Periodontitis and diabetes are complex chronic diseases, linked by an established bidirectional relationship. Risk for periodontitis is increased two to three times in people with diabetes compared to individuals without, and the level of glycaemic control is key in determining risk. In people who do not have diabetes, periodontitis is associated with higher glycated haemoglobin (HbA1c) and fasting blood glucose levels, and severe periodontitis is associated with increased risk of developing diabetes. In people with type 2 diabetes, periodontitis is associated with higher HbA1c levels and worse diabetes complications. Treatment of periodontitis in people with diabetes has been shown to result in improved glycaemic control, with HbA1c reductions of 3-4 mmol/mol (0.3-0.4%) in the short term (3-4 months) post-treatment. Given that treatment of periodontitis results in clinically relevant reductions in HbA1c, the dental team has an important role in the management of patients with diabetes. Improved interprofessional working in relation to diabetes and periodontitis has been advocated by professional and scientific organisations, though practical and systemic barriers make this challenging. This paper reviews current evidence linking periodontitis and diabetes, and considers the role of the dental team in the wider context of management of patients with diabetes and periodontitis.

Gingivitis and chronic periodontitis are highly prevalent chronic inflammatory diseases. Gingivitis affects the majority of people, and advanced periodontitis is estimated to affect 5-15% of adults. The detection and diagnosis of these common diseases is a fundamentally important component of oral health care. All patients should undergo periodontal assessment as part of routine oral examination. Periodontal screening using methods such as the Basic Periodontal Examination/Community Periodontal Index or Periodontal Screening Record should be performed for all new patients, and also on a regular basis as part of ongoing oral health care. If periodontitis is identified, full periodontal assessment is required, involving recording of full mouth probing and bleeding data, together with assessment of other relevant parameters such as plaque levels, furcation involvement, recession and tooth mobility. Radiographic assessment of alveolar bone levels is driven by the clinical situation, and is required to assess bone destruction in patients with periodontitis. Risk assessment (such as assessing diabetes status and smoking) and risk management (such as promoting smoking cessation) should form a central component of periodontal therapy. This article provides guidance to the oral health care team regarding methods and frequencies of appropriate clinical and radiographic examinations to assess periodontal status, to enable appropriate detection and diagnosis of periodontal conditions.

Novel nicotine products, particularly electronic cigarettes (e-cigarettes), have become increasingly popular over the past decade. E-cigarettes are sometimes regarded as a less harmful alternative to tobacco smoking, and there is some evidence of their potential role as a smoking cessation aid. However, there are concerns about their health consequences, particularly in users who are not tobacco smokers, and also when used long term. Given the mode of delivery of these products, there is potential for oral health consequences. Over the past few years, there have been an increasing number of studies conducted to explore their oral health effects. In vitro studies have reported a range of cellular effects, but these are much less pronounced than those resulting from exposure to tobacco smoke. Microbiological studies have indicated that e-cigarette users have a distinct microbiome, and there is some indication this may be more pathogenic compared to nonusers. Evidence of oral health effects from clinical trials is still limited, and most studies to date have been small in scale and usually cross-sectional in design. Epidemiological studies highlight concerns over oral dryness, irritation, and gingival diseases. Interpreting data from e-cigarette studies is challenging, given the different populations that have been investigated and the continual emergence of new products. Overall, studies reveal potential oral health harms, underscoring the importance of efforts to reduce use in nonsmokers. However, in smokers who are using e-cigarettes as an aid to help them quit, the benefits of quitting tobacco smoking may outweigh any negative oral health impacts of e-cigarette use, particularly in the short term. Future research is needed to understand the clinical significance of some of the biological changes observed by following different cohorts of users longitudinally in carefully designed clinical studies and pragmatic trials supported by high-quality in vitro studies.

Porphyromonas gingivalis lipopolysaccharide (LPS) (strain W50) interacts with Toll-like receptor 2 (TLR-2) leading to cytokine expression and inflammation, and thereby plays a key role in the pathogenesis of periodontal disease. The aims of this study were to investigate gene expression of key regulatory mediators of innate immune responses in a human monocytic cell line (THP-1) to P. gingivalis LPS and to compare these results with those obtained using the TLR-4 ligand, Escherichia coli LPS. Custom-made Taqman low-density arrays were used for expression profiling of 45 different cytokine-related genes. Both types of LPS highly up-regulated interleukin (IL)-1α and IL-1β, IL-18 receptor (IL-18R), IL-18R accessory protein and IL-1 family (IL-1F)9. Expression levels of IL-1F6, IL-1F7 and caspase-1 were unaltered by either LPS. Genes for tumour necrosis factor-α, IL-6, leukaemia inhibitory factor and IL-32 were also highly induced by both LPS. For a subset of genes, including CXC chemokine ligand 5 (CXCL5), expression was induced only by E. coli LPS or was up-regulated more highly by E. coli compared with P. gingivalis LPS in THP-1 monocytes. A similar expression pattern was also observed in dendritic cells. Analysis of signalling pathways which lead to CXCL5 expression indicated that the mechanisms underpinning the differential responses did not involve the recruitment of different adaptor proteins by TLR-2 and TLR-4, and therefore occur downstream of the receptor–adaptor complex. We conclude that differences in signalling pathways activated by TLR-2 and TLR-4 ligands lead to differential innate immune responses which may be important in polymicrobial diseases such as periodontal disease.