Oral conditions such as gingivitis and chronic periodontitis are found worldwide and are among the most prevalent microbial diseases of mankind. The cause of these common inflammatory conditions is the complex microbiota found as dental plaque, a complex microbial biofilm. Despite 3000 years of history demonstrating the influence of oral status on general health, it is only in recent decades that the association between periodontal diseases and systemic conditions such as coronary heart disease and stroke, and a higher risk of preterm low birth-weight babies, has been realised. Similarly, recognition of the threats posed by periodontal diseases to individuals with chronic diseases such as diabetes, respiratory diseases and osteoporosis is relatively recent. Despite these epidemiological associations, the mechanisms for the various relationships remain unknown. Nevertheless, a number of hypotheses have been postulated, including common susceptibility, systemic inflammation with increased circulating cytokines and mediators, direct infection and cross-reactivity or molecular mimicry between bacterial antigens and self-antigens. With respect to the latter, cross-reactive antibodies and T-cells between self heat-shock proteins (HSPs) and Porphyromonas gingivalis GroEL have been demonstrated in the peripheral blood of patients with atherosclerosis as well as in the atherosclerotic plaques themselves. In addition, P. gingivalis infection has been shown to enhance the development and progression of atherosclerosis in apoE-deficient mice. From these data, it is clear that oral infection may represent a significant risk-factor for systemic diseases, and hence the control of oral disease is essential in the prevention and management of these systemic conditions.

In terms of the pathogenesis of cardiovascular disease (CVD) the focus has traditionally been on dyslipidemia. Over the decades our understanding of the pathogenesis of CVD has increased, and infections, including those caused by oral bacteria, are more likely involved in CVD progression than previously thought. While many studies have now shown an association between periodontal disease and CVD, the mechanisms underpinning this relationship remain unclear. This review gives a brief overview of the host-bacterial interactions in periodontal disease and virulence factors of oral bacteria before discussing the proposed mechanisms by which oral bacterial may facilitate the progression of CVD.

Dark‐colored fruit berries are a rich source of polyphenols that could provide innovative bioactive molecules as natural weapons against dental caries. High‐quality extracts of cranberry, blueberry, and strawberry, and a combination of the three berry extracts (Orophenol), were used to treat 24‐h‐old Streptococcus mutans biofilms. The grown biofilms were treated with the berry extracts at concentrations ranging from 62.5 to 500 μg ml−1. Treated biofilms were assessed for metabolic activity, acidogenicity, biovolumes, structural organization, and bacterial viability. The biofilms treated with the cranberry and Orophenol extracts exhibited the most significant reductions in metabolic activity, acid production, and bacterial/exopolysaccharide (EPS) biovolumes, while their structural architecture appeared less compact than the control‐treated biofilms. The blueberry extract produced significant reductions in metabolic activity and acidogenicity only at the highest concentration tested, without significantly affecting bacterial/EPS biovolumes or biofilm architecture. Strawberry extracts had no significant effects on S. mutans biofilms. None of the berry extracts were bactericidal for S. mutans. The results indicate that cranberry extract was the most effective extract in disrupting S. mutans virulence properties without significantly affecting bacterial viability. This suggests a potential ecological role for cranberry phenols as non‐bactericidal agents capable of modulating pathogenicity of cariogenic biofilms.

Aim To determine the relationship between periodontal pathogen load and anti‐human heat shock protein 60 (hHSP60) antibodies in patients with established cardiovascular disease (CVD). Materials and Methods Participants were cardiovascular patients (n = 74) with a previous hospital admission for myocardial infarction. Concurrent periodontal pathogen load of Porphyromonas gingivalis, Fusobacterium nucleatum, Tannerella forsythia and Aggregatibacter actinomycetemcomitans was determined using quantitative real‐time PCR. Serum antibodies to these pathogens, GroEL and hHSP60 were determined using an ELISA. Results There was a trend for increasing anti‐hHSP60 antibody as the number of bacterial species increased. The strongest positive correlations were found between anti‐hHSP60 levels and numbers of T. forsythia (r = 0.43; p < 0.001) and between anti‐hHSP60 and anti‐GroEL levels (r = 0.39; p = 0.001). Patients with extensive periodontal pocketing (≥4 mm) had higher numbers of P. gingivalis and T. forsythia (p < 0.05) and a higher subgingival pathogen load (p < 0.05) than patients with minimal pocketing (≤1 site ≥ 4 mm). They also had significantly elevated anti‐hHSP60 levels (p < 0.05). Overall, the highest anti‐hHSP60 levels were seen in patients with extensive periodontal pocketing and all four bacterial species. Conclusions In cardiovascular patients, a greater burden of subgingival infection with increased levels of P. gingivalis and T. forsythia is associated with modestly higher anti‐hHSP60 levels.

Sodium lauryl sulphate is the major bacterial inhibitory compound in children's dentifrices.