Methods: From smoking and non-smoking periodontitis patients venous blood was collected and the whole blood aliquots were diluted 10 fold for whole blood cell cultures (WBCC). WBCC were stimulated for 18 hours with a 1:100 sonic extract of Porphyromonas gingivalis (Pg-SE) and with 1 µg/ml lipooligosaccharide from Neisseria meningitidis (Nm-LOS). The release of the pro-inflammatory cytokines IL-1, IL-6, IL-8, as well as the T cell directing cytokines IL-10 and IL-12p40 were measured in the culture supernatants.
Results: To date 6 patients (3 smokers and 3 non-smokers, mean age 52 years) are included in the study. On average, after stimulation with Pg-SE, higher levels respectively of IL-1 (327 pg/ml vs. 185 pg/ml), IL-6 (3203 pg/ml vs. 1969 pg/ml) and IL-8 (31194 pg/ml vs. 12109 pg/ml) were observed for the smokers. The T cell directing cytokine IL-10 was also somewhat higher in smokers than non-smokers (56 pg/ml vs. 29 pg/ml respectively), while IL-12p40 was lower in smokers than non-smokers (145 pg/ml vs. 335 pg/ml, respectively). Comparable results were obtained when Nm-LOS stimulus was used in stead of Pg-SE. For both stimuli the IL-12p40/IL-10 ratio was lower in smokers than non-smokers.
Conclusion: Periodontitis patients who smoke may produce higher levels of pro-inflammatory cytokines. They also show a lower IL-12p40/IL-10 ratio, which may suppress the TH1 response pathway, and could exacerbate the periodontal lesion through activation of the TH2 pathway. These preliminary findings could be one of several explanations why smoking aggravates periodontitis.