Stages of Dental plaque formation

Stages of Dental plaque formation

Plaque is a tenaciously adherent deposit that forms on tooth surfaces. It consists of an organic matrix containing a dense concentration of bacteria.

In microbiological terms, plaque is a biofilm. Biofilms consist of a hydrated viscous phase formed from bacteria and their extracellular polysaccharide matrices. In such a film, molecules and ions exist in concentrations that can be widely different from those of the surrounding fluid phase (saliva). Bacteria in biofilms can also exhibit cooperative activity and behave differently from the same species in isolation in a culture medium. As a consequence, a biofilm may be resistant to antimicrobials or to immunological defences to which the individual bacteria are normally sensitive. Bacterial plaque must therefore be regarded as a living entity and not as a mere collection of bacteria. In particular, the ability of dental plaque to concentrate and retain acid was recognised long before the special properties of biofilms were discovered.

Clinically, bacterial plaque is a tenaciously adherent deposit on the teeth. It resists the friction of food during mastication, and can only be readily removed by toothbrushing. However, neither toothbrushing nor fibrous foods will remove plaque from inaccessible surfaces or pits .
Plaque becomes visible, particularly on the labial surfaces of the incisors, when toothbrushing is stopped for 12-24 hours. It appears as a translucent film with a matt surface that dulls the otherwise smooth and shiny enamel. It can be made obvious when stained with disclosing agents. Little plaque forms under conditions of starvation but it forms rapidly and abundantly on a high-sucrose diet.
In stagnation areas where it is undisturbed, plaque bacteria can form acid from sugars over sufficiently long periods as to
attack tooth surfaces. Adhesion of bacteria to the teeth from which they would otherwise be washed away is an essential requirement for the
colonisation of enamel. Attachment depends on complex mechanisms and depends on such molecules as glucans and/or glucosyltransferase. Components of plaque which act as adhesion receptors, include a group of proline-rich proteins (PRPs) from the saliva.

If teeth are thoroughly cleaned by polishing with an abrasive, plaque quickly re-forms.

Stages of formation of bacterial plaque
• Deposition of structureless cell-free, pellicle of salivary glycoprotein
• Further deposition of pellicle enhanced by bacterial action precipitating salivary proteins
• Colonisation of the cell-free layer by bacteria, particularly by S. sanguis and S. mutans strains within 24 hours
• Progressive build-up of plaque substance by bacterial polysaccharides
• Proliferation of filamentous and other bacteria as the plaque matures

Sucrose diffuses rapidly into plaque, and acid production quickly follows. These changes have been measured directly in the human mouth using microelectrodes in direct contact with plaque. It has been shown by this means that, after rinsing the mouth with a 10% glucose solution, the pH falls within 2-5 minutes, often to a level sufficient to decalcify enamel. Even though no more sucrose may be taken and the surplus is washed away by the saliva, the pH level remains at a low level for about 15-20 minutes; it returns only gradually to the resting level after about an hour. These changes (the so-called Stephan curve) are shown diagramatically in Figure 3.7. The rapidity with which the pH falls is a reflection of the speed with which sucrose can diffuse into plaque and the activity of the concentration of enzymes produced by the great numbers of bacteria in the plaque.

Factors contributing to maintenance of low plaque pH
• Rapid production of a high concentration of acid within the plaque, temporarily overcomes local buffering
• Escape of acid into the saliva, delayed by the diffusion-limiting properties of plaque and its thickness
• Diffusion of salivary buffers into plaque hampered by the diffusion-limiting properties of plaque and its thickness
• Continued sugar production from bacterial intracellular polysaccharides

As discussed in relation to the pathology of dental caries, it is clear that acid production is responsible for the carious attack. Lactic acid is mainly responsible. When plaque is sampled after exposure to sucrose, lactic acid is the quantitatively predominant acid during plaque activity, particularly during the trough of the Stephan curve. Lactic acid has a lower pK constant and causes a greater fall in pH than equimolar solutions of acetic or propionic acids that may also be detected in plaque.

Category: Oral Pathology