Definition and Significance
In spite of the worldwide decline in dental caries rates, there persists a segment of the population who are still ravaged by the disease. The National Health and Nutrition Examination Survey for 1999-2002 recorded that 21% of children and 23% of adults had untreated dental caries in the permanent dentition.1 Ten percent of adults had untreated root caries. Declines in dental caries rates in the primary dentition seen in earlier surveys had leveled off for this study period, and, for children two to five years old, dental caries rates had actually increased.
Among this group of caries-active individuals is a smaller fraction that experiences a particularly aggressive form of the disease. Referred to by the clinician as rampant caries, the clinical picture involves (1) caries lesions on many, if not all, of the teeth in a dentition, (2) an alarming speed of lesions progression, and (3) a relentless course that seems resistant to traditional preventive methods (Figures 1-4). There are no specific criteria with regard to the number of caries lesions or the rate of cavity development that constitutes rampant caries. Rather, the term is somewhat loosely applied to any clinical case marked by an alarming amount of carious destruction or remarkably rapid attack rate. If there is concern about the dental caries rate exceeding the pace of restorative treatment, that patient has rampant caries. In part because of the lack of strict diagnostic criteria, there is little published data on the incidence and prevalence of rampant caries. Although confined to a relatively minor proportion of society, it is nonetheless a devastating and debilitating oral condition and the bane of practicing dentists.
Rampant caries patients can present with different patterns of decay depending upon the etiological factors at play. Some individuals may present with a preponderance of lesions that developed from cervical cavities; others may have caries lesions confined almost exclusively to root surfaces. Typically the lesions affect surfaces and teeth otherwise rarely involved, such as the facial surfaces of anterior teeth and the interproximal surfaces of lower incisors.2,3 In the variant known as early childhood caries (ECC; formerly baby bottle syndrome, baby bottle mouth, or baby bottle caries), there is rapid destruction of the primary dentition. In a review of 94 clinical studies of ECC, no consensus was found about diagnostic criteria. Even destruction of anterior teeth was insufficient since this is but one of several patterns of ECC destruction. Rampant caries involving pit and fissures, smooth surfaces, and anterior teeth to varying degrees all occur in the teeth of preschool children.4 The natural history of these various patterns is similar, involving widespread rapid tissue morbidity.
Rampant caries as a pathological entity is different in many ways from milder forms of the disease. Although there are many risk factors associated with dental caries, aggressive patterns of the disease seem to correlate most strongly with a subset of these risk factors. Individuals with aggressive dental caries have not appeared to benefit from the public health efforts that are thought to have been responsible for the general decline in dental caries rates. Similarly, the therapeutic measures employed by many dental practices to prevent dental caries seem ineffective against the relentless clinical course of rampant caries.
Dental caries is a multi-factorial, infectious disease. Caries risk arises from many factors that can be grouped into four general categories: (1) inadequate salivary output, (2) frequent exposure to fermentable carbohydrates, (3) suboptimal fluoride exposure, and (4) a history of caries activity. Aggressive forms of dental caries tend to be strongly associated with inadequate salivary output or frequent exposure to fermentable carbohydrates.
Inadequate salivary flow promotes dental caries because it leads to diminished ability to buffer acids, reduces clearance of food, microorganisms, and microbial byproducts, gross impairment of remineralization capabilities, loss of salivary-based host defense mechanisms, and compensatory and deleterious alterations in eating and drinking habits.
Inadequate saliva output can arise from certain systemic diseases, disease treatments, or as a side effect of medications. Examples of diseases often associated with oral dryness include Sjogren’s syndrome,5,6,7,8 rheumatoid arthritis,9 systemic lupus erythematosus,10 scleroderma,11 primary biliary cirrhosis,5 Parkinson’s disease,12 anxiety,13 depression,5,14 anorexia nervosa,15 cystic fibrosis,16 human immunodeficiency virus (AIDS),17 diabetes mellitus18,19 sarcoidosis,20 malignant lymphoma,21 and Down syndrome.5 Disease treatments that are associated with significant oral dryness include radiation for cancer of the head and neck,22,23 chemotherapy,24,25 bone marrow transplants,26 and neurologic surgery.
