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Oncotarget. 2016 Oct 11;7(41):66700-66712. doi: 10.18632/oncotarget.11449.

Effect of Helicobacter pylori infection on chronic periodontitis by the change of microecology and inflammation.

Hu Z1, Zhang Y1, Li Z2, Yu Y3,4, Kang W1,5, Han Y2, Geng X2, Ge S1,5, Sun Y2.

Author information

1
Shandong Provincial Key Laboratory of Oral Tissue Regeneration, School of Stomatology, Shandong University, Jinan, Shandong 250012, People's Republic of China.
2
Department of Microbiology, Key Laboratory for Experimental Teratology of Chinese Ministry of Education, School of Medicine, Shandong University, Jinan, Shandong 250012, People's Republic of China.
3
Shanghai Southwest Weiyu Middle School, Shanghai 200233, People's Republic of China.
4
Laboratory of Oral Tumor Biology, Shanghai Research Institute of Stomatology Ninth People Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, People's Republic of China.
5
Department of Periodontology, School of Stomatology, Shandong University, Jinan, Shandong 250012, People's Republic of China.

Abstract

Helicobacter pylori (H. pylori), a pathogen inducing peptic disease, is recently found to be binding to the progress of periodontitis. Most previous studies are case-controlled, and they investigate the risk of H. pylori infection in disease the development of while few studies evaluate the correlation between H. pylori and periodontal pathogens. Therefore, we investigated the correlation between H. pylori infection with periodontal parameters, periodontal pathogens and inflammation. The results indicated that patients with H. pylori showed significantly higher probing depth and attachment loss than those without (p < 0.05). Among 28 subgingival plaque samples from 14 patients, the frequencies of Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum and Treponema denticola were significantly higher with H. pylori infection than those without H. pylori infection (p < 0.05). However, the frequency of Aggregatibacter actinomycetemcomitans was lower (p < 0.05). Furthermore, after human acute monocytic leukemia cell line (THP-1) was stimulated with cagA-positive standard strains (cagA+ H. pylori 26695), the expression of periodontitis-related molecules Wnt5a, interleukin 8 (IL-8), interleukin 6 (IL-6) and interferon gamma (IFN-γ) significantly increased (p < 0.05). Conversely, the expression of tumor necrosis factor alpha (TNF-α) was almost stable. Meanwhile, cagA+ H. pylori promoted significantly higher expression of IL-8 and Wnt5a than isogenic cagA mutants strains (cagA- H. pylori 26695) did. Taken together, our data suggested that H. pylori might promote the growth of some periodontal pathogens and aggravate the progress of chronic periodontitis.

KEYWORDS:

IL-8; Wnt5a; chronic periodontitis; inflammation; Helicobacter pylori

PMID:
27602578
PMCID:
PMC5341831
DOI:
10.18632/oncotarget.11449
[Indexed for MEDLINE]
Free PMC Article

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