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NIH: Consensus Development Conference on Diagnosis and Management of Dental Caries Throughout Life: Background

NIH organized conference that produced consensus statements on important and controversial topics in medicine and dentistry.

Clinical Decision-Making for Coronal Caries Management in the Permanent Dentition

Kenneth J. Anusavice, Ph.D., D.M.D.:

Clinical decisions on caries diagnosis and appropriate treatment are quite variable. Because of the limitations of diagnostic devices and uncertainty in interpreting images and tactile responses, treatment decisions can lead to both overtreatment and undertreatment. Overtreatment is of major concern because premature or unnecessary restoration eliminates the chance for remineralization and does not necessarily reduce the caries risk of patients. Undertreatment, on the other hand, may lead to undetected progression of caries lesions and result in larger restorations. For low-risk patients, however, more conservative treatment decisions are justifiable, and the consequences of undertreatment should be less significant for them than the consequences of undertreatment for high-risk patients.

In this era of evidence-based dentistry, decisions to place initial restorations or to replace "faulty" ones are being questioned. As the prevalence of caries has declined, we have realized that it is critically important that patients at low risk for caries should not be prescribed the same treatment as high-risk patients. In addition, we now know that noncavitated enamel lesions can be arrested, and that noncavitated tooth enamel can be remineralized and hardened. We have also learned that caries lesions generally progress rather slowly. Thus, questionable or early caries lesions can be monitored for several years before a decision is made to intervene surgically. There is considerable uncertainty in diagnosing early lesions accurately because of the rather low sensitivity of current diagnostic methods. For a successful treatment decision to be made, the presence of a lesion must be determined at a sufficiently high level of certainty. It is not sufficient simply to determine the