Collaborative Research Reveals Surprising Bacterial Species Linked to Tooth Decay

Collaborating scientists from 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 have made an unexpected discovery regarding the development of tooth decay. 

Traditionally, the bacterial species Streptococcus mutans was considered the primary cause of dental caries. However, in a recent study published in Nature Communications, the research teams demonstrated that Selenomonas sputigena, previously associated only with gum disease, can significantly enhance the cavity-causing abilities of S. mutans when they work together. 

Their findings were published under the title “Selenomonas sputigena acts as a pathobiont mediating spatial structure and biofilm virulence in early childhood caries”.

Identifying Specific Selenomonas Species in Tooth Decay

Tooth decay, or dental caries, is considered the most common chronic disease among children and adults globally. It occurs when acid-producing bacteria, including S. mutans, form a protective biofilm, or plaque, on teeth, primarily due to inadequate oral hygiene practices. 

Previous studies have identified various bacterial species within plaque, in addition to S. mutans. Among these species are different types of Selenomonas, which are typically associated with gum disease and are anaerobic bacteria that do not require oxygen to survive. However, this recent study is the first to identify a specific Selenomonas species as a contributor to tooth decay.

Bacterium Capable of Worsening Caries

The researchers integrated various omics analyses of supragingival biofilm samples collected from 416 preschool-age children to identify disease-relevant interactions between different microbial species. Through advanced imaging techniques and virulence assays, the team examined the behavior and metabolic activity of S. sputigena, Prevotella salivae, and Leptotrichia wadei, both individually and in combination with S. mutans. 

Their findings showed that S. sputigena, an anaerobic bacterium with an undiscovered role in supragingival biofilm, became trapped within the exoglucans produced by S. mutans. Although incapable of causing caries independently, S. sputigena, when co-infected with S. mutans, contributes to extensive tooth enamel lesions and worsens the severity of the disease. 

Study co-senior author Hyun (Michel) Koo, DDS, PhD, Co-Director of the Center for Innovation & Precision Dentistry at Penn Dental Medicine, expressed the significance of this unexpected finding.

“This gives us new insights into the development of caries, highlights potential future targets for cavity prevention, and reveals novel mechanisms of bacterial biofilm formation that may be relevant in other clinical contexts,” said Koo.

Possibilities for Cavity Prevention

The discovery of this complex microbial interaction provides a deeper understanding of the development of childhood cavities and opens up new possibilities for cavity prevention strategies. Koo suggests that disrupting the protective superstructures formed by S. sputigena using specific enzymes or more effective tooth-brushing methods could be potential approaches for preventing cavities.

Kimon Divaris, PhD, DDS, a professor at UNC’s Adams School of Dentistry, another of the co-senior authors, emphasized the importance of the collaborative effort, stating, “This was a perfect example of collaborative science that couldn’t have been done without the complementary expertise of many groups and individual investigators and trainees.”

Moving forward, the researchers plan to investigate in greater detail how S. sputigena, an anaerobic and motile bacterium, ends up in the oxygen-rich environment of the tooth surface. Koo believes that this phenomenon, where bacteria from one environment enter and interact with bacteria in a different environment, resulting in the formation of remarkable superstructures, will be of significant interest to microbiologists.

Click here to read the full article.