ETIOLOGY OF DENTAL CARIES

For as long as the science of dentistry has existed, there has been theorizing about the cause of dental caries. Today, all experts on dental caries generally agree that it is an infectious and communicable disease and that multiple factors influence the initiation and progression of the disease. The disease is recognized to require a host (tooth in the oral environment), a dietary substrate, and aciduric bacteria.⁶ The saliva (also considered a host component), the substrate, and the bacteria form a biofilm (plaque) that adheres to the tooth surface. Over time the presence of the substrate serves as a nutrient for the bacteria, and the bacteria produce acids that can demineralize the tooth. The flow, dilution, buffering, and remineralizing capacity of saliva are also recognized to be critical factors that affect, and in some ways regulate, the progression and regression of the disease. If the oral environment is balanced and favorable, saliva can contribute to strengthening of the tooth by supplying the components known to help build strong apatite structure. If the oral environment is unfavorable (too much acid is produced too often), an adequate flow of saliva can help dilute and buffer the acid, and thus slow the rate of damage to the tooth or even repair it. The critical pH for dissolution of enamel has been shown to be about 5.5. Once the process reaches dentin, dissolution can occur at a considerably higher pH. In addition, we know of many anatomic, behavioral, dietary, genetic, social, cultural, socioeconomic, and therapeutic variables that can significantly influence the level of caries activity favorably or unfavorably.

We recognize dental caries as a preventable disease. Furthermore we know that the disease typically begins in enamel and progresses slowly in the early stages of the process. Rampant caries is an exception to the typical course and is discussed later. Cavitation of the tooth structure is quite a late stage of the disease. Before cavitation, the progress of the disease may be arrested and/or reversed if a favorable oral environment can be achieved. Even after cavitation occurs, if the pulp is not yet involved and if the cavitated area is open enough to be self-cleansing (plaque-free), the caries process can halt and become an “arrested lesion.” Arrested lesions typically exhibit much coronal destruction, but the remaining exposed dentin is hard and usually very dark, there is no evidence of pulpal damage, and the patient has no pain. We also must emphasize that treating a carious tooth by providing a restoration does not cure the disease. If the unfavorable oral environment that caused the cavity persists, so will the disease, and more restorations will be required in time. Treating the oral infection by reducing the number of cariogenic microorganisms and establishing a favorable oral environment to promote predominantly remineralization of tooth structure over time will stop the caries process and cure the disease. Curing the disease currently requires modifications by the patient and/or caretaker and relies on their compliance in making the necessary modifications. Research efforts are ongoing to find a feasible method of achieving caries immunity that would be far less dependent on patient compliance.

Studies by Orland⁷ and by Fitzgerald and colleagues⁸ demonstrated that dental caries do not occur in the absence of microorganisms. Animals maintained in a germ-free environment did not develop caries even when fed a high-carbohydrate diet. However, dental caries did develop in these animals when they were inoculated with microorganisms from caries-active animals and then fed cariogenic diets.

A number of microorganisms can produce enough acid to demineralize tooth structure, particularly aciduric streptococci, lactobacilli, diphtheroids, yeasts, staphylococci, and certain strains of sarcinae. Streptococcus mutans has been implicated as one of the major and most virulent of the caries-producing organisms. Consequently S. mutans has been targeted in a large share of research. Loesche conducted an extensive review of the literature regarding the etiology of caries.⁹ He concluded that the evidence suggests that S. mutans, possibly Streptococcus sobrinus, and lactobacilli are human odontopathogens. He stated that aciduricity appears to be the most consistent attribute of S. mutans and is associated with its cariogenicity. He also observed that other aciduric species such as S. sobrinus may be more important in smooth-surface decay and are perhaps associated with rampant caries. Loesche concluded the review with the suggestion that treatment strategies that interfere with the colonization of S. mutans may have a profound effect on the incidence of caries in humans.⁹ As caries research proceeds, there seems to be increasing evidence that disease may result from a group of microbial species in the tooth-adhering biofilm. It is not clear which combinations of organisms are most blameworthy.

