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Periodontitis may impair the homeostasis of systemic bone through regulation of gut microbiota in ApoE-/- mice.

AIM
To investigate whether periodontitis impacts bone homeostasis via gut microbiota regulation.


MATERIALS AND METHODS
Experimental periodontitis was induced by ligatures (LIG group). ApoE-/- mice were employed as a model with weakened bone homeostasis. Bone turnover was evaluated through micro-CT, HE-stained sections, osteoblasts and osteoclasts biomarkers in the bone and serum. Gut microbiota was analyzed through 16S rRNA gene sequencing. Serum concentrations of cytokines were detected by ELISA. The role of gut microbiota was evaluated through their transplantation into antibiotic-treated mice.


RESULTS
Periodontitis significantly increased the number of osteoclasts and the expression of the osteoclasts biomarkers in the proximal tibia of ApoE-/- mice, with the RANKL/OPG (receptor activator of nuclear factor-κB ligand/ osteoprotegerin) ratio significantly increased, which indicated the osteoclastic activity overwhelmed osteogenesis. Meanwhile, periodontitis altered the composition of gut microbiota and induced low-grade inflammation in the colon and blood circulation. Interestingly, the concentration of circulating TNF-α, IL-6, IL-1β, IL-17A, and MCP-1 were positively correlated with fecal α1-Antitrypsin and calprotectin, as well as serum OPG and RANKL. Furthermore, transplantation of gut microbiota from mice with periodontitis to antibiotic-treated mice could partially recapitulate the phenotypes in the bone and colon.


CONCLUSION
Periodontitis may impair systemic bone homeostasis through gut microbiota.