Introduction
Molecular aggregation in dental plaque involves the accumulation and interaction of various molecules, primarily microbial cells and their extracellular products, on the surfaces of teeth. Dental plaque is a biofilm—a structured community of microorganisms encapsulated within a self-produced extracellular polymeric substance (EPS) matrix. The molecular interactions between microorganisms in dental plaque are crucial for the development, stability, and pathogenicity of the biofilm. These interactions include physical attachments, chemical signaling, and exchange of genetic material.
Adhesion and coaggregation of microorganisms
Surface proteins on bacteria (e.g., adhesins) bind to specific receptors on other microbial cells or host tissues. Streptococcus mutans has adhesins like antigen I/II that bind to salivary glycoproteins in the acquired pellicle. These bacteria produce enzyme glucansucrase that help in converting sucrose into a sticky, extracellular, dextran-based polysaccharide. This sticky matrix allows S. mutans cells to cohere, forming the foundation of dental plaque. Another important bacteria that plays a major role in plaque formation is Fusobacterium nucleatum. It acts as a bridge organism, coaggregating with both early and late colonizers through various adhesins and receptors. A. actinomycetemcomitans is a key pathogen in periodontitis and plays a significant role in biofilm formation and interactions with other microorganisms in dental plaque. These bacteria adhere to early colonizers such as Streptococcus gordonii and Actinomyces species. It can also coaggregate with other periodontopathogens like Porphyromonas gingivalis and Fusobacterium nucleatum. Porphyromonas gingivalis is a key pathogen in the development of periodontitis and plays a critical role in the biofilm dynamics of dental plaque. It can adhere to early colonizers such as Streptococcus gordonii and Actinomyces species. This interaction is mediated by adhesins like fimbriae and specific receptors on the surface of the colonizers. P. gingivalis also coaggregates with other periodontopathogens like Tannerella forsythia and Treponema denticola, forming a pathogenic consortium. P. gingivalis can metabolize peptides and amino acids released by other bacteria in the biofilm. It is an asaccharolytic bacterium, relying on protein degradation for nutrition. P. gingivalis requires heme for growth and can obtain it from lysed red blood cells, often facilitated by synergistic interactions with other bacteria that induce hemolysis. It engages in horizontal gene transfer with other bacteria in the biofilm, leading to the spread of antibiotic resistance genes and virulence factors. It can take up extracellular DNA from the environment, enhancing genetic diversity and adaptability.
Tannerella forsythia, a member of the “red complex” bacteria, plays a significant role in severe periodontitis. It thrives as a late colonizer in the oral biofilm. T. forsythia coaggregates with P. gingivalis through specific adhesins and receptors. This interaction is significant for the pathogenic synergy between these two bacteria, contributing to biofilm maturation and virulence. T. forsythia also interacts with T. denticola, another key periodontal pathogen, enhancing the overall pathogenicity of the biofilm. It contributes to the EPS matrix of the biofilm, which includes polysaccharides, proteins, and extracellular DNA (eDNA). This matrix provides structural integrity and protection to the biofilm. T. forsythia can modulate the host immune response, creating an environment that favors its survival and that of other pathogenic bacteria.
Treponema denticola is a spirochete bacterium associated with periodontal diseases. Its interactions with other bacteria in the biofilm are crucial for its survival, integration, and pathogenicity. T. denticola participates in quorum sensing, producing and responding to signaling molecules that coordinate gene expression and behavior within the biofilm. T. denticola benefits from the metabolic activities of other bacteria. For example, it can utilize amino acids and peptides generated by the proteolytic activities of P. gingivalis and T. forsythia.
Synergistetes species have been found to interact with other bacteria in biofilms, contributing to the complexity and pathogenicity of the microbial community. They coaggregate with P. gingivalis, a keystone pathogen in periodontal disease. This interaction may facilitate the integration of Synergistetes into the biofilm and enhance the pathogenic potential of both organisms. Along with this, Synergistetes may support the survival and pathogenic activities of other bacteria by creating a more favorable microenvironment within the biofilm.
Conclusion
The bacteria in dental biofilms interact through adhesion, coaggregation, quorum sensing, metabolic cooperation, genetic exchange, and antagonistic mechanisms. These interactions enhance the biofilm’s structural integrity, resistance to external stresses, and pathogenic potential, contributing to the development and progression of periodontal diseases. In summary, understanding coaggregation and the dynamics of dental plaque biofilms is crucial for understanding pathogenesis of periodontal diseases. Understanding these molecular interactions is essential for developing targeted strategies to disrupt plaque formation and combat oral diseases.