Neutrophils Orchestrate the Periodontal Pocket

The subgingival biofilm attached to tooth surfaces triggers and maintains periodontitis. Previously, late-onset periodontitis has been considered a consequence of dysbiosis and a resultant polymicrobial disruption of host homeostasis. However, a multitude of studies did not show “healthy” oral micro...

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Autores principales: Ljubomir Vitkov, Luis E. Muñoz, Janina Schoen, Jasmin Knopf, Christine Schauer, Bernd Minnich, Martin Herrmann, Matthias Hannig
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/09f6f2d40de245ad84d0c676a891723a
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spelling oai:doaj.org-article:09f6f2d40de245ad84d0c676a891723a2021-11-30T19:11:00ZNeutrophils Orchestrate the Periodontal Pocket1664-322410.3389/fimmu.2021.788766https://doaj.org/article/09f6f2d40de245ad84d0c676a891723a2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.788766/fullhttps://doaj.org/toc/1664-3224The subgingival biofilm attached to tooth surfaces triggers and maintains periodontitis. Previously, late-onset periodontitis has been considered a consequence of dysbiosis and a resultant polymicrobial disruption of host homeostasis. However, a multitude of studies did not show “healthy” oral microbiota pattern, but a high diversity depending on culture, diets, regional differences, age, social state etc. These findings relativise the aetiological role of the dysbiosis in periodontitis. Furthermore, many late-onset periodontitis traits cannot be explained by dysbiosis; e.g. age-relatedness, attenuation by anti-ageing therapy, neutrophil hyper-responsiveness, and microbiota shifting by dysregulated immunity, yet point to the crucial role of dysregulated immunity and neutrophils in particular. Furthermore, patients with neutropenia and neutrophil defects inevitably develop early-onset periodontitis. Intra-gingivally injecting lipopolysaccharide (LPS) alone causes an exaggerated neutrophil response sufficient to precipitate experimental periodontitis. Vice versa to the surplus of LPS, the increased neutrophil responsiveness characteristic for late-onset periodontitis can effectuate gingiva damage likewise. The exaggerated neutrophil extracellular trap (NET) response in late-onset periodontitis is blameable for damage of gingival barrier, its penetration by bacteria and pathogen-associated molecular patterns (PAMPs) as well as stimulation of Th17 cells, resulting in further neutrophil activation. This identifies the dysregulated immunity as the main contributor to periodontal disease.Ljubomir VitkovLjubomir VitkovLuis E. MuñozLuis E. MuñozJanina SchoenJanina SchoenJasmin KnopfJasmin KnopfChristine SchauerChristine SchauerBernd MinnichMartin HerrmannMartin HerrmannMatthias HannigFrontiers Media S.A.articledysbiosisdysregulated immunityNET formationcaspase 4caspase 11bacterial membrane vesiclesImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic dysbiosis
dysregulated immunity
NET formation
caspase 4
caspase 11
bacterial membrane vesicles
Immunologic diseases. Allergy
RC581-607
spellingShingle dysbiosis
dysregulated immunity
NET formation
caspase 4
caspase 11
bacterial membrane vesicles
Immunologic diseases. Allergy
RC581-607
Ljubomir Vitkov
Ljubomir Vitkov
Luis E. Muñoz
Luis E. Muñoz
Janina Schoen
Janina Schoen
Jasmin Knopf
Jasmin Knopf
Christine Schauer
Christine Schauer
Bernd Minnich
Martin Herrmann
Martin Herrmann
Matthias Hannig
Neutrophils Orchestrate the Periodontal Pocket
description The subgingival biofilm attached to tooth surfaces triggers and maintains periodontitis. Previously, late-onset periodontitis has been considered a consequence of dysbiosis and a resultant polymicrobial disruption of host homeostasis. However, a multitude of studies did not show “healthy” oral microbiota pattern, but a high diversity depending on culture, diets, regional differences, age, social state etc. These findings relativise the aetiological role of the dysbiosis in periodontitis. Furthermore, many late-onset periodontitis traits cannot be explained by dysbiosis; e.g. age-relatedness, attenuation by anti-ageing therapy, neutrophil hyper-responsiveness, and microbiota shifting by dysregulated immunity, yet point to the crucial role of dysregulated immunity and neutrophils in particular. Furthermore, patients with neutropenia and neutrophil defects inevitably develop early-onset periodontitis. Intra-gingivally injecting lipopolysaccharide (LPS) alone causes an exaggerated neutrophil response sufficient to precipitate experimental periodontitis. Vice versa to the surplus of LPS, the increased neutrophil responsiveness characteristic for late-onset periodontitis can effectuate gingiva damage likewise. The exaggerated neutrophil extracellular trap (NET) response in late-onset periodontitis is blameable for damage of gingival barrier, its penetration by bacteria and pathogen-associated molecular patterns (PAMPs) as well as stimulation of Th17 cells, resulting in further neutrophil activation. This identifies the dysregulated immunity as the main contributor to periodontal disease.
format article
author Ljubomir Vitkov
Ljubomir Vitkov
Luis E. Muñoz
Luis E. Muñoz
Janina Schoen
Janina Schoen
Jasmin Knopf
Jasmin Knopf
Christine Schauer
Christine Schauer
Bernd Minnich
Martin Herrmann
Martin Herrmann
Matthias Hannig
author_facet Ljubomir Vitkov
Ljubomir Vitkov
Luis E. Muñoz
Luis E. Muñoz
Janina Schoen
Janina Schoen
Jasmin Knopf
Jasmin Knopf
Christine Schauer
Christine Schauer
Bernd Minnich
Martin Herrmann
Martin Herrmann
Matthias Hannig
author_sort Ljubomir Vitkov
title Neutrophils Orchestrate the Periodontal Pocket
title_short Neutrophils Orchestrate the Periodontal Pocket
title_full Neutrophils Orchestrate the Periodontal Pocket
title_fullStr Neutrophils Orchestrate the Periodontal Pocket
title_full_unstemmed Neutrophils Orchestrate the Periodontal Pocket
title_sort neutrophils orchestrate the periodontal pocket
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/09f6f2d40de245ad84d0c676a891723a
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