Primary Preventive Dentistry 6th Ed. (2004)
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Objectives At the end of this chapter it will be possible to 1. Differentiate between organic coatings of endogenous and exogenous (acquired) origin. 2. Explain why dental plaque is not unique among naturally occurring microbial layers. 3. Discuss some of the mechanisms proposed to explain bacterial adhesion to the acquired pellicle. 4. Distinguish between primary and secondary bacterial colonizers in dental plaque, and cite examples of each. 5. Identify the prime sites of calculus formation, explain how calculus forms, and detail the differences between supragingival and subgingival calculus. 6. Explain the basis for the involvement of the acquired pellicle, bacterial dental plaque, and dental calculus in caries and the inflammatory periodontal diseases. Introduction The dental profession has to deal with two of the most widespread of all human maladies, dental caries (tooth decay), and inflammatory diseases of the periodontium (i.e., the supporting tissues of the teeth), gingivitis, and periodontitis (Figure 2-1). These conditions are known to have a bacterial etiology. Unlike some other infectious diseases, these diseases are not caused by a single pathogenic microorganism. Dental caries and inflammatory periodontal diseases result from the accumulation of many different bacteria that form dental plaque,1,2 a naturally acquired bacterial biofilm that develops on the teeth (Figure 2-2). Some bacterial species in dental plaque may be of greater relevance to caries and periodontal diseases than others. Dental plaque cannot be removed by rinsing alone but can be removed by mechanical debridement. The proportions of different bacteria in plaque from a healthy mouth are different from those in plaque associated with caries, and both are different from the dental plaque of an individual with inflammatory periodontal disease.3,4 If the role of dental plaque in caries and inflammatory periodontal diseases is to be understood,5,6 the logical place to start is by examining how dental plaque forms and, as will be discussed in later chapters, how changes in the proportions of different plaque bacteria lead to oral disease.
^ Most natural surfaces have their own coating of microorganisms or biofilm adapted to its individual habitat. The features of dental plaque formation are by no means unique and merely reflect a single instance of a widespread and ancient natural phenomenon. One of the first known examples of life are mineralized bacteria or algae7,8 found on rocks from the Precambrian era. These are quite similar to dental calculus. The physicochemical and biochemical interactions that underlie bacterial adhesion elsewhere in nature are the same as those observed in plaque formation.9-11 For example, all living cells, including bacterial cells, have a net negative surface charge. The cells can, therefore, be attracted to oppositely charged surfaces on such items as rocks in a stream, skin, or teeth. As with plaque bacteria, organisms in other environments can produce extracellular coatings or slime layers, or a variety of surface fibrils or appendages extending from their cell walls that mediate their attachment to the substrate.9,12 In response to environmental conditions and interactions with other members of the microbial community, biofilm bacteria behave differently from planktonic (liquid-phase) cells. This has significant clinical implications. Current research indicates that bacteria growing in biofilms are more resistant to the effects of host defense mechanisms and exogenous antimicrobial agents when compared to the same cells in a liquid suspension.13,14,15 Thus, it becomes of paramount importance to mechanically disturb the biofilm when utilizing antimicrobial therapy. ^ Microorganisms initially colonize the mouth during birth, being naturally acquired from the mother. Thereafter, bacteria are acquired from the atmosphere, food, human contact, and even from animal contacts (e.g., pets). The bacteria subsequently colonize interfaces between saliva and both oral soft (e.g., gingiva, tongue, cheeks, and alimentary tract) and hard tissues (e.g., erupted teeth). Mucosal surfaces of the tongue and tonsils may serve as reservoirs for dental plaque-forming organisms, including those related to disease.16 With increasing age and improper toothbrushing, gingival recession may occur and result in the exposure of root cementum and dentin. These surfaces, like enamel, may become colonized by oral bacteria that can trigger dental caries. Prior to eruption, the enamel is lined by remnants of the enamel-forming organ, namely the reduced enamel epithelium and the basal lamina that connects it to the enamel surface. The basal lamina is also continuous with organic material that fills the microscopic voids in the superficial enamel. This subsurface material appears as a fringe attached to the basal