Cardiovascular disease (CVD) is the leading cause of death worldwide and has been confirmed to be associated with a common oral bacterial infection-chronic apical periodontitis (CAP). However, the detailed mechanisms remain controversial. CAP can potentially alter systemic inflammation, lipid metabolism, and gut microbiota, all of which contribute to the progression of the aortic inflammatory response. This study aimed to explore the differential effects between E. faecalis and P. gingivalis-CAP on the aortic inflammatory response, which focused on changes in systemic inflammation, lipid metabolism, and gut microbiota, to explore potential mechanisms linking oral disease to CVD. Our result showed P. gingivalis-CAP could activate more serious aortic inflammatory cytokine mRNA expression (TNF-α, MCP-1, and ICAM-1) than E. faecalis-CAP by promoting higher serum inflammation (TNF-α, IL-6, IL-1α, and MCP-1) and lipid (LDL-C and TC) level. Simultaneously, there was no significant change in gut microbiota between them. Furthermore, all serum inflammatory cytokines showed substantial correlations with aortic inflammatory cytokine mRNA expression, and certain serum lipid indicators showed significant correlations, but only two gut microorganisms (Ruminococcaceae and Prevotellaceae) showed significant correlations. The combined results suggest that CAP might activate the aortic inflammatory response in association with changes in the three potential mechanisms. However, the promotion of gut microbiota might be relatively weak. Using experimental CAP induced by specific bacteria, in which bacteria are sequestered in the medullary cavity, avoids the direct influence of blood or intestinal pathways, and provides new perspectives for studying the mechanism of CVD associated with oral disease. Overall, these findings suggest that CAP may exacerbate systemic inflammation and serum lipid levels in patients with CVD, highlighting the importance of educating such patients on oral hygiene.
Read full abstract