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.