Interconnections between the Oral and Gut Microbiomes: Reversal of Microbial Dysbiosis and the Balance between Systemic Health and Disease

Abstract

The human microbiota represents a complex array of microbial species that influence the balance between the health and pathology of their surrounding environment. These microorganisms impart important biological benefits to their host, such as immune regulation and resistance to pathogen colonization. Dysbiosis of microbial communities in the gut and mouth precede many oral and systemic diseases such as cancer, autoimmune-related conditions, and inflammatory states, and can involve the breakdown of innate barriers, immune dysregulation, pro-inflammatory signaling, and molecular mimicry. Emerging evidence suggests that periodontitis-associated pathogens can translocate to distant sites to elicit severe local and systemic pathologies, which necessitates research into future therapies. Fecal microbiota transplantation, probiotics, prebiotics, and synbiotics represent current modes of treatment to reverse microbial dysbiosis through the introduction of health-related bacterial species and substrates. Furthermore, the emerging field of precision medicine has been shown to be an effective method in modulating host immune response through targeting molecular biomarkers and inflammatory mediators. Although connections between the human microbiome, immune system, and systemic disease are becoming more apparent, the complex interplay and future innovations in treatment modalities will become elucidated through continued research and cross-disciplinary collaboration.

Oral Microbiota of Children Is Conserved across Han, Tibetan and Hui Groups and Is Correlated with Diet and Gut Microbiota

“…Recently, Balakrishnan et al reported an ethnicity-specific association in both the gut and oral microbial profiles between African American and European American children although no correlation analysis was conducted between the oral and gut microbiota within each group [ 55 ]. Khor et al proposed two hypotheses to (at least partially) explain how oral bacteria may be transmitted to the lower digestive tract including the hematogenous route and the enteral route [ 56 ]. Given that the oral microbiotas are constantly swallowed along with saliva and delivered to the gut, we hypothesized that the oral microbiota would share a positive association with the gut microbiota.…”

“…This finding supported those of Nakajima et al [ 65 ] and Kato et al [ 66 ] who reported that the oral administration of Porphyromonas gingivalis could significantly alter the gut microbiota composition in mice. This apparent interaction between P. gingivalis and the gut microbiota is plausible because P. gingivalis has been shown to be tolerant of a low pH (i.e., as in the stomach environment) and could therefore actively migrate and proliferate from the oral cavity through the intestinal tract [ 56 , 67 ]. Moreover, the oral administration of P. gingivalis in mice was also found to significantly exacerbate endotoxemia while reducing the transcription of genes such as ZO-1 , occludin and Tjp1 tight junction proteins in the small intestine.…”

PplD is a de-N-acetylase of the cell wall linkage unit of streptococcal rhamnopolysaccharides

“…In the oral cavity, nitrite is actively concentrated by salivary glands reaching up to 2 mM after a dietary nitrate load 58 . The Streptococcus genus dominates the majority of oral surfaces 59 . These bacteria produce by-products of fermentation, lactic and acetic acids, that cause a significant decrease in pH level to 5.5 and below.…”

Infective Endocarditis: A Focus on Oral Microbiota

“…Periodontitis is a chronic inflammatory disease that can lead to non-reversible damage of supportive tissues (cementum, periodontal ligament, and alveolar bone) surrounding the teeth and tooth loss [80,81]. Mechanistically, the increased concentration of pathogenic bacteria (dysbiosis) within the dental plaque activates a massive deleterious immune response [82]. Indeed, the augmented concentration of bacterial lipopolysaccharides (LPS) and other virulence factors stimulate the production of inflammatory mediators and cytokines (e.g., interleukins (ILs), prostaglandin E2 (PGE2) and tumor necrosis factor-alpha (TNF-α)) and promote the release of the matrix metalloproteinases (MMPs) that contribute to the extracellular matrix remodeling and alveolar bone reabsorption by osteoclasts [83].…”