ORAL MICROBIOTA IN SMOKERS AND NONSMOKERS IN NATURAL AND EXPERIMENTALLY-INDUCED GINGIVITIS

The present study primarily aimed at investigating the oral microbiota in smokers and non-smokers with established gingivitis and monitoring its composition during experimental gingivitis. Secondly it aimed at examining whether the composition of the microbiota is associated with different levels of gingival inflammation during this experimental gi ngivitis trial. For this purpose, 25 nondental university students wit h gingivitis were recruited. 11 subjects were smokers and 14 were non- smokers. After achieving gingival health, they entered a 14-day experi mental gingivitis trial. Plaque and bleeding were assessed before ente ring into the study (intake), at day 0, day 5 and at day 14 of the exp eriment. Microbiological samples from mucosal sites and dental plaque (taken at intake, day 0, and day 14) were analysed for the presence of Actinomyces species, Actinobacillus actinomycetemcomitans, Bacteroide s forsythus, Campylobacter rectus, Fusobacterium nucleatum, Peptostrep tococcus micros, Porphyromonas gingivalis, Prevotella intermedia and S treptococcus species. At day 14 of the experimental period, the level of plaque formation was not different between smokers and nonsmokers, but bleeding scores were lower in smokers than in non- smokers (15% an d 30% respectively, p=0.01). The change from natural gingivitis to a s tate of gingival health and a subsequent change from gingival health t o experimentally induced gingivitis was accompanied by quantitative al terations in the cultivable microbiota in both groups. Changes were mo st prominent in the transition from gingival health to experimental gi ngivitis and were found in dental plaque for Actinomyces species, C. r ectus, F. nucleatum, and P. intermedia. Within the group of non-smoker s, a distinction was made between subjects with a 'weak' or 'strong' i nflammatory response. No relationship with a single bacterial species could be established which would likely explain the differences in lev els of inflammation. It is concluded that differences in response to e xperimental gingivitis are not caused by major differences in the comp osition of the oral microbiota.