Researchers at the University of Minnesota School of Dentistry are exploring how oral bacteria communicate and whether disrupting this "chatter" may prevent plaque formation and support a healthy oral microbiome and prevent periodontal diseases.
Furthermore, using specialized enzymes to remove certain signaling molecules may promote the growth of healthy dental species, according to a university news release dated November 17.
“Understanding how bacterial communities communicate and organize themselves may ultimately give us new tools to prevent periodontal disease,” Mikael Elias, PhD, an associate professor at the university and lead author of a recently published study, said in the release.
Bacteria in the mouth constantly chat with each other through a process called quorum sensing. Many of these species communicate using signaling molecules known as N-acyl homoserine lactones (AHLs). Researchers sought to alter bacterial communication to prevent poor oral health outcomes, according to the release.
They found that bacteria in dental plaque produce AHL signals in aerobic environments that require oxygen to survive, such as above the gumline, and that these signals can be received by bacteria in anaerobic environments that do not require oxygen beneath the gumline. Removing AHL signals with specialized enzymes called lactonases enriched health-associated dental plaque species.
When AHL signaling was blocked under aerobic conditions, levels of beneficial bacteria increased. In contrast, adding AHLs under anaerobic conditions promoted the growth of disease-associated late colonizers, according to the release.
These findings suggest quorum sensing plays different roles above and below the gumline, with important implications for periodontal treatment. By disrupting bacterial signaling, it may be possible to keep dental plaque in a health-associated state and maintain a balanced oral microbiome.
However, further research is needed to understand how bacterial communication varies across the mouth and stages of periodontal disease, according to the release.
“By disrupting the chemical signals bacteria use to communicate, one could manipulate the plaque community to remain or return to its health-associated stage," Elias said.
