| Summary: | Introduction
Cigarette users are more susceptible than non-smokers to periodontitis,
a bacterial-induced, inflammation-driven, destructive disease of the supporting
tissues of the teeth. We hypothesized that clinical periodontal findings and
microbiological and/or inflammatory marker levels would be intermediate in
those exposed to environmental tobacco smoke compared to active smokers and
non-smokers.
Methods
Sixty individuals were recruited from a University periodontal clinic and
assigned as non-smokers, active smokers or passive-smokers according to their
self reports. Clinical periodontal measurements, comprising plaque index, probing
depth (PD), clinical attachment level (CAL) and bleeding on probing, were
recorded at six sites per tooth. Cotinine levels were determined in whole saliva
samples 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
Study groups were subsequently reassigned in accordance with the cotinine
data. The smoker group exhibited higher mean PD and CAL values compared to
the non-smoker group (p<0.05). Passive-smokers exhibited PD and CAL values
smaller than those of the active smokers and greater than those of the nonsmokers,
but the differences were not statistically significant. PD and CAL values
correlated with cotinine concentrations (p 0.05).
Conclusions
The present clinical periodontal findings provide further support for
a negative, dose-related effect of tobacco exposure on periodontal health. The
tendency for a more prevalent detection of T. denticola and for a suppressed
inflammatory response observed in the smokers may partly explain the increased
susceptibility to periodontal tissue destruction, but needs to be verified in larger
scale studies.
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