A joint study by researchers at the University of Pennsylvania School of Dental Medicine and the Adams School of Dentistry and Gillings School of Global Public Health at the University of North Carolina has found that a bacterial species called Selenomonas sputigena can have a key impact on causing tooth decay. This marks a departure from long-established research that has concentrated on another bacterial species, the plaque-forming, acid-making Streptococcus mutans, as the primary instigator of dental caries. The team showed that S. sputigena, formerly only associated with gum disease, can act as a key partner of S. mutans, significantly enhancing its cavity-creating power.
The findings highlight new areas of research into caries, emphasize potential future targets for cavity prevention, and reveal the novel mechanisms of microbial biofilm generation that could have relevance in other clinical situations.
Caries is considered one of the most common chronic diseases affecting both children and adults in the US and globally. This arises from insufficient removal of S. mutans and other acid-making bacteria by brushing and other dental care methods. These can end up forming protective biofilm on teeth. Within the biofilm, the bacteria consume sugars from food or drink, converting them into acids that if left it in place for too long can erode tooth enamel, ultimately resulting in cavities.
Additional species other than S. mutans have been identified in the past in studies of plaque bacterial contents. These include certain species of Selenomonas, which are more commonly found beneath the gum in gum disease. This new research pinpoints a specific Selenomonas bacterium as a contributor to tooth decay.
The North Carolina researchers sourced plaque samples from the teeth of 300 children aged between three and five, half of whom had caries, and, with input from the Pennsylvania lab, analysed the samples using an array of advanced tests. These included sequencing the bacterial gene activity in the samples, and direct microscopic imaging. Subsequently, the researchers validated their findings on another set of plaque samples from 116 children age three to five.
These results showed that although S. sputigena only constitutes one of several caries-linked bacterial species in plaque beside S. mutans, and it does not cause caries when present on its own, it has a remarkable ability to team-up with S. mutans to significantly boost the caries process. Scientists knew S. mutans used available sugar to build sticky constructions called glucans within the protective plaque environment and subsequently found that S. sputigena, with small appendages enabling it to move on surfaces, can get snagged by glucans. Once trapped, the bacterium multiples quickly, using its own cells to encase and safeguard S. mutans. The result is an unexpected partnership that substantially increases and concentrates acid production, which exacerbates the condition of the cavity.
Since disrupting the protective superstructures built by S. sputigena with specific enzymes or, more effective tooth-brushing methods, could be a way to address the problem, the research team is focusing on exploring this area further. The team plans to study how this anaerobic motile bacterium ends up present in the aerobic environment of the tooth surface.
The team’s findings show a more complex microbial interaction than was previously thought to occur and offer a greater understanding of how childhood cavities develop. This insight could facilitate improved preventive measures against cavities in the future.
“Selenomonas sputigena acts as a pathobiont mediating spatial structure and biofilm virulence in early childhood caries” was co-authored by Di Wu, Kimon Divaris, Zhi Ren, Hunyong Cho, M. Andrea Azcarate-Peril, Poojan Shrestha, Bridget Lin, Alena Orlenko, Miguel Simancas-Pallares, Jeffrey Roach, Jeannie Ginnis, Apoena Aguiar Ribeiro, Kari North, Chuwen Liu, Andrea Ferreira Zandona and Hyun “Michel” Koo. The work was partly funded via the National Institutes of Health.
