Hans Preber

Tobacco Use as a Risk Factor

Tobacco, particularly tobacco smoking, has a substantial influence on periodontal health and disease. It is associated with an increased disease rate in terms of periodontal bone loss, periodontal attachment loss, as well as periodontal pocket formation. In addition, it exerts a masking effect on gingival symptoms of inflammation. Risk assessment based on an increasing body of investigations over the past few years suggests that the tobacco attributable risk is considerable, estimated odds ratios being of the order 2.5 to 6.0 or even greater. Although the mechanisms by which tobacco exerts its influence are obscure, information available to date does not support the view that its action simply relates to other environmental factors such as the dental plaque or some specific microflora. It seems more likely that it primarily has a systemic influence affecting host response or susceptibility. The chief novelty of the present report is that current data suggest that, although the overall disease prevalence is decreasing, the proportion of periodontal disease attributed to tobacco is stable or even increasing. This seems to be analogous to what has been observed for other smoking-associated chronic diseases. This, in turn, indicates that periodontal disease behaves like several other chronic diseases and, further, that tobacco should be considered a major risk factor for chronic periodontal disease. J Periodontol 1994;65:545-550.

Occurrence of gingival bleeding in smoker and non-smoker patients

The objective of the present investigation was to study the influence of cigarette smoking on the occurrence of gingival bleeding. The occurrence of bleeding was evaluated by probing at a standardized pressure of 60 g. The bleeding occurrence of each patient was indicated by the number of sites bleeding on probing as a percentage of the total. Twenty patients with moderate to severe periodontitis, 10 smokers and 10 non-smokers, participated in the study. The smoker patients had been regular smokers for at least 15 years, their present tobacco consumption being 20 cigarettes a day or more. The results showed that, although they had a significantly greater plaque index, smokers displayed a significantly lower bleeding occurrence than non-smokers, the average being 27% and 40%, respectively. The present findings suggest that gingival bleeding as measured by probing with a pressure of 60 g is reduced in smokers with periodontitis.

Effect of non-surgical treatment on gingival bleeding in smokers and non-smokers

According to previous findings, gingival bleeding seems to be reduced under the influence of cigarette smoking. The present study deals with the effect of non-surgical therapy on gingival bleeding in smokers and non-smokers. The underlying hypothesis was that the therapeutic effect in terms of reduction of gingival bleeding might differ in smokers and non-smokers. Twenty patients with moderate to severe periodontitis, 10 smokers and 10 non-smokers, took part in the study. Gingival bleeding was assessed by probing under a standardized pressure (60 g), and measurements were performed before and 1 month after the completion of active treatment. The active treatment included debridement of supra- and sub-gingival deposits by means of hand instrumentation. The treatment caused a reduction in plaque index and gingival bleeding both in smokers and in non-smokers. The plaque reduction was significantly greater in smokers. Nevertheless, the reduction in gingival bleeding was significantly less pronounced than that attained in non-smokers. The findings suggest that the gingival bleeding response to treatment is reduced in smokers. It would seem that in response to a given amount of plaque reduction the changes in gingival bleeding will be less apparent under the influence of smoking.

Periodontal Condition of Epileptic Adults Treated Long-Term with Phenytoin or Carbamazepine

The periodontal condition of 40 adult epileptic subjects (mean age 51 years) receiving long‐term therapy (mean 18 years) with phenytoin (PHT) or carbamazepine (CBZ) was studied. The subjects completed a questionnaire and underwent clinical and radiologic examination. Patients receiving PHT exhibited the same level of alveolar bone loss as those receiving CBZ. Patients receiving PHT exhibited more units with gingival overgrowth, reflected by the significantly higher number of gingival units with increased probing depth (p < 0.05). The results indicate that long‐term PHT does not result in increased risk for alveolar bone loss as compared with CBZ.