lamina and is composed of residual enamel matrix proteins (Figures 2-3, 2-4). It is referred to as a subsurface pellicle. Because it originates from local cells during tooth formation, it is considered to be of endogenous origin. When the tooth emerges into the oral cavity, the remnants of the reduced enamel epithelium are worn off or digested by salivary and bacterial enzymes. The underlying enamel becomes exposed to saliva and the oral microbiota. Salivary components become adsorbed to exposed enamel within seconds, forming a microscopic coating over the exposed tooth surface. This thin coating can subsequently become colonized by oral bacteria. Because this coating originates from salivary proteins rather than the dental organ, it is considered to be of exogenous origin. Thus, the tooth surface is almost always coated by a variety of structures that are either of endogenous origin (i.e., derived from cells of the dental organ) or of exogenous origin (i.e., acquired following eruption of the teeth into the oral cavity).17
^ The coating of salivary origin that forms on exposed tooth surfaces is called the acquired pellicle.18,19 It is acellular and consists primarily of glycoproteinsa derived from saliva (Figure 2-3). The pellicle also occupies the millions of microscopic voids in the erupted tooth caused by chemical and mechanical interactions of the tooth surface with the oral environment. Collectively these organic fringe-like projections form a subsurface pellicle, which is of exogenous or acquired origin. Oral fluids and small molecules can slowly diffuse through the acquired pellicle into the superficial enamel. If the pellicle is displaced, for example by a prophylaxis, it begins to reform immediately.20,21 It takes about a week for the pellicle to develop its condensed, mature structure which may also incorporate bacterial products.22-24 An acquired pellicle also forms on artificial surfaces, including dental restorations and dentures. These organic coatings are similar to the pellicles on natural teeth and may be colonized by bacteria.25-27 Colonization of the acquired pellicle can be beneficial for the bacteria because the pellicle components can serve as nutrients.28 For example, proline-rich salivary proteins may be degraded by bacterial collagenases,29 releasing peptides, free amino acids, and salivary mucins that may enhance the growth of dental plaque organisms, such as actinomycetes and spirochetes.30 The carbohydrate components of certain pellicle glycoproteins may serve as receptors for bacterial-binding proteins such as adhesins, thereby contributing to bacterial adhesion to the tooth.31-33 There is competition for the binding sites on the pellicle, not only by receptors on bacteria, but also from host proteins, including immunoglobulins (i.e., antibodies), proteins of the complement system, and the enzyme lysozyme. These host proteins originate from saliva and gingival sulcus fluid.34,35 Once a pellicle site is occupied by one of the competing entities, occupancy by another is inhibited.36 Not only does competition arise for occupancy of binding sites, but an antagonistic relationship often exists between different types of bacteria competing for the binding sites. For example, it has been shown that some streptococci synthesize and release bacteriocins, which can inhibit some strains of Actinomyces37 and Actinobacillus species.38 aA glycoprotein is a protein molecule that includes an attached carbohydrate component. ^ All bacteria that initiate plaque formation come in contact with the organically coated tooth surface fortuitously. Forces exist that tend to allow bacteria to accumulate on teeth or to remove them. Shifts in these forces determine whether more or less plaque accumulates at a given site on a tooth. Many factors influence the build-up of plaque,39 ranging from simple factors, such as mechanical displacement, stagnation (i.e., colonization in a sheltered or undisturbed environment), and availability of nutrients, to complex factors, including interactions between the microbes and the host's inflammatory-immune systems. Bacteria tend to be removed from the teeth during mastication of foods, by the tongue, toothbrushing, and other oral-hygiene activities. For this reason, bacteria tend to accumulate on teeth in sheltered, undisturbed environments (sites at risk), such as the occlusal fissures, the surfaces apical to the contact between adjacent teeth, and in the gingival sulcus. Question 1 Which of the following statements, if any, are true? A. The acquired pellicle is a layer of cells on the external surface of the clinical crown of the tooth. B. Salivary glycoproteins are a major source of organic materials in the acquired pellicle. C. Bacteria produce enzymes that may degrade some of the acquired pellicle components such as proteins. D. It usually takes several days before the acquired pellicle is reformed after a prophylaxis. E. The presence of