Dental Caries

Etiology, Clinical Characteristics, Risk Assessment, and Management

André V. Ritter, R. Scott Eidson and Terence E. Donovan

This chapter presents basic definitions and information on dental caries, clinical characteristics of the caries lesion, caries risk assessment, and caries management, in the context of clinical operative dentistry.

What is Dental Caries?

Dental caries is a multifactorial, transmissible, infectious oral disease caused primarily by the complex interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface over time. Traditionally, this tooth-biofilm-carbohydrate interaction has been illustrated by the classical Keyes-Jordan diagram (Fig. 2-1).¹ However, dental caries onset and activity are, in fact, much more complex than this three-way interaction, as not all persons with teeth, biofilm, and consuming carbohydrates will have caries over time. Several modifying risk and protective factors influence the dental caries process, as will be discussed later in this chapter.

Fig. 2-1 Modified Keyes-Jordan diagram. As a simplified description, dental caries is a result of the interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface (host) over time. However, dental caries onset and activity are, in fact, much more complex, as not all persons with teeth, biofilm, and who are consuming carbohydrates will have caries over time. Several modifying risk factors and protective factors influence the dental caries process. *(Modified from Keyes PH, Jordan HV: Factors influencing initiation, transmission and inhibition of dental caries. In Harris RJ, editor:* Mechanisms of hard tissue destruction, New York, 1963, Academic Press.)

At the tooth level, caries activity is characterized by localized demineralization and loss of tooth structure (Figs. 2-2 and 2-3). Cariogenic bacteria in the biofilm metabolize refined carbohydrates for energy and produce organic acid by-products. These organic acids, if present in the biofilm ecosystem for extended periods, can lower the pH in the biofilm to below a critical level (5.5 for enamel, 6.2 for dentin). The low pH drives calcium and phosphate from the tooth to the biofilm in an attempt to reach equilibrium, hence resulting in a net loss of minerals by the tooth, or demineralization. When the pH in the biofilm returns to neutral and the concentration of soluble calcium and phosphate is supersaturated relative to that in the tooth, mineral can then be added back to partially demineralized enamel, in a process called remineralization. At the tooth surface and sub-surface level, therefore, dental caries results from a dynamic process of attack (demineralization) and restitution (remineralization) of the tooth matter. These events take place several times a day over the life of the tooth and are modulated by many factors, including number and type of microbial flora in the biofilm, diet, oral hygiene, genetics, dental anatomy, use of fluorides and other chemotherapeutic agents, salivary flow and buffering capacity; and inherent resistance of the tooth structure and composition that will differ from person to person, tooth to tooth, and site to site. The balance between demineralization and remineralization has been illustrated in terms of pathologic factors (i.e., those favoring demineralization) and protective factors (i.e., those favoring remineralization) (Fig. 2-4).² Individuals in whom the balance tilts predominantly toward protective factors (remineralization) are much less likely to develop dental caries than those in which the balance is tilted toward pathologic factors (demineralization). Understanding the balance between demineralization and remineralization is key to caries management.

Fig. 2-2 A, Young adult with multiple active caries lesions involving teeth No. 8-10. B, Cavitated areas (a) are surrounded by areas of extensive demineralization that are chalky and opaque (b). Some areas of noncavitated caries have superficial stain.

Fig. 2-3 Extensive active caries in a young adult (same patient as in Fig. 2-2). A, Mirror view of teeth No. 20-22. B, Cavitated lesions (a) are surrounded by extensive areas of chalky, opaque demineralized areas (b). The presence of smooth-surface lesions such as these is associated with rampant caries. Occlusal and interproximal smooth-surface caries usually occur in advance of facial smooth-surface lesions. The presence of these types of lesions should alert the dentist to the possibility of extensive caries activity elsewhere in the mouth. The interproximal gingiva is swollen red and would bleed easily on probing. These gingival changes are the consequence of long-standing irritation from the plaque adherent to the teeth.

