Chronic apical periodontitis exacerbates atherosclerosis in apolipoprotein E‐deficient mice and leads to changes in the diversity of gut microbiota

Abstract Aim To investigate the impact of chronic apical periodontitis (CAP) on atherosclerosis and gut microbiota by establishing a Porphyromonas gingivalis ( P . gingivalis )‐induced CAP in an apolipoprotein E‐deficient (apoE −/− ) mice model. Methodology Twenty‐eight male apoE −/− mice were divided into two groups with 14 in each: CAP group and control group. In the CAP group, sterile cotton wool containing 10 8 colony‐forming units of P . gingivalis was placed into the pulp chamber after pulp exposure followed by coronal resin filling in bilateral maxillary first and second molars. The mice were fed with a chow diet to induce atherosclerosis. Animals were euthanized 16 weeks after the operation, and the periapical lesions of bilateral maxillary first and second molars were assessed by micro‐CT. After collection of aortic arches, atherosclerotic lesions were measured by Oil Red O staining. Serum levels of high‐density lipoprotein cholesterol (HDL‐C), low‐density lipoprotein cholesterol (LDL‐C), total cholesterol (TC), and triglycerides (TG) were measured. Stools were collected to detect alterations in gut microbiota by 16S rRNA gene sequencing. Independent samples t ‐test was used to calculate the difference between the two groups. Results CAP was observed in 98.2% of molars. A significant increase in atherosclerotic plaque formation in the aortic arches was found in the CAP groups (CAP: 2.001% ± 0.27%, control: 0.927% ± 0.22%, p = .005). No significant difference was observed between sevum level of HDL‐C (CAP: 2.295 ± 0.31 mmol/L, Control: 3.037 ± 0.55 mmol/L, p = .264) or LDL‐C (CAP: 17.066 ± 3.95 mmol/L, Control: 10.948 ± 1.69 mmol/L, p = .177) in CAP group and Control group. There were no significant differences in TG (CAP: 1.076 ± 0.08 mmol/L, control: 1.034 ± 0.13 mmol/L, p = .794) or TC (CAP: 6.372 ± 0.98 mmol/L, control: 6.679 ± 0.75 mmol/L, p = .72) levels between the two groups ( p > .05). The alpha diversity was elevated in the CAP group. In terms of beta diversity, the CAP and control groups were clearly distinguished by the microbial community. Conclusion In a mouse experimental model, pulp infection with P . gingivalis ‐induced CAP, thus aggravating the development of atherosclerosis. Meanwhile, CAP increased alpha diversity and altered the beta diversity of the gut microbiota.