A number of bacterial species are involved in the aetiology of periodontitis and include Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus and Treponema denticola. Several studies have shown differences in the microflora between the various forms of periodontal disease. It is recognised that smoking is a risk factor for periodontal disease, but there are conflicting reports on whether or not smoking has an effect on the periodontal microflora. We utilised the polymerase chain reaction to determine the presence of A. actinomycetemcomitans, P. gingivalis, P. intermedia, B. forsythus and T. denticola in subgingival plaque samples in 33 adult periodontitis (AP) patients and 24 generalized early-onset periodontitis (GEOP) patients prior to treatment. When GEOP and AP patients were compared there were significant differences in the number of positive patients and sites for both A. actinomycetemcomitans and B. forsythus (p=0.0023 and 0.00001, respectively). No statistically significant differences in the prevalence of these organisms were found between smoker and non-smoker groups. These results confirm that AP and GEOP sites harbour varied microflora, but show that B. forsythus and A. actinomycetemcomitans were detected to a significantly greater extent in this group of GEOP than in the AP patients investigated. Our findings do not support the hypothesis that smokers have significant differences in the prevalence of periodontal pathogens from non-smokers.

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.

The 2017 World Workshop Classification system for periodontal and peri-implant diseases and conditions was developed in order to accommodate advances in knowledge derived from both biological and clinical research, that have emerged since the 1999 International Classification of Periodontal Diseases. Importantly, it defines clinical health for the first time, and distinguishes an intact and a reduced periodontium throughout. The term "aggressive periodontitis" was removed, creating a staging and grading system for periodontitis that is based primarily upon attachment and bone loss and classifies the disease into 4 stages based on severity (I, II, III or IV) and 3 grades based on disease susceptibility (A, B or C). The British Society of Periodontology convened an implementation group to develop guidance on how the new classification system should be implemented in clinical practice. A particular focus was to describe how the new classification system integrates with established diagnostic parameters and pathways, such as the Basic Periodontal Examination (BPE). This implementation plan focusses on clinical practice; for research, readers are advised to follow the international classification system as described in the Journal of Clinical Periodontology (Vol 45, suppl 20, pp s1-s291). In this paper we describe a diagnostic pathway for plaqueinduced periodontal diseases that is consistent with established guidance and accommodates the novel 2017 classification system, as recommended by the BSP implementation group. Case vignettes are discussed as examples of the application of this guidance in clinical practice.

Early onset periodontitis (EOP) is considered to have a substantial genetic basis, although the gene or genes involved have not been elucidated. The aim of the present study was to investigate possible links between generalized EOP (GEOP) and genes regulating expression of the cytokines tumour necrosis factor (TNF) and interleukin-10 (IL-10). Microsatellite marker DNA sequences corresponding to phenotypic variations in cytokine response were analysed. Genotypic variations in cytokine response have been shown in vitro for TNF and IL-10, and specific alleles are implicated in diseases such as systemic lupus erythmatosus (SLE) and rheumatoid arthritis (RA). Two microsatellites at the IL-10 locus, IL10.R and IL10.G, and 1 microsatellite at the TNF locus, TNFa, were typed for 77 GEOP patients in the West of Scotland. Due to the highly polymorphic nature of the microsatellite loci, a statistical comparison with ethnically matched healthy controls (TNFa, n = 91, IL10.R, n = 94, IL10.G, n = 102) was conducted using a Monte Carlo simulation for each marker. No significant differences were observed for any of the 3 markers, although there were possible indications of trends similar to those observed in SLE for the IL10.G marker. In conclusion, no links were found between GEOP and microsatellites at TNFa, IL10.R or IL10.G loci.

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.