Microbes and Dental Disease

Bacteriology at UW- Madison

The Microbial World

University of Wisconsin - Madison

Microbes and Dental Disease

© 2008 Kenneth Todar University of Wisconsin-Madison Department of Bacteriology

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Normal Flora of the Human Oral Cavity

The presence of nutrients, epithelial debris and secretions makes the mouth a favorable habitat for a great variety of bacteria. Oral bacteria include mainly streptococci, lactobacilli, staphylococci, corynebacteria and a great number of anaerobes, especially bacteroides. Hundreds of different bacteria have been identified in the oral cavity although this does not imply that they are not transients.

The mouth presents a succession of different ecological situations with age, and this corresponds with changes in the composition of the normal flora. At birth the oral cavity is composed solely of the soft tissues of the lips, cheeks, tongue and palate, which are kept moist by the secretions of the salivary glands. At birth the oral cavity is sterile but rapidly becomes colonized from the environment, particularly from the mother in the first feeding. Streptococcus salivarius is dominant and may make up 98% of the total oral flora until the appearance of the teeth (6 - 9 months in humans). The eruption of the teeth during the first year leads to colonization by S. mutans and S. sanguis. These bacteria require a nondesquamating (nonepithelial) surface in order to colonize. They will persist as long as teeth remain. Other strains of streptococci adhere strongly to the gums and cheeks but not to the teeth. The creation of the gingival crevice area (supporting structures of the teeth) increases the habitat for the variety of anaerobic species found. The complexity of the oral flora continues to increase with time, and bacteroides and spirochetes colonize around puberty.

Various streptococci in a biofilm in the oral cavity.

Several oral bacteria have been implicated in diseases of the oral cavity, including dental caries and gum diseases such as gingivitis and periodontitis. In the U.S. these are among the most costly and econmically important bacterial diseases in our culture.

The oral bacteria can invade compromised tissues in their hosts and produce disease outside the oral cavity. Oral bacteria invade deeper tissues they may cause abscesses of alveolar bone, lung, brain, or the extremities. Such infections usually contain mixtures of bacteria with Bacteroides melaninogenicus often playing a dominant role. If oral streptococci are introduced into wounds created by dental manipulation or treatment, they may adhere to heart valves and initiate subacute bacterial endocarditis or other heart disease.

Dental Plaque, Caries, Gingivitis and Periodontal Disease

Dental plaque, which is material adhering to the teeth, consists of bacterial cells (60-70% the volume of the plaque), salivary polymers, and bacterial extracellular products. Plaque is a naturally-constructed biofilm, in which the consortia of bacteria may reach a thickness of 300-500 cells on the surfaces of the teeth. These accumulations subject the teeth and gingival tissues to high concentrations of bacterial metabolites, which result in dental disease.

Bacteria involved in dental caries and periodontitis produce three forms of toxins: soluble protein toxins (exotoxins) which work as extracellular enzymes; endotoxins, which are lipolysaccharides in the Gran-negative cell wall; products of bacterial metabolism (e.g. metabolites) which may be toxic. The latter include volatile sulfur compounds such as hydroghen sulfide and methylmercaptan; polyamines with names like putrescine, cadaverine and spermidine; and fatty acids such as lactic acid, propionic acid and butyric acid.

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Porphyromonas gingivalis. Transmission EM 60,000. A common bacterium found in periodontal infections. Virulence factors of the bacterium include endotoxin, fimbrial adhesins and production of extracellular enzymes including proteases and phpsphatase.

Dental plaque, scanning electron micrograph illustrating the diversity of microbes in plaque.

By far the dominant bacterial species in dental plaque are Streptococcus sanguis and Streptococcus mutans, both of which are considered responsible for plaque.

Streptococcus mutans. Gram stain. CDC.

Plaque formation is initiated by a weak attachment of the streptococcal cells to salivary glycoproteins forming a pellicle on the surface of the teeth. This is followed by a stronger attachment by means of extracellular sticky polymers of glucose (glucans) which are synthesized by the bacteria from dietary sugars, principally sucrose. An enzyme on the cell surface of Streptococcus mutans, glycosyl transferase, is involved in initial attachment of the bacterial cells to the tooth surface and in the conversion of sucrose to dextran polymers (glucans) which form plaque.

Dental Caries is the destruction of the enamel, dentin or cementum of teeth due to bacterial activities. Caries are initiated by direct demineralization of the enamel of teeth due to lactic acid and other organic acids which accumulate in dental plaque. Lactic acid bacteria in the plaque produce lactic acid from the fermentation of sugars and other carbohydrates in the diet of the host. Streptococcus mutans has most consistently been associated with the initiation of dental caries, but other lactic acid bacteria are probably involved as well. These organisms normally colonize the occlusal fissures and contact points between the teeth, and this correlates with the incidence of decay on these surfaces.

Cross section of a tooth illustrating the various structural regions susceptible to colonization or attack by microbes.

The bacterium Streptococcus mutans has a number of physiological and biochemical properties which implicate it in the initiation of dental caries.

2. It contains the enzyme glycosyl transferase that probably serves as the bacterial ligand for attachment, and that polymerizes glucose obtained from dietary sucrose to glucans which leads directly to the formation of plaque.

3. It produces lactic acid from the utilization of dietary carbohydrate which demineralizes tooth enamel. S. mutans produces more lactic acid and is more acid-tolerant than most other streptococci.

4. It stores polysaccharides made from dietary sugars which can be utilized as reserve carbon and energy sources for production of lactic acid. The extracellular glucans formed by S. mutans are, in fact, bacterial capsular polysaccharides that function as carbohydrate reserves. The organisms can also form intracellular polysaccharides from sugars which are stored in cells and then metabolized to lactic acid.

Streptococcus mutans appears to be important in the initiation of dental caries because its activities lead to colonization of the tooth surfaces, plaque formation, and localized demineralization of tooth enamel. It is not however, the only cause of dental decay. After initial weakening of the enamel, various oral bacteria gain access to interior regions of the tooth. Lactobacilli, Actinomyces, and various proteolytic bacteria are commonly found in human carious dentin and cementum, which suggests that they are secondary invaders that contribute to the progression of the lesions.

Actinomyces israelii

Periodontal Diseases are bacterial infections that affect the supporting structures of the teeth (gingiva, cementum, periodontal membrane and alveolar bone). The most common form, gingivitis, is an inflammatory condition of the gums. It is associated with accumulations of bacterial plaque in the area. Increased populations of Actinomyces have been found, and they have been suggested as the cause.

Diseases that are confined to the gum usually do not lead to loss of teeth, but there are other more serious forms of periodontal disease that affect periodontal membrane and alveolar bone resulting in tooth loss. Bacteria in these lesions are very complex populations consisting of Gram-positive organisms (including Actinomyces and streptococci) and Gram-negative organisms (including spirochetes and Bacteroides). The mechanisms of tissue destruction in periodontal disease are not clearly defined but hydrolytic enzymes, endotoxins, and other toxic bacterial metabolites seem to be involved.