Fig. 2-4 The caries balance. The balance between demineralization and remineralization is illustrated in terms of pathologic factors (i.e., those favoring demineralization) and protective factors (i.e., those favoring remineralization). *(Modified from Featherstone JDB: Prevention and reversal of dental caries: Role of low level fluoride,* Community Dent Oral Epidemiol *27:31–40, 1999.)*

Repeated demineralization events may result from a predominantly pathologic environment causing the localized dissolution and destruction of the calcified dental tissues, evidenced as a caries lesion or a “cavity.” Severe demineralization of enamel results in the formation of a cavitation in the enamel surface. Severe demineralization of dentin results in the exposure of the protein matrix, which is denatured initially by host matrix metalloproteinases (MMPs) and is subsequently degraded by MMPs and other bacterial proteases. Demineralization of the inorganic phase and denaturation and degradation of the organic phase result in dentin cavitation.³

It is essential to understand that caries lesions, or cavitations in teeth, are signs of an underlying condition, an imbalance between protective and pathologic factors favoring the latter. In clinical practice, it is very easy to lose sight of this fact and focus entirely on the restorative treatment of caries lesions, failing to treat the underlying cause of the disease (Table 2-1). Although symptomatic treatment is important, failure to identify and treat the underlying causative factors allows the disease to continue. This chapter emphasizes the components of a caries management program that is based first on risk assessment and then on modifying the biofilm ecology to enhance protective factors and minimize pathologic factors.⁴

Table 2-1

Caries Management Based on the Medical Model

Primary Etiology	Cariogenic Biofilm (Infection)
Symptoms	Demineralization lesions in teeth
Treatment, symptomatic	Restoration of cavitated lesions
Treatment, therapeutic	Improvement of host resistance by (1) biofilm control, (2) elevating biofilm pH, and (3) enhancing remineralization
Post-treatment assessment, symptomatic	Examination of teeth for new lesions
Post-treatment assessment, therapeutic	Re-evaluation of etiologic conditions and primary and secondary risk factors; and continuous management based on findings

This chapter also presents information on clinical characteristics of caries lesion as they relate to clinical operative dentistry. Use of correct and consistent terms when referring to caries lesions is important. Box 2-1 summarizes the most common terms used in this textbook to define caries lesions based on their location, cavitation status, and activity status.

Box 2.1 Caries Lesion Definitions

This box summarizes the most common terms used in this textbook to define caries lesions based on their location, cavitation status, and activity status.

Caries lesion. Tooth demineralization as a result of the caries process. Other texts may use the term carious lesion. Laypeople may use the term cavity.

Smooth-surface caries. A caries lesion on a smooth tooth surface.

Pit-and-fissure caries. A caries lesion on a pit-and-fissure area.

Occlusal caries. A caries lesion on an occlusal surface.

Proximal caries. A caries lesion on a proximal surface.

Enamel caries. A caries lesion in enamel, typically indicating that the lesion has not penetrated into dentin. (Note that many lesions detected clinically as enamel caries may very well have extended into dentin histologically.)

Dentin caries. A caries lesion into dentin.

Coronal caries. A caries lesion in any surface of the anatomic tooth crown.

Root caries. A caries lesion in the root surface.

Primary caries. A caries lesion not adjacent to an existing restoration or crown.

Secondary caries. A caries lesion adjacent to an existing restoration, crown, or sealant. Other term used is caries adjacent to restorations and sealants (CARS). Also referred to as recurrent caries, implying that a primary caries lesion was restored but that the lesion reoccurred.

Residual caries. Refers to carious tissue that was not completely excavated prior to placing a restoration. Sometimes residual caries can be difficult to differentiate from secondary caries.

Cavitated caries lesion. A caries lesion that results in the breaking of the integrity of the tooth, or a cavitation.

Non-cavitated caries lesion. A caries lesion that has not been cavitated. In enamel caries, non-cavitated lesions are also referred to as “white spot” lesions.

(Clinically, the distinction between a cavitated and a noncavitated caries lesion is not as simple as it may seem. Although historically any roughness detectable with a sharp explorer has been considered a cavitated lesion, more recent caries detection guidelines establish that only lesions in which a blunt probe (e.g., WHO[World Health Organization]/CPI[Communty Periodonatal Index]/PSR[Periodontal Screening and Recording] probe) penetrates are to be considered cavitated. This distinction has important implications on lesion management.)

Active caries lesion. A caries lesion that is considered to be biologically active, that is, lesion in which tooth demineralization is in frank activity at the time of examination.

Inactive caries lesion. A caries lesion that is considered to be biologically inactive at the time of examination, that is, in which tooth demineralization caused by caries may have happened in the past but has stopped and is currently stalled. Also referred to as arrested caries, meaning that the caries process has been arrested but that the clinical signs of the lesion itself are still present.

