BACKGROUND: We examined whether smoking status could influence growth of potentially pathogenic bacteria in the periodontal environment of treated and untreated periodontal patients.
METHODS: We have previously reported effects of treatment status on marker bacteria in our patients. We established a history of any smoking during 6 months prior to microbiological sampling (F-ME, 16 smokers out of 64; MHM, 70 smokers out of 185). We used a commercial immunoassay to quantitate Porphyromonas gingivalis, Prevotella intermedia, and Actinobacillus actinomycetemcomitans in paper point samples from periodontal sites.
RESULTS: Logistic regression showed that in smokers, neither P. gingivalis nor A. actinomycetemcomitans was quantitatively increased, while P intermedia was somewhat increased. Multiple regression demonstrated that smoking disrupts the positive relationship between increasing probing depth and increasing bacterial growth that is found in non-smokers. In smokers, growth of marker bacteria at shallow sites (< or =5 mm) was significantly increased to the levels found at deeper sites (>5 mm) in both smokers and non-smokers. Supragingival plaque biofilm was identified as a reservoir for marker bacteria; smokers and nonsmokers had equal ranges of oral cleanliness.
CONCLUSIONS: Smoking-associated periodontitis is not simply a reflection of oral cleanliness. Smoking extends a favorable habitat for bacteria such as P. gingivalis, P. intermedia, and A. actinomycetemcomitans to shallow sites (< or =5 mm). Molecular byproducts of smoking interfere with mechanisms that normally contain growth of damaging bacteria at the surface of the oral mucosa in gingival crevices. In this way, smoking can promote early development of periodontal lesions.
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