Wan and colleagues have published a series of three papers that report on 111 infants whom they observed to 2 years of age. They found S. mutans colonization in infants as young as 3 months, and more than 50% of the predentate infants were infected by 6 months of age. By 24 months of age, 84% of the children harbored the bacteria.^10–12 Investigations by Davey and Rogers¹³ and by Berkowitz and Jones¹⁴ have confirmed that S. mutans is transmitted orally from mother to infant, whereas Brown and colleagues¹⁵ have demonstrated a relationship between the numbers of S. mutans present in mothers and infants. Research by Kohler and colleagues demonstrated that reducing the numbers of oral S. mutans in mothers delayed the colonization of the organisms in the mouths of their children.¹⁶ Their findings also showed that 52% of the children who carried S. mutans at 3 years of age had caries, whereas only 3% of the children without demonstrable S. mutans had caries at the same age. In 1988, these same investigators reported that, the earlier the colonization of S. mutans in the mouths of children, the higher the caries prevalence at 4 years of age.¹⁷ Caufield and colleagues suggested the possibility of a “window of infectivity” between 19 and 33 months of age during which most children acquire the cariogenic organisms.¹⁸ The mother was the most common source of transmission of the bacteria to the child. In a group of 122 children 6 to 24 months of age, Mohan and colleagues found oral mutans streptococci colonization in 20% of the children younger than 14 months of age.¹⁹ In addition, logistic regression models that controlled for both age and number of teeth indicated that children who consumed sweetened beverages in their baby bottle were four times more likely to have mutans streptococci than children who only consumed milk. Although investigations to elucidate how and when mutans streptococci are transmitted to children are continuing, essentially all experts agree that the earlier transmission occurs, the higher the caries risk.

The acids that initially demineralize the enamel have a pH of 5.5 to 5.2 or less and are formed in the plaque material, which has been described as an organic nitrogenous mass of microorganisms firmly attached to the tooth structure. This film, which exists primarily in the susceptible areas of the teeth, has received a great deal of attention. Considerable emphasis is currently being given to plaque and its relationship to oral disease. Methods of chemical plaque control are being investigated. The method that has received the most attention during the past decade is the use of antimicrobial agents whose action is selective against certain types of microorganisms, including S. mutans. Chlorhexidine and other agents are available in antimicrobial oral rinse solutions. Another approach involves the use of monomolecular layers on the tooth surface that prevent the adherence of microorganisms. Perhaps by learning how to make enamel resistant to bacterial colonization (plaque formation), both caries and gingival disease can be reduced.

The acids involved in the initiation of the caries process are normal metabolic by-products of the microorganisms and are generated by the metabolism of carbohydrates. Because the outer surface of enamel is far more resistant to demineralization by acid than is the deeper portion of enamel, the greatest amount of demineralization occurs 10 to 15 mm beneath the enamel surface (Fig. 10-1). The continuation of this process results in the formation of an incipient subsurface enamel lesion that is first observed clinically as a so-called white spot. Unless the demineralization is arrested or reversed (remineralization), the subsurface lesion continues to enlarge, with the eventual collapse of the thin surface layer and the formation of a cavitated lesion.

Figure 10-1 Polarized light appearance of natural subsurface caries lesion. A, Blue/green line represents surface zone; yellow/brown represents the most demineralized area, the body of the lesion. B, More advanced natural subsurface lesion reaching to the dentino-enamel junction (DEJ).

(Courtesy Dr. James Wefel.)

Remineralization of incipient subsurface lesions may occur as long as the surface layer of the enamel remains intact. Saliva, which is supersaturated with calcium and phosphate and has acid-buffering capability, diffuses into plaque, where it neutralizes the microbial acids and repairs the damaged enamel. The time required for remineralization to replace the hydroxyapatite lost during demineralization is determined by the age of the plaque, the nature of the carbohydrate consumed, and the presence or absence of fluoride. For example, it has been suggested that, in the presence of dental plaque that has developed for 12 hours or less, the enamel demineralization resulting from a single exposure to sucrose will be remineralized by saliva within about 10 minutes. In contrast, a period of at least 4 hours is required for saliva to repair the damage to enamel resulting from a similar exposure to sucrose in the presence of dental plaque that is 48 or more hours old. The presence of fluoride has a profound effect on the remineralization process; not only does fluoride greatly enhance the rate of remineralization of enamel by saliva but it also results in the formation of a fluorohydroxyapatite during the process, which increases the resistance of the remineralized enamel to future attack by acids. Fluoride also has antimicrobial effects.

