The bacteria that cause tooth decay protect themselves by hiding in a multilayered community of other bacteria and polymers, researchers in the US have found.
They did so by using a combination of super-resolution confocal and scanning electron microscopy with computational analysis to study how Streptococcus mutans arranges itself within the sticky biofilm we know as dental plaque.
This allowed them to examine the biofilm layer by layer, creating a 3D picture of the specific architectures.
They discovered that S. mutans most often appeared arranged in a mound against the tooth’s surface. It formed an inner core, with other commensal bacteria, such as S. oralis, forming additional outer layers precisely arranged in a crownlike structure.
Supporting and separating these layers was an extracellular scaffold made of sugars produced by S. mutans, effectively encasing and protecting the disease-causing bacteria.
“We found this highly ordered community with a dense accumulation of S. mutans in the middle surrounded by these halos of different bacteria, and wondered how this could cause tooth decay,” says Michael Koo from the University of Pennsylvania, co-senior author of a paper in the journal PNAS.
To learn more, the team attempted to recreate the natural plaque formations on a toothlike surface in the lab using S. mutans, S. oralis and a sugar solution. They grew rotund-shaped architecture then measured levels of acid and demineralisation associated with them.
“What we discovered, and what was exciting for us, is that the rotund areas perfectly matched with the demineralised and high acid levels on the enamel surface,” says Koo.
“This mirrors what clinicians see when they find dental caries: punctuated areas of decalcification known as white spots. The domelike structure could explain how cavities get their start.”
In a final set of experiments, the team put the rotund community to the test, applying an antimicrobial treatment and observing how the bacteria fared.
When the rotund structures were intact, the S. mutans in the inner core largely avoided dying from the antimicrobial treatment. Only breaking up the scaffolding material holding the outer layers together enabled the antimicrobial to penetrate and effectively kill the cavity-causing bacteria.
The findings, the researchers say, may not only help more effectively target the pathogenic core of dental biofilms, but also have implications for other fields.
“It demonstrates that the spatial structure of the microbiome may mediate function and the disease outcome, which could be applicable to other medical fields dealing with polymicrobial infections,” says Michael Koo.
“It’s not just which pathogens are there but how they’re structured that tells you about the disease that they cause,” adds Marvin Whiteley, from Georgia Tech. “Bacteria are highly social creatures and have friends and enemies that dictate their behaviours.”
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