There are several hundred medications with oral dryness listed as a common side effect.27 Use of two or more of these medications concomitantly increases the effect. These medications represent many varied and disparate drug families. However, there are a few medication categories that have a preponderance of xerogenic drugs, such as cardiac medications, antihypertensive medications, psychotropic medications (for mental or emotional problems), and cold and allergy medications.
Additionally, many illicit recreational drugs reduce salivary flow. Most notable among these are marijuana (hashish, THC),28,29 methamphetamine (speed),30 methylene-dioxymethamphetamine (MDMA, ecstasy, XTC),31,32 and cocaine (crack).33 Caffeine, present in coffee, tea, soft drinks, and energy drinks, also causes oral dryness.
Dental caries is a diet-supported disease. The Vipeholm study34 in the 1950’s dramatically demonstrated the role diet plays in the etiology of rampant caries. Children who consumed sweets frequently during the day developed aggressive dental caries patterns, whereas children who consumed the same amount of sweets but confined them to the three meals did not develop such decay. Similarly, sticky sweets, like toffees and caramels, were more cariogenic than less retentive forms. There is no question that the rampant caries seen today - whether related to habitual consumption of caffeinated soda, methamphetamine abuse, or head and neck radiation treatment — is related to frequent (more than at meal times) or prolonged (sucking hard candies, chewing sugar-containing gum, or sipping sweetened beverages) exposure of the dentition to fermentable carbohydrates. Attempts to control rampant caries will not be successful unless there is diet modification.
Certain aspects of the diet contribute to caries risk. A diet that contributes to caries risk is referred to as a cariogenic diet. To be cariogenic, the frequency and consistency (retentiveness) are more important than absolute quantity of sugar in the diet. Common aspects of the diet that contribute to caries risk include:
1. Habitual use of sweetened beverages such as coffee, tea, pop, fruit juices, fruit drinks, energy drinks, sports drinks, and vitamin water.35
2. Protracted use of sugared chewing gum.
3. Protracted use of hard candy, breath mints, throat lozenges, and antacids.
4. Regular use of sweets that are sticky or retentive, such as caramel or raisins.
5. Regular consumption of sweet snacks before bedtime.
The most cariogenic diets often involve beverages containing both sugar and caffeine, most notably caffeinated soft drinks.36 Caffeine causes oral dryness and thirst and has the ability to encourage habitual consumption.37 Caffeinated soft drinks tend to be consumed in a pattern involving habitual use on a daily or near daily basis, frequent consumption throughout the day, and repeated sipping in an attempt to make the beverage last longer. It is likely that this combination of frequent and relentless consumption and reduced salivary flow leads to the aggressive pattern of decay. Individuals who regularly drink caffeinated soft drinks are much more likely to experience rampant caries than those who drink non-caffeinated soft drinks.
Similar cariogenic potential exists in the consumption of coffee and tea if sweetened with sugar or honey. Additionally, non-dairy creamers are potentially cariogenic because they contain corn syrup solids and maltodextrin,38 which are cariogenic.39,40
In addition to sweet foods and beverages, regular exposure to fermentable carbohydrates may be provided by extra-dietary sources. Frequent and protracted use of sugar-containing medications can provide a substantial caries risk. Such medications include pediatric formulations (used at times by adults who have difficulty swallowing pills - analgesics, decongestants, antihistamines), anti-diarrheal suspensions, sore throat lozenges, antacids, and Emetrol [McNeil-PPC, Inc.] (for nausea).
Some diseases are commonly associated with dietary changes that can promote dental caries. These include bulimia and anorexia nervosa,41 poorly controlled diabetes mellitus,42 and depression.43,44 The frequent binging associated with bulimia often involves sugar-laden foods and beverages. Frequent purging leads to acid erosion of the teeth. The associated hypersensitivity from this process leads to avoidance of oral hygiene practices, which deprives the dentition of regular fluoride exposure and allows retentive sweets to remain against the teeth. Dehydration associated with abuse of laxatives and diuretics and with induced vomiting can lead to oral dryness, which increases risk for dental caries.
