Biofilm on Teeth: Key Facts and Latest Insights

Biofilm on teeth is a sticky layer of bacteria and other microorganisms that significantly impacts oral health. While it naturally forms as part of the mouth’s ecosystem, its buildup can lead to cavities and gum disease if not properly managed. Research continues to reveal new details about its development and interaction with various factors in the mouth, helping refine strategies for oral hygiene and disease prevention.

Key Components of Formation

Biofilm formation begins with the acquired pellicle, a thin, protein-rich layer that quickly coats enamel surfaces after brushing or professional cleaning. Composed mainly of salivary glycoproteins, phosphoproteins, and lipids, this layer facilitates bacterial adhesion by providing binding sites for early colonizers like Streptococcus sanguinis and Streptococcus mitis, which use adhesins to anchor to the tooth surface.

Once initial colonization occurs, bacterial proliferation and co-aggregation shape the biofilm’s structure. Early colonizers establish a foundation that allows secondary and late colonizers to attach through co-adhesion and quorum sensing. Fusobacterium nucleatum acts as a bridge, linking early streptococcal species with more pathogenic bacteria like Porphyromonas gingivalis. This process follows a coordinated sequence, where microbial interactions dictate the biofilm’s composition and architecture.

As bacterial communities expand, they produce extracellular polymeric substances (EPS), a matrix of polysaccharides, proteins, and extracellular DNA. This matrix provides structural integrity and enhances microbial resistance to environmental stressors, including antimicrobial agents and mechanical disruption. The biofilm’s biochemical environment also influences its stability and pathogenic potential. Organic acids from bacterial metabolism lower pH, leading to enamel demineralization, while anaerobic conditions in deeper layers promote the growth of bacteria associated with periodontal disease. EPS further limits antimicrobial diffusion, making mature biofilms highly resistant to conventional oral hygiene measures. Disrupting biofilm formation in its early stages is crucial to preventing its progression into a resilient and pathogenic structure.

Microbial Composition

The bacterial communities in dental biofilm are diverse and dynamic, shaped by nutrient availability, oxygen gradients, and interspecies interactions. Early colonizers like Streptococcus sanguinis and Streptococcus mitis initiate biofilm formation, creating conditions for more complex microbial assemblages. These facultative anaerobes survive in both oxygen-rich and oxygen-limited environments. As the biofilm matures, oxygen levels decrease in deeper layers, fostering obligate anaerobes such as Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, which are linked to periodontal disease.

Metabolic interactions further shape the microbial landscape. Fusobacterium nucleatum facilitates the transition from early to late colonizers by co-aggregating with both aerobic and anaerobic microorganisms. Metabolic byproducts, including organic acids and volatile sulfur compounds, create localized microenvironments that selectively promote the growth of acidogenic and proteolytic bacteria. This biochemical stratification results in distinct ecological niches, where specific species dominate based on their ability to tolerate or exploit the surrounding conditions.

Beyond bacteria, dental biofilm also harbors fungi and viruses. Candida albicans, a fungal species common in the oral cavity, integrates into biofilm structures, particularly in individuals with weakened immune defenses or dental prosthetics, enhancing biofilm resilience against antifungal agents and mechanical disruption. Bacteriophages—viruses that infect bacteria—regulate bacterial populations. Studies suggest that phages targeting Streptococcus mutans, a major cariogenic species, may modulate its abundance, potentially influencing cavity formation.

Role of Salivary Flow

Salivary flow regulates biofilm dynamics by influencing its composition and structural integrity. Continuous saliva secretion physically dislodges loosely attached microorganisms, preventing excessive accumulation. This effect is most pronounced during eating and speaking when increased salivary production enhances bacterial and food debris clearance. Reduced salivary flow, as seen in xerostomia (dry mouth) caused by medications or medical conditions, accelerates biofilm formation, increasing the risk of cavities and gum disease.

Beyond mechanical effects, saliva contains proteins, enzymes, and antimicrobial peptides that influence biofilm stability. Lysozyme, lactoferrin, and histatins exhibit bacteriostatic and bactericidal properties, disrupting bacterial cell walls and inhibiting microbial growth. Salivary immunoglobulin A (IgA) interferes with bacterial adhesion, limiting colonization by opportunistic pathogens. Saliva’s buffering capacity, driven by bicarbonate and phosphate ions, helps maintain oral pH. When biofilm bacteria metabolize dietary sugars, they produce acids that lower pH and contribute to enamel demineralization. Saliva counteracts this by neutralizing excess hydrogen ions, reducing cavity risk. Individuals with impaired salivary buffering, such as those undergoing radiation therapy for head and neck cancers, experience a more cariogenic biofilm environment.

Saliva composition varies based on hydration, diet, and circadian rhythms, affecting biofilm characteristics. Higher protein concentrations, particularly mucins, enhance bacterial aggregation, promoting the formation of larger, less adhesive biofilm structures that are more easily removed by saliva. Conversely, systemic conditions like diabetes increase glucose levels in oral fluids, providing additional nutrients that promote cariogenic bacteria like Streptococcus mutans. This highlights the intricate connection between systemic health and oral biofilm formation.

Physical Influences in the Mouth

The structural and mechanical environment of the mouth shapes biofilm formation and persistence. The topography of teeth, including pits, fissures, and interproximal spaces, creates sheltered regions where biofilm develops with minimal disruption. Molars, particularly their occlusal surfaces, are prone to biofilm accumulation due to their complex structure. Areas less accessible to natural cleaning mechanisms, such as the lingual surfaces of mandibular molars or the distal aspects of third molars, often have higher biofilm density.

Mastication and speech also influence biofilm dynamics. Chewing stimulates mechanical abrasion, helping dislodge loosely adhered bacterial cells, particularly on occlusal and incisal surfaces. The extent of removal varies based on diet composition. Fibrous foods like raw vegetables and whole grains provide a mild cleansing effect by increasing friction against enamel. In contrast, diets high in refined carbohydrates promote biofilm persistence by supplying fermentable substrates for bacterial metabolism. Studies indicate that individuals with softer diets develop more extensive biofilm layers due to reduced mechanical stimulation.

Maturation Over Time

As biofilm develops, its composition and structure evolve, increasing its resilience and pathogenicity. Early colonization is dominated by primary adherents like Streptococcus sanguinis and Streptococcus mitis, forming a thin, loosely attached layer. Over time, microbial diversity increases as secondary colonizers, including Fusobacterium nucleatum and Veillonella species, integrate into the biofilm. These bacteria contribute to biofilm expansion by facilitating co-aggregation and modifying the local environment to support anaerobic growth. The accumulation of extracellular polymeric substances (EPS) stabilizes the biofilm, making it more resistant to mechanical removal and antimicrobial agents.

As biofilm matures, metabolic activity intensifies, leading to localized shifts in pH and oxygen availability. Acidogenic bacteria like Streptococcus mutans and Lactobacillus species metabolize dietary sugars into organic acids, lowering pH and promoting enamel demineralization. Simultaneously, deeper biofilm layers become increasingly anaerobic, fostering the growth of obligate anaerobes such as Porphyromonas gingivalis and Treponema denticola, which contribute to periodontal disease. These changes not only drive cavity formation and gum inflammation but also increase biofilm persistence by making it more resistant to host defenses and oral hygiene measures. The longer biofilm remains undisturbed, the more complex and pathogenic it becomes, emphasizing the need for regular mechanical disruption through brushing, flossing, and professional cleanings.