Infectious disease specialists looking for breakthrough findings have something to, well, sink their teeth into.
A review published October 30, 2017, in the journal Trends in Microbiology, highlights the importance of biofilms in improved understanding of the “local microenvironment where pathogens and commensals interact.” As the authors, from the Division of Community Oral Health at University of Pennsylvania Dental Medicine; the Center for Oral Biology at the University of Rochester (NY); and the Department of Oral Biology in the College of Dentistry at the University of Florida note, tooth decay (known clinically as “dental caries”) is arguably the most well-known example of a “polymicrobial biofilm disease,” as it is “driven by the diet” (namely sugar, which serves as a catalyst for emerging pathogens) and “microbiota-matrix interactions… on a solid surface.” Of course, polymicrobial diseases are infections that involve multiple agents; examples include respiratory infections, gastroenteritis, and conjunctivitis.
“Biofilms are more than just piled-up assemblages of different microorganisms,” review co-author Hyun (Michel) Koo, DDS, MS, PhD, a professor in Department of Orthodontics Divisions of Pediatric Dentistry and Community Oral Health at the University of Pennsylvania told Contagion®. “Rather, biofilms are self-constructed ecosystems where microorganisms are embedded in a complex extracellular matrix that provides a supportive scaffold as well as a heterogeneous and protected environment… against antimicrobials and [fosters] conditions for survival of pathogenic bacteria to cause disease. In dental caries, polymicrobial biofilms containing pathogenic bacteria embedded in a glue-like polymeric matrix create a sticky biofilm accumulation and… localized acidic pH microenvironment that erode the enamel of the adjacent teeth, leading to tooth decay. Thus, the matrix helps biofilm to ‘cling’ onto teeth and create localized acidic pH despite being ‘bathed’ by buffering saliva.”
Dr. Koo and his colleagues summarize recent advances in the understanding of the role of the biofilm matrix and interactions between opportunistic pathogens and commensals in the pathogenesis of tooth decay, hoping to use the disease as a model for biofilm involvement in infectious diseases in general. They also describe existing research into the role matrix-producing organisms play in “driving the disease process” in other infections linked with polymicrobial biofilms.
While they emphasize that existing research has determined that the “assembly” of the extracellular polymeric substances matrix and “synergistic multispecies efforts triggered by the host’s dietary sugars” both play a vital role in cariogenic biofilm development, future studies are needed to better understand the “molecular and functional diversity” of the extracellular matrix and its links with polymicrobial interactions as disease develops. How the matrix provides structural support and protection for pathogens, and assists in the generation of local microenvironments or niches for disease, remains unknown. The authors believe that further analysis of the “structural and functional interaction between the many components of the biofilm matrix, the local microbiome, and host factors” will enhance understanding of the pathogenesis of all polymicrobial diseases, hopefully fostering the development of targeted therapies designed to prevent or treat them.
“Although microbiome-based studies [to date have] provided great strides to understand the complexity of the biofilm microbiota, future research on dissecting the matrix composition and function as well as how the various microorganisms interact with the matrix components may lead to further understanding about the pathogenic mechanisms of biofilms in infectious diseases,” Dr. Koo said. “Furthermore, more effective therapies will probably need to target the matrix and the biofilm microenvironment as well as the individual microbial cells within.”