Evidence map›Paper›PMID 42165292›Full record

ArticleInternational endodontic journal2026

Apical Periodontitis May Exacerbate Ulcerative Colitis via Neutrophil Extracellular Trap-Mediated Systemic Inflammation and Intestinal Barrier Disruption in Mice.

Yu Zeng, Yulin Zhang, Yutong Xiong, Peining Zheng, Huachen Wang, Shiyu Zhang, Shihan Lin, Yufang Luo, Huaxiang Lei, Shuai Chen and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International endodontic journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Yu ZengFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Yulin ZhangFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Yutong XiongFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Peining ZhengFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Huachen WangFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Shiyu ZhangFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Shihan LinFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Yufang LuoFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Huaxiang LeiFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Shuai ChenFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Zhiyu CaiDepartment of Stomatology, Fujian Medical University Union Hospital, Fuzhou, China.
Guowu GanFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.ORCID 0000-0002-3189-9915
Xiaojing HuangFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatology Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.

Funding

Fujian Provincial Health Technology Project 2022QNA073National Natural Science Foundation of China 81970926Natural Science Foundation of Fujian Province 2023J01709
6 · The paper itself

Abstract

aimThis study investigated the impact of apical periodontitis (AP) on ulcerative colitis (UC) progression and elucidated the roles of intestinal barrier dysfunction and neutrophil extracellular traps (NETs) in a mouse model, providing new evidence and perspectives for oral-systemic diseases. METHODOLOGY: Thirty-two male ICR mice were randomized into four groups (n = 8 per group): Ctrl, AP, UC and AP + UC. AP was induced by lipopolysaccharide application to the bilateral maxillary first and second molars. UC was established via dextran sulphate sodium administration. Disease activity index (DAI), colon length and histopathology were assessed. Serum levels of C-reactive protein (CRP), interleukin (IL)-6, IL-10, IL-1β, immunoglobulin G (IgG) and NETs were measured by ELISA. Intestinal tight junction proteins (ZO-1 and Claudin) and NETs were analysed via immunofluorescence. Gut microbiota composition was evaluated by 16S rRNA sequencing.

resultsAP + UC mice exhibited significantly higher DAI scores (p < 0.01 vs. UC), shortened colon length (p < 0.05 vs. UC) and exacerbated histopathological damage (p < 0.01 vs. UC). Serum CRP, IL-1β and IL-6 levels were elevated in AP + UC mice (p < 0.05 vs. UC). Levels of NETs increased significantly in AP + UC serum (p < 0.05 vs. UC) and colonic tissue. AP and AP + UC groups showed reduced goblet cell areas (p < 0.01 AP vs. Ctrl, p < 0.01 AP + UC vs. UC) and diminished tight junction protein expression. Gut microbiota analysis revealed increased alpha diversity and altered genus-level composition in AP + UC mice, with significant correlations between specific bacteria and NETs levels/goblet cell areas.

conclusionAP may exacerbate UC severity through intestinal barrier impairment and systemic NETs elevation, accompanied by gut microbiota dysbiosis.

Indexed as

Colitis, UlcerativeExtracellular TrapsInflammationPeriapical PeriodontitisAnimalsDisease Models, AnimalIntestinal Barrier FunctionMaleMiceMice, Inbred ICRanimal modelapical periodontitisneutrophil extracellular trapsoral‐systemic diseasesulcerative colitis

Identifiers

PMID42165292
PMCPMC13462424

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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.