Background and Objective: Diabetes mellitus is believed to increase the risk and severity of periodontitis. However, less evidence is available on the converse effects of periodontitis on diabetes. The objective of the study was to investigate to what degree experimental periodontitis induced by Porphyromonas gingivalis might influence the onset and severity of diabetes in different mouse models.Material and Methods: Twenty‐eight male Tallyho/JngJ mice (type 2 diabetes), 20 male streptozotocin‐induced diabetes C57BL/6J mice (type 1 diabetes) and 20 male C57BL/6J mice at 4 wks of age were evenly divided into two groups: periodontal infection and sham infection. Periodontitis was induced by Porphyromonas gingivalis W50 (P. gingivalis) oral inoculation before the development of diabetes. Sham‐infected mice received vehicle as control. P. gingivalis in the oral cavity were identified by quantitative polymerase chain reaction. Fasting glucose, body weight and food intake levels were monitored and glucose tolerance tests were performed to assess glucose homeostasis for the onset and progression of diabetes. The level of alveolar bone loss and tumor necrosis factor‐alpha were determined in week 20 when mice were killed.Results: Mice in the infection groups developed more alveolar bone loss than those in sham‐infection groups (Tallyho p = 0.021; C57‐STZ p = 0.014; C57 p = 0.035). Hyperglycemic mice exhibited significantly more bone loss compared to those normal glucose mice (Tallyho vs. C57 p = 0.029; C57‐STZ vs. C57 p = 0.024). The level of tumor necrosis factor‐alpha was consistent with that of periodontal bone loss and hyperglycemia. There was no significant effect of mouse species on the amount of bone loss at the same level of blood glucose. No statistically significant difference or trend in glucose metabolism was found between the infection and sham‐infection group.Conclusion: Diabetes enhanced the risk for periodontal disease induced by P. gingivalis. However, no converse impact was found between this periodontal infection and onset and severity of diabetes in both type 1 and 2 diabetes mice.

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