Periodontal sources of citrullinated antigens and TLR agonists related to RA

Vitkov, Ljubomir; Hannig, Matthias; Minnich, Bernd; Herrmann, Martin

doi:10.1080/08916934.2018.1527907

Cited by 24 publications

(22 citation statements)

References 82 publications

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“…Additionally, the suggested generation of NETs in the periodontium leads to increased inflammation and can be considered another virulence strategy used by P. gingivalis. The presentation of intracellular self-antigens modified by gingipains may have immunological consequences, as the excessive presentation of cryptic antigens creates a developed part of systemic diseases associated with periodontitis [78]. Hirschfeld et al indicated that some bacteria (Propionibacterium acnes, Veillonella parvula and Streptococcus gordonii) led to an enhancement of NET-derived DNA production, via NADPH oxidase-independent mechanisms [71].…”

Section: Microbial Agents Alter Net Formationmentioning

confidence: 99%

“…In a recent study from the same authors, they hypothesize that there is a dissemination phenomenon of bacterial species, LPS and antigens citrullinated by NETs from the infected periodontal tissue. This dissemination could contribute to exacerbated autoimmune diseases such as RA via the activation of TLR receptors [78]. Therefore, both mechanisms of NET formation may be responsible for tissue destruction [88].…”

Section: Defective Neutrophils and Impaired Net Formation In Periodonmentioning

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: Microbial Agents Alter Net Formationmentioning

confidence: 99%

Section: Defective Neutrophils and Impaired Net Formation In Periodonmentioning

confidence: 99%

Neutrophil Extracellular Traps in Periodontitis

Magán‐Fernández

Al-Bakri

O’Valle

et al. 2020

Cells

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“…In spite of differences in the etiologies of RA (autoimmune) and PD (dysbiotic microbial biofilm), there are similar biological processes involved, such as citrullination and autoantibody response [7,8] and the pivotal role of bacterial dysbiosis, which may represent direct links between these two conditions [1,9,10,11]. Citrullination of peptides is mediated by peptidylarginine deiminase (PAD) and is considered a key event in RA [12,13].…”

Section: Introductionmentioning

confidence: 99%

Linkage of Periodontitis and Rheumatoid Arthritis: Current Evidence and Potential Biological Interactions

Molon

Rossa

Thurlings

et al. 2019

IJMS

136

109

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The association between rheumatoid arthritis (RA) and periodontal disease (PD) has been the focus of numerous investigations driven by their common pathological features. RA is an autoimmune disease characterized by chronic inflammation, the production of anti-citrullinated proteins antibodies (ACPA) leading to synovial joint inflammation and destruction. PD is a chronic inflammatory condition associated with a dysbiotic microbial biofilm affecting the supporting tissues around the teeth leading to the destruction of mineralized and non-mineralized connective tissues. Chronic inflammation associated with both RA and PD is similar in the predominant adaptive immune phenotype, in the imbalance between pro- and anti-inflammatory cytokines and in the role of smoking and genetic background as risk factors. Structural damage that occurs in consequence of chronic inflammation is the ultimate cause of loss of function and disability observed with the progression of RA and PD. Interestingly, the periodontal pathogen Porphyromonas gingivalis has been implicated in the generation of ACPA in RA patients, suggesting a direct biological intersection between PD and RA. However, more studies are warranted to confirm this link, elucidate potential mechanisms involved, and ascertain temporal associations between RA and PD. This review is mainly focused on recent clinical and translational research intends to discuss and provide an overview of the relationship between RA and PD, exploring the similarities in the immune-pathological aspects and the possible mechanisms linking the development and progression of both diseases. In addition, the current available treatments targeting both RA and PD were revised.

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“…Citrullination of proteins and systemic autoimmunity against these novel autoantigens occurs via enzymes like peptidylarginine deiminase 4 (PAD4), which can exemplarily be induced by cigarette smoke, partly explaining the elevated risk of smokers to develop RA. Vitkov et al [3] investigated PD, as it exhibits two sources of citrullination, PAD4 of periodontal neutrophils and neutrophil extracellular traps (NETs) as well as the PAD of Porphyromonas gingivalis (PPAD). They hypothesize that PD leads to an increased responsiveness to autoantigens via TLR4 activation participating in the development and propagation of RA.…”

Section: Nets As Source Of Autoantigens In Autoimmune Diseasesmentioning

confidence: 99%

“…In this article, they contrast NET formation with other types of cell death pathways that may affect autoimmunity (Figure 1). [3] linked PD to NET formation and ACPA generation. Applegren et al [4] found NETs on mitral valves in a patient with severe SLE.…”

Section: Net Involvement In Disease Onset Progression and Severitymentioning

confidence: 99%