Rampant caries. Term used to describe the presence of extensive and multiple cavitated and active caries lesions in the same person. Typically used in association with “baby bottle caries,” “radiation therapy caries,” or “meth-mouth caries.” These terms refer to the etiology of the condition.

Ecologic Basis of Dental Caries: The Role of the Biofilm

Dental plaque is a term historically used to describe the soft, tenacious film accumulating on the surface of teeth. Dental plaque has been more recently referred to as a plaque biofilm, or simply biofilm, which is a more complete and accurate description of its composition (bio) and structure (film).⁵ Biofilm is composed mostly of bacteria, their by-products, extracellular matrix, and water (Figs. 2-5 to 2-9). Biofilm is not adherent food debris, as is widely and erroneously thought, nor does it result from the haphazard collection of opportunistic microorganisms. The accumulation of biofilm on teeth is a highly organized and ordered sequence of events. Many of the organisms found in the mouth are not found elsewhere in nature. Survival of microorganisms in the oral environment depends on their ability to adhere to a surface. Free-floating organisms are cleared rapidly from the mouth by salivary flow and frequent swallowing. Only a few specialized organisms, primarily streptococci, are able to adhere to oral surfaces such as the mucosa and tooth structure.

Fig. 2-5 A, Composite diagram illustrating the relationship of plaque biofilm (p) to the enamel in a smooth-surface noncavitated lesion. A relatively cell-free layer of precipitated salivary protein material, the acquired pellicle (ap), covers the perikymata ridges (pr). The plaque bacteria attach to the pellicle. Overlapping perikymata ridges can be seen on surface of enamel (see Fig. 2-6). Figs. 2-7 to 2-9 are photomicrographs of cross-sections of plaque biofilm. The enamel is composed of rod-like structures (er) that course from the inner dentinoenamel junction (DEJ) to the surface of the crown. Striae of Retzius (sr) can be seen in cross-sections of enamel. B, Higher power view of the cutout portion of enamel in A. Enamel rods interlock with each other in a head-to-tail orientation. The rod heads are visible on the surface as slight depressions on the perikymata ridges. The enamel rods comprise tightly packed crystallites. The orientation of the crystallites changes from being parallel to the rod in the head region to being perpendicular to the rod axis in the tail end. Striae of Retzius form a descending diagonal line, descending cervically. C, Drawings 1 through 5 illustrate the various stages in colonization during plaque formation on the shaded enamel block shown in B. The accumulated mass of bacteria on the tooth surface may become so thick that it is visible to the unaided eye. Such plaques are gelatinous and tenaciously adherent; they readily take up disclosing dyes, aiding in their visualization for oral hygiene instruction. Thick plaque biofilms (4 and 5) are capable of great metabolic activity when sufficient nutrients are available. The gelatinous nature of the plaque limits outward diffusion of metabolic products and serves to prolong the retention of organic acid metabolic byproducts.

Fig. 2-6 A, Scanning electron microscope view (×600) of overlapping perikymata (P) in sound enamel from unerupted molar. B, Higher power view (×2300) of overlapped site rotated 180 degrees. Surface of noncavitated enamel lesions has “punched-out” appearance. *(From Hoffman S: Histopathology of caries lesions. In Menaker L, editor:* The biologic basis of dental caries, New York, 1980, Harper & Row.)

Fig. 2-7 Photomicrograph of one-day old plaque biofilm. This plaque biofilm consists primarily of columnar microcolonies of cocci (C) growing perpendicular to crown surface (S) (×1350). *(From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. A light and electron microscopic study,* J Periodontol *46(1):10–26, 1975.)*

Fig. 2-8 Plaque biofilm formation at 1 week. Filamentous bacteria (f) appear to be invading cocci microcolonies. Plaque near gingival sulcus has fewer coccal forms and more filamentous bacteria (×860). *(From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. A light and electron microscopic study,* J Periodontol *46(1):10–26, 1975.)*

Fig. 2-9 At 3 weeks old, plaque biofilm is almost entirely composed of filamentous bacteria. Heavy plaque formers have spiral bacteria (a) associated with subgingival plaque (¥660). *(From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. A light and electron microscopic study,* J Periodontol *46(1):10–26, 1975.)*

Significant differences exist in the biofilm communities found in various habitats (ecologic environments) within the oral cavity (Fig. 2-10). Teeth normally have a biofilm community dominated by Streptococcus sanguis and S. mitis. The population size of mutans streptococci (MS) on teeth varies. Normally, it is a small percentage of the total biofilm population, but it can be one-half the facultative streptococcal flora in other biofilms. Mature plaque biofilm communities have tremendous metabolic potential and are capable of rapid anaerobic metabolism of any available carbohydrates (Fig. 2-11).