Although studies that looked at diabetes and caries risk have historically been equivocal, when studies began separating the poorly controlled and well-controlled diabetics, caries risk was more easily demonstrated.42,45,46 Gestational diabetes is also associated with increased caries risk.47 Some diabetics, particularly those showing poor disease control, indulge in frequent snacking on sugar-containing foods and beverages in an attempt to avoid hypoglycemia and have an increased risk for dental caries.48
Late-life depression occurs in individuals older than age 65. This form of depression results in a loss of pleasure from life, marked sadness, and an inability to function normally. This includes interest in providing normal oral hygiene and adequate nutrition. Food choices often involve convenient, sugar-laden foods and beverages. Frequently people suffering from this disease present with significant dental problems, including advanced periodontal disease and rampant caries.43,44 Many of the medications used to treat depression cause oral dryness, which exacerbates dental caries.27
Certain life situations are also associated with deleterious dietary change which may impart a risk for dental caries, among them pregnancy, retirement, death of a spouse, smoking cessation, going away to school, marijuana use, and drug addiction. Pregnancy, contrary to folk wisdom, does not “steal calcium from the teeth”. Rather, pregnancy leads to hormonal changes that affect appetite and cravings. The dietary changes that result can be quite drastic, and often involve more frequent consumption of fermentable carbohydrates. Going away to school, retirement, disability leave, and death of a spouse can favor shifts in the diet toward convenient, more easily consumed foods, which are often high in sugar and may be low in nutrient density. During attempts to quit smoking and other addictions, it is not uncommon for these individuals to combat nicotine cravings with frequent use of hard candies or soft drinks. Marijuana,51 methamphetamine,52,53 and other illicit drugs, either through the effect on salivation or through direct central nervous system effects on eating habits, lead to binging on sugary foods and beverages.
Patients who present with rampant caries can be placed in a disease control program. Elements of this type of program have been described in the literature to contain the following elements.54
1. Caries risk assessment and evaluation, with reassessment throughout the program.
2. Restoration of all cavitated lesions and use of fluoride releasing materials.
3. Preventive and therapeutic control strategies, including diet modification.
The initial risk assessment identifies all caries lesions, including smooth surface, pit and fissure, secondary or marginal, and root caries. This, together with an assessment of the periodontal condition, can identify methods by which oral hygiene must be improved. Dietary analysis is necessary to identify the source(s) of fermentable carbohydrates, and diet counseling tailored to these findings should be provided. Other risk factors, such as xerostomia (medication induced or not), motor skill, or compliance with oral hygiene protocols can be used to modify the plan.
The second phase of treatment requires the surgical removal of all carious tooth structure to lessen the infectivity of the mouth and halt any further progression of the caries process. In this phase of treatment, compliance in the use of oral hygiene protocols can be measured.
Multi-Pronged Treatment Strategy
The third phase of treatment involves employment of strategies to control the underlying disease. Dental caries cannot be cured. However, it can be controlled. Curing the disease would involve eradication of the pathogen from the oral cavity. Currently there are no methods available to predictably and reliably do this. However, these organisms can be suppressed and the conditions that favor their proliferation and pathogenesis altered so that tissue morbidity (frank cavitation) is avoided.
The treatment of rampant caries needs to be aggressive and multi-pronged, employing both preventive and therapeutic strategies. Preventive treatment is low in intensity and open ended (i.e., for the life of the patient). Therapeutic treatment is high intensity, short term, and to a defined endpoint (such as pathogen suppression or remineralization). Multi-pronged treatment refers to attacking the pathology on several different fronts simultaneously. Possible prongs in this attack are listed in Table 1.
Attempts to control rampant caries will not be successful unless there is diet modification. To modify a patient’s diet first requires diet analysis. Often the dietary excesses are obvious, and simple questioning can elicit the dietary culprit. Suggested questions for this purpose include:
1. Do you regularly drink sweetened beverages such as coffee, tea, pop, fruit juices, fruit drinks, energy drinks, sports drinks, or vitamin water?
