1. Anti-Plaque Activity

Anti-Plaque Activity

It is widely acknowledged that mechanical hygiene is the most common method to remove plaque, however mechanical plaque removal is not enough (Bellamy et al. 2014). Stannous fluoride hemotherapeutically inhibits plaque regrowth and metabolism to improve plaque control.

The development of supragingival plaque can be divided into several distinct phases (Marsh 2006, Liljemark & Bloomquist 1996, Hojo et al. 2009, Lovegrove 2004):

  • Formation of the acquired pellicle. The pellicle consists mainly of salivary glycoproteins that are adsorbed onto the tooth surface within minutes of exposure of the surface to saliva (e.g., after cleaning). It is acellular, membranous and appears to be unstructured.
  • Attachment of primary plaque-forming bacteria to pellicle-coated tooth surfaces. Bacterial colonization begins with Gram-positive cocci and rods which loosely adhere within an hour.
  • Bacterial growth to form micro-colonies on the pellicle. The bacteria also produce an extra-cellular matrix that facilitates the attachment and division of bacteria (co-aggregation) and protects the micro-colonies from host defenses and antimicrobial agents. Co-adhesion enables other bacteria to adhere to the earlier colonizers. By 8–12 hours, the plaque has become multi-layered.
  • Maturation of the dental plaque (dental biofilm): it is in this phase of development that the plaque may become pathogenic. At 24–48 hours, only Gram-positive cocci and rods are present and the plaque increases in thickness, however by day five Gramnegative filaments increase in number and begin to coaggregate with the Gram-positive microorganisms and form a more complex structure.

Subgingival plaque develops subsequent to supragingival plaque development. The presence of plaque at the gingival margin results in an inflammatory reaction, which affects the composition of the plaque. The structure of the plaque becomes highly organised with micro-colonies interspersed with voids and channels that allow nutrients and other agents to circulate through the plaque (Figure 2). Different bacterial species also function synergistically or antagonistically within the plaque. Three to twelve weeks after plaque begins to form, Gram-negative cocci and rods, filamentous bacteria and spirochaetes collectively become dominant in the subgingival plaque.

Dental plaque contributes to the development of gingivitis. The onset of gingivitis coincides with an increase in the bacterial load and complexity of plaque as it matures. Stannous fluoride chemotherapeutically acts against the bacteria that cause plaque.

Figure 2. The structure of dental plaque

The structure of dental plaque

Mechanism of action of stannous fluoride and anti-bacterial activity

Scientific evidence indicates the anti-bacterial activity of stannous fluoride against both Gram-positive and Gram-negative bacteria and inhibits bacterial metabolism. Bacteria exposed to stannous fluoride retain large amounts of tin, and bacterial metabolism could be affected through several different mechanisms. Exposure to stannous fluoride reduces bacterial growth, bacterial adhesion, and the production of acids and other metabolic toxins that contribute to gingivitis. Active levels of tin in plaque persist for up to twelve hours following exposure to stabilized stannous fluoride dentifrice, consistent with the plaque and gingivitis reductions observed for the dentifrice and indicative of a sustained mechanism of action with twice-daily use (Ramji et al. 2005, Otten et al. 2012).

Early studies of stannous fluoride suggest that it affects bacterial adhesion. Plaque bacteria produce extracellular polysaccharides (EPS) which are responsible for the adhesiveness of the plaque. Busscher et al. (2008) demonstrated that stabilized stannous fluoride dentifrice significantly reduced EPS production in vivo compared to a regular sodium fluoride dentifrice. This helps to prevent bacterial adhesion and cohesion, thus reducing the thickness and stickiness of plaque.

One important mechanism that has been proposed for stannous fluoride’s anti-bacterial action is the oxidation by stannous of thiol groups in the enzymes involved in bacterial glycolysis (Ellingsen et al. 1980) In vivo plaque glycolysis and regrowth models have shown that stabilized stannous fluoride dentifrice exerts strong inhibitory actions on plaque acid production and regrowth relative to a regular sodium fluoride dentifrice (Ramji et al. 2005). A minimum metabolic inhibitory concentration was determined for stannous by measuring the reduction in acid production by bacteria in human saliva samples; 99% inhibition of metabolic activity occurred as low as 20 ppm stannous.

Most recently, research has shown that stannous fluoride makes plaque less toxic, or less virulent, by neutralizing lipopolysaccharides (LPS), or bacterial endotoxins (Haught et al. 2016a, Haught et al. 2016b, Huggins et al. 2016, Klukowska et al. 2017). LPS are responsible for activating toll-like receptors, which trigger the host response and inflammatory cascade associated with periodontal disease. By blocking the reactivity of LPS with tissue receptors that trigger inflammation, stannous fluoride decreases the pathogenicity of plaque.

Stannous Fluoride inhibits plaque by killing bacteria, Inhibiting plaque metabolism/acid production/regrowth, reducing bacterial adhesion and cohesion, reducing plaque virulence, sustained activity (retained up to 12 hours)
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