Fig. 2-10 Approximate proportional distribution of predominant cultivable flora of four oral habitats. *(Redrawn from Morhart R, Fitzgerald R: Composition and ecology of the oral flora. In Menaker L, editor:* The biologic basis of dental caries, New York, 1980, Harper & Row.)

Fig. 2-11 A, Mature plaque biofilm communities have tremendous metabolic potential and are capable of rapid anaerobic metabolism of any available carbohydrates. Classic studies by Stephan show this metabolic potential by severe pH drops at the plaque-enamel interface after glucose rinse. It is generally agreed that a pH of 5.5 is the threshold for enamel demineralization. Exposure to a glucose rinse for an extreme caries activity plaque results in a sustained period of demineralization (pH 5.5). Recording from a slight caries activity plaque shows a much shorter period of demineralization. B, The frequency of sucrose exposure for cariogenic plaque greatly influences the progress of tooth demineralization. The top line illustrates pH depression, patterned after Stephan’s curves in A. Three meals per day results in three exposures of plaque acids, each lasting approximately 1 hour. The plaque pH depression is relatively independent of the quantity of sucrose ingested. Between-meal snacks or the use of sweetened breath mints results in many more acid attacks, as illustrated at the bottom. The effect of frequent ingestion of small quantities of sucrose results in a nearly continuous acid attack on the tooth surface. The clinical consequences of this behavior can be seen in Fig. 2-35. C, In active caries, a progressive loss of mineral content subjacent to the cariogenic plaque occurs. Inset illustrates that the loss is not a continuous process. Instead, alternating periods of mineral loss (demineralization) occur, with intervening periods of remineralization. The critical event for the tooth is cavitation of the surface, marked by the vertical dashed line. This event marks an acceleration in caries destruction of the tooth and irreversible loss of tooth structure. For these reasons, restorative intervention is required. *(A, adapted and redrawn from Stephan RM: Intra-oral hydrogen-ion concentration associated with dental caries activity,* J Dent Res *23:257, 1944.)*

Many distinct habitats may be identified on individual teeth, with each habitat containing a unique biofilm community (Table 2-2). Although the pits and fissures on the crown may harbor a relatively simple population of streptococci, the root surface in the gingival sulcus may harbor a complex community dominated by filamentous and spiral bacteria. Facial and lingual smooth surfaces and proximal surfaces also may harbor vastly different biofilm communities. The mesial surface of a molar may be carious and have a biofilm dominated by large populations of MS and lactobacilli, whereas the distal surface may lack these organisms and be caries-free. Generalization about biofilm communities is difficult. Nevertheless, the general activity of biofilm growth and maturation is predictable and sufficiently well known to be of therapeutic importance in the prevention of caries.

Table 2-2

Oral Habitats *

Habitat	Predominant Species	Environmental Conditions within Plaque
Mucosa	S. mitis	Aerobic
	S. sanguis	pH approximately 7
	S. salivarius	Oxidation-reduction potential positive
Tongue	S. salivarius	Aerobic
	S. mutans	pH approximately 7
	S. sanguis	Oxidation-reduction potential positive
Teeth (non-carious)	S. sanguis	Aerobic
		pH 5.5
		Oxidation-reduction negative
Gingival crevice	Fusobacterium	Anaerobic
	Spirochaeta	pH variable
	Actinomyces	Oxidation-reduction very negative
	Veillonella
Enamel caries	S. mutans	Anaerobic
		pH <5.5
		Oxidation-reduction negative
Dentin caries	S. mutans	Anaerobic
	Lactobacillus	pH <5.5
		Oxidation-reduction negative
Root caries	Actinomyces	Anaerobic
		pH <5.5
		Oxidation-reduction negative

^*The micro-environmental conditions in the habitats associated with host health are generally aerobic, near neutrality in pH, and positive in oxidation-reduction potential. Significant micro-environmental changes are associated with caries and periodontal disease. The changes are the result of the plaque community metabolism.