2. Do you regularly use sugared gum?
3. Do you regularly use hard candy, throat lozenges, breath mints, or antacids?
4. Are you in the habit of having snacks before bedtime?
If these questions fail to elucidate the source of frequent or prolonged fermentable carbohydrate exposure, then a detailed diet history should be employed.
As appropriate, patients should be counseled to avoid between-meal sweets and avoid snacks within one hour of bedtime. Soft drink consumers should be encouraged to drink only sugar-free (i.e., diet) soft drinks, and gum chewers should be encouraged to chew sugar-free gum. Those who regularly consume coffee between meals should avoid sugar and non-dairy creamers instead drinking the coffee black, with milk, or with sugar substitutes.
Central to a large number of rampant caries patients is daily consumption of caffeinated soft drinks. Regular consumers of caffeinated soft drinks can develop dependence and a pattern of frequent consumption. This pattern will include nearly daily episodes of use with repeated sipping in an effort to make the drink last longer. The diet versions of these beverages do not cause dental caries.
For the heavy user of caffeinated soft drinks, breaking the habit can be very difficult. One effective strategy for quitting involves substituting a diet soft drink that still contains caffeine. By providing caffeine, the diet soda will satisfy some of the patient’s cravings without supplying fermentable carbohydrates to the teeth. Heavy users of caffeinated soft drinks demonstrate strong brand preference. When switching to a diet caffeinated soft drink, success will be better if a brand other than the usual soda-of-choice is employed.
Low-Intensity Fluoride Treatment
The key to the effectiveness of fluoride in controlling dental caries is its presence at the tooth surface. This is different from early concepts of the mode of action of fluoride which purported that the incorporation of fluoride into developing tooth structures early in life led to dental hard tissues that were less acid soluble. The current view is that the principal effect of systemic fluorides is a topical one: Ingested fluoride becomes systemically disseminated and is secreted in the saliva; fluoride in the saliva then bathes the teeth and exerts its principal cariostatic action by catalyzing remineralization at the tooth surface.56 This is important because it means that there is benefit to adults from exposure to fluoride.
Systemic administration of fluoride early in life does not impart a lifetime protection from dental caries. Epidemiological studies have demonstrated that children raised in optimally fluoridated communities who subsequently move to sub-optimally fluoridated communities gradually lose their caries resistance and adopt a caries rate commensurate with the new community.57 For the caries-prone individual, keeping teeth caries free appears to require continuous exposure to low concentrations of fluoride throughout life.
Fluoride ions in the liquid phase at the surface of dental hard tissues catalyze remineralization. Fluoride ions are incorporated into remineralizing incipient lesions. Arrested (remineralized) lesions thus can be more resistant to acid dissolution than the adjacent unaffected tooth structure.
The importance of fluoride-containing dentifrice cannot be overstated. There is evidence that the worldwide decline in dental caries rates that has been recorded in most industrialized countries in the last 30 years is attributable to the widespread use of fluoride-containing dentifrice.58 Even when fluoride is ingested from a fluoridated water supply or in the form of fluoride supplements, use of fluoride-containing dentifrice still provides additional benefit, because topical and systemic fluorides have an additive effect.59,60 Over-the-counter fluoride mouth rinses are another source of fluoride available for controlling dental caries. The addition of these rinses to a diligent brushing schedule with a fluoride dentifrice may not have a great additional benefit. However, to the less-than-diligent brusher — and many caries-active individuals are — an easily utilized additional source of fluoride has the potential to be very beneficial.
All rampant caries patients should be brushing with a fluoride-containing dentifrice at least twice daily: in the morning, and immediately before retiring to bed. Benefits can be increased by using higher concentrations of fluoride (1,500 ppm F) and brushing more frequently (3-4 times per day). Over-the-counter fluoride rinses should be used twice daily as well, generally in the morning and immediately before bed, following brushing and flossing. For both the dentifrice and mouthwash, the bedtime dose is the most important dose because of increased dwell-time in the oral cavity allowed by nocturnal salivary flow reduction.
