Might smoking assuage the pro-inflammatory effect of diabetes in periodontal sites?

This study evaluated the effects of type 2 diabetes mellitus (DM), smoking, and these two factors combined on gingival crevicular fluid levels and ratios of pro-/anti-inflammatory cytokines. Associations between cytokines with each other and with key periodontal pathogens in periodontal sites under the challenge of one or both of these risk factors were also assessed.

A total of 102 subjects with periodontitis were included in this cross-sectional study and assigned to one of the following groups: non-diabetic non-smokers (control group, n = 25), non-smokers with DM (DM group, n = 30), non-diabetic smokers (S group, n = 26), and smokers with DM (S + DM group, n = 21). The levels of 13 pro-inflammatory (IFN-γ, TNF-α, MIP-1α, GM-CSF, IL-1β, IL-2, IL-6, IL-7, IL-8, IL-12, IL-17, IL-21, and IL-23) and 5 anti-inflammatory (IL-4, IL-5, IL-10, IL-13, and TGF-β) cytokines were assessed in healthy and diseased sites, using multiplex immunoassay. Ratios of pro-/anti-inflammatory cytokines were obtained in all possible permutations. The levels of 7 key periodontal pathogens were evaluated by qPCR.

Overall, the ratios of pro-/anti-inflammatory cytokines were higher in healthy and diseased sites of the DM group and in healthy sites of the S + DM group, and lower in diseased sites of the S group, compared with the control (p < .05). The proportion of the pro-inflammatory cytokines in relation to the 18 cytokines studied was higher in the DM group and lower in the S group, whereas the proportion of the anti-inflammatory cytokines was lower in both diabetic groups and higher in the S group, compared to the control (p < .05). A cluster of six common cytokines (IL-4, IL-5, IL-12, IL-13, IL-21, and IL-23) was observed in the diseased sites of all groups studied. Eight common cytokines (IL-4, IL-5, IL-12, IL-13, IL-17, IL-21, IL-23, and IFN-γ) grouped closely in the healthy sites of both diabetic groups. Significant associations between pathogens and cytokines occurred mainly in the diseased sites of the S + DM group (p < .05).

Diabetes mellitus induced an overall pro-inflammatory state, while smoking mainly stimulated immunosuppression in periodontal sites. When the two risk factors overlapped, smoking seemed to partially assuage the hyperinflammatory effect of DM.