Thus the development of dental caries may be considered as a continuous dynamic process involving repeating periods of demineralization by organic acids of microbial origin and subsequent remineralization by salivary components (or therapeutic agents), but in which the overall oral environment is imbalanced toward demineralization. Several factors influence the degree of vulnerability of the tooth.

CARIES PREVALENCE IN PRESCHOOL CHILDREN

Weddell and Klein examined 441 children who ranged in age from 6 to 36 months and resided in a community with water fluoridation.²⁰ They found dental caries in 4.2% of the children 12 to 17 months of age, 19.8% of those 24 to 29 months of age, and 36.4% of those 30 to 36 months of age. Children in the middle and middle-low socioeconomic groups showed a trend toward higher caries frequencies. Edelstein and Tinanoff found that 30.5% of 200 preschool children had caries detectable by visual or radiographic examination.²¹ These children were recruited from a private pediatric dental office and ranged in age from 5 months to 5 years 11 months (mean, 3 years 8 months).

Douglass and colleagues determined the caries prevalence in children 3 to 4 years of age from a fluoridated community in Connecticut who were enrolled in the same Head Start program.²² They compared the caries prevalence in 517 children enrolled in 1999 with that in 311 children enrolled in 1991. They found a caries prevalence of 38% in the children enrolled in 1999 and 49% in those enrolled in 1991. They noted, however, that the children enrolled in 1999 had a greater severity of maxillary anterior caries. Tang and colleagues performed dental caries examinations on 5171 preschool children recruited from public health assistance programs in Arizona.²³ They found caries in 6.4% of 1-year-olds, nearly 20% of 2-year-olds, 35% of 3-year-olds, and 49% of 4-year-old children in the study.

In general, other reports of caries prevalence among children in various parts of the world show rates that seem to be comparable to those cited here. Another common element of caries prevalence in the United States and throughout the world is that children from families in low socioeconomic groups consistently have greater caries prevalences than their peers from families at a higher socioeconomic level. Vargas and colleagues reported that 27.4% of a sample of 3889 children 2 to 5 years of age had at least one decayed or filled primary tooth.²⁴ These children were part of a larger sample of individuals included in the third National Health and Nutrition Examination Survey (NHANES III, 1988-1994). This sample of children was 51.4% male and 48.6% female, with an ethnic distribution of 64.1% non-Hispanic white, 16.0% black, 9.5% Mexican American, and 10.4% other ethnicity. The family incomes for these children were distributed into four groups categorized from low to high, and these groups comprised 27.9%, 25.5%, 21.6%, and 24.9% of the sample, respectively.

In a longitudinal evaluation of caries patterns in 317 children followed an average of 7.8 years in private dental practices, Greenwell and colleagues made several noteworthy discoveries.²⁵ They found that 84% of the children who were caries-free in the primary dentition remained caries-free in the mixed dentition. Children with pit and fissure caries in the primary dentition were more likely to develop smooth-surface caries of primary teeth than the caries-free children. Fifty-seven percent of the children with proximal lesions in primary molars in the primary dentition developed additional primary molar proximal lesions in the mixed dentition. Children with faciolingual decay (nursing caries) were at the highest risk of any group for developing additional carious lesions. These investigators also discovered levels of caries susceptibility in children that can be characterized as caries-free, pit and fissure caries, and proximal molar caries patterns.

CARIES PREVALENCE IN SCHOOL CHILDREN

The report by Vargas and colleagues provides additional representative data for school children as well.²⁴ Their report revealed that 61% of the sample of children 6 to 12 years of age had at least one decayed or filled primary tooth. Furthermore, in the sample of 4116 children 6 to 14 years of age, 40% had at least one decayed or filled permanent tooth. Of the 1383 children 15 to 18 years of age, 89.8% had at least one decayed or filled permanent tooth. The ethnic and family income distributions for children in these different age groups were comparable to those outlined in detail for the preschool children. This information, along with that in many other published reports, clearly indicates that managing the disease of dental caries among children remains a formidable task despite the advances made in various preventive programs. Edelstein and Douglass have noted, “The popular statement that half of U.S. school children have never experienced tooth decay fails profoundly to reflect the extremity and severity of this still highly prevalent condition of childhood.”²