Xylitol Chewing Gum
Xylitol, a naturally occurring sugar-substitute, has demonstrated an ability to interfere with dental caries. The anti-caries abilities of xylitol have been studied most notably in chewing gum and candy vehicles.61,62 Dental caries is an infectious disease of the teeth involving proliferation of mutans streptococci (MS) in response to certain dietary excesses and host conditions. Frequent use of chewing gum with high levels of xylitol has been shown to prevent dental caries and harden even advanced caries lesions, even in the face of a highly cariogenic diet.63,64 Frequent use of chewing gum with high levels of xylitol has been shown to reduce MS loads on the dentition, and presumably this is the mechanism by which it exerts its cariostatic effect.57
Chewing gum use in this country is widespread, and compliance with chewing gum recommendations is high.65 Commercially available chewing gums advertised as “sugar-free” generally contain sorbitol as the sole or major sweetener. Although sometimes promoted as “cavity fighting”, these chewing gums do not predictably reduce, and may in fact promote, proliferation of oral MS.66 In individuals with low salivary flow rates, frequent use of sorbitol may in fact cause caries lesions.67 To be effective, the chewing gum must be sweetened solely with xylitol. Chewing gums sweetened with combinations of xylitol and other sugar alcohols produce no measurable caries-inhibiting effect.63
The recommended dose of xylitol is achieved by chewing two pellets or one stick (depending on the form) five separate times each day for a minimum of five minutes each time. A daily regimen of chewing gum usage may not be appropriate for individuals prone to temporomandibular joint disorders or who wear removable prostheses. Xylitol-sweetened mints, gel, and dentifrices are also available for those who cannot chew gum.
Xylitol and fluoride have synergistic inhibitory effects on acid production by mutans streptococci.68 Xylitol inhibits the upper part of the glycolytic pathway, while fluoride inhibits the lower. This means that xylitol products can be used along with fluoride products for an increased therapeutic effect in treating dental caries.
High-Intensity Fluoride Treatment
High intensity fluoride treatment refers to professionally applied topical fluoride gels, foams, or varnishes, or to prescription-strength fluoride gels or mouth rinses for home use. High-intensity fluoride treatments have been shown to be valuable in preventing dental morbidity in patients with the most aggressive forms of dental caries and in stimulating the remineralization of incipient lesions.69 High-intensity fluoride products are much more effective at preventing dental morbidity in caries-active individuals than are low-intensity products.70,71,72,73
Prescription-strength fluoride gels and mouth rinses for home use provide a high concentration of fluoride to the dentition, which is valuable for remineralizing early caries lesions. These products can be used daily for a limited period, until remineralization is achieved. Patients should be recalled every three months during remineralization therapy to evaluate the lesions. Complete remineralization may take 12 to 18 months. For the fluoride gels, there are two global application techniques: (1) brush on with a toothbrush for one full minute, or (2) apply with full arch trays, either custom-fitted or standard-sized, for five minutes. Alternatively, specific sites (spot) application can be directed to individual incipient caries lesions.
High-intensity fluoride mouth rinses (0.2% NaF or 0.09% F) are about four times as concentrated as the over-the-counter rinses (0.05% NaF or 0.02% F). They were originally designed to be used once per week as an alternative to the daily rinsing schedule with over-the-counter rinses. Research has shown that used in this way they are equally as effective in impeding caries activity.74 High-intensity fluoride rinses may be of value as an alternative to the gels in remineralization therapy for individuals with impaired manual dexterity or where lesions are scattered throughout the mouth. For remineralization therapy, these rinses would be used once daily.
High-intensity fluoride dentifrices (e.g., PreviDent 5000 plus, Colgate Oral Pharmaceuticals) are also available (1.1% NaF or 0.5% F). These products have been specifically formulated for head and neck radiation patients with post-radiation xerostomia so that they are gentle on the tender tissues experiencing oral mucositis. The advantage of a high-intensity fluoride dentifrice is that it replaces the two-step procedure of brushing with a dentifrice and then applying a high-intensity fluoride product.
