Evidence map›Paper›PMID 41057450›Full record

ArticleScientific reports2025

Periodontitis associated with Porphyromonas gingivalis infection is a risk factor for infertility through uterine hypertrophy.

Chiaki Kamei-Nagata, Kazuhiro Omori, Hidefumi Sako, Kyosuke Sakaida, Masa-Aki Nakayama, Toshiaki Ohara, Hiroki Mandai, Moyuka Kubota-Takamori, Fumiko Kiyama, Takayuki Ishii and 13 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

Chiaki Kamei-NagataDepartment of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Kazuhiro OmoriDepartment of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan. kazu@okayama-u.ac.jp.
Hidefumi SakoDepartment of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital, Okayama, 700-8558, Japan.
Kyosuke SakaidaDepartment of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital, Okayama, 700-8558, Japan.
Masa-Aki NakayamaDepartment of Oral Microbiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Toshiaki OharaDepartment of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8558, Japan.
Hiroki MandaiDepartment of Pharmacy, Faculty of Pharmacy, Gifu University of Medical Science, Gifu, 509-0293, Japan.
Moyuka Kubota-TakamoriDepartment of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Fumiko KiyamaDepartment of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Takayuki IshiiDepartment of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Kimito HiraiDepartment of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Atsushi IkedaDepartment of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital, Okayama, 700-8558, Japan.
Kazu Takeuchi-HatanakaDepartment of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital, Okayama, 700-8558, Japan.
Yuki Shinoda-ItoDepartment of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Masako Tai-TokuzenDepartment of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital, Okayama, 700-8558, Japan.
Ai SakamotoCenter for Reproductive Medicine, Miyake Clinic, Okayama, 701-0204, Japan.
Machiko KiyokawaCenter for Reproductive Medicine, Miyake Clinic, Okayama, 701-0204, Japan.
Tomomi YamanishiCenter for Reproductive Medicine, Miyake Clinic, Okayama, 701-0204, Japan.
Takashi OdaCenter for Reproductive Medicine, Miyake Clinic, Okayama, 701-0204, Japan.
Masayuki TakigawaMiyake Hello Dental Clinic, Pediatric Dentistry and Orthodontics, Okayama, 701-0204, Japan.
Tadashi YamamotoThe Center for Graduate Medical Education (Dental Division), Okayama University Hospital, Okayama, 700-8558, Japan.
Takahito MiyakeCenter for Reproductive Medicine, Miyake Clinic, Okayama, 701-0204, Japan.
Shogo TakashibaDepartment of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.

Funding

Japan Society for the Promotion of Science 21K16992Japan Society for the Promotion of Science 23K27773
6 · The paper itself

Abstract

Periodontitis has recently been recognized as a potential risk factor for infertility due to its adverse effect on conception, although the underlying mechanisms remain unclear. This study investigated serum IgG antibody titers against periodontopathogenic bacteria in women with unexplained infertility and investigated how periodontal inflammation affects pregnancy and uterine function using a ligature-induced periodontitis mouse model infected with Porphyromonas gingivalis (Pg). IgG antibody titers against seven periodontopathogenic bacteria strains were measured by ELISA in 76 spontaneously pregnant women and 70 women undergoing infertility treatment. In the in vivo study, periodontitis mice were bred four weeks after periodontitis induction. Birth numbers, newborn weights, and gestation periods were assessed. To evaluate periodontal inflammation, alveolar bone, serum, and uterus was collected before mating. Uterine tissue was evaluated through histological and immunohistochemical staining. Women receiving infertility treatment were significantly older and had higher IgG titers against three Pg strains. Periodontitis mice had fewer births, lower newborn weights, and increased uterine cross-sectional areas. Additionally, elevated estrogen receptor α and progesterone receptor expression levels were observed in endometrial and stromal tissues. These results suggest that periodontitis may cause uterine hypertrophy and hormone receptor changes, potentially impairing pregnancy.

Indexed as

Bacteroidaceae InfectionsInfertility, FemalePeriodontitisPorphyromonas gingivalisUterusAdultAnimalsAntibodies, BacterialDisease Models, AnimalFemaleHumansHypertrophyImmunoglobulin GMicePregnancyRisk FactorsAntibodies, BacterialImmunoglobulin GChronic inflammationInfertilityPeriodontitisPorphyromonas gingivalisSex hormone receptorUterus

Identifiers

PMID41057450
PMCPMC12504428

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.