Identification of the cause of the development and progression of periodontitis has received extensive attention, with notable advances over the past decade in clinical, microbiological, immunological, biochemical, and behavioral knowledge. However, it is still largely unknown which factors lead to the conversion of non-destructive forms of periodontal disease into destructive forms and disease progression. Chronic adult periodontitis is believed to be influenced by an interaction of host defense and environmental factors. Although these variables have been studied extensively, no study has employed randomized controlled prospective human or randomized controlled community intervention designs, methodologies necessary to prove a variable to be a cause of periodontitis. Owing to the absence of literature employing rigorous experimental design, this article assesses systematically observational, cross-sectional and longitudinal studies to examine the potential causal association between cigarette smoking and periodontitis. The methodology of Sir Bradford Hill's criteria for causation was used as the framework. Results suggest that cigarette smoking is causally associated with periodontitis. That is, cigarette smoking is consistently associated with an increased prevalence/severity of periodontitis and is suspected on theoretical grounds of playing a causal role. Hill's criteria provide a useful methodology to better understand the pathogenesis of periodontal diseases and may be applied to study the pathogenesis of other dental diseases as well.

The anti-plaque, anti-gingivitis and anti-microbial efficacies of a phenolic compound (Listerine) and 2 different amine/stannous fluoride mouthwashes (Meridol I, II) were compared when these solutions were used in addition to usual tooth cleaning. A placebo preparation was utilized as a negative control and a chlorhexidine solution as a positive control in this double-blind study. After professional tooth cleaning, 49 volunteers continued their habitual, self-performed and non-supervised oral hygiene for a period of 2 weeks, in order to have a more standard baseline. At day 0, they began to rinse twice daily with 1 of the 5 mouthwashes. After 3 weeks of rinsing, plaque indices remained the lowest in the chlorhexidine and the Meridol I groups, while subjects using Listerine or Meridol II demonstrated similar indices significantly lower than that of individuals rinsing with the placebo solution. Through this period, the gingival index scores were similar in the Meridol, Listerine and chlorhexidine groups. At day 21, the mean GI scores in the chlorhexidine group were significantly lower than the scores in the placebo group. The plaque vitality scores showed a bacterial effect in vivo of chlorhexidine and, to a lesser extent, of the Meridol solutions. No substantial evidence of an antibacterial effect in vivo was found for Listerine. This study has demonstrated that when mouthrinses are used to supplement habitual mechanical oral hygiene, chlorhexidine remains the most powerful solution. Furthermore, it was also shown that a combination of habitual self-performed and non-supervised oral hygiene with Meridol or Listerine is more beneficial for plaque control than the use of mechanical oral hygiene alone.

The VAS pain scores showed that the anaesthetic gel 5% was statistically more effective than the placebo in reducing pain during periodontal debridement.

In this small population, regular maintenance treatment in a cross-section of highly motivated subjects with chronic periodontitis seemed to be equally successful in preventing progressive periodontal tissue destruction in current smokers and current non-smokers.

The present systematic review concludes that the evidence for an additional benefit of adjunctive antibiotic therapy in smokers with chronic periodontitis is insufficient and inconclusive. Additional well-designed RCTs are required to assess the effect of antibiotics in conjunction with periodontal treatments in smokers.