10-27
• Subjects: chronic periodontitis -- NET degradation -- neutrophil extracellular traps -- neutrophils; Periodontics -- Periodicals; 617.6
• DOI: 10.1111/jcpe.12628
• Languages: English
• ISSNs: 0303-6979

Abstract

Abstract: Aims: To investigate ex vivo peripheral neutrophil extracellular trap (NET) production and their subsequent degradation by plasma in chronic periodontitis patients, and periodontally and systemically healthy‐matched controls. Materials and Methods: Chronic periodontitis patient and control ( n = 40 pairs) peripheral blood neutrophils (PBN) were stimulated for NET quantification. A subset of patients received non‐surgical periodontal therapy ( n = 19) and NETs were quantified 3 months later alongside controls. Blood plasma was collected from patients and controls to quantify plasma‐induced NET degradation ( n = 19 pairs). Subsequent experiments quantified plasma concentrations of DNase‐1, immunoglobulin G (IgG), free light chains (FLCs), and cystatin C. Results: No differences were observed in NET production between patients and controls. However, NET production decreased significantly in patients post‐treatment. Plasma NET degradation was significantly lower in patients than controls, which may be due to significantly reduced DNase‐1 levels as demonstrated, or potentially due to elevated IgG/FLC concentrations in patients. NET degradation post‐periodontal treatment was comparable between patients and controls. Conclusions: NET production was comparable between patients and controls; however, non‐surgical therapy causes attenuated NETs. NET degradation by plasma is impaired in untreated chronic periodontitis, potentially increasing the chronic NET burden, which may enhance antimicrobial function, or conversely, increase the risk of autoimmune/inflammatory responses.