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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Frontiers Media S.A.
2021
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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) |
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dysbiosis dysregulated immunity NET formation caspase 4 caspase 11 bacterial membrane vesicles Immunologic diseases. Allergy RC581-607 |
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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 |
work_keys_str_mv |
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1718406303881101312 |