Dental plaque is a general term for the diverse microbial community (predominantly bacteria) found on the tooth surface, embedded in a matrix of polymers of bacterial and salivary origin. Plaque develops naturally on teeth, and forms part of the defence systems of the host by helping to prevent colonisation of enamel by exogenous (and often pathogenic) microorganisms (colonisation resistance). Plaque is an example of a biofilm; current research is showing that the properties of bacteria associated with a surface in a biofilm can be markedly different than those of the same cells growing in liquid broth (planktonic cells). Plaque is found preferentially at protected and stagnant surfaces, and these are at the greatest risk of disease.
MECHANISMS OF PLAQUE FORMATION
The attachment, growth, removal and reattachment of bacteria to the tooth surface is a continuous and dynamic process. However, several distinct processes can be recognised:
PLAQUE COMPOSITION & STRUCTURE
Environmental conditions on a tooth are not uniform. Differences exist in the degree of protection from oral removal forces and in the gradients of many biological and chemical factors that influence the growth of the resident microfiora. These differences will be reflected in variations in the composition of the microbial community, particularly at sites so obviously distinct as the gingival crevice, approximal regions, smooth surfaces, and pits and fissures. For example, fissure plaque will be influenced more by saliva than other sites, whereas gingival crevicular fluid (GCF) has a greater impact on plaque in the gingival crevice. This latter site also has a lower redox potential (Eh) and is colonised by higher numbers of anaerobes, especially proteolytic species which obtain key growth factors from the catabolism of host proteins and glycoproteins in GCF.
Plaque structure has been studied mainly by electron microscopy. A heterogeneous and a colonial type of sub-structure have been observed in sections of smooth surface plaque.
The heterogeneous type is associated with pallisaded regions where filaments and cocci appear to be aligned in parallel at right angles to the enamel surface. Micro-colonies, presumably of single populations, have also been observed. In addition, horizontal stratification has been described. The early stages of development results in a condensed layer of apparently a limited number of bacterial types. From 7 to 14 days, the bulk layer forms which shows less orientation but a higher morphological diversity. This layering has been attributed directly to bacterial succession (see below). In mature plaque, organisms have been seen in direct contact with the enamel due to enzymic attack on the pellicle. Electron microscopy has confirmed the presence of an inter-bacterial matrix of polysaceharide.
MICROBIAL INTERACTIONS AND SUCCESSION IN PLAQUE
In a biofilm such as dental plaque, micro-organisms are in close proximity to one another and interact as a consequence. These interactions can be beneficial to one or more of the interacting populations, while others can be antagonistic. Microbial metabolism within plaque will produce gradients in factors affecting the growth of other species, including the depletion of essential nutrients with the simultaneous accumulation of toxic or inhibitory byproducts. These gradients lead to the development of vertical and horizontal stratifications within the plaque biofilm. Such environmental heterogeneity enables organisms with widely differing requirements to grow, and ensures the co-existence of species that would be incompatible with one another in a homogeneous habitat.
Beneficial interactions include the concerted action of two or more species to metabolise host macromolecules, such as mucin (individual species are unable to catabolise such molecules), the development of food chains (e.g. lactate consumption by Veillonella spp), and coaggregation. Antagonistic interactions include the production of inhibitory substances such as bacteriocins, H2O2, and organic acids.
Early colonisers of the tooth surface are mainly Neisseria spp. and streptococci. The growth and metabolism of these pioneer species changes local environmental conditions (e.g. Eh, pH, coaggregation, substrate availability). thereby enabling more fastidious organisms to colonise, e.g. obligate anaerobes tend to be late colonisers in plaque, only able to grow once favourable gradients in O2 or Eh have developcd in the biofilm.
MICROBIAL IMBALANCES IN HEALTH AND DISEASE
Plaque develops naturally on teeth, and gives benefit to the host by providing colonisation resistance. Once established at a site, the plaque flora remains relatively stable with time despite regular environmental challenges. This stability (microbial homeostasis) is not due to any metabolic indifference by the resident microflora but is due to a dynamic balance being established among the resident members of this microbial community.
On occasions, homeostasis breaks down and imbalances in the microflora can occur which predispose a site to disease. For example, the repeated intake of fermentable sugar in the diet produces frequent conditions of low pH in plaque which inhibits the growth of many of the species associated with dental health, and selects for the highly acidogenic (acid-producing) and aciduric (“acid-loving") species, such as mutans streptococci and lactobacilli, associated with dental caries. In periodontal diseases, there is a shift in the composition of the plaque microfiora to a more proteolytic Gram negative anaerobic community, which can induce damage to tissues either indirectly via the “sidc-effects" of an inflammatory host response or directly by the production of proteases, cytotoxins and other virulence factors.
Dental caries is the localised destruction of the tissues of the tooth by acid produced from the bacterial degradation of fermentable sugars. One of the main difficulties in determining the bacterial aetiology of caries is because disease occurs at sites with an existing diverse resident microflora.
MICROBIAL AETIOLOGY OF CARIES
Evidence that micro-organisms are involved in the aetiology of dental caries has come from animal studies and human clinical trials. Gnotobiotic animal studies showed that caries could be induced by specific bacteria, especially members of the mutans streptococci-group (eg. Streptococcus mutans and Strep. sobrinus), but only when fed a cariogenic (high sucrose) diet. These studies also showed the potential for transmission from animal to animal, and that protection could be achieved by antimicrobial agents and vaccination. Primate models have confirmed the role of mutans streptococci, and that protection can occur by various vaccination routes and by passive immunisation (when antibodies from another source are applied to teeth).
Cross-sectional and longitudinal studies of a range of patient groups have shown a strong relationship between the presence of mutans streptococci and the initiation of a lesion in humans (Table). This association is strongest for fissure and rampant caries; the evidence for approximal surfaces is less strong, possibly due to problems of sampling plaque and diagnosing lesions at this inaccessible site. However, lesions can be detected at all sites in the apparent absence of mutans streptococci, while these bacteria can be present at a site at relatively high levels without evidence of demineralisation (Table), suggesting that the disease does not have an absolute specificity in terms of microbial aetiology.
Advanced lesions oflen have a high proportion of lactobacilli, while dentinal lesions have a diverse microflora with many fastidious Gram positive (Actinomyces naeslundii, A. odontolyticus, Propionibacterium spp., Eubacterium spp.) and Gram negative (Fusobacterium spp. Capnocytophage spp, Veillonella spp.) bacteria.
Root surface caries was originally associated with Actinomyces spp. but recent studies suggest a similar aetiology to enamel caries, namely, mutans streptococci and lactobacilli, with possibly a role for A. naeslundii.
Rampant caries can occur in xerostomic patients and in infants fed with high levels of sugar in pacifiers (nursing bottle caries). The plaque contains high levels of mutans streptococci and lactobacilli.
PATHOGENIC DETERMINANTS OF CARIOGENIC BACTERIA
A striking feature of the main cariogenic bacteria (mutans streptococci and lactobacilli) is their combined acidogenicity and aciduricity; mutans streptococci but not lactobacilli produce EPS.