Myocardial infarction risk is increased by periodontal pathobionts: a cross-sectional study

C Joshi; A Mezincescu; M Gunasekara; A Rudd; H Botchorichvili; S Sabir; C Dospinescu; A Noman; D Hogg; G Cherukara; D McLernon; K Hijazi; D Dawson

doi:10.1038/s41598-022-19154-z

Myocardial infarction risk is increased by periodontal pathobionts: a cross-sectional study

C Joshi, A Mezincescu, M Gunasekara, A Rudd, H Botchorichvili, S Sabir, C Dospinescu, A Noman, D Hogg, G Cherukara, D McLernon, K Hijazi^* (Corresponding Author), D Dawson^* (Corresponding Author)

^*Corresponding author for this work

University of Aberdeen

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

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Abstract

To establish the role of periodontal pathobionts as a risk factor for myocardial infarction, we examined the contribution of five periodontal pathobionts and their virulence genes’ expressions to myocardial injury (Troponin-I) and coronary artery disease burden (SYNTAX-I scores) using hierarchical linear regression. Pathobiont loads in subgingival-plaques and intra-coronary-thrombi were compared. Troponin-I release increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 6.8×10-6, 95% CI = 1.1×10-7-2.1×10-5), one-fold increased expressions of fimA (β = 14.3, 95% CI = 1.5-27.1), bioF-3 (β = 7.8, 95% CI = 1.1-12.3), prtH (β = 1107.8, 95% CI = 235.6-2451.3), prtP (β = 6772.8, 95% CI = 2418.7-11126.9), ltxA (β = 1811.8, 95% CI = 217.1-3840.8), cdtB (β = 568.3, 95% CI = 113.4-1250.1), all p < 0.05. SYNTAX-I score increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 3.8×10-9, 95% CI = 3.6×10-10-1.8×10-8), one-fold increased expressions of fimA (β = 1.2, 95% CI = 1.1-2.1), bioF-3 (β = 1.1, 95% CI = 1-5.2), prtP (β = 3, 95% CI = 1.3-4.6), ltxA (β = 1.5, 95% CI = 1.2-2.5), all p < 0.05. Within-subject Porphyromonas gingivalis and Tannerella forsythia from intra-coronary-thrombi and subgingival-plaques correlated (rho = 0.6, p < 0.05). Higher pathobiont load and/or upregulated virulence are risk factors for myocardial infarction.
Trial registration: ClinicalTrials.gov Identifier: NCT04719026

Original language	English
Article number	18608
Number of pages	11
Journal	Scientific Reports
Volume	12
Early online date	3 Nov 2022
DOIs	https://doi.org/10.1038/s41598-022-19154-z
Publication status	Published - Dec 2022

Bibliographical note

Acknowledgements The authors thank the laboratory and administrative staff at the Institute of Dentistry and the Institute of Medical Sciences of the University of Aberdeen for their help. We are grateful to Dr Pirkko Pussinen (Institute of Dentistry, University of Turku, Finland) for sharing the P. gingivalis-antibody positive serum samples and a detailed ELISA protocol. We would like to thank all Consultant Cardiologists at Aberdeen Royal Infirmary for identifying suitable patients during the acute on-call: Dr Andrew Hannah, Dr Andrew Stewart, Dr Adelle Dawson, Dr Deepak Garg, Dr Paul Broadhurst, Dr Nicola Ryan. Lastly, we are grateful to all the participating patients.

Funding: “Periodontal health in patients acutely admitted for myocardial infarction study” was funded by the Elphinstone Award to Dr Hijazi. Dr Dawson is supported by the British Heart Foundation (FS/RTF/20/30009, NH/19/1/34595, PG/18/35/33786, CS/17/4/32960, PG/15/88/31780, PG/17/64/33205), Chest Heart and Stroke Scotland (19/53), Tenovus Scotland (G.18.01), Friends of Anchor and Grampian NHS-Endowments.

Data Availability Statement

The corresponding author has full access to all the datasets used for analysis and it will be shared at a reasonable request.

