Evidence map›Paper›PMID 41225099›Full record

ReviewAdvances in experimental medicine and biology2026

Immunological Diagnosis and Treatments of Periodontitis in Patients with Type 2 Diabetes Mellitus.

Koki Yoshida, Kengo Iwasaki, Osamu Uehara, Satsuki Kato, Shintaro Shimizu, Kohei Sato, Nodoka Sugiyama, Yukichi Okada, Yoshiki Fujimoto, Sho Hirose and 11 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2026. 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. Review
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

21 authors.

Koki YoshidaDivision of Oral Medicine and Pathology, Department of Human Biology and Pathophysiology, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Kengo IwasakiDivision of Creative and Integrated Medicine, Advanced Medical Research Center, Translational Research Institute for Medical Innovation (TRIMI), Osaka Dental University, Hirakata, Osaka, Japan.
Osamu UeharaDivision of Disease Control & Molecular Epidemiology Department of Oral Growth & Development, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Satsuki KatoDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Shintaro ShimizuDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Kohei SatoDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Nodoka SugiyamaDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Yukichi OkadaDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Yoshiki FujimotoDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Sho HiroseDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Norihiro NakamotoDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Yuko MatsukiDivision of Advanced Clinical Education, Department of Integrated Dental Education, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Takashi KadoDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Yukie MurataDivision of Disease Control & Molecular Epidemiology Department of Oral Growth & Development, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Katsuya KawanishiDivision of Advanced Clinical Education, Department of Integrated Dental Education, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Hirofumi MatsuokaDivision of Disease Control & Molecular Epidemiology Department of Oral Growth & Development, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Hiroko MiuraDivision of Disease Control & Molecular Epidemiology Department of Oral Growth & Development, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Keiji NaganoDivision of Microbiology, Department of Oral Biology, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Yoshihiro AbikoDivision of Oral Medicine and Pathology, Department of Human Biology and Pathophysiology, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Yasushi FuruichiDepartment of Integrated Dental Education Division of Dental Education Development School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan.
Toshiyuki NagasawaDivision of Periodontology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, Health Sciences University of Hokkaido, Kanazawa, Hokkaido, Japan. nagasawa@hoku-iryo-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The oral mucosa is a key barrier and entry point for microorganisms into the gastrointestinal tract. Interleukin-17 (IL-17) and T helper 17 (Th17) cells contribute to mucosal defense against bacterial and fungal pathogens. Gingival fibroblasts recruit neutrophils, construct a mechanical barrier of gingival tissue, and produce osteoprotegerin, which prevents bone resorption. In periodontitis, inflammatory cytokines induce RANKL expression by osteoblasts and periodontal ligament fibroblasts, resulting in alveolar bone resorption. In diabetes mellitus, excessive IL-17 activity increases the risk of periodontal tissue destruction and fungal infections. In patients with diabetes, periodontitis worsens insulin resistance and glycemic control while introducing periodontopathic bacteria and Th17 cells to the gut, exacerbating intestinal inflammation. Infection with periodontopathic bacteria sharing homology with β2 glycoprotein I (β2GPI) may induce antibodies against β2GPI, increasing blood clot risk. Thus, in patients with diabetes and periodontitis, symptoms vary due to localized and systemic immune responses to bacteria and fungi, necessitating a comprehensive understanding for accurate diagnosis and treatment. The biopsychosocial model aids in addressing these complexities, while the common risk approach and cognitive-behavioral therapy address social and psychological challenges. Therefore, comprehensive treatment strategies are necessary for managing periodontitis in patients with diabetes, considering both microbial factors and immune responses.

Indexed as

Diabetes Mellitus, Type 2PeriodontitisHumansDiabetesIL-17Immune responseOral mucosaPeriodontitis

Identifiers

PMID41225099

What OpenQuestion holds

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Registered trials

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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.