Background and objective: The purpose of this study was to determine if chronic periodontitis (CP) may induce hyperinsulinemia and may have the effect of on pancreatic β-cell proliferation in a rat model.
Materials and methods: Twelve male Sprague-Dawley rats were divided into two groups: the CP group and the control group (Con group). The following contents were evaluated: pathological changes in periodontal soft and hard tissues; serum lipopolysaccharide (LPS) level, serum fasting insulin (FINS) level, fasting blood glucose (FBG) level, and homeostasis model assessment (HOMA) β (HOMA-β) index; histopathological examination of islets; immunohistochemistry of insulin and p-Smad2 expression in islets; immunofluorescence of changes in the relative number of β-cells and the number of Ki67-positive β-cells. Western blotting was used to analyze p-Smad2/Smad2 levels. Results were analyzed by two independent samples t tests.
Results: Increased serum LPS level, FINS level, and HOMA-β index were observed in the rats of the CP group; FBG level did not change significantly; histological assessments showed an enlarged islet area, increased insulin content, relatively increased β-cells, increased Ki67-positive β-cells, and decreased p-Smad2 expression in islets in the rats of the CP group.
Conclusion: Our study results link CP-induced hyperinsulinemia with changes in islets, such as islet hyperplasia and compensatory β-cell proliferation, by using a CP rat model.
Keywords: cell proliferation; chronic periodontitis; hyperinsulinemia; islets of Langerhans; β-cells.
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