Fluoride varnish has special applicability for root caries risk or to remineralize root caries lesions. Applied by the dentist to exposed root surfaces, these varnishes offer an effective remineralization treatment.65,66
Chlorhexidine Mouth Rinse
In the late 1940’s, chlorhexidine was discovered by scientists seeking to develop anti-malarial agents.67 Although never utilized in the treatment of malaria, chlorhexidine has been widely used in the practice of medicine since the early 1950’s for the treatment of burns and disinfection of the skin. Chlorhexidine rinses were subsequently used in dentistry to remove plaque from the teeth. Use for this purpose fell into disfavor when prolonged use led to development of resistant dental plaque. However, it was recognized that periodic episodes of chlorhexidine rinsing had the ability to reduce caries rates. Historically, many antimicrobial agents have been studied in an attempt to suppress oral MS levels. Chlorhexidine was one of the most safe and effective agents discovered for this purpose.
Part of the reason for the marked antimicrobial action of chlorhexidine in vivo is its substantivity. Substantivity is the ability of an agent to prolong its presence in a given environment. The duration of action of chlorhexidine is prolonged by its ability to adsorb to oral structures. The chlorhexidine molecule possesses a strong positive charge. It adsorbs to the negatively charged oral tissues. It is slowly released into the oral environment for up to 24 hours after a brief therapeutic dose. This decreased oral clearance has the effect of maintaining the drug in contact with the plaque microorganisms for a prolonged period of time.78 On the other hand, this strong positive charge prevents the molecule from penetrating well. Chlorhexidine will not penetrate into caries lesions. This is why it is recommended that all cavitated lesions be restored before prescribing chlorhexidine rinses.
Chlorhexidine has a broad-spectrum antimicrobial activity. Even so, mutans streptococci (MS) are more susceptible to its killing action than are other members of the normal oral flora.79 Relative specificity for MS is important because those bacteria, which survive antimicrobial therapy in large numbers, have an advantage in repopulating the treated area. Mutans streptococci have a greater difficulty establishing on surfaces already occupied by other bacteria.80,81,82 If MS are suppressed more strongly than other members of the resident flora, re-growth of other organisms may help to impede re-growth of MS.83 Chlorhexidine appears to have enough specificity that it can suppress the proportions of MS in the microflora on a dentition initially harboring high levels of these organisms. In those subjects most favorably affected by treatment, MS can remain suppressed for many months after treatment ceases.84,85,89 However, not all individuals respond optimally to chlorhexidine treatment. Once chlorhexidine treatment ceases, the rapidity of return of MS to pretreatment levels varies considerably from subject to subject,86,87 and appears to be primarily due to incomplete eradication of, rather than re-inoculation with, the pathogen.88,89 The average rate of rebound to pre-treatment levels is in the range of two weeks to six months.85,86,90,91
Various methods of prolonging the effects of a chlorhexidine regimen have been explored. It has been recognized that MS can survive on toothbrush bristles and on toothpaste tubes, providing a mechanism for re-inoculation of the dentition.92 It is therefore recommended that a new toothbrush be provided at the commencement of a chlorhexidine regimen. Similarly, removable appliances should be disinfected at the same time in dilute chlorhexidine rinse.
To maintain MS suppression for a period of several months requires either repeated chlorhexidine treatment or some other form of intervention. Sugar restriction in a hamster model demonstrated the ability to prevent MS return following chlorhexidine suppression.93 However, compliance with dietary recommendations involving sucrose restriction is far better among captive laboratory animals than it is among human patients. Topical fluoride treatments are capable of prolonging MS suppression for up to 12 weeks following chlorhexidine treatment.94 However, the relatively modest results required a vigorous fluoride regimen. Chewing xylitol gum after meals has been shown to prolong the suppression of mutans streptococci following chlorhexidine treatment for at least three months.95
In using available 0.12% chlorhexidine mouth rinses for the control of dental caries, the regimen used for the control of gingival disease is adequate for MS-suppression: Rinse with one capful (15 ml) for 30 seconds twice daily, after brushing and flossing, after breakfast and before bed for two weeks (1 pint, 475 ml bottle). Using chlorhexidine and sodium fluoride treatments concomitantly has been shown to be more effective at reducing caries rates than using either treatment alone.96 The fluoride product should be used first, in order to avoid removal of the flavor-masking agent in the chlorhexidine rinse.
