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Integrated hypothesis of dental caries and periodontal diseases

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Integrated hypothesis of dental caries and periodontal diseases. / Nyvad, Bente; Takahashi, Nobuhiro.

In: Journal of Oral Microbiology, Vol. 12, No. 1, 1710953, 2020.

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Nyvad, B & Takahashi, N 2020, 'Integrated hypothesis of dental caries and periodontal diseases', Journal of Oral Microbiology, vol. 12, no. 1, 1710953. https://doi.org/10.1080/20002297.2019.1710953

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Nyvad, Bente ; Takahashi, Nobuhiro. / Integrated hypothesis of dental caries and periodontal diseases. In: Journal of Oral Microbiology. 2020 ; Vol. 12, No. 1.

Bibtex

@article{39b960564b4243f1ad9ba59e29056ff7,
title = "Integrated hypothesis of dental caries and periodontal diseases",
abstract = "This review considers an integrated hypothesis of dental caries and periodontal diseases that builds on theoretical ecological principles. The backbone of the hypothesis is based on the dynamic stability stage of the oral microbiota, at which intrinsic (mainly saliva and gingival crevicular fluid) and bacterial (mainly metabolic) resilience factors maintain ecological dynamic stability, compatible with clinical health. However, loss of intrinsic resilience factors and/or prolonged changes in the availability of microbial metabolic substrates may shift the ecological balance of the microbiota into either saccharolytic (acidogenic) or amino acid-degrading/proteolytic (alkalinogenic) stages, depending on the nature of the predominant substrates, leading to clinical diseases. Therefore, to maintain and restore the dynamic stability of the oral microbiota, it is necessary to control the drivers of disease, such as salivary flow and influx of bacterial nutrients into the oral cavity. Contrary to conventional wisdom, excessive intake of fermentable carbohydrates may contribute to inflammation in periodontal tissues resulting from hyperglycaemia. An integrated hypothesis emphasizes that both dental caries and periodontal diseases originate in the dynamic stability stage and emerge in response to nutritional imbalances in the microbiota. Periodontal diseases may belong to the sugar driven inflammatory diseases, similar to diabetes, obesity, and cardiovascular diseases.",
keywords = "Dental caries, carbohydrates, dynamic stability stage, ecological hypothesis, ecosystem, gingival crevicular fluid, microbiota, periodontal diseases, resilience factor",
author = "Bente Nyvad and Nobuhiro Takahashi",
year = "2020",
doi = "10.1080/20002297.2019.1710953",
language = "English",
volume = "12",
journal = "Journal of Oral Microbiology",
issn = "2000-2297",
publisher = "Taylor & Francis ",
number = "1",

}

RIS

TY - JOUR

T1 - Integrated hypothesis of dental caries and periodontal diseases

AU - Nyvad, Bente

AU - Takahashi, Nobuhiro

PY - 2020

Y1 - 2020

N2 - This review considers an integrated hypothesis of dental caries and periodontal diseases that builds on theoretical ecological principles. The backbone of the hypothesis is based on the dynamic stability stage of the oral microbiota, at which intrinsic (mainly saliva and gingival crevicular fluid) and bacterial (mainly metabolic) resilience factors maintain ecological dynamic stability, compatible with clinical health. However, loss of intrinsic resilience factors and/or prolonged changes in the availability of microbial metabolic substrates may shift the ecological balance of the microbiota into either saccharolytic (acidogenic) or amino acid-degrading/proteolytic (alkalinogenic) stages, depending on the nature of the predominant substrates, leading to clinical diseases. Therefore, to maintain and restore the dynamic stability of the oral microbiota, it is necessary to control the drivers of disease, such as salivary flow and influx of bacterial nutrients into the oral cavity. Contrary to conventional wisdom, excessive intake of fermentable carbohydrates may contribute to inflammation in periodontal tissues resulting from hyperglycaemia. An integrated hypothesis emphasizes that both dental caries and periodontal diseases originate in the dynamic stability stage and emerge in response to nutritional imbalances in the microbiota. Periodontal diseases may belong to the sugar driven inflammatory diseases, similar to diabetes, obesity, and cardiovascular diseases.

AB - This review considers an integrated hypothesis of dental caries and periodontal diseases that builds on theoretical ecological principles. The backbone of the hypothesis is based on the dynamic stability stage of the oral microbiota, at which intrinsic (mainly saliva and gingival crevicular fluid) and bacterial (mainly metabolic) resilience factors maintain ecological dynamic stability, compatible with clinical health. However, loss of intrinsic resilience factors and/or prolonged changes in the availability of microbial metabolic substrates may shift the ecological balance of the microbiota into either saccharolytic (acidogenic) or amino acid-degrading/proteolytic (alkalinogenic) stages, depending on the nature of the predominant substrates, leading to clinical diseases. Therefore, to maintain and restore the dynamic stability of the oral microbiota, it is necessary to control the drivers of disease, such as salivary flow and influx of bacterial nutrients into the oral cavity. Contrary to conventional wisdom, excessive intake of fermentable carbohydrates may contribute to inflammation in periodontal tissues resulting from hyperglycaemia. An integrated hypothesis emphasizes that both dental caries and periodontal diseases originate in the dynamic stability stage and emerge in response to nutritional imbalances in the microbiota. Periodontal diseases may belong to the sugar driven inflammatory diseases, similar to diabetes, obesity, and cardiovascular diseases.

KW - Dental caries

KW - carbohydrates

KW - dynamic stability stage

KW - ecological hypothesis

KW - ecosystem

KW - gingival crevicular fluid

KW - microbiota

KW - periodontal diseases

KW - resilience factor

UR - http://www.scopus.com/inward/record.url?scp=85077624215&partnerID=8YFLogxK

U2 - 10.1080/20002297.2019.1710953

DO - 10.1080/20002297.2019.1710953

M3 - Review

C2 - 32002131

VL - 12

JO - Journal of Oral Microbiology

JF - Journal of Oral Microbiology

SN - 2000-2297

IS - 1

M1 - 1710953

ER -