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OBJECTIVES: To compare the effects of scaling and root planing (SRP) on clinical and microbiological parameters at selected sites in smoker and non-smoker chronic and generalized aggressive periodontitis patients. MATERIALS AND METHODS: Clinical parameters including probing depth (PD), relative attachment level (RAL), and bleeding upon probing (BOP), and subgingival plaque samples were taken from four sites in 28 chronic periodontitis (CP) and 17 generalized aggressive periodontitis (GAgP) patients before and after SRP. Polymerase chain reaction assays were used to determine the presence of A. actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythensis, Prevotella intermedia and Treponema denticola. RESULTS: Both CP and GAgP non-smokers had significantly greater reduction in pocket depth (1.0+/-1.3 mm in CP smokers versus 1.7+/-1.4 mm in non-smokers, p=0.007 and 1.3+/-1.0 in GAgP smokers versus 2.4+/-1.2 mm in GAgP non-smokers, p lt 0.001) than respective non-smokers, with a significant decrease in Tannerella forsythensis in CP sites (smokers 25% increase and non-smokers 36.3% decrease, p lt 0.001) and Prevotella intermedia at GAgP sites (smokers 25% reduction versus 46.9% in non-smokers, p=0.028). CONCLUSION: SRP was effective in reducing clinical parameters in both groups. The inferior improvement in PD following therapy for smokers may reflect the systemic effects of smoking on the host response and the healing process. The lesser reduction in microflora and greater post-therapy prevalence of organisms may reflect the deeper pockets seen in smokers and poorer clearance of the organisms. These detrimental consequences for smokers appear consistent in both aggressive and CP. (c) Blackwell Munksgaard, 2005.

Objectives: In order to elucidate the genetic background to EOP it is useful to investigate associations with genetic polymorphisms of immune response genes, whose products play a role in the inflammatory process. The aim of this study was to examine IL1A and IL1B genetic polymorphisms in unrelated European white Caucasian patients with generalised early-onset periodontitis (GEOP). Material and methods: Polymerase chain reaction (PCR) amplification of the IL1A (−889) gene and IL1B (+3953) gene (56 patients, 56 controls) was carried out and PCR products subjected to restriction fragment length polymorphism (RFLP) analysis. Results: There were no significant differences between patients and controls for any of the genotype or allele frequencies investigated (p=1.0). Smoking status was also included as a covariate but this did not alter the results. Furthermore, expression of the composite genotype described by Kornman and coworkers was also investigated in these subjects. No significant differences were found between patients and controls whether smoking was included as a covariate or not. Conclusion: The lack of any association between the IL1 polymorphisms and GEOP, in the population presented here, brings into doubt the usefulness of these candidate genes as markers of susceptibility to this form of periodontitis.