A Bacterium That Acts Like a Toothbrush

Researchers have identified a new ally in the war against tooth decay: an enzyme produced by a mouth bacterium that prevents plaque formation. The finding could eventually lead to the development of toothpaste that harnesses the body's own plaque-fighting tools.

The human mouth is awash with bacteria. More than 700 species thrive in the hot, moist conditions, including Streptococcus mutans, one of the main components of plaque. Clinging to the teeth in thin layers called biofilms, S. mutans digests sugars and produces acids that can eat into enamel and cause cavities. Other bacteria are more gracious guests. In 2009, for example, scientists found that S. salivarius, a type of bacterium found on the tongue and other soft tissues in the mouth, decreases the buildup of S. mutans biofilms.

Hidenobu Senpuku, a biologist at the National Institute of Infectious Diseases in Tokyo, and colleagues wanted to know what substance conferred S. salivarius's cavity-fighting powers. Using chromatography, a method that divides the molecules in a mixture based on charge or size, they separated out individual proteins from samples of the microbe. The scientists then mixed each kind of protein with S. mutans cells and measured which cultures grew the smallest amount of biofilm on plates in the lab. The protein FruA, an enzyme that breaks apart complex sugars, was the most powerful biofilm blocker.

The researchers also found that a form of FruA, produced by the common fungus Aspergillus niger and available off-the-shelf, stymies plaque equally well. This commercial FruA worked despite the fact that its amino acid sequence is somewhat different from that of S. salivarius FruA. That might speed the development of toothpastes that include FruA, says Senpuku.

The findings, reported in Applied and Environmental Microbiology, are not a license to eat all the candy you want, however. When researchers increased the concentration of sucrose, a type of sugar, in mixtures containing S. salivarius FruA and S. mutans, the beneficial bacterium lost its ability to prevent biofilm formation. The authors write that this observation may help explain why a 1996 study found that FruA contributed to cavity formation in rats.

Mary Ellen Davey, a microbiologist at the Forsyth Institute in Cambridge, Massachusetts, agrees that the findings could spur the development of better toothpaste. But she says that won't be an easy task. Finding "the formulation that would 'guarantee' that the enzyme remained enzymatically active on the shelf of your favorite drug store is a big challenge," she says.