Many components of our oral hygiene regimens are meant to keep cariogenic bacteria at bay: sodium fluoride in ACT interferes with electron transport and ATP synthesis, the essential oils in Listerine have antiseptic effects, and abrasives – small, insoluble particles in toothpaste – help remove plaque and calculus when you brush your teeth. Eliminating oral bacteria helps fight cavities, gingivitis, and periodontitis, but cavities (also called dental caries) aren’t caused by all oral microbes. The main culprit, Streptococcus mutans, causes caries by acidifying its environment, which demineralizes the enamel protecting our teeth.
Of course, S. mutans resides together with the rest of our oral microbes, where it forms multispecies biofilms that constitute the dental plaque (see right) that can lead to caries. Caries are generated when S. mutans ferments sucrose, found in our diets, into lactic acid, and this process occurs inside a biofilm that also contains other viridans streptococci and Actinomycetes. New research now published in the Journal of Bacteriology suggests that addition of L-Arginine can change the chemical makeup of the biofilm, specifically inhibiting caries without disrupting the rest of the oral microbial flora.
The research takes advantage of an arginolytic oral bacterium, Streptotoccus gordonii, that breaks down arginine to produce ammonia. This ammonia can prevent the pH from dropping, thereby negating the effects of the acid produced by S. mutans. First author Jinzhi He and lead scientist Hyun Koo were aware of previous research correlating higher salivary levels of arginine in caries-free people, and hypothesized that supplementing additional L-arginine might further decrease the risk of cavities. They tested in vitro mixed biofilms of S. mutans, S. gordonii, and Actinomyces naeslundii to represent three of the major oral bacterial species found in healthy people.
The biofilms were grown in the presence of sucrose, with or without L-arginine supplementation. The researchers observed that the pH of the biofilm was nearly tenfold higher with the arginine addition, as they had expected. The authors also found that arginine promoted S. gordonii dominance and maintained A. naeslundii growth, while preventing S. mutans outgrowth. This suggests a means to control the disease-causing members of a mixed bacterial population without having negative effects on the remaining members – minimal disturbance to the oral microbiome.
The effects weren’t limited to growth, however. Biofilms are encased in an extracellular matrix, and S. mutans contributes insoluble exopolysaccharides to this matrix in part through GtfB-mediated production. Arginine exposure repressed normal levels of S. mutans gtfB expression, resulting in less extracellular polysaccharide surrounding the biofilms (see image, left). So in addition to decreasing the pathogenic bacterial presence, the arginine-exposed biofilms are less protected by their extracellular matrix, and could potentially be more susceptible to antimicrobial molecules or removal by mechanical processes (like brushing your teeth!).
Arginine is already known to be an effective therapy for dentin hypersensitivity, and is generally recognized as safe (GRAS) at up to 20g/d. However, a number of experiments, such as in vivo studies, remain before we start adding L-arginine to all our toothpastes and mouthwashes. A biofilm disruptor such as L-arginine may go a long ways toward decreasing dental caries and increasing oral health, with minimal disruption to other oral microbes. This is the first step in applying a promising finding toward improving human health.
-- Julie Wolf