Periodontal therapy increases neutrophil extracellular trap degradation

Moonen, Carolyn G. J.; Buurma, Kirsten Gd; Faruque, Mouri R. J.; Balta, Maria G.; Liefferink, Erol; Bizzarro, Sergio; Nicu, Elena A.; Loos, Bruno G.

doi:10.1177/1753425919889392

Cited by 12 publications

(13 citation statements)

References 58 publications

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“…A key to this process is that the mechanism of NET removal is similar to that of apoptosis, whereby macrophages do not release pro-inflammatory cytokines [59]. Recently it has been reported that NET degradation is increased in treated periodontitis patients, what indicates that NET degradation contributes to a decreased pro-inflammatory state [60,61].…”

Section: Removal Of Netsmentioning

confidence: 99%

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Neutrophil Extracellular Traps in Periodontitis

Magán‐Fernández

Al-Bakri

O’Valle

et al. 2020

Cells

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Neutrophils are key cells of the immune system and have a decisive role in fighting foreign pathogens in infectious diseases. Neutrophil extracellular traps (NETs) consist of a mesh of DNA enclosing antimicrobial peptides and histones that are released into extracellular space following neutrophil response to a wide range of stimuli, such as pathogens, host-derived mediators and drugs. Neutrophils can remain functional after NET formation and are important for periodontal homeostasis. Periodontitis is an inflammatory multifactorial disease caused by a dysbiosis state between the gingival microbiome and the immune response of the host. The pathogenesis of periodontitis includes an immune-inflammatory component in which impaired NET formation and/or elimination can be involved, contributing to an exacerbated inflammatory reaction and to the destruction of gingival tissue. In this review, we summarize the current knowledge about the role of NETs in the pathogenesis of periodontitis.

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Section: Removal Of Netsmentioning

confidence: 99%

“…The formation of NETs could promote thrombosis via histones [61]. NETs in combination with platelets may damage the blood vessels during sepsis, destroying endothelial cells and causing vascular occlusions [76,89].…”

Section: Role Of Nets In Systemic Diseasesmentioning

confidence: 99%

Neutrophil Extracellular Traps in Periodontitis

Magán‐Fernández

Al-Bakri

O’Valle

et al. 2020

Cells

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“…Multivariate logistic regression analysis showed that the peripheral blood NET level was significantly positively associated with moderate to severe PD (Kaneko et al, 2018). Degradation of NETs in plasma is increased after periodontal therapy in PD patients (Moonen et al, 2020). Periodontal pathogens and excessive NETs produced during PD may participate in the progression of AS after entering the circulation.…”

Section: Neutrophil Extracellular Trapsmentioning

confidence: 99%

PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets

Zhu

Huang

Zhao

2022

Front. Cell Dev. Biol.

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Atherosclerosis is a chronic artery disease characterized by plaque formation and vascular inflammation, eventually leading to myocardial infarction and stroke. Innate immunity plays an irreplaceable role in the vascular inflammatory response triggered by chronic infection. Periodontitis is a common chronic disorder that involves oral microbe-related inflammatory bone loss and local destruction of the periodontal ligament and is a risk factor for atherosclerosis. Periodontal pathogens contain numerous pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide, CpG DNA, and Peptidoglycan, that initiate the inflammatory response of the innate immunity depending on the recognition of pattern-recognition receptors (PRRs) of host cells. The immune-inflammatory response and destruction of the periodontal tissue will produce a large number of damage-associated molecular patterns (DAMPs) such as neutrophil extracellular traps (NETs), high mobility group box 1 (HMGB1), alarmins (S100 protein), and which can further affect the progression of atherosclerosis. Molecular patterns have recently become the therapeutic targets for inflammatory disease, including blocking the interaction between molecular patterns and PRRs and controlling the related signal transduction pathway. This review summarized the research progress of some representative PAMPs and DAMPs as the molecular pathological mechanism bridging periodontitis and atherosclerosis. We also discussed possible ways to prevent serious cardiovascular events in patients with periodontitis and atherosclerosis by targeting molecular patterns.

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“…2016; Doke et al, 2017;Obama et al, 2019;Moonen et al, 2020). There are other DNA releasing activities, such as necrosis, which would confound the results.…”

Section: Measurement and Removal Of Netsmentioning

confidence: 99%

The Role of Neutrophil Extracellular Traps in Periodontitis

Wang

Zhou

Ren

et al. 2021

Front. Cell. Infect. Microbiol.

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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.

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Periodontal therapy increases neutrophil extracellular trap degradation

Cited by 12 publications

References 58 publications

Neutrophil Extracellular Traps in Periodontitis

Neutrophil Extracellular Traps in Periodontitis

PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets

The Role of Neutrophil Extracellular Traps in Periodontitis

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