Events in Plaque Formation

Varios

==========

Events in Plaque Formation

http://www.ncl.ac.uk/dental/oralbiol/oralenv/images/transparent.gif

Dental plaque

Dental plaque is a mixed microbial biofilm growing on teeth and is the prime aetiological agent of the two main oral diseases, dental caries and periodontal disease. The microbial composition of plaque varies between individuals and the location on the tooth and generally reflects the complex nature of the ecology of the mouth.

In common with other biofilms, the microbial composition of dental plaque is capable of change in response to changes in the environment, notably the diet. These responses are modulated by homeostatic mechanisms inherent in the plaque in ways which are, as yet, poorly understood.

The major sites of plaque accumulation are in the fissures of molar teeth, in the area bounded by the margin of the gum and the tooth and between adjacent teeth. In addition, plaque can cause gingival inflammation which may result in loss of epithelial attachment to the tooth leading to the formation of sub-gingival pockets. These pockets may also harbour dental plaque which is significantly different from supra-gingival plaque in a number of important respects in particular a much lower redox potential which selects for a variety of anaerobic bacterial species.

Plaque formation

Although dental plaque varies considerably in composition, it has been possible to piece together a sequence of events which lead to its establishment. The consensus view of plaque development begins with a clean tooth surface covered by a conditioning film of salivary proteins and glycoproteins, called the tooth pellicle, being colonised by so-called "pioneer species". These multiply forming, first a monolayer and, subsequently, palisades of cells perpendicular to the tooth surface.

During and after this outgrowth period secondary colonisation by a variety of Gram positive and negative species occurs leading to a large increase in the species diversity. Foremost among the events contributing to this secondary colonisation is the process known as co-aggregation whereby colonising microbes attach to cells already part of the developing biofilm. This allows species which can not attach, or can attach only poorly, to the tooth pellicle to participate in the biofilm. At 24 hours the maturing dental plaque contains a wide variety of bacteria and it is possible to detect easily identifiable inter-species associations such as the well documented "corn-cob-configurations", although a wide variety of other inter-species associations will be present.

Further colonisation and growth of established bacteria takes place as the plaque matures to form a stable, climax, community. This pattern of development leading to a climax community has been termed "bacterial succession". The resulting community consists of individual microbes and microcolonies acting in complex consortia which can convey a range of beneficial properties. These include feeding synergies, improved antibiotic resistance and a host of cooperative mechanisms which are the subject of much current research.

Events in plaque formation

1. Colonisation by pioneer species

2. Outgrowth

3. Secondary colonisation

4. Climax community

http://www.ncl.ac.uk/dental/oralbiol/oralenv/images/transparent.gif

Microbial adhesion

Probably the single most important phenomenon in the development of a biofilm is the process of microbial adhesion either to the substratum or to other adhering cells be they of the same or another species. Microbial adhesion is now recognised as a crucial step in the pathogenicity of a wide range of bacterial diseases and this has generated enormous interest into the mechanisms by which it is achieved.

In the case of some mono-specific diseases such as those caused by Salmonellae, enteropathogenic Escherichia coli or Neisseria gonorrhoeae it has been possible to piece together a highly detailed picture of the process. In situations where diseases is associated with biofims, whether mono-specific eg infective endocarditis, or multi-specific eg dental caries, the process is very much more complex and we are less certain of the details.

The adhesion of a microbe to a surface, including another microbe, appears to be governed by two major forces. The first is shear force which tends to sweep bacteria away from or off a surface. The second is electrostatic repulsion which works in combination with van de Waal's forces to provide areas of weak attraction which are thought to be important in the overall adhesion process. The current view of the adhesion process is that it takes place in two distinct phases.

Phase 1

In Phase 1 the microbe is held, for a brief period, by a weakly attractive force some 10nm from the surface . Shear force or Brownian Motion may disrupt this initial attraction. On the other hand, a number of specific adhesion mechanisms may hold the cell close to the surface for a significant time period. These specific interactions may be a combination of lectin-like , electrostatic and hydrophobic interactions which in some instances may involve delicate structures called fibrils or fimbriae which project from the cell surface.

Phase 2

In Phase 2, the adhesion is rendered essentially irreversible by the synthesis of extracellular polymers. Ultimately these polymers form a significant part of the biofilm matrix. In the case of dental plaque, these polymers comprise soluble and insoluble high molecular weight polysaccharides synthesised from sucrose by extracellular glucosyl- and fructosyltransferases. In view of the established