IADR Abstract Archives
KetoC Targets on Gut Microbiota Thereby Preventing Periodontitis
Objectives: Oral-gut bacterial dysbiosis facilitates the connection between periodontitis and systemic disease. A bioactive metabolite generated by intestinal bacteria, KetoC, possesses beneficial roles in maintaining homeostasis. Nevertheless, its function to oral-gut dysbiosis in periodontitis remains unclear. We investigated whether gut microbiota is affected in periodontitis model. Moreover, we demonstrated that KetoC shows an indirect mechanism to restore gut bacterial alteration leading to the periodontal homeostasis.
Methods: A total of 31 eight-week-old male C57BL/6N mice were randomly divided into four groups (non-ligation, non-ligation + KetoC, ligation + Porphyromonas gingivalis (P. gingivalis), and ligation + P. gingivalis + KetoC) (n = 7/8 mice/group) and given a daily oral gavage of KetoC (15 mg/mL) or vehicle for two weeks. On day 7, a 5-0 silk ligature was placed on the maxillary left second molar and P. gingivalis W83 (109 CFU) was delivered orally every three days to induce periodontitis. On day 14, fresh fecal samples were collected, then all mice were euthanized. Alveolar bone resorption was determined from the level of the cementoenamel junction to the alveolar bone crest at the mesial and distal sites of maxillary second molar. Gut microbial diversity and composition in the feces were analyzed by metagenomics assay. Statistical analyses were performed accordingly.
Results: Periodontitis model was successfully obtained in this model as alveolar bone destruction was observed. Periodontitis group exhibited less gut bacterial diversity than non-ligation groups. In the periodontitis group, at the phylum level, Verrucomicrobia and Firmicutes were upregulated and downregulated, respectively; while, Ruminococcus and Akkermansia were downregulated and upregulated at the genus level, respectively. KetoC administration in the periodontitis group significantly reduced alveolar bone destruction and restored gut bacterial alteration.
Conclusions: This metabolite prevents alveolar bone loss and improves gut bacterial diversity and composition in the oral-gut dysbiosis-related periodontitis model, as its indirect mechanism.
Methods: A total of 31 eight-week-old male C57BL/6N mice were randomly divided into four groups (non-ligation, non-ligation + KetoC, ligation + Porphyromonas gingivalis (P. gingivalis), and ligation + P. gingivalis + KetoC) (n = 7/8 mice/group) and given a daily oral gavage of KetoC (15 mg/mL) or vehicle for two weeks. On day 7, a 5-0 silk ligature was placed on the maxillary left second molar and P. gingivalis W83 (109 CFU) was delivered orally every three days to induce periodontitis. On day 14, fresh fecal samples were collected, then all mice were euthanized. Alveolar bone resorption was determined from the level of the cementoenamel junction to the alveolar bone crest at the mesial and distal sites of maxillary second molar. Gut microbial diversity and composition in the feces were analyzed by metagenomics assay. Statistical analyses were performed accordingly.
Results: Periodontitis model was successfully obtained in this model as alveolar bone destruction was observed. Periodontitis group exhibited less gut bacterial diversity than non-ligation groups. In the periodontitis group, at the phylum level, Verrucomicrobia and Firmicutes were upregulated and downregulated, respectively; while, Ruminococcus and Akkermansia were downregulated and upregulated at the genus level, respectively. KetoC administration in the periodontitis group significantly reduced alveolar bone destruction and restored gut bacterial alteration.
Conclusions: This metabolite prevents alveolar bone loss and improves gut bacterial diversity and composition in the oral-gut dysbiosis-related periodontitis model, as its indirect mechanism.