Table 1.
Studies assessing the influence of Helicobacter pylori (H. pylori) infection on oral microbiota.
| Author, year | Study groups | Age | Sample | Microorganisms’ changes after H. pylori infection | Main findings | |
|---|---|---|---|---|---|---|
| Increased | Decreased | |||||
| (Li et al., 2021) | Oral lichen planus (OLP) and negative control (NC): 21 were H. pylori (+) OLP, 9 were H. pylori (−) OLP, 11 were H. pylori (+) NC, 10 were H. pylori (−) NC | Adult | Saliva | phylum: Bacteroidetes genus: Alloprevotella, Haemophilus |
phylum: Proteobacteria, Firmicutes genus: Actinomyces |
• H. pylori affects erosive OLP by inducing the secretion of cytokines IL-6, IL-17, and IL-8, which causes the abundance of oral microorganisms in OLP patients to change. |
| (Ji et al., 2020) | 34 were H. pylori (+), 24 were H. pylori (−) | Adult | Saliva | Acinetobacter, Ralstonia, Leptothrix, Sphingomonas, Ochrobactrum, Afipia, Leptotrichia, Oribacterium, Moryella | Alloprevotella, Aggregatibacter, Klebsiella, Leptotrichlaceae:G_1_, Fusobacterium, Parvimonas, Peptococcus | • H. pylori produces large amounts of urease, which reduces the acidic environment in the stomach thereby altering the oral microbial community and structure. |
| (Kadota et al., 2020) | 29 were H. pylori (+), 10 were H. pylori (−) | Adult, elder | Saliva, dental plaque, dental pulp |
P. gingivalis, T. denticola, T. forsythia | P. intermedia, Prevotella nigrescens, Campylobacter rectus | • The planting of H. pylori in the oral cavity related to the existence of the red complex (P. gingivalis, T. denticola, and T. forsythia). • Low pathogenic periodontal bacteria have an inhibitory effect on H. pylori, such as orange complex (P. intermedia, P. nigrescens, and C. rectus), and green complex (Capnocytophage ochracea, Capnocytophage sputigena, A. actinomycetemcomitans, and Eikenella corrodens). • H. pylori is associated with the formation of periodontal pockets. |
| (Zhao et al., 2019) | Gastritis: 13 were (CagA−) H. pylori (+), 35 were (CagA +) H. pylori (+), 32 were H. pylori (−) | Adult, elder | Tongue plaque | After (CagA−) H. pylori infection | • CagA positive strains of H. pylori can reduce the structural complexity of oral microorganisms, leading to a reduction in structural stability. | |
| Bacteroidetes, Firmicutes, Fusobacteria | Actinobacteria, Proteobacteria | |||||
| After (CagA +) H. pylori infection | ||||||
| Actinobacteria, Proteobacteria | Bacteroidetes, Firmicutes, Fusobacteria | |||||
| (Chua et al., 2019) | 10 were H. pylori (+), 14 were H. pylori (−) | Adult | Cheek mucosa | Pseudomonas, Roseomonas | Fusobacterium, Solobacterium, Streptococcus, Haemophilus | • H. pylori-positive individuals show more differences than negative in both alpha and beta diversity during the daytime. • H. pylori disrupts the balance of the oral microbiota only during the day by affecting systemic metabolic and immune factors. • H. pylori secretes proteins and metabolites, as well as alters the nutrient supply and pH in the oral cavity through proliferation, which affects the growth and structure of the oral microbiome during the day. |
| (Schulz et al., 2018) | Gastritis: 16 were H. pylori (+), 24 were H. pylori (−) | Adult, elder | Saliva | genus: Treponema | genus: Haemophilus
species: P. acnes, P. oris |
• Bacteria can migrate continuously through the upper gastrointestinal tract, demonstrating that saliva is a major source of gastric microorganisms. |
| (Hu et al., 2016) | Chronic periodontitis: 13 were H. pylori (+), 15 were H. pylori (−) | Adult | Plaque | P. gingivalis, P. intermedia, F. nucleatum, T. denticola | A. actinomycetemcomitans | • H. pylori infection increases the risk of periodontal disease by increasing the proportion of total periodontal pathogens in dental plaque. |
| (Umeda et al., 2003) | Once or now suffering from gastritis and peptic ulcer: 45 were H. pylori (+), 12 were H. pylori (−) | Adult, elder | Saliva, supragingival plaque, tongue plaque | Bacteroides forsythus, A. actinomycetemcomitans | P. gingivalis, P. intermedia | • Supragingival plaque and shallow periodontal pockets provide a good environment for H. pylori and also promote the co-aggregation of H. pylori with oral microorganisms, thus increasing the prevalence of H. pylori. |
| (Ishihara et al., 1997) | Peptic ulcer or gastritis: 54 were H. pylori (+), 48 were H. pylori (−) | Adult, elder | Saliva, plaque, | F. nucleatum, P. gingivalis | – | • Antagonism of oral bacteria against H. pylori can lead to its low detection rate |
| (Ji et al., 2020) | 34 were H. pylori (+), 24 were H. pylori (−) | Adult | Saliva | After H. pylori eradication | • H. pylori produces large amounts of urease, which reduces the acidic environment in the stomach thereby altering the oral microbial community and structure. | |
| Increased | Decreased | |||||
| phylum: Fusobacteria genus: Leptotrichia, Campylobacter, Pseucomonas |
genus: Alloprevotella, Aggregatibacter | |||||