Professional tooth cleaning is intended to control biofilm (plaque) and prevent disease. After professional removal of all organic material and bacteria from the tooth surface, a new coating of organic material begins to accumulate immediately. Within 2 hours, a cell-free, structureless organic film, the acquired enamel pellicle (AEP, see Figs. 2-5, A and C), can cover the previously denuded area completely. The pellicle is formed primarily from the selective precipitation of various components of saliva. The functions of the pellicle are believed to be as follows: (1) to protect the enamel, (2) to reduce friction between teeth, and (3) possibly to provide a matrix for remineralization.⁶

Tooth Habitats for Cariogenic Biofilm

The tooth surface is unique because it is not protected by the surface shedding mechanisms (continual replacement of epithelial cells) used throughout the remainder of the alimentary canal. The tooth surface is stable and covered with the pellicle of precipitated salivary glycoproteins, enzymes, and immunoglobulins. It is the ideal surface for the attachment of many oral streptococci. If left undisturbed, biofilm rapidly builds up to sufficient depth to produce an anaerobic environment adjacent to the tooth surface. Tooth habitats favorable for harboring pathogenic biofilm include (1) pits and fissures (Fig. 2-12); (2) the smooth enamel surfaces immediately gingival to the proximal contacts and in the gingival third of the facial and lingual surfaces of the clinical crown (Fig. 2-13); (3) root surfaces, particularly near the cervical line; and (4) subgingival areas (Fig. 2-14). These sites correspond to the locations where caries lesions are most frequently found.

Fig. 2-12 Developmental pits, grooves, and fissures on the crowns of the teeth can have complex and varied anatomy. A and B, The facial developmental groove of the lower first molar often terminates in a pit. The depth of the groove and the pit varies. C and D, The central groove extends from the mesial pit to the distal pit. Sometimes grooves extend over the marginal ridges. E, The termination of pits and fissures may vary from a shallow groove (a) to complete penetration of the enamel (b). The end of the fissure may end blindly (c) or open into an irregular chamber (d).

Fig. 2-13 Plaque biofilm formation on posterior teeth and associated caries lesions. A, Teeth No. 19 and No. 20 in contacting relationship. B, The crown of tooth No. 20 has been removed at the cervix. The proximal contact and subcontact plaque can be seen on the mesial surface of tooth No. 19. A facial plaque also is illustrated. C, During periods of unrestricted growth, the mesial and facial plaques become part of a continuous ring of plaque around teeth. D, A horizontal cross-section through teeth No. 19 and No. 20 with heavy plaque. Inset shows the interproximal space below the contact area filled with gelatinous plaque. This mass of interproximal plaque concentrates the effects of plaque metabolism on the adjacent tooth smooth surfaces. All interproximal surfaces are subject to plaque accumulation and acid demineralization. In patients exposed to fluoridated water, most interproximal lesions become arrested at a stage before cavitation.

Pits and Fissures

Pits and fissures are particularly susceptible surfaces for caries initiation (see Fig. 2-12; Figs. 2-15 to 2-19; see also Fig. 2-12). The pits and fissures provide excellent mechanical shelter for organisms and harbor a community dominated by S. sanguis and other streptococci.⁷ The relative proportion of MS most probably determines the cariogenic potential of the pit-and-fissure community. The appearance of MS in pits and fissures is usually followed by caries 6 to 24 months later. In susceptible patients, sealing the pits and fissures just after tooth eruption may be the most important event in their resistance to caries.

Fig. 2-16 A, Mandibular first molar has undermined discolored enamel owing to extensive pit-and-fissure caries. The lesion began as illustrated in Fig. 2-15 and has progressed to the stage illustrated in Fig. 2-15, D. B, Discolored enamel is outlined by broken line in the central fossa region.

Fig. 2-17 Progression of pit-and-fissure caries. A, The mandibular right first molar (tooth No. 30) was sealed. Note radiolucent areas under the occlusal enamel in A and B. The sealant failed, and caries progressed slowly during the next 5 years; the only symptom was occasional biting-force pain. C and D, Note the extensive radiolucency under the enamel and an area of increased radiopacity below the lesion, suggesting sclerosis.