immunoglobulins in the acquired pellicle guarantees that the acquired pellicle will remain free from bacterial colonization. Therefore, it is no coincidence that the major plaque-based diseases, caries and inflammatory periodontal diseases, arise at these sites where plaque is most abundant and stagnant. Initial plaque formation may take as long as 2 hours.40 Binding sites and individual strain affinity for a given surface vary considerably.41,42 Colonization begins as a series of isolated colonies, often confined to microscopic tooth surface irregularities.23 With the aid of nutrients from saliva and host food, the colonizing bacteria begin to multiply. About 2 days are then required for the plaque to double in mass, during which time, the bacterial colonies have been coalescing.43 The most dramatic change in bacterial numbers occurs during the first 4 or 5 days of plaque formation.44,45 After approximately 21 days, bacterial replication slows so that plaque accumulation becomes relatively stable.46 The increasing thickness of the plaque limits the diffusion of oxygen to the entrapped original, oxygen-tolerant populations. As a result, the organisms that survive in the deeper aspects of the developing plaque are either facultative or obligate anaerobes.b The forming bacterial colonies are rapidly covered by saliva.47 When seen with the scanning electron microscope, growing colonies protrude from the surface of the plaque as domes, giving the appearance of a cluster of igloos beneath newly fallen snow (Figure 2-5). In individuals with poor oral hygiene, superficial dental plaque may incorporate food debris and mammalian cells such as desquamated epithelial cells and leukocytes. This debris is called materia alba (literally, "white matter"). Unlike plaque, it is usually removed easily by rinsing with water.18 At times, the plaque demonstrates staining, with the discoloration being caused by sources including tea, heavy metal salts, drugs, and chromogenic bacteria. b Facultative anaerobes can exist in an environment with or without oxygen; obligate anaerobes cannot exist in an environment with oxygen.
Molecular Mechanisms of Bacterial Adhesion The initial bacterial attachment to the acquired pellicle (^ A) is thought to involve physicochemical interactions (e.g., electrostatic forces and hydrophobic bonding)48-51 between molecules or portions of molecules, such as the side chains of the amino acids phenylalanine and leucine. It has been suggested that the hydrophobicity of some streptococci, a major plaque group, is caused by cell wall-associated molecules including glucosyltransferase, an enzyme that converts the glucose portion of the sugar, sucrose, into extracellular polysaccharide. Some glucosyltransferases have been designated as hydrophobins.52 Another molecular mechanism of bacterial adhesion is calcium bridging53-55 which links negatively charged bacterial cell surfaces to the negatively charged acquired pellicle (Figure 2-6 B) via interposed positively charged, divalent calcium ions from the saliva. Calcium bridging may only be important in early plaque formation, because recently formed plaque is readily disrupted by exposure to a calcium-complexing (chelating) agent, such as ethylenediaminetetraacetic acid (EDTA).56 Some of the streptococci in plaque use the enzyme glucosyltransferase to synthesize extracellular polysaccharides (ECP). Among these are "sticky" glucans that, through hydrogen bonding, are thought to contribute to the mediation of bacterial adhesion (Figure 2-6 C).57 Once the bacteria adhere, they are often "entombed" as additional glucan is produced.58 Bacteria also exhibit external cell surface proteins termed adhesins,33,59 that have lectin-likec activity as they can bind to carbohydrate components of glycoproteins.32,60 These molecules, which some researchers have suggested may be located on bacterial surface appendages, such as fimbriae61 (Figur e 2-6 D), are believed to facilitate colonization of the acquired pellicle.62 Fimbria-associated adhesins probably mediate bacterial adhesion via ionic or hydrogen-bonding interactions. Adhesins and fimbriae may function together to promote bacterial attachment to pellicle-coated surfaces.63 For example, pilin, a structural protein that constitutes the bulk of some fimbriae, is hydrophobic because of its amino-acid content.64 These fibrillar surface appendages extend from the bacterial surface and may reduce or mask the repelling effect of the net negative surface charges. Carbohydrate-binding adhesins have been shown to link actinomycetes to streptococci in early dental-plaque formation.65,66 While some or all of the above-described mechanisms may play a role in the attachment of bacteria to one another and to the tooth surface, the nature of the actual linking molecules in plaque, or between plaque and tooth surface coatings is not known. cLectins are plant proteins with receptor sites that bind specific sugars.
