Those studies suggest that by-products originated from tobacco oxidation modify the clinical characteristics and the progression of periodontal diseases, and described smoking habit as a risk factor for periodontal diseases.
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Some early studies indicated that smoking patients showed more intense inflammatory gingival signs than non-smoking ones.
This finding was generally interpreted as related to a less efficient oral hygiene and its consequent intense plaque accumulation in smokers. Conversely, high tobacco consumption seemed to reduce gingival bleeding.
Later studies confirmed the reduction of inflammatory signs in smokers, suggesting that smoking could modify the inflammatory response to dental plaque accumulation.
The gingivitis experimental model in smoking and non-smoking patients showed that the plaque formation rate was similar in both groups.
However, smokers displayed a less pronounced gingival inflammatory reaction as compared with non-smokers.
The reduction of clinical inflammatory signsis confirmed by the decrease in gingival bleeding and suppuration on probing tissue redness, edema and the amount of blood vessels in the marginal gingival tissue.