Fig. 2-18 A young patient with extensive caries. A and B, The occlusal pits of the first molar and second premolar are carious. An interproximal caries lesion is seen on the second premolar. The second premolar is rotated almost 90 degrees, bringing the lingual surface into contact with the mesial surface of the first molar. Normally, the lingual surfaces of mandibular teeth are rarely attacked by caries, but here, the tooth rotation makes the lingual surface a proximal contact and, consequently, produces an interproximal habitat, which increases the susceptibility of the surface to caries. C and D, The first and second molars have extensive caries in the pits and fissures. E and F, On the bitewing radiograph, not only can the extensive nature of the caries in the second premolar be seen but also seen is a lesion on the distal aspect of the first molar, which is not visible clinically. (Dark areas in B, D, and F indicate caries.)

Fig. 2-19 Example of occlusal caries that is much more extensive than is apparent clinically. A and B, Clinical example. C and D, A bitewing radiograph further reveals an extensive area of demineralization undermining the distofacial cusp.

Smooth Enamel Surfaces

The proximal enamel surfaces immediately gingival to the contact area are the second most susceptible areas to caries (Figs. 2-20 and 2-21; see also Figs. 2-14 and 2-18). These areas are protected physically and are relatively free from the effects of mastication, tongue movement, and salivary flow. The types and numbers of organisms composing the proximal surface biofilm community vary. Important ecologic determinants for the biofilm community on the proximal surfaces are the topography of the tooth surface, the size and shape of the gingival papillae, and the oral hygiene of the patient. A rough surface (caused by caries, a poor-quality restoration, or a structural defect) restricts adequate biofilm removal. This situation favors the occurrence of caries or periodontal disease at the site.

Fig. 2-20 Bitewing radiograph of normal teeth, free from caries. Note the uniform density of the enamel on the interproximal surfaces. A third molar is impacted on the distal aspect of the lower second molar. The interproximal bone levels are uniform and located slightly below the cementoenamel junctions, suggesting a healthy periodontium.

Fig. 2-21 Longitudinal sections (see inset for A) showing initiation and progression of caries on interproximal surfaces. A, Initial demineralization (indicated by the shading in the enamel) on the proximal surfaces is not detectable clinically or radiographically. All proximal surfaces are demineralized to some degree, but most are remineralized and become immune to further attack. The presence of small amounts of fluoride in the saliva virtually ensures that remineralization and immunity to further attack will occur. B, When proximal caries first becomes detectable radiographically, the enamel surface is likely still to be intact. An intact surface is essential for successful remineralization and arrest of the lesion. Demineralization of the dentin (indicated by the shading in the dentin) occurs before cavitation of the surface of the enamel. Treatment designed to promote remineralization can be effective up to this stage. C, Cavitation of the enamel surface is a critical event in the caries process in proximal surfaces. Cavitation is an irreversible process and requires restorative treatment and correction of the damaged tooth surface. Cavitation can be diagnosed only by clinical observation. The use of a sharp explorer to detect cavitation is problematic because excessive force in application of the explorer tip during inspection of the proximal surfaces can damage weakened enamel and accelerate the caries process by creating cavitation. Separation of the teeth can be used to provide more direct visual inspection of suspect surfaces. Fiberoptic illumination and dye absorption also are promising new evaluation procedures, but neither is specific for cavitation. D, Advanced cavitated lesions require prompt restorative intervention to prevent pulpal disease, limit tooth structure loss, and remove the nidus of infection of odontopathic organisms.

Root Surfaces

The proximal root surface, particularly near the cementoenamel junction (CEJ), often is unaffected by the action of hygiene procedures such as flossing because it may have concave anatomic surface contours (fluting) and occasional roughness at the termination of the enamel. These conditions, when coupled with exposure to the oral environment (as a result of gingival recession), favor the formation of mature, cariogenic biofilm and proximal root-surface caries. Likewise, the facial or lingual root surfaces (particularly near the CEJ), when exposed to the oral environment (because of gingival recession), are often both neglected in hygiene procedures and usually not rubbed by the bolus of food. Consequently, these root surfaces also frequently harbor cariogenic biofilm. Root-surface caries is more common in older patients because of niche availability and other factors sometimes associated with senescence, such as decreased salivary flow and poor oral hygiene as a result of lowered digital dexterity and decreased motivation. Caries originating on the root is alarming because (1) it has a comparatively rapid progression, (2) it is often asymptomatic, (3) it is closer to the pulp, and (4) it is more difficult to restore.