Keywords

Humans
Cross-Sectional Studies
RNA, Ribosomal, 16S/genetics
Troponin I
Porphyromonas gingivalis
Myocardial Infarction/epidemiology
DNA

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Cite this

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title = "Myocardial infarction risk is increased by periodontal pathobionts: a cross-sectional study",

abstract = "To establish the role of periodontal pathobionts as a risk factor for myocardial infarction, we examined the contribution of five periodontal pathobionts and their virulence genes{\textquoteright} expressions to myocardial injury (Troponin-I) and coronary artery disease burden (SYNTAX-I scores) using hierarchical linear regression. Pathobiont loads in subgingival-plaques and intra-coronary-thrombi were compared. Troponin-I release increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 6.8×10-6, 95% CI = 1.1×10-7-2.1×10-5), one-fold increased expressions of fimA (β = 14.3, 95% CI = 1.5-27.1), bioF-3 (β = 7.8, 95% CI = 1.1-12.3), prtH (β = 1107.8, 95% CI = 235.6-2451.3), prtP (β = 6772.8, 95% CI = 2418.7-11126.9), ltxA (β = 1811.8, 95% CI = 217.1-3840.8), cdtB (β = 568.3, 95% CI = 113.4-1250.1), all p < 0.05. SYNTAX-I score increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 3.8×10-9, 95% CI = 3.6×10-10-1.8×10-8), one-fold increased expressions of fimA (β = 1.2, 95% CI = 1.1-2.1), bioF-3 (β = 1.1, 95% CI = 1-5.2), prtP (β = 3, 95% CI = 1.3-4.6), ltxA (β = 1.5, 95% CI = 1.2-2.5), all p < 0.05. Within-subject Porphyromonas gingivalis and Tannerella forsythia from intra-coronary-thrombi and subgingival-plaques correlated (rho = 0.6, p < 0.05). Higher pathobiont load and/or upregulated virulence are risk factors for myocardial infarction.Trial registration: ClinicalTrials.gov Identifier: NCT04719026",

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author = "C Joshi and A Mezincescu and M Gunasekara and A Rudd and H Botchorichvili and S Sabir and C Dospinescu and A Noman and D Hogg and G Cherukara and D McLernon and K Hijazi and D Dawson",

note = "Acknowledgements The authors thank the laboratory and administrative staff at the Institute of Dentistry and the Institute of Medical Sciences of the University of Aberdeen for their help. We are grateful to Dr Pirkko Pussinen (Institute of Dentistry, University of Turku, Finland) for sharing the P. gingivalis-antibody positive serum samples and a detailed ELISA protocol. We would like to thank all Consultant Cardiologists at Aberdeen Royal Infirmary for identifying suitable patients during the acute on-call: Dr Andrew Hannah, Dr Andrew Stewart, Dr Adelle Dawson, Dr Deepak Garg, Dr Paul Broadhurst, Dr Nicola Ryan. Lastly, we are grateful to all the participating patients. Funding: “Periodontal health in patients acutely admitted for myocardial infarction study” was funded by the Elphinstone Award to Dr Hijazi. Dr Dawson is supported by the British Heart Foundation (FS/RTF/20/30009, NH/19/1/34595, PG/18/35/33786, CS/17/4/32960, PG/15/88/31780, PG/17/64/33205), Chest Heart and Stroke Scotland (19/53), Tenovus Scotland (G.18.01), Friends of Anchor and Grampian NHS-Endowments.",

year = "2022",

month = dec,

doi = "10.1038/s41598-022-19154-z",

language = "English",

volume = "12",

journal = "Scientific Reports",

issn = "2045-2322",

publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Myocardial infarction risk is increased by periodontal pathobionts

T2 - a cross-sectional study

AU - Joshi, C

AU - Mezincescu, A

AU - Gunasekara, M

AU - Rudd, A

AU - Botchorichvili, H

AU - Sabir, S

AU - Dospinescu, C

AU - Noman, A

AU - Hogg, D

AU - Cherukara, G

AU - McLernon, D

AU - Hijazi, K

AU - Dawson, D

N1 - Acknowledgements The authors thank the laboratory and administrative staff at the Institute of Dentistry and the Institute of Medical Sciences of the University of Aberdeen for their help. We are grateful to Dr Pirkko Pussinen (Institute of Dentistry, University of Turku, Finland) for sharing the P. gingivalis-antibody positive serum samples and a detailed ELISA protocol. We would like to thank all Consultant Cardiologists at Aberdeen Royal Infirmary for identifying suitable patients during the acute on-call: Dr Andrew Hannah, Dr Andrew Stewart, Dr Adelle Dawson, Dr Deepak Garg, Dr Paul Broadhurst, Dr Nicola Ryan. Lastly, we are grateful to all the participating patients. Funding: “Periodontal health in patients acutely admitted for myocardial infarction study” was funded by the Elphinstone Award to Dr Hijazi. Dr Dawson is supported by the British Heart Foundation (FS/RTF/20/30009, NH/19/1/34595, PG/18/35/33786, CS/17/4/32960, PG/15/88/31780, PG/17/64/33205), Chest Heart and Stroke Scotland (19/53), Tenovus Scotland (G.18.01), Friends of Anchor and Grampian NHS-Endowments.

