Serum IgG titers against periodontal pathogens are associated with cerebral hemorrhage growth and 3-month outcome.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2020
Historique:
received: 30 04 2020
accepted: 12 10 2020
entrez: 28 10 2020
pubmed: 29 10 2020
medline: 15 12 2020
Statut: epublish

Résumé

To assess the influence of periodontal disease on cerebral hemorrhage and its clinical course, we examined the association of the serum IgG titer of periodontal pathogens with hemorrhage growth and 3-month outcome. We consecutively enrolled 115 patients with acute cerebral hemorrhage (44 females, aged 71.3 ± 13.1 years) and used ELISA to evaluate the serum IgG titers of 9 periodontal pathogens: Porphyromonas gingivalis, Aggregatibacter (A.) actinomycetemcomitans, Prevotella intermedia, Prevotella nigrescens, Fusobacterium (F.) nucleatum, Treponema denticola, Tannerella forsythensis, Campylobacter rectus, and Eikenella corrodens. Significant hematoma growth was defined as an increase in the volume of >33% or an absolute increase in the volume of >12.5 mL. A poor outcome was defined as a 3 or higher on the modified Rankin Scale. We observed hemorrhage growth in 13 patients (11.3%). Multivariate analysis revealed that increased IgG titers of A. actinomycetemcomitans independently predicted the elevated hemorrhage growth (odds ratio 5.26, 95% confidence interval 1.52-18.25, p = 0.01). Notably, augmented IgG titers of F. nucleatum but not A. actinomycetemcomitans led to a poorer 3-month outcome (odds ratio 7.86, 95% confidence interval 1.08-57.08, p = 0.04). Thus, we demonstrate that elevated serum IgG titers of A. actinomycetemcomitans are an independent factor for predicting cerebral hemorrhage growth and that high serum IgG titers of F. nucleatum may predict a poor outcome in patients with this disease. Together, these novel data reveal how systemic periodontal pathogens may affect stroke patients, and, should, therefore, be taken into consideration in the management and treatment of these individuals.

Identifiants

pubmed: 33112888
doi: 10.1371/journal.pone.0241205
pii: PONE-D-20-12711
pmc: PMC7592768
doi:

Substances chimiques

Antibodies, Bacterial 0
Immunoglobulin G 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0241205

Déclaration de conflit d'intérêts

Hirofumi Maruyama reports research support from Eisai, Pfizer, Takeda Pharmaceutical, Otsuka Pharmaceutical, Nihon Pharmaceutical, Shionogi, Teijin Pharma, Fuji Film, Boehringer Ingelheim, Sumitomo Dainippon Pharma, Nihon Medi-Physics, Bayer, MSD, Daiichi Sankyo, Kyowa Hakko Kirin, Sanofi, Novartis, Kowa Pharmaceutical, Astellas Pharma, Tsumura, Japan Blood Products Organization, Mitsubishi Tanabe Pharma, and Mylan which are unrelated to the submitted work. This does not alter our adherence to PLOS ONE policies on sharing data and materials. All other authors declare that they have no conflicts of interest.

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Auteurs

Masahiro Nakamori (M)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
Department of Neurology, Suiseikai Kajikawa Hospital, Hiroshima, Japan.

Naohisa Hosomi (N)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
Department of Neurology, Chikamori Hospital, Kochi, Japan.
Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.

Hiromi Nishi (H)

Department of General Dentistry, Hiroshima University Hospital, Hiroshima, Japan.

Shiro Aoki (S)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.

Tomohisa Nezu (T)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.

Yuji Shiga (Y)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.

Naoto Kinoshita (N)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.

Kenichi Ishikawa (K)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
Department of Neurology, Suiseikai Kajikawa Hospital, Hiroshima, Japan.

Eiji Imamura (E)

Department of Neurology, Suiseikai Kajikawa Hospital, Hiroshima, Japan.

Tomoaki Shintani (T)

Center of Oral Examination, Hiroshima University Hospital, Hiroshima, Japan.

Hiroki Ohge (H)

Department of Infectious Diseases, Hiroshima University Hospital, Hiroshima, Japan.

Hiroyuki Kawaguchi (H)

Department of General Dentistry, Hiroshima University Hospital, Hiroshima, Japan.

Hidemi Kurihara (H)

Department of Periodontal Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Shinichi Wakabayashi (S)

Department of Neurosurgery, Suiseikai Kajikawa Hospital, Hiroshima, Japan.

Hirofumi Maruyama (H)

Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.

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