Oral Hygiene and Its Role in the Caries Process

Oral hygiene, accomplished primarily by proper tooth brushing and flossing, is another ecologic determinant of caries onset and activity. Careful mechanical cleaning of teeth disrupts the biofilm and leaves a clean enamel surface. The cleaning process does not destroy most of the oral bacteria but merely removes them from the surfaces of teeth. Large numbers of these bacteria subsequently are removed from the oral cavity during rinsing and swallowing after flossing and brushing, but sufficient numbers remain to recolonize teeth. Some fastidious organisms and obligate anaerobes may be killed by exposure to oxygen during tooth cleaning. No single species is likely to be entirely eliminated, however. Although all the species that compose mature biofilm continue to be present, most of these are unable to initiate colonization on the clean tooth surface.

Saliva: Nature’s Anticaries Agent

Saliva is an extremely important substance for the proper digestion of foods, and it also plays a key role as a natural anticaries agent (Table 2-3). Many medications are capable of reducing salivary flow and increasing caries risk (Table 2-4). The importance of saliva in the maintenance of the oral health is illustrated dramatically by observing changes in oral health after therapeutic radiation to the head and neck. After radiation, salivary glands become fibrotic and produce little or no saliva, leaving the patient with an extremely dry mouth, a condition termed xerostomia (xero, dry; stoma, mouth). Such patients may experience near-total destruction of the teeth in just a few months after radiation treatment.^8,9 Salivary protective mechanisms that maintain the normal oral flora and tooth surface integrity include bacterial clearance, direct antibacterial activity, buffers, and remineralization.¹⁰

Table 2-3

Elements of Saliva that Control Plaque Biofilm Communities

Names	Action	Effects on Plaque Biofilm Community
SALIVARY ENZYMES
Amylase	Cleaves—1,4 glucoside bonds	Increases availability of oligosaccharides
Lactoperoxidase	Catalyzes hydrogen peroxide–mediated oxidation; adsorbs to hydroxyapatite in active form	Lethal to many organisms: suppresses plaque formation on tooth surfaces
Lysozyme	Lyses cells by degradation of cell walls, releasing peptidoglycans; binds to hydroxyapatite in active conformation	Lethal to many organisms; peptidoglycans activate complement; suppresses plaque formation on tooth surfaces
Lipases	Hydrolysis of triglycerides to free fatty acids and partial glycerides	Free fatty acids inhibit attachment and growth of some organisms
NON-ENZYME PROTEINS
Lactoferrin	Ties up free iron	Inhibits growth of some iron-dependent microbes
Secretory immunoglobulin A(IgA) (smaller amounts of IgM, IgG)	Agglutination of bacteria inhibits bacterial enzymes	Reduces numbers in saliva by precipitation; slows bacterial growth
Glycoproteins (mucins)	Agglutination of bacteria	Reduces numbers in saliva by precipitation

Table 2-4

Medications with Potential to Cause Hyposalivation or Dry Mouth (Xerostomia)

Action/Medication Group	Medicaments
SYMPATHOMIMETIC
Antidepressants	Ventafaxine Duloxetine Reboxetine Bupropion

ANTICHOLINERGIC Tricyclic antidepressants

Muscarinic receptor antagonists

Oxybutynin

Alpha-receptor antagonists

Antipsychotics

Antihistamines

ANTICHOLINERGIC, DEHYDRATION Diuretics

SYMPATHOMIMETIC Antihypertensive agents

Metroprolol

Monoxidine

Rilmenidine

Appetite suppressants

Decongestants

Bronchodilators

Skeletal muscle relaxants

Tizanidine

Antimigraine agents

Rizatriptan

SYNERGISTIC MECHANISM Opioids, hypnotics

UNKNOWN H2 antagonists, proton pump inhibitors

Cytotoxic drugs

Anti-HIV drugs, protease inhibitors

Didanosine

(Adapted from the Kois Center, Support Materials, Always Pages, http://koiscenter.com/store/supmatlist.aspx, accessed January 13, 2012.)

