Research Topic

PMN and Biofilm Interactions in Late-Onset (Earlier Denoted Chronic) Periodontitis

About this Research Topic

Chronic periodontitis (CPD) has been characterized by dysregulated inflammation, triggered by polymicrobial dysbiotic communities (biofilms) that form on subgingival tooth sides. However, CPD cannot be regarded as a canonical bacterial infection as it is not caused by any specific exogenous pathogen(s). Both ...

Chronic periodontitis (CPD) has been characterized by dysregulated inflammation, triggered by polymicrobial dysbiotic communities (biofilms) that form on subgingival tooth sides. However, CPD cannot be regarded as a canonical bacterial infection as it is not caused by any specific exogenous pathogen(s). Both excess of pathogen-associated molecular patterns (PAMPs) (e.g. due to dental biofilm accumulation) and polymorphonuclear neutrophils (PMN) hyperactivity may cause an exaggerated immune response in CPD.

The PMN hyperactivity demonstrated in CPD is related to the altered PMN transcriptional activity in CPD, and in particular the up-regulation of Toll-like receptor (TLR) signalling pathways. The tissue destruction in CPD is mainly mediated by the exaggerated inflammatory response of the host to the bacterial challenge. This response is characterized by an excessive PMN efflux into the periodontal crevice and neutrophil extracellular trap (NET) formation. The host then becomes unable to control the dental biofilm formation, and its exaggerated response is deleterious to the host tissues.

The PMNs are the first line of host immunity and are the most abundant inflammatory cells directly interacting with the dental biofilm, its toxins, and metabolic products. For this reason, PMNs/bacteria interactions are of particular interest in improving our understanding of the pathology of periodontitis and introducing novel treatment approaches. Consequently, the following questions arise: (i) which dental plaque components (solved and dispersed ones) trigger NET formation and to what extent? (ii) what are the signalling pathways responsible for NET formation? (iii) is there a relationship between bone resorption and the quantities of lipopolysaccharide (LPS) and prokaryotic RNA in whole blood of animal models? (iv) does the modulation of NET response affect bone resorption?

In this Research Topic, we therefore seek Reviews, Perspectives, and Original Research articles on cutting-edge research that explores these questions and helps expand our knowledge on solved and dispersed PAMPs of dental plaque, and the PMN signalling pathways responsible for dental plaque PAMPs.

The sub-topics of interest include, but are not limited to:

• Growing PMN culture from orally healthy subjects and CPD patients; quantification of NET response to certain dental plaque PAMPs.
• Exploration of PMN signalling pathways responsible for the NET response to certain PAMPs of dental plaque.
• In vivo (mouse model) modulation of NET response by inhibition of PMN hyperactivity in order to explore novel treatment approaches for CPD.


Keywords: NETs, PAMPs, PMN Responsiveness, Inhibitors of PMN Responsiveness, Bone Resorption, Periodontitis


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Submission Deadlines

10 December 2020 Manuscript
15 April 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

10 December 2020 Manuscript
15 April 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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