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Periodontal microorganisms and Alzheimer disease – A causative relationship?

In the initiation or exacerbation of Alzheimer disease, the dissemination of oral microorganisms into the brain tissue or the low‐level systemic inflammation have been speculated to play a role. However, the impact of oral microorganisms, such as Porphyromonas gingivalis, on the pathogenesis of Alzh...

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Autores principales: Jungbauer, Gert, Stähli, Alexandra, Zhu, Xilei, Auber Alberi, Lavinia, Sculean, Anton, Eick, Sigrun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9314828/
https://www.ncbi.nlm.nih.gov/pubmed/35244967
http://dx.doi.org/10.1111/prd.12429
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author Jungbauer, Gert
Stähli, Alexandra
Zhu, Xilei
Auber Alberi, Lavinia
Sculean, Anton
Eick, Sigrun
author_facet Jungbauer, Gert
Stähli, Alexandra
Zhu, Xilei
Auber Alberi, Lavinia
Sculean, Anton
Eick, Sigrun
author_sort Jungbauer, Gert
collection PubMed
description In the initiation or exacerbation of Alzheimer disease, the dissemination of oral microorganisms into the brain tissue or the low‐level systemic inflammation have been speculated to play a role. However, the impact of oral microorganisms, such as Porphyromonas gingivalis, on the pathogenesis of Alzheimer disease and the potential causative relationship is still unclear. The present review has critically reviewed the literature by examining the following aspects: (a) the oral microbiome and the immune response in the elderly population, (b) human studies on the association between periodontal and gut microorganisms and Alzheimer disease, (c) animal and in vitro studies on microorganisms and Alzheimer disease, and (d) preventive and therapeutic approaches. Factors contributing to microbial dysbiosis seem to be aging, local inflammation, systemic diseases, wearing of dentures, living in nursing homes and no access to adequate oral hygiene measures. Porphyromonas gingivalis was detectable in post‐mortem brain samples. Microbiome analyses of saliva samples or oral biofilms showed a decreased microbial diversity and a different composition in Alzheimer disease compared to cognitively healthy subjects. Many in‐vitro and animal studies underline the potential of P gingivalis to induce Alzheimer disease‐related alterations. In animal models, recurring applications of P gingivalis or its components increased pro‐inflammatory mediators and β‐amyloid in the brain and deteriorated the animals' cognitive performance. Since periodontitis is the result of a disturbed microbial homoeostasis, an effect of periodontal therapy on the oral microbiome and host response related to cognitive parameters may be suggested and should be elucidated in further clinical trials.
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spelling pubmed-93148282022-07-30 Periodontal microorganisms and Alzheimer disease – A causative relationship? Jungbauer, Gert Stähli, Alexandra Zhu, Xilei Auber Alberi, Lavinia Sculean, Anton Eick, Sigrun Periodontol 2000 Review Articles In the initiation or exacerbation of Alzheimer disease, the dissemination of oral microorganisms into the brain tissue or the low‐level systemic inflammation have been speculated to play a role. However, the impact of oral microorganisms, such as Porphyromonas gingivalis, on the pathogenesis of Alzheimer disease and the potential causative relationship is still unclear. The present review has critically reviewed the literature by examining the following aspects: (a) the oral microbiome and the immune response in the elderly population, (b) human studies on the association between periodontal and gut microorganisms and Alzheimer disease, (c) animal and in vitro studies on microorganisms and Alzheimer disease, and (d) preventive and therapeutic approaches. Factors contributing to microbial dysbiosis seem to be aging, local inflammation, systemic diseases, wearing of dentures, living in nursing homes and no access to adequate oral hygiene measures. Porphyromonas gingivalis was detectable in post‐mortem brain samples. Microbiome analyses of saliva samples or oral biofilms showed a decreased microbial diversity and a different composition in Alzheimer disease compared to cognitively healthy subjects. Many in‐vitro and animal studies underline the potential of P gingivalis to induce Alzheimer disease‐related alterations. In animal models, recurring applications of P gingivalis or its components increased pro‐inflammatory mediators and β‐amyloid in the brain and deteriorated the animals' cognitive performance. Since periodontitis is the result of a disturbed microbial homoeostasis, an effect of periodontal therapy on the oral microbiome and host response related to cognitive parameters may be suggested and should be elucidated in further clinical trials. John Wiley and Sons Inc. 2022-03-04 2022-06 /pmc/articles/PMC9314828/ /pubmed/35244967 http://dx.doi.org/10.1111/prd.12429 Text en © 2022 The Authors. Periodontology 2000 published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Articles
Jungbauer, Gert
Stähli, Alexandra
Zhu, Xilei
Auber Alberi, Lavinia
Sculean, Anton
Eick, Sigrun
Periodontal microorganisms and Alzheimer disease – A causative relationship?
title Periodontal microorganisms and Alzheimer disease – A causative relationship?
title_full Periodontal microorganisms and Alzheimer disease – A causative relationship?
title_fullStr Periodontal microorganisms and Alzheimer disease – A causative relationship?
title_full_unstemmed Periodontal microorganisms and Alzheimer disease – A causative relationship?
title_short Periodontal microorganisms and Alzheimer disease – A causative relationship?
title_sort periodontal microorganisms and alzheimer disease – a causative relationship?
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9314828/
https://www.ncbi.nlm.nih.gov/pubmed/35244967
http://dx.doi.org/10.1111/prd.12429
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