Dental plaque is one of the most familiar biofilms in the human body, and one of the most studied. It forms on teeth every day and is removed, at least in part, by brushing and cleaning between teeth. Under the microscope, plaque is not a random mix of microbes. It is assembled in a fairly ordered way, with different bacteria arriving at different stages and using specific adhesins to attach both to the tooth and to each other.
Step One: The Acquired Pellicle
Clean tooth enamel is quickly coated by a thin film of proteins and glycoproteins from saliva. This layer is called the acquired pellicle. It includes molecules such as proline-rich proteins, statherin, mucins and salivary amylase. Bacteria do not usually bind bare enamel directly; they bind receptors in this pellicle.
Step Two: Early Colonizers
The first bacteria to attach are known as early colonizers. Streptococci, particularly species in the mitis group such as Streptococcus sanguinis and Streptococcus gordonii, are prominent, along with Actinomyces species.
These bacteria carry surface adhesins that recognize pellicle components. Examples include:
- Large streptococcal surface proteins of the antigen I/II family, which bind salivary glycoproteins.
- Fimbriae on Actinomyces that bind proline-rich proteins and certain sugar chains.
- Serine-rich repeat glycoproteins that bind sialic acid-containing structures.
For a broader look at how adhesins drive surface colonization, see our article on biofilm formation.
Step Three: Coaggregation
Once the first layer is in place, new arrivals often attach not to the pellicle but to bacteria already there. This cell-to-cell binding between genetically different bacteria is called coaggregation. It usually involves a protein adhesin on one cell recognizing a carbohydrate receptor on the other, a lectin-like interaction.
Coaggregation is quite specific. A given strain will pair with some partners but not others, and the interactions can often be blocked in the laboratory by adding simple sugars such as lactose or galactose, which compete for the adhesin's binding site. This specificity helps explain why plaque communities develop in a predictable sequence.
Fusobacterium as a bridge
Fusobacterium nucleatum is a key example of a bridging organism. It can coaggregate with many early colonizers and also with many later colonizers. Because it binds both groups, it is thought to link the early community to the bacteria that arrive later, many of which cannot attach to the early colonizers directly.
Step Four: Late Colonizers
Late colonizers include anaerobic, often Gram-negative bacteria such as Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola. These organisms are associated with gum disease (periodontitis) when they become abundant beneath the gum line.
Their success depends partly on the community that came before. Early colonizers consume oxygen, creating low-oxygen pockets where anaerobes can grow, and the bridging bacteria provide places to attach. Porphyromonas gingivalis, for example, uses fimbriae and other surface proteins to bind streptococci and host tissue.
The Matrix and Community Behavior
As plaque matures, bacteria produce an extracellular matrix rich in polysaccharides. Some streptococci, including Streptococcus mutans, make glucans from dietary sucrose, which help bacteria stick together and to the tooth. The matrix gives plaque its sticky texture and makes the community harder to remove by rinsing alone, which is why mechanical cleaning matters.
Within plaque, bacteria also exchange metabolites and signaling molecules. The waste of one species can be the food of another, reinforcing the partnerships that coaggregation began.
Why This Matters
Understanding plaque as an organized biofilm helps explain several everyday observations. Regular brushing and cleaning between teeth disrupt the community before late colonizers become established. Sugar intake can shift the balance toward acid-producing species linked to tooth decay. Researchers have also explored whether blocking particular adhesins or coaggregation partners could change how plaque develops. Our glossary defines terms such as pellicle and lectin.
Key Takeaways
- Plaque forms on a saliva-derived pellicle, not on bare enamel.
- Early colonizers such as streptococci and Actinomyces bind pellicle receptors with specific adhesins.
- Coaggregation lets later bacteria attach to earlier ones, with Fusobacterium nucleatum acting as a bridge.
- Late colonizers, including bacteria linked to gum disease, depend on the community built before them.
Educational information only, not medical advice. Always follow the advice of a qualified healthcare professional or dental professional about oral health; in an emergency call your local emergency number.