ArticleHistology and histopathology2020
Chronic atrophic gastritis aggravate chronic periodontitis with Helicobacter pylori infection and CD4+Th cytokines infiltration.
Article in Histology and histopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed, 2 syntheses or guidelines pooled it, 6 citations in OpenAlex.
- Pooled it
- Possible Association of Periodontal Diseases WithFrontiers in medicine · 2022Pooled it
- Serum level of (interleukin (IL)-2, IL-10, tumor necrosis factor (TNF)-a, motilin (MTL), gastrin (GAS), pepsinogen (PG), after adjunctive treatment in patients with chronic atrophic gastritis.Journal of medical biochemistry · 2025Article
- Oral manifestations associated with gastrointestinal diseases - A review.Bioinformation · 2025Article
- Clinical manifestations of gastrointestinal diseases in the oral cavity.The Saudi dental journal · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo investigate the potential effect of chronic atrophic gastritis on chronic periodontitis and further explore the possible mechanism.
methodsLocal periodontal lesions were collected from periodontitis tissues of 30 CAG patients and 35 control adults without CAG (non-CAG). Clinical periodontal parameters were recorded, and the expression levels of distinct CD4+ Th specific cytokines at local periodontitis lesions were evaluated by real time PCR (RT-PCR). Helicobacter pylori (H. pylori) detection was carried out in both gastric and periodontitis lesions of CAG and non CAG patients.
resultsClinical parameters analysis showed that the level of clinical attachment loss in periodontitis lesions of CAG group was significantly higher than non-CAG group. It was observed that the infection rate of H. pylori in the CAG group was higher than non-CAG group. Further cytokine analysis showed that Th17 associated cytokines IL-17, IL-21 and IL-23 were increased in periodontal lesions of CAG patients when compared with non-CAG patients. However, Th1, Th2, Th9 and Treg cells specific cytokines were not significantly increased in CAG group when compared with non-CAG group.
conclusionsPatients with CAG demonstrated that significant elevated attachment loss in periodontitis lesions, while elevated Th17 cytokines IL-17, IL-21 and IL-23 participate in immunopathogenesis of both diseases.
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Registered trials
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