Introduction:
Cigarette users are more susceptible than non-smokers to chronic periodontitis, a bacterial-induced, inflammation-driven, destructive disease of the supporting tissues of the teeth. Limited evidence suggests that environmental smoke may similarly predispose to periodontal diseases. We hypothesized that levels of microbiological mediators and / or inflammatory markers of chronic periodontitis would be intermediate in those exposed to environmental tobacco smoke compared to active and non-smokers.

Material and Methods:
Self-reported non-smokers (n = 20), current smokers (n = 20) and environmentally-exposed (n = 20) individuals were recruited from a University periodontal clinic. Clinical periodontal measurements, comprising plaque index, probing depth, clinical attachment level and bleeding on probing, were recorded at four sites per tooth. Whole saliva samples were collected and cotinine levels determined by EIA. Treponema denticola and Porphyromonas gingivalis infection was determined by PCR, while matrix metalloproteinase-8 (MMP-8) and interleukin-8 (IL-8) concentrations were determined by ELISA.

Results:
Smoking groups were subsequently reassigned in accord with biochemical data. P. gingivalis infection was noted in most subjects, irrespective of smoking status. T. denticola infection was noted in 4/23 (17%) smokers, 0/16 (0%) environmentally-exposed recruits and 2/21 (10%) non-smokers. MMP-8 and IL-8 were significantly lower in smokers compared to both non-smokers and environmentally-exposed individuals (all p < 0.05).

Conclusions:
In this pilot study, where clinical parameters and bacterial infection were similar in all groups, active smoking was associated with a reduced inflammatory response, as determined by salivary MMP-8 and IL-8 burden, compared to non-smokers and environmentally-exposed smokers.