^ Plaque bacteria vary in number and proportions from time to time and from site to site within the mouth of any one individual. The diversity is even greater between individuals,67 between races,68 and between supra- and subgingival plaques.69 The only abundant bacteria found almost universally in the mouths of humans and animals are streptococci and actinomycetes. The bacteria colonize the teeth in a reasonably predictable sequence. The first to adhere are primary colonizers, sometimes referred to as pioneer species. These are microorganisms that are able to stick directly to the acquired pellicle. Those that arrive later are secondary colonizers. They may be able to colonize an existing bacterial layer, but they are unable to act as primary colonizers. Generally speaking, the primary colonizers are not pathogenic. If the plaque is allowed to remain undisturbed, it eventually becomes populated with secondary colonizers that are the likely etiologic agents of caries, gingivitis, and periodontitis, the destructive form of inflammatory periodontal disease. The earliest colonizers are overwhelmingly cocci (i.e., spherical cells),1,69,70 especially streptococci, which constitute 47 to 85% of the cultivable cells found during the first 4 hours after professional tooth cleaning.71 These tend to be followed by short rods and filamentous bacteria. Because of stagnation, the most abundant colonization is on the proximal surfaces, in the fissures of teeth, and in the gingival sulcus region.72 Cocci are probably the first to adhere because they are small and round and, therefore, have a smaller energy barrier to overcome than other bacterial forms.73 The first or primary colonizers tend to be aerobic (i.e., oxygen-tolerant) bacteria including Neisseria and Rothia. The streptococci, the Gram-positive facultative rods, and the actinomycetes are the main organisms in both early fissure and approximal plaque.73-75 As plaque oxygen levels fall, the proportions of Gram-negative rods, for example fusobacteria, and Gram-negative cocci such as Veillonella tend to increase. Of the early colonizers, Streptococcus sanguis often appears first,76 followed by S. mutans. Both depend on a sheltered environment for growth and the presence of extracellular carbohydrate (e.g., sucrose). Sucrose is used to synthesize intracellular polysaccharides that serve as an internal source of energy, as well as external polysaccharide coats.77,78 The polysaccharide coating helps protect the cell from the osmotic effects of sucrose. In addition, it reduces the inhibitory effect of toxic metabolic end products, such as lactic acid, on bacterial survival. Whereas nonmotile cells, including streptococci and actinomycetes, come into contact with the tooth randomly, motile cells such as the spirochetes are likely to be attracted by chemotactic factors (e.g., nutrients). Surface receptors probably provide a means of attachment for secondary colonizers onto the initial bacterial layer.79 Bacteria that cannot adhere easily to the tooth initially via organic coatings can probably attach by strong lectin-like, cell-to-cell interactions with similar or dissimilar bacteria that are already attached (i.e., the primary colonizers).33,80,81 Gram-negative, anaerobic (e.g., oxygen-intolerant) species predominate in the subgingival plaque during the later phases of plaque development,82 but they may also be present in early plaque, for example, ^ and Fusobacterium species. There is evidence that oxygen does not penetrate more than 0.1 mm into the dental plaque,83,84 a fact that may explain the presence of anaerobic bacteria in early plaque. Question 2 Which of the following statements, if any, are correct? A. An important criterion for successful bacterial colonization of teeth is the availability of an unoccupied binding site. B. Sites on teeth at risk for dental plaque formation include the occlusal fissures, approximal surfaces apical to the contact point between adjacent teeth, and the gingival sulcus region. C. An operational definition for materia alba is "the adherent material on tooth surfaces that can be removed by rinsing." D. During initial formation of dental plaque, negative charges on bacterial cells are attracted to the negative charges of the acquired pellicle. E. The observation that calcium-complexing agents release recently formed dental plaque from the teeth supports the argument for calcium bridging. ^ A great variety of factors affect the colonization of the teeth by bacteria. Dental plaque consists of different species of bacteria that are not uniformly distributed, since different species colonize the tooth surface at different times and under different circumstances. The newly formed supragingival biofilm frequently exhibits "palisades" (i.e., columnar microcolonies of cells) of firmly attached cocci, rods, or filaments. The organisms are positioned perpendicular to the tooth surface,1,69,85 the result of competitive colonization. The bacterial cells in the biofilm are surrounded by an intercellular plaque matrix (Figure 2-7).56 The matrix is composed of both organic and inorganic components that originate primarily from the bacteria. Polysaccharides derived from bacterial metabolism of carbohydrates are a major constituent of the matrix while salivary and serum proteins/glycoproteins represent minor components. The bacteria in the subgingival biofilm consist of several motile species that do not form distinctive microcolonies. They tend to be located on the surface of the adherent bacterial layer and are separated by an abundant intercellular matrix. Some bacteria on the surface of the biofilm aggregate into distinctive structures that include arrangements of cocci ("corn-cob" configurations) and rods ("test-tube brush" configurations)1,2,69,86 radially arranged around a central filament (Figure 2-8).
Dental-Plaque Metabolism For metabolism to occur, a source of energy is required. For the caries-related S. mutans and many other acid-forming organisms, this energy source can be sucrose.87 Almost immediately following exposure of these microorganisms to sucrose, they produce (1) acid, (2) intracellular polysaccharides (ICP), that provide a reserve source of energy for each bacterium, much like glycogen does for human cells,88 and (3) extracellular polysaccharides including glucans (dextran)89 and fructans (levan).90 Glucans can be viscid substances that help anchor the bacteria to the pellicle, as well as stabilize the plaque mass. Fructans can act as an energy source for any bacteria having the enzyme levanase.91,92 Quantitatively, the glucans constitute up to approximately 20% of plaque dry weight, levans about 10%, and bacteria the remaining 70 to 80%. As mentioned previously, the glucans and fructans are major contributors to the intercellular plaque matrix.92 Plaque organisms grow under adverse environmental conditions. These include pH, temperature, ionic strength, oxygen tension, nutrient levels, and antagonistic elements, such as competing organisms and the host inflammatory-immune response. To cope with this hostile environment, the plaque organisms must find a safe haven in relation to their neighbors and the oral environment. Such a favorable location is termed an ecologic niche.5 Normally, once the niches are established, the bacteria of the resident microbiota coexist with the host and the surrounding microcosm. This symbiosis results in a resistance to colonization by subsequent nonindigenous organisms. In this manner, the resident microbiota can protect the host against infection by major primary pathogens, e.g., Corynebacterium diphtheria and Streptococcus pyogenes. With dietary sugars entering the plaque, anaerobic glycolysis results in acid production (acidogenesis) and accumulation of acid in the plaque.5 If no acid-consuming organisms (e.g., Veillonella) are available to utilize the acids, the plaque pH drops rapidly from 7.0 to below 4.5. This drop is important because enamel begins to demineralize between pH 5.0 and 5.5. One possible outcome of the drop in pH may be the dissolution of the mineralized tooth surface adjacent to the plaque, resulting in carious cavitation of the tooth.77 This process provides the bacteria access to the inorganic elements (e.g., calcium and phosphate) needed for their nutritional requirements. By adhering to the tooth surface via an organic layer of salivary origin, dental plaque bacteria can gain access to a supply of organic nutrients, a widespread phenomenon.47 The same search for nutrients may explain the extension of bacteria from the supragingival plaque into the gingival sulcus.93,94 To prevent or reduce subgingival colonization, the host tissues defend against the bacterial challenge with antibacterial strategies, such as the passage of antibodies and the emigration of polymorphonuclear neutrophils from the adjacent connective tissue into the gingival sulcus. The continued metabolic activity of plaque in the subgingival environment initiates the inflammatory response of the gingival tissues (gingivitis)95 and also may eventually lead to progressive destruction of the periodontium (periodontitis)96. Until supragingival plaque mineralizes as dental calculus, it can be removed by toothbrushing and flossing.97 As the plaque matures, it becomes more resistant to removal with a toothbrush. In one study, at 24, 48, and 72 hours after formation, 5.5, 7.8, and 14.0 g/cm2 of pressure, respectively, were required to dislodge the plaquealmost three times as much pressure to remove it on the third day as on the first.98 Once dental calculus is formed, professional instrumentation is necessary for its removal. |
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