Christopher G. Daly

Bacteraemia due to dental flossing

AIMS The aims of this study were to (1) investigate the incidence of bacteraemia following flossing in subjects with chronic periodontitis or periodontal health; (2) identify the micro-organisms in detected bacteraemias; and (3) identify any patient or clinical factors associated with such bacteraemia. MATERIAL AND METHODS Baseline blood samples were obtained from 30 individuals with chronic periodontitis (17 M:13 F, 29-75 years) and 30 with periodontal health (17 M:13 F, 28-71 years) following a non-invasive examination. Each subjects teeth were then flossed in a standardized manner and blood samples obtained 30 s and 10 min. after flossing cessation. Blood samples were cultured in a BACTEC system and positive samples subcultured for identification. RESULTS Forty per cent of periodontitis subjects and 41% of periodontally healthy subjects tested positive for bacteraemia following flossing. Viridans streptococci, which are commonly implicated in infective endocarditis (IE), were isolated from 19% of positive subjects and accounted for 35% of microbial isolates. Twenty per cent of subjects had a detectable bacteraemia at 10 min. post-flossing. No patient or clinical factors were significantly associated with post-flossing bacteraemia. CONCLUSIONS Dental flossing can produce bacteraemia in periodontally healthy and periodontally diseased individuals at a rate comparable with that caused by some dental treatments for which antibiotic prophylaxis is given to prevent IE.

Incidence and magnitude of bacteraemia caused by flossing and by scaling and root planing

AIM (1) Investigate incidence, magnitude and bacterial diversity of bacteraemia due to flossing compared with scaling and root planing (SRP) and (2) Identify any associations with clinical parameters. MATERIALS AND METHODS Full-mouth flossing and single quadrant SRP were performed at separate visits for 30 patients with chronic periodontitis. Baseline blood samples and at 30 s and 10 min. after completion of flossing, 5 min. after initiation of SRP and 30 s and 10 min. after completion of SRP were obtained. Total bacteraemia and viridans streptococcal bacteraemia (VSB) were investigated. RESULTS Total bacteraemia incidence was 30% for flossing and 43.3% for SRP (no significant difference; p = 0.21). Flossing and SRP caused the same incidence of VSB (26.7%). Flossing caused a higher mean magnitude of total bacteraemia than SRP (7.4 ± 16.2 CFU/ml versus 2 ± 3.4 CFU/ml), but the difference was not significant (p = 0.2). Flossing caused a higher mean magnitude of VSB than SRP (1.2 ± 1.6 CFU/ml versus 0.4 ± 0.2 CFU/ml), but the difference was not significant (p = 0.09). Viridans streptococci comprised 11.4% of flossing bacteraemia isolates and 7.6% in SRP. No correlations were found between clinical parameters and incidence or magnitude of bacteraemia following flossing. Gingival inflammation was significantly associated with incidence of total bacteraemia (p = 0.01) and VSB (p = 0.001) following SRP. No correlations were found for any parameter and magnitude of total bacteraemia or VSB following SRP. CONCLUSIONS No differences were found between flossing and SRP in the incidence or magnitude of total bacteraemia or VSB. This finding is important in the ongoing re-evaluation of antibiotic prophylaxis to prevent infective endocarditis.

A change of heart: the new infective endocarditis prophylaxis guidelines

New Australian guidelines for the prevention of infective endocarditis were published in July 2008. The guidelines were revised by a multidisciplinary group to reflect recent changes in international recommendations regarding antibiotic prophylaxis for infective endocarditis. The reasons for the changes are explored in this review and the implications for dental practice are discussed.

Alveolar bone and the bisphosphonates

Bisphosphonate associated osteonecrosis of the jaws (ONJ) usually commences at the alveolus. Comparison is made between the structure and function of long bones and alveolar bone and the differing susceptibilities of the bisphosphonates at these different sites are explored. Current concepts of the causation of ONJ are discussed. The clinical implications of these findings to dentists managing periodontal conditions are presented.

Gingival enlargements and localized gingival overgrowths

Gingival enlargements are a common clinical finding and most represent a reactive hyperplasia as a direct result of plaque related inflammatory gingival disease. These generally respond to conservative tissue management and attention to plaque control. However, a small group are distinct from these and whilst they also represent a reactive tissue response, this occurs at the level of the superficial fibres of the periodontal ligament. These epulides grow from under the free gingival margin and not as a result of a primary inflammatory gingival enlargement. This distinct aetiopathogenesis separates this group of lesions both in terms of their specific clinical presentation and behaviour and their propensity for recurrence if managed inadequately.