Dental plaque, which has come to be viewed and managed as a complex biofilm, can be defined simplistically as an adherent deposit that forms on the tooth surface composed almost entirely of bacteria derived from the normal flora of the mouth (Figure 1). Dental plaque is the most prevalent and densest of human biofilms. The advantages for the microbes in the biofilm include protection from environ mental hazards (including antimicrobials) and optimization of spatial arrangements that maximize energy through movement of nutrients. Organisms within the biofilm interact dynamically at multiple metabolic and molecular levels. The biofilm first forms in relation to the dental pellicle, which is a physiologic thin organic film covering the mineralized tooth surface composed of proteins and glycoproteins derived from saliva and other oral secretions (see Figure 1). As the plaque biofilm evolves, it does so in relation to the pellicle and not the mineralized tooth itself. Plaque formation takes place in stages and layers at two levels. The first is the anatomical location of the plaque in relation to the gingival line; the earliest plaque is supragingival, which may then extend to subgingival plaque. The second level is the layering within the plaque, the bacterial species involved, and the bacteria–pellicle and bacteria–bacteria binding mechanisms involved. The initial colonizing organisms are mainly Gram-positive bacteria that use specific ionic and hydrophobic interactions as well as lectin-like surface structures to adhere to the pellicle and to each other. The prototype early colonizer is Streptococcus sanguis, but other streptococci (Streptococcus mutans, Streptococcus mitis, Streptococcus salivarius, Streptococcus oralis, Streptococcus gordonii), lactobacilli, and Actinomyces species are usually present. Late colonizers can appear in the biofilm in as little as 2–4 days and consist primarily of Gram-negative anaerobes (eg, Porphyromonas, Prevotella, Fusobacterium, Veillonella species), including anaerobic spirochetes (eg, Treponema denticola), and more Actinomyces species. These bacteria use similar mechanisms to bind to the early colonizers and to each other. High-molecular-weight extracellular glucan polymers are synthesized, which act like a cement binding the plaque biofilm together. The carbohydrate polymers (glucans) are produced mainly by streptococci (S. mutans), perhaps in association with Actinomyces species. In all, there are thought to be 300–400 bacterial species present in mature dental plaque.

Fig1. Dental plaque biofilm. The stages of formation of the bacterial biofilm called dental plaque are shown. Early colonizers bind to the pellicle, and late colonizers bind to the other bacteria. (Reproduced with permission from Willey J, Sherwood L, Woolverton C [editors]: Prescott’s Principles of Microbiology. McGraw-Hill, 2008. © McGraw-Hill Education.)

Caries is a disintegration of the teeth beginning at the surface and progressing inward. First the surface enamel, which is entirely noncellular, is demineralized. This has been attributed to the effect of acid products of glycolytic metabolic activity when the plaque bacteria are fed the right substrate. Subsequent decomposition of the dentin and cementum of the exposed root surface involves bacterial digestion of the protein matrix. S. mutans is considered to be the dominant organism for the initiation of caries; however, multiple members of the plaque biofilm participate in the evolution of the lesions. These include other streptococci (S. salivarius, S. sanguis, Streptococcus sobrinus), lactobacilli (Lactobacillus acidophilus, Lactobacillus casei), and actinomycetes (Actinomyces viscosus, Actinomyces naeslundii). The large amounts of organic acid products produced from car bohydrates by the interaction of S. mutans with these other species in plaque are the underlying cause of caries. The accumulation of these acid products causes the pH of the plaque to drop to levels sufficient to react with the hydroxy apatite of the enamel, demineralizing it to soluble calcium and phosphate ions. Production of acid and decreased pH is maintained until the substrate is depleted after which the plaque pH returns to its more neutral pH resting level and some recovery can take place.

Dietary monosaccharides (eg, glucose, fructose) and disaccharides (eg, sucrose, lactose, and maltose) provide an appropriate substrate for bacterial glycolysis and acid production to cause tooth demineralization. Foods with high sugar content, particularly sucrose, which adhere to the teeth and have long oral clearance times, are more cariogenic than less retentive food stuffs such as sugar containing liquids. A possible advantage for S. mutans is its ability to metabolize sucrose more efficiently than other oral bacteria. An additional factor is that sucrose is also used for the synthesis of extracellular polyglycans such as dextrans and levans by transferase enzymes on the bacterial cell surface. Polyglycan production contributes to aggregation and accumulation of S. mutans on the tooth surface and may also serve as an extracellular storage form of substrate for other plaque bacteria.

Periodontal pockets in the gingiva are particularly rich sources of organisms, including anaerobes that are rarely encountered elsewhere. Plaque-induced periodontal disease encompasses two separate disease entities, gingivitis and chronic periodontitis. Both conditions are caused by bacteria in the subgingival dental plaque found within the gingival crevice or the sulcus around the necks of the teeth. Periodon titis is a biofilm-induced chronic inflammatory disease which affects the tooth-supporting tissues. Although the tooth associated biofilm plays a crucial role in the initiation and progression of periodontitis, it is primarily the host inflammatory response that is responsible for the damage to the periodontium, leading to tooth loss in some cases. It has been hypothesized that Porphyromonas gingivalis impairs innate immunity in ways that alter the growth and development of the entire biofilm, triggering a breakdown in the normally homeostatic host–microbiota interplay in the periodontium. A recent study established a correlation between the presence of periodontal disease and the presence of archaeal DNA, the severity of periodontal disease and the relative abundance of archaeal DNA in the subgingival plaque, and between disease resolution and diminished archaeal DNA abundance. The Archaea were comprised of two distinct phylotypes within the genus Methanobrevibacter. A causative association has not been established.

Although the microorganisms within the biofilm may participate in periodontal disease and tissue destruction, attention is drawn to them when they are implanted elsewhere (eg, producing infective endocarditis or bacteremia in a gran ulocytopenic host). Examples are Capnocytophaga species and Rothia dentocariosa. Capnocytophaga species are fusiform, Gram-negative, gliding anaerobes; Rothia species are pleomorphic, aerobic, Gram-positive rods. In granulocytopenic immunodeficient patients, they can lead to serious opportunistic lesions in other organs.

Control of caries involves physical removal of plaque, limitation of sucrose intake, good nutrition with adequate protein intake, and reduction of acid production in the mouth by limitation of available carbohydrates and frequent cleansing. The application of fluoride to teeth or its ingestion in water results in enhancement of acid resistance of the enamel. Control of periodontal disease requires removal of calculus (calcified deposit) and good mouth hygiene.

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