PY - 2022/12

Y1 - 2022/12

N2 - To establish the role of periodontal pathobionts as a risk factor for myocardial infarction, we examined the contribution of five periodontal pathobionts and their virulence genes’ expressions to myocardial injury (Troponin-I) and coronary artery disease burden (SYNTAX-I scores) using hierarchical linear regression. Pathobiont loads in subgingival-plaques and intra-coronary-thrombi were compared. Troponin-I release increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 6.8×10-6, 95% CI = 1.1×10-7-2.1×10-5), one-fold increased expressions of fimA (β = 14.3, 95% CI = 1.5-27.1), bioF-3 (β = 7.8, 95% CI = 1.1-12.3), prtH (β = 1107.8, 95% CI = 235.6-2451.3), prtP (β = 6772.8, 95% CI = 2418.7-11126.9), ltxA (β = 1811.8, 95% CI = 217.1-3840.8), cdtB (β = 568.3, 95% CI = 113.4-1250.1), all p < 0.05. SYNTAX-I score increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 3.8×10-9, 95% CI = 3.6×10-10-1.8×10-8), one-fold increased expressions of fimA (β = 1.2, 95% CI = 1.1-2.1), bioF-3 (β = 1.1, 95% CI = 1-5.2), prtP (β = 3, 95% CI = 1.3-4.6), ltxA (β = 1.5, 95% CI = 1.2-2.5), all p < 0.05. Within-subject Porphyromonas gingivalis and Tannerella forsythia from intra-coronary-thrombi and subgingival-plaques correlated (rho = 0.6, p < 0.05). Higher pathobiont load and/or upregulated virulence are risk factors for myocardial infarction.Trial registration: ClinicalTrials.gov Identifier: NCT04719026

AB - To establish the role of periodontal pathobionts as a risk factor for myocardial infarction, we examined the contribution of five periodontal pathobionts and their virulence genes’ expressions to myocardial injury (Troponin-I) and coronary artery disease burden (SYNTAX-I scores) using hierarchical linear regression. Pathobiont loads in subgingival-plaques and intra-coronary-thrombi were compared. Troponin-I release increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 6.8×10-6, 95% CI = 1.1×10-7-2.1×10-5), one-fold increased expressions of fimA (β = 14.3, 95% CI = 1.5-27.1), bioF-3 (β = 7.8, 95% CI = 1.1-12.3), prtH (β = 1107.8, 95% CI = 235.6-2451.3), prtP (β = 6772.8, 95% CI = 2418.7-11126.9), ltxA (β = 1811.8, 95% CI = 217.1-3840.8), cdtB (β = 568.3, 95% CI = 113.4-1250.1), all p < 0.05. SYNTAX-I score increased with one 16S rRNA gene copy/ng DNA of Porphyromonas gingivalis (β = 3.8×10-9, 95% CI = 3.6×10-10-1.8×10-8), one-fold increased expressions of fimA (β = 1.2, 95% CI = 1.1-2.1), bioF-3 (β = 1.1, 95% CI = 1-5.2), prtP (β = 3, 95% CI = 1.3-4.6), ltxA (β = 1.5, 95% CI = 1.2-2.5), all p < 0.05. Within-subject Porphyromonas gingivalis and Tannerella forsythia from intra-coronary-thrombi and subgingival-plaques correlated (rho = 0.6, p < 0.05). Higher pathobiont load and/or upregulated virulence are risk factors for myocardial infarction.Trial registration: ClinicalTrials.gov Identifier: NCT04719026

KW - Humans

KW - Cross-Sectional Studies

KW - RNA, Ribosomal, 16S/genetics

KW - Troponin I

KW - Porphyromonas gingivalis

KW - Myocardial Infarction/epidemiology

KW - DNA

U2 - 10.1038/s41598-022-19154-z

DO - 10.1038/s41598-022-19154-z

M3 - Article

C2 - 36329042

SN - 2045-2322

VL - 12

JO - Scientific Reports

JF - Scientific Reports

M1 - 18608

ER -

Myocardial infarction risk is increased by periodontal pathobionts: a cross-sectional study

Abstract

Bibliographical note

Data Availability Statement

Keywords

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