Exogenous Calcium Phosphate
Most sources of calcium, such as antacids and calcium supplements, do not dissociate rapidly enough to provide bio-available calcium and phosphate for remineralization of caries lesions. However, a milk-derived protein has been found which can provide bio-available calcium and phosphate to the teeth. It is called casein-phosphopeptide amorphous calcium-phosphate (CPP-CP) [trade name Recaldent].
Exogenous calcium phosphate appears to be beneficial to any caries-active patient.97,98 However, this strategy has particular applicability to cases of profound oral dryness.99 Without saliva, the tooth has no remineralization capabilities. Fluoride in these instances has limited efficacy since its chief mode of action is to catalyze remineralization. It makes more sense in cases of extremely dry mouth to provide an exogenous source of calcium phosphate along with the fluoride. CPP-CP is available as a prophylaxis paste and in a chewing gum vehicle.
Prospec MI Paste [GC America] is 10% CPP-CP in a vehicle of polishing and cleaning agents. It has the consistency of thin toothpaste. This material is purchased by the dentist and dispensed to the patient for home use. The paste may be brushed on with a toothbrush or applied in full arch trays. There is no need to rinse afterward, and it is safe to swallow. Specific site application to individual incipient caries lesions with the finger is also possible. The product is safe for those lactose-intolerant.
Trident White chewing gum [Cadbury Adams USA LLC] contains CPP-CP. The gum is available at most stores where gum is sold. Chewing gum appears to be an economical and effective way of supplying exogenous calcium phosphate.100,101,102
Fluoride containing restorative materials, such as glass ionomer, offers significant benefit in preventing recurrent caries.104 To maximize the benefit, these materials may require recharging of the fluoride by supplemental use of topical fluorides. The therapeutic use of glass ionomer materials in pediatric patients, high caries risk patients, xerostomic patients, elderly or infirm patients susceptible to root caries, and rampant caries patients all can benefit significantly from the use of glass ionomer restorations. In some high-risk caries patients — e.g., methamphetamine abusers — where compliance may be a significant issue, placement of viscous glass ionomer as the initial restorative material offers some significant benefits in maintaining dental health, allowing time to assess compliance and improve oral hygiene and diet.
Following successful implementation of control strategies and failure of new lesions to develop, glass ionomer restorations in stress-bearing areas may be replaced with more definitive, durable restorations as required. Glass ionomer bases, liners, and luting agents can be employed in this process. Glass ionomer restorations may be left in non-stress bearing areas as definitive restorations. In esthetic areas, glass ionomer restorations may be veneered with composite materials to improve the surface durability. Although the fluoride release from glass ionomer materials has no effect on the caries risk of distant sites, it can help prevent recurrent caries around that particular restoration.104,106
Rampant caries is an aggressive, relentless, destructive process that requires aggressive and multi-pronged therapeutic strategies. To be successful, the diet must be modified. Preventive and therapeutic agents can be employed from several different fronts simultaneously, tailored to the source of the caries risk. Restorative procedures can utilize fluoride-releasing materials to reduce the chances of recurrent decay.
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*Dr. Hildebrandt is Clinical Associate Professor and Director, Division of Operative Dentistry, Department of Restorative Sciences, University of Minnesota School of Dentistry, Minneapolis, Minnesota 55455.
**Dr. Larson is Associate Professor, Division of Operative Dentistry, Department of Restorative Sciences, University of Minnesota School of Dentistry, Minneapolis, Minnesota 55455. E-mail is firstname.lastname@example.org.