Fig. 3.

Schematic summarizing hypothesized pathways where the oral microbiome mediates cardiovascular risk and disease in response to smoking. A An increased RA of multiple bacteria associated with smoking including Fusobacterium, Porphyromonas, Lachnoanaerobaculum Parvimonas, Mogibacterium Streptococcus, Selenomonas, and Rothia in the oral microbiome have been positively associated with increased proinflammatory cytokine levels. A smoking-associated increase in the RA of Alloprevotella, Filifactor, Fusobacterium, Porphyromonas, Veillonella, Treponema, and Parvimonas was associated with LPS levels or biosynthesis genes, while Parvimonas was associated with CRP. Increases in local and systemic cytokines, along with elevated CRP and LPS are associated with an increased risk of CVD. B Increased RA of Rothia and Porphyromonas, both elevated in the oral cavities of smokers versus non-smokers, are potentially associated with decreased tyrosine and tryptophan levels through different hypothesized mechanisms. Prevotella RA was increased in smokers, which is positively associated with increased Apolipoprotein B levels. Both decreases in tyrosine/tryptophan and increased Apolipoprotein B is associated with increased cardiovascular risk. C An increase in the oral RA of Prevotella and Veillonella, and a decrease in the RA of Neisseria that was documented in smokers versus non-smokers is associated with decrease nitrate levels that ultimately lead to decreased nitric oxide levels. Decreased nitic oxide levels are associated with alterations in blood pressure and CVD, and may lead to a compensatory increase in oral Rothia abundance in association with smoking. Figure created with BioRender.com