Microbiota of Plaque Microcosm Biofilms: Effect of Three Times Daily Sucrose Pulses in Different Simulated Oral Environments

Abstract

Aim: To explore the Ecological Plaque Hypothesis for dental caries. To test modification of the microbiota of dental plaque microcosm biofilms by sucrose pulsing during growth in two different simulated oral fluids, and with a urea-induced plaque pH elevation. Methods: Plaque microcosm biofilms were cultured in an ‘artificial mouth’ with and without 6-min 5% w/v sucrose pulses every 8 h in an environment of continuously supplied saliva-like defined medium with mucin (DMM), or basal medium mucin (BMM, a high-peptone-yeast extract oral fluid analogue), and also in DMM + 10 mmol/l urea, with sucrose pulsing. Forty plaque species were quantified by checkerboard DNA:DNA hybridization analysis. Results: Sucrose pulsing extended rapid plaque growth in DMM and BMM, inducing major microbiota changes in DMM but not in BMM. In DMM, some streptococci and lactobacilli were unaffected while others implicated in caries, together with Candida albicans and Capnocytophaga gingivalis, increased. Aerobic, microaerophilic and major anaerobic species decreased. Elevation of the pH_max from 6.4 to 7.0 had almost no effect on the microbiota. BMM plaques were distinct from DMM plaques with particularly low levels of Candida albicans and Actinomyces. Conclusions: Modest sucrose exposure in a saliva-like environment causes profound changes in the developmental self-organization of plaque microcosms, supporting the Ecological Plaque Hypothesis. Nevertheless, there is significant stability in microbial composition with varying pH near neutrality. Increases in levels of specific bacteria in response to sucrose could be characteristic of organisms particularly important in caries.

Bacterial sucrose isomerases: properties and structural studies

“…Currently, sucrose is widely used in many agro-alimentary products. However, this disaccharide is efficiently metabolized, which highly influences the glycaemia of the body and promotes dental caries (Sissons et al 2007). Such effects are undesirable for health and especially for those suffering from obesity and diabetes (Saris 2003;Schulze et al 2004).…”

Oral health in South East Queensland Koalas: Prevalence of periodontal disease and other pathologies

“…Microbial factors such as adherence, retention and coaggregation t he microbial intra-and interspecies interactions, clonal heterogeneity and virulence mechanisms create a dynamic and complex ecosystem (Kuramitsu et al, 2007, Kolenbrander et al, 2006, Marsh, 2005, Overman, 2000, Rosan and Lamont, 2000, Socransky and Haffajee, 2002, Ten carte, 2006, Sissons et al, 2007.…”

The Microbial Aetiology of Periodontal Diseases

“…With specific microbial species demonstrating tropism for specific tissues (Aas et al, 2005;Gibbons, 1996;Mager et al, 2003;Van Houte et al, 1970), all of which interact with each other as well as with the oral environment, the oral cavity meets the criteria for the definition of a microbial ecosystem (Konopka, 2006;Marsh, 1992;Raes & Bork, 2008). Factors which determine the oral microflora include environmental factors (temperature, oxygen tension, pH, availability of nutrients), host factors (host tissues and fluids, genetics, diet) and microbial factors (adherence, retention and coaggregation, microbial intra-and interspecies interactions, clonal heterogeneity, virulence mechanisms) thus creating a dynamic and complex ecosystem (Kuramitsu et al, 2007;Marsh, 2005;Overman, 2000;Rosan & Lamont, 2000;Sissons et al, 2007;Socransky & Haffajee, 2002;Ten Carte, 2006). Dental plaque is a dynamic biofilm formed by the ordered succession of > 700 bacterial species.…”

“…Plaque biofilm formation has been described as a highly ordered sequential attachment of specific species over time, a process found to occur at the same rate for everyone (Palmer 2003). However, the architecture and function is person-specific and even though the same bacterial species may often be found in the same site of many different individuals, each individual may have a unique microbial fingerprint (Dethlefsen et al, 2007), which dictates the outcome of disease progression and response to treatment (Filoche et al, 2007(Filoche et al, , 2008Haffajee et al, 2006;Preza et al, 2008;Sissons et al, 2007;Teles et al, 2006). Not only do different persons harbour different oral microbiota, but different sites within the same mouth as well as different sites of the same tooth in the same mouth also differ in microbial composition due to environmental differences (Dawes et al, 2008;Haffajee et al, 2006Haffajee et al, , 2009Mager et al, 2003;Mineoka et al, 2008).…”