Abstract
We examined whether colonization of selected oral pathogens is associated with gastric precancerous lesions in a cross-sectional study. A total of 119 participants were included, of which 37 were cases of chronic atrophic gastritis, intestinal metaplasia, or dysplasia. An oral examination was performed to measure periodontal indices. Plaque and saliva samples were tested with real-time quantitative PCR for DNA levels of pathogens related to periodontal disease (Porphyromonas gingivalis, Tannerella forsythensis, Treponema denticola, Actinobacillus actinomycetemcomitans) and dental caries (Streptococcus mutans and S. sobrinus). There were no consistent associations between DNA levels of selected bacterial species and gastric precancerous lesions, although an elevated but non-significant odds ratio (OR) for gastric precancerous lesions was observed in relation to increasing colonization of A. actinomycetemcomitans (OR = 1.36 for one standard deviation increase, 95% Confidence Interval = 0.87–2.12), P. gingivalis (OR = 1.12, 0.67–1.88) and T. denticola (OR = 1.34, 0.83–2.12) measured in plaque. To assess the influence of specific long-term infection, stratified analyses by levels of periodontal indices were conducted. A. actinomycetemcomitans was significantly associated with gastric precancerous lesions (OR = 2.51, 1.13–5.56) among those with ≥ median of percent tooth sites with PD≥3 mm, compared with no association among those below the median (OR = 0.86, 0.43–1.72). A significantly stronger relationship was observed between the cumulative bacterial burden score of periodontal disease-related pathogens and gastric precancerous lesions among those with higher versus lower levels of periodontal disease indices (p-values for interactions: 0.03–0.06). Among individuals with periodontal disease, high levels of colonization of periodontal pathogens are associated with an increased risk of gastric precancerous lesions.
Highlights
Gastric cancer is the fourth most common cancer and second highest in mortality worldwide [1]
We considered microbes that are etiologically linked with periodontal diseases [21], including Porphyromonas gingivalis, a gram-negative oral anaerobe commonly associated with adult periodontal disease [22]; Tannerella forsythensis, an anaerobic gram-negative member of the Cytophaga-Bacteroides family implicated in periodontal diseases, Treponema denticola, a motile and highly proteolytic bacterium associated with the incidence and severity of human periodontal disease, and Actinobacillus actinomycetemcomitans, a gram-negative facultative anaerobe, which is a typical cause of periodontitis and associated with systemic infections [23], [24]
We observed that the means of log-transformed periodontal pathogen DNA levels in plaque increased across tertiles of periodontal indices (Table S3)
Summary
Gastric cancer is the fourth most common cancer and second highest in mortality worldwide [1]. For the most common ‘‘intestinal’’ subtype of gastric adenocarcinomas, which account for approximately 70% of gastric cancer cases [2], [6], a pre-neoplastic sequence has been defined from chronic superficial gastritis through atrophic gastritis, intestinal metaplasia, and to dysplasia and adenocarcinoma [7], [8]. Studies of gastric precancerous lesions can be used to identify risk factors that play a role in the development of gastric cancer. Several case-control studies of gastric precancerous lesions, predominantly atrophic gastritis and intestinal metaplasia, have identified common risk factors for gastric cancer such as cigarette smoking, old age, and low levels of fruit or vitamin C intake [9,10,11,12,13,14]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