RAMPANT DENTAL CARIES

There is no complete agreement on the definition of rampant caries or on the clinical picture of this condition. It has been generally accepted, however, that the disease referred to as rampant caries is, in terms of human history, relatively new. Rampant caries has been defined by Massler as a “suddenly appearing, widespread, rapidly burrowing type of caries, resulting in early involvement of the pulp and affecting those teeth usually regarded as immune to ordinary decay.”²⁶

There is no evidence that the mechanism of the decay process is different in rampant caries or that it occurs only in teeth that are malformed or inferior in composition. On the contrary, rampant caries can occur suddenly in teeth that were previously sound for many years. The sudden onset of the disease suggests that an overwhelming imbalance of the oral environment has occurred, and some factors in the caries process seem to accelerate it so that it becomes uncontrollable; it is then referred to as rampant caries.

When a patient has what is considered an excessive amount of tooth decay, one must determine whether that person actually has a high susceptibility and truly rampant caries of sudden onset or whether the oral condition represents years of neglect and inadequate dental care. Young teenagers seem to be particularly susceptible to rampant caries, although it has been observed in both children and adults of all ages (Fig. 10-2).

Figure 10-2 A, Early childhood caries (ECC). B, Occlusal ECC in mandible. C, Occlusal and interproximal ECC in maxilla (mirror image). D, Rampant dental caries and evidence of dental neglect in a preschool child. E, Palatal caries on maxillary incisor teeth.

There is considerable evidence that emotional disturbances may be a causative factor in some cases of rampant caries. Repressed emotions and fears, dissatisfaction with achievement, rebellion against a home situation, a feeling of inferiority, a traumatic school experience, and continuous general tension and anxiety have been observed in children and adults who have rampant dental caries. Because adolescence is often considered to be a time of difficult adjustment, the increased incidence of rampant caries in this age group lends support to this theory. An emotional disturbance may initiate an unusual craving for sweets or the habit of snacking, which in turn might influence the incidence of dental caries. On the other hand, a noticeable salivary deficiency is not an uncommon finding in tense, nervous, or disturbed persons. Indeed, various forms of stress in both children and adults, as well as various medications (e.g., tranquilizers and sedatives) that are commonly taken to help cope with stress, are associated with decreased salivary flow and decreased caries resistance caused by impaired remineralization. It is well known that radiation therapy to the head and neck often results in significantly diminished salivary function and may place patients at high risk for severe caries development.

EARLY CHILDHOOD CARIES, SEVERE EARLY CHILDHOOD CARIES, NURSING CARIES, BABY BOTTLE TOOTH DECAY

The American Academy of Pediatric Dentistry (AAPD) defines early childhood caries (ECC) as the presence of one or more decayed (noncavitated or cavitated), missing (as a result of caries), or filled tooth surfaces in any primary tooth in a child 71 months of age or younger. The AAPD also specifies that, in children younger than 3 years of age, any sign of smooth-surface caries is indicative of severe early childhood caries (S-ECC).²⁷

For many years it has been recognized that, after eruption of the primary teeth begins, excessively frequent bottle feedings and/or prolonged bottle or breast-feeding is often associated with early and rampant caries. The clinical appearance of the teeth in S-ECC in a child 2, 3, or 4 years of age is typical and follows a definite pattern.²⁸ There is early carious involvement of the maxillary anterior teeth, the maxillary and mandibular first primary molars, and sometimes the mandibular canines (Fig. 10-3). The mandibular incisors are usually unaffected. A discussion with the parents often reveals an inappropriate feeding pattern: the child has been put to bed at afternoon nap time and/or at night with a nursing bottle holding milk or a sugar-containing beverage. The child falls asleep, and the liquid becomes pooled around the teeth (the lower anterior teeth tend to be protected by the tongue). It would seem that the carbohydratecontaining liquid provides an excellent culture medium for acidogenic microorganisms. Salivary flow is also decreased during sleep, and clearance of the liquid from the oral cavity is slowed.

Figure 10-3 Radiographs illustrating early childhood caries. A, Maxillary incisors (interproximal). B, Mandibular incisors. C, Deep caries in mandibular molar. D, Maxillary molar distally and on mandibular first molar.

Gardner and colleagues reported four case histories in which the same pattern of caries was observed, and in each child the condition was attributed to a specific breast-feeding habit.²⁹ In each case the mother explained that human milk was the main source of nutrition. The investigators recommend that from birth the infant should be held while feeding. The child who falls asleep while nursing should be burped and then placed in bed. In addition, the parent should start brushing the child’s teeth as soon as they erupt.

