Role of Smoking and Type 2 Diabetes in the Immunobalance of Advanced Chronic Periodontitis

Background : This study evaluates the tissue levels of interleukin (IL)‐17⁺, IL‐15⁺, Foxp3⁺ cells, fibrosis, and plasma B‐cell infiltration in sites with chronic periodontitis in smokers and subjects with type 2 diabetes. Methods: Gingival biopsies were harvested from the following groups: systemically and periodontally healthy subjects (healthy group, n = 10); non‐smokers and subjects with advanced periodontitis and without diabetes (non‐risk factor/periodontitis group, n = 10); heavy smokers with advanced periodontitis and without diabetes (smoking/periodontitis group, ≥20 cigarettes per day for at least the past 5 years, n = 10); and non‐smoking poorly controlled subjects with diabetes (glycated hemoglobin levels ≥9%) with advanced periodontitis (diabetes mellitus/periodontitis group DMP], n = 10). The number of IL‐17⁺, IL‐15⁺, and Foxp3⁺ cells was analyzed by immunohistochemistry, whereas the amount of fibrosis and plasma B‐cell infiltration in gingival tissue was analyzed by histomorphometry. Results: The number of Foxp3⁺ cells was significantly higher in the periodontitis groups compared to the healthy group (P <0.05). The DMP group presented higher levels of Foxp3⁺ cells than other periodontitis groups (P <0.05). The levels of IL‐15⁺ and IL‐17⁺ cells and the amount of fibrosis were higher in the DMP group than in the other groups (P <0.05). There was a trend for a decreased B‐cell infiltration in the DMP group (P >0.05). There was a slightly significant negative correlation between B‐cell infiltration and the amount of fibrosis (P <0.05). Conclusion: Upregulation of IL‐17⁺, IL‐15⁺, and Foxp3⁺ cells and increased amounts of fibrosis were observed in chronic periodontitis sites in subjects with type 2 diabetes, suggesting that periodontitis development in these subjects may be influenced by the T helper 17/T regulatory axis.