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.
Highlights
Periodontitis is one of the most prevalent diseases, and it influences up to 90% people in the world [1]
28 samples from 14 patients with chronic periodontitis were involved in our study, and real-time PCR was performed to determine if they were infected with H. pylori
The result indicated that patients with and without H. pylori infection did not differ in plaque index (PLI) and bleeding index (BI) (p > 0.05) (Table 2), while patients with H. pylori exhibited deeper probing depth (PD) and more attachment loss (AL) than those without (p < 0.05) (Table 2)
Summary
Periodontitis is one of the most prevalent diseases, and it influences up to 90% people in the world [1]. Varying from other infectious diseases, periodontitis is a multiple bacteria-related disease. As the most important etiology, periodontal pathogens have been studied for decades. Multiple experimental methods have been used in detecting periodontal pathogens. Techniques such as PCR, sequencing and DNA hybridization have been used to identify bacterial species in samples such as plaque and soil [3], and about 1,000 bacterial species have been found in human oral cavity [4], which led to a development in the area of periodontitis as well. Previous studies found that periodontal diseases occurred due to the change of periodontitis-related bacterial species in subgingival plaque [5]. The effect of Helicobacter pylori (H. pylori) on periodontitis became a new hotspot
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