The AAPD endorses the policy statement of the American Academy of Pediatrics (AAP) on breast-feeding and the use of human milk.³⁰ The AAP statement includes the acknowledgment that “breast-feeding ensures the best possible health as well as the best development and psychosocial outcomes for the infant.” However, both organizations discourage extended or excessive frequency of feeding times (from the breast or bottle) and encourage appropriate oral hygiene measures for infants and toddlers.

Dilley and colleagues observed a large number of children with prolonged nursing habit caries and concluded that there was no association between the nursing habit and family background, except that the families were predominantly from lower socioeconomic groups.³¹ All subjects demonstrated prolonged breast-feeding or bottle feeding, with milk reported to be the liquid most often used in the bottle. Parents indicated that they did not know when weaning should occur and when oral hygiene should be instituted. The authors also observed nearly symmetric caries patterns.

Hallonsten and colleagues screened 3,000 18-month-old children for dental caries and ongoing breastfeeding.³² Twelve (19.7%) of the 61 children still being breast-fed had caries, while 51 (1.7%) of the 2,939 children not being breast-fed had caries. The authors found that children who experience prolonged breast-feeding tend to develop unsuitable dietary habits that put them at risk for caries at an early age.

There is considerable scientific evidence from experiments in vitro and in animal models to suggest that some dairy products such as bovine milk and cheese, as well as human breast milk, are not cariogenic and may actually be protective to tooth structure and promote remineralization under certain conditions. Similar experiments show that many infant formulas, with refined food additives, do promote caries. There is much still to learn about caries progression in both the more typical disease and this rampant form. It is prudent to counsel parents to practice good oral hygiene measures for the child and to avoid inappropriate feeding habits that are associated with S-ECC.

S-ECC may be prevented by early counseling of the parents. This is one reason for suggesting that children receive their first dental examination between 6 and 12 months of age when S-ECC is not likely to have developed. In a comprehensive report prepared for the Oral Health Subcommittee of the Healthy Mothers–Healthy Babies Coalition, Ripa states, “Priority needs to be given to a major national educational program directed toward educating the public about nursing caries.”³³ The educational program must involve direct contact with pregnant women, parents, and other caregivers in population subgroups with a high prevalence of nursing caries.

ADDITIONAL FACTORS KNOWN TO INFLUENCE DENTAL CARIES

SALIVA

Although saliva was identified in the etiology section earlier as part of the host component and thus a primary part of the caries process, the role of saliva overall is so unique and special that further discussion is warranted here regarding its influence on several aspects of the caries process that may help produce favorable environments to combat the process. Any patient with a salivary deficiency, from any cause, is at higher risk for caries activity.

It is generally accepted that the dental caries process is controlled to a large extent by a natural protective mechanism inherent within the saliva. Many properties of saliva have been investigated to learn their possible role in the caries process. Considerable importance has been placed on the salivary pH, the acid-neutralizing power, and the calcium, fluoride, and phosphorus content. It has long been suggested that in addition to these properties the rate of flow and the viscosity of saliva may influence the development of caries. The normal salivary flow aids in the solution of food debris on which microorganisms thrive. In addition, the saliva manifests a variety of antibacterial and other anti-infectious properties. All known characteristics of saliva seem somehow relevant to the process of dental caries.

Saliva is secreted by three paired masses of cells—the submaxillary, sublingual, and parotid glands. Small accessory glands are also scattered over the oral mucous membranes. Each of these has its own duct.

The salivary glands are under the control of the autonomic (involuntary) nervous system, receiving fibers from both its parasympathetic and sympathetic divisions. Stimulation of either the parasympathetic (chorda tympani) fibers or the sympathetic fibers to the submaxillary or sublingual gland causes a secretion of saliva. The secretion resulting from parasympathetic stimulation is profuse and watery in most animals. Sympathetic stimulation, however, causes a scanty secretion of a thick, mucinous juice. Stimulation of the parasympathetic fibers to the parotid gland causes a profuse, watery secretion, but stimulation of the sympathetic fibers causes no secretion.

