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Published on: November 1, 2019
The Role of Neutrophil Extracellular Traps in Periodontitis
Jingyi Wang1, Yucong Zhou1, Biao Ren1
1State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, National Clinical Research Center for Oral Diseases, Sichuan University, Chengdu, China.
Abstract:
Periodontitis is a chronic, destructive disease of periodontal tissues caused by multifaceted, dynamic interactions. Periodontal bacteria and host immunity jointly contribute to the pathological processes of the disease. The dysbiotic microbial communities elicit an excessive immune response, mainly by polymorphonuclear neutrophils (PMNs). As one of the main mechanisms of PMN immune response in the oral cavity, neutrophil extracellular traps (NETs) play a crucial role in the initiation and progression of late-onset periodontitis. NETs are generated and released by neutrophils stimulated by various irritants, such as pathogens, host-derived mediators, and drugs. Chromatin and proteins are the main components of NETs. Depending on the characteristics of the processes, three main pathways of NET formation have been described. NETs can trap and kill pathogens by increased expression of antibacterial components and identifying and trapping bacteria to restrict their spread. Moreover, NETs can promote and reduce inflammation, inflicting injuries on the tissues during the pro-inflammation process. During their long-term encounter with NETs, periodontal bacteria have developed various mechanisms, including breaking down DNA of NETs, degrading antibacterial proteins, and impacting NET levels in the pocket environment to resist the antibacterial function of NETs. In addition, periodontal pathogens can secrete pro-inflammatory factors to perpetuate the inflammatory environment and a friendly growth environment, which are responsible for the progressive tissue damage. By learning the strategies of pathogens, regulating the periodontal concentration of NETs becomes possible. Some practical ways to treat late-onset periodontitis are reducing the concentration of NETs, administering anti-inflammatory therapy, and prescribing broad-spectrum and specific antibacterial agents. This review mainly focuses on the mechanism of NETs, pathogenesis of periodontitis, and potential therapeutic approaches based on interactions between NETs and periodontal pathogens.
Insights
Neutrophil extracellular traps (NETs) are key in periodontitis. Periodontal pathogens resist NETs, causing tissue damage, but targeting NETs may offer new treatments for this chronic gum disease.
Area of Science:
- Oral microbiology
- Immunology
- Periodontology
Background:
- Periodontitis is a chronic inflammatory disease damaging periodontal tissues.
- Dysbiotic oral microbial communities trigger excessive host immune responses, particularly involving polymorphonuclear neutrophils (PMNs).
- Neutrophil extracellular traps (NETs), a key PMN mechanism, are implicated in the initiation and progression of periodontitis.
Purpose of the Study:
- To review the mechanism of NET formation and function in periodontitis.
- To explore how periodontal pathogens interact with and resist NETs.
- To discuss potential therapeutic strategies targeting NETs for periodontitis treatment.
Main Methods:
- Review of existing literature on NETs, periodontitis pathogenesis, and host-pathogen interactions.
- Analysis of the role of NETs in both host defense and tissue damage.
- Examination of bacterial resistance mechanisms against NETs.
Main Results:
- NETs play a dual role, trapping pathogens but also contributing to inflammation and tissue injury.
- Periodontal pathogens have evolved strategies to degrade NETs and promote inflammation.
- These interactions create a pro-inflammatory environment conducive to progressive tissue damage.
Conclusions:
- Understanding the interplay between NETs and periodontal pathogens is crucial.
- Therapeutic approaches could involve modulating NET levels, anti-inflammatory treatments, and targeted antimicrobials.
- Regulating NET concentration presents a potential strategy for managing late-onset periodontitis.
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