Bacterial Clearance

Secretions from various salivary glands pool in the mouth to form whole or mixed saliva. The amount of saliva secreted varies greatly over time. When secreted, saliva remains in the mouth for a short time before being swallowed. While in the mouth, saliva lubricates oral tissues and bathes teeth and the biofilm. The secretion rate of saliva may have a bearing on caries susceptibility and calculus formation. Adults produce 1-1.5 L of saliva a day, very little of which occurs during sleep. The flushing effect of this salivary flow is, by itself, adequate to remove virtually all microorganisms not adherent to an oral surface. The flushing is most effective during mastication or oral stimulation, both of which produce large volumes of saliva. Large volumes of saliva also can dilute and buffer biofilm acids.

Direct Antibacterial Activity

Salivary glands produce an impressive array of antimicrobial products (see Table 2-3). Lysozyme, lactoperoxidase, lactoferrin, and agglutinins possess antibacterial activity. These salivary proteins are not part of the immune system but are part of an overall protection scheme for mucous membranes that occurs in addition to immunologic control. These protective proteins are present continuously at relatively uniform levels, have a broad spectrum of activity, and do not possess the “memory” of immunologic mechanisms. The normal resident oral flora apparently has developed resistance to most of these antibacterial mechanisms.

Although the antibacterial proteins in saliva play an important role in the protection of soft tissue in the oral cavity from infection by pathogens, they have little effect on caries because similar levels of antibacterial proteins can be found in caries-active and caries-free individuals.11,12 It is suggested that caries susceptibility in healthy individuals is not related to saliva composition. Individuals with decreased salivary production (owing to illness, medication, or irradiation) may have significantly higher caries susceptibility (see Table 2-4).

Buffer Capacity

The volume and buffering capacity of saliva available to tooth surfaces have major roles in caries protection.¹³ The buffering capacity of saliva is determined primarily by the concentration of bicarbonate ion. Buffering capacity can be estimated by titration techniques and may be a useful method for assessment of saliva in caries-active patients. The benefit of the buffering is to reduce the potential for acid formation.

In addition to buffers, saliva contains molecules that contribute to increasing biofilm pH. These include urea and sialin, which is a tetrapeptide that contains lysine and arginine. Hydrolysis of either of these basic compounds results in production of ammonia, causing the pH to increase.

Because saliva is crucial in controlling the oral flora and the mineral content of teeth, salivary testing should be done on patients with high caries activity. A portion of the salivary sample also may be used for bacteriologic testing, as will be described later in this chapter.

Remineralization

Saliva and biofilm fluid are supersaturated with calcium and phosphate ions. Without a means to control precipitation of these ions, the teeth literally would become encrusted with mineral deposits. Saliva contains statherin, a proline-rich peptide that stabilizes calcium and phosphate ions and prevents excessive deposition of these ions on teeth.¹⁴ This supersaturated state of the saliva provides a constant opportunity for remineralizing enamel and can help protect teeth in times of cariogenic challenges.

Diet and Caries

High-frequency exposure of fermentable carbohydrates such as sucrose may be the most important factor in producing cariogenic biofilm and, ultimately, caries lesions. Frequent ingestion of fermentable carbohydrates begins a series of changes in the local tooth environment that promotes the growth of highly acidogenic bacteria and eventually leads to caries. In contrast, when ingestion of fermentable carbohydrates is severely restricted or absent, biofilm growth typically does not lead to caries. Dietary sucrose plays a leading role in the development of pathogenic biofilms and may be the most important factor in disruption of the normal healthy ecology of dental biofilm communities. Because the eventual metabolic product of cariogenic diet is acid, and the acid leads to the development of caries, the exposure to acidity from other sources (e.g., dried fruits, fruit drinks, or other acidic foods and drinks) also may result in caries. The dietary emphasis must include all intakes that result in acidity, not just sucrose.

Clinical Characteristics of the Caries Lesion

The caries lesion is the product of disequilibrium between the demineralization and remineralization processes discussed previously. When the tooth surface becomes cavitated, a more retentive surface area becomes available to the biofilm community. The cavitation of the tooth surface produces a synergistic acceleration of the growth of the cariogenic biofilm community and the expansion of the demineralization with ensuing expanded cavitation. This situation results in a rapid and progressive destruction of the tooth structure. When enamel caries penetrates to the dentinoenamel junction (DEJ), rapid lateral expansion of the caries lesion occurs because dentin is much less resistant to acid demineralization. This sheltered, highly acidic, and anaerobic environment provides an ideal niche for cariogenic bacteria.