Salivary Deficiency

One of the first descriptions of a severe salivary deficiency with its deleterious effect on the dentition was reported by Hutchinson in 1888.³⁴ Since that time, many reports have emphasized the importance of a normal flow of saliva in preventing a breakdown of the dentition. A reduction in the salivary flow may be temporary or permanent. When the quantity is only moderately reduced, the oral structures may appear normal. A pronounced reduction or complete absence of saliva, however, results in an acidic environment with rampant caries (Fig. 10-4). In addition to the rapid destruction of the teeth, there may be dryness and cracking of the lips, with fissuring at the corners of the mouth, burning and soreness of the mucous membranes, crusting of the tongue and palate, and sometimes paresthesia of the tongue or mucous membrane.

Figure 10-4 Progression of early childhood caries illustrated in three different children. A, Restorable with resins. B, Restorable with crown forms (possibly). C, Nonrestorable.

There are many reasons for a reduction in salivary flow. Acquired salivary dysfunction may be the result of a psychological or emotional disturbance and, again, may be either temporary or permanent. During the acute stages, mumps may cause a temporary reduction in salivary flow. Immune disorders, such as Sjögren syndrome, and genetic conditions, such as hypohidrotic ectodermal dysplasia, often exhibit chronic xerostomia. Many oncology patients receive head and neck or total-body irradiation that also results in salivary gland dysfunction. An interruption in the central pathways of the secretory nerves has been suggested as a cause of salivary failure, but this is usually overshadowed by definite neurologic signs and symptoms. Similarly, a deficiency of vitamin B complex has been reported as a cause of salivary gland dysfunction.

One study indicated that the minimum effective dose of many of the antihistaminic drugs can reduce salivary flow by as much as 50%.³⁵ Dryness of the mouth may occur after the use of a variety of tranquilizers and antihistamines. It has likewise been observed that dry mouth and rampant caries may accompany a systemic condition, such as myasthenia gravis. In this disease, the acetylcholine that is necessary for the proper transmission of nerve impulses is destroyed; as a result, the salivary glands do not receive adequate stimulation.

Previous work has shown a great deal of individual variation in the amount of saliva produced by stimulation of the glands. The range is from less than a measurable amount in patients with acquired or congenital dysfunction of the salivary glands to 65 mL during a 15-minute period of stimulation and collection. Patients with deficient salivary flow often have excessive or rampant caries. In contrast, patients with greater than average salivary flow are usually relatively free from dental caries.

Determination of Salivary Flow

If a patient has no known existing conditions that may cause hyposalivation and if the clinician notices a small pool of saliva in the floor of the mouth during oral examination, it is not unreasonable to assume that the patient has adequate salivary quantity and flow. Little information is available about salivary flow rates in children, but Crossner reported that in children 5 to 15 years of age, the rate of mixed whole stimulated saliva increases with age, and boys have consistently higher rates than girls.³⁶ If inadequate salivary flow is known to exist or is suspected, measurement of salivary flow can provide a baseline useful for comparing with later measurements after implementation of adjunctive therapy.

To evaluate the adequacy of salivary flow, Zunt recommends establishing the unstimulated salivary flow (USF) rate.³⁷ The USF rate is measured after a period of 1 hour without eating, drinking, chewing gum, or brushing the teeth. Sitting in the “coachman” position, on the edge of the dental chair, the patient passively drools into a funnel inserted into a graduated cylinder for 5 minutes. The eyes should remain open except for blinking during the 5-minute collection period. The head and neck should be bent, and the arms should rest comfortably on the thighs or knees. The volume of saliva collected in the cylinder after 5 minutes is divided by 5 to determine the USF. A USF rate of less than 0.1 mL per minute is diagnostic of salivary gland hypofunction. If the USF rate is less than 0.1 mL per minute, the next step is to measure the stimulated salivary flow (SSF). The patient should chew unflavored paraffin for 45 chews or 1 minute and expectorate into a funnel inserted into a graduated cylinder. The SSF rate should be 1 to 2 mL per minute; less than 0.5 mL per minute is scored as an abnormal rate. A convenient alternative method for measuring USF is the modified Schirmer technique, which uses a calibrated paper test strip to collect saliva in the floor of the mouth.

In patients who are known or suspected to have salivary deficiency, it is not unusual to find a salivary flow ranging from slightly below normal to practically a dry mouth. If there is a deficiency of saliva or a dry mouth, the cause should be sought. Sometimes the cause is readily determinable; sometimes it is obscure. An emotional disturbance should not be overlooked as a cause in a patient of any age. Psychotherapy may be helpful in these cases. If the cause cannot readily be determined, perhaps it should be assumed that the sparse flow is related to inadequacies in the diet, particularly a vitamin deficiency or excessive sugar consumption to the exclusion of needed foods. Monthly quantitative analyses of the saliva should be performed to determine whether dietary improvement is accompanied by an increased flow.

If the salivary glands have not undergone degenerative or metaplastic change and if the nerve pathways between the central nervous system and the salivary glands are still intact, salivary stimulants may be recommended. If dryness of the mouth is attributable to dehydration, increased fluid intake should be recommended. The use of gustatory stimulants (sugar-free candy) or masticatory stimulants (xylitol gum) has been suggested as an adjunct to encourage salivation. Prescription sialagogue medications, also known as secretagogues, such as pilocarpine and cevimeline may be of benefit in improving the salivary flow rate in patients with Sjögren syndrome or with radiation damage to salivary glands. The use of sialagogue medications has not been studied in pediatric populations, but these agents are considered safe for most adult patients and have been used successfully in older children. The use of salivary substitutes has been suggested by Shannon and colleagues as helpful in preventing soft tissue problems associated with dry mouth.³⁸ Saliva substitutes, as well as fluoride and chlorhexidine rinses, are also reported to enhance remineralization and promote resistance to demineralization of tooth surfaces, and may help prevent radiationinduced caries.

Viscosity of Saliva

It has long been suggested that the viscosity of saliva is related to the rate of dental decay. Both thick, ropy saliva and thin, watery saliva have been blamed for rampant dental caries. Previous work has shown a statistically significant direct relationship between the viscosity of saliva and the number of decayed, missing, and filled teeth.³⁹ This relationship held true for all members of the observation group, regardless of age. Patients with thick, ropy saliva invariably had poor oral hygiene. The teeth were covered with stain or plaque, and the rate of dental caries ranged from greater than average to rampant.

No evidence exists that viscosity changes with age under normal conditions. This property of the saliva is governed not only by the particular set of glands stimulated but also by the type of nervous stimulation and the amount of mucin (glycoprotein) present.

Children who consume excessive amounts of carbohydrates often have not only a sparse flow but also viscous saliva. Even minimal doses of some antihistaminic drugs will result in a greatly increased viscosity of saliva in some persons.³⁵

There are apparently only a limited number of ways to alter the viscosity of saliva. Reduction of refined sugar intake may be effective in some patients.

Although relatively little information specific to salivary function, flow, and viscosity in children is available, an excellent review article by Leone and Oppenheim provides much additional information regarding the relationship between saliva and dental caries.⁴⁰

EARLY DETECTION OF DISEASE ACTIVITY

Traditionally, dentists have relied upon a visual-tactileradiographic procedure for the detection of dental caries. This procedure involves the visual identification of demineralized areas (typically white spots) or suspicious pits or fissures and the use of the dental explorer to determine the presence of a loss of continuity or breaks in the enamel and assess the softness or resilience of the enamel. Carious lesions located on interproximal tooth surfaces have generally been detected with the use of bite-wing radiographs. These procedures have been used routinely in virtually every dental office in the United States for the past 50 years.

Because the reversal of the caries process depends on an intact surface layer of the lesion and the typical use of the dental explorer to probe the suspicious areas often results in the rupture of the surface layer covering early lesions, the use of the dental explorer to probe enamel is no longer recommended. The recommended use of the dental explorer is to judiciously remove plaque and debris to permit visual inspection of pits and fissures.

Tactile probing procedures are no longer used for caries detection in most European countries and this protocol has now been adopted by many U.S. dental schools. The primary concerns that led to the discontinuation of the probing procedure were (1) the insertion of the probe into the suspected lesion inevitably disrupts the surface layer covering very early lesions, thereby eliminating the possibility for remineralizing the decalcified area; (2) the probing of lesions and suspected lesions results in the transport of cariogenic bacteria from one area to another; and (3) frank lesions requiring restoration are generally apparent visually without the need for probing. The clinical caries detection procedures commonly used in Europe have been described by several clinical investigators.^47–51

Carious lesions are detected visually on the basis of their location (decalcification can only occur in areas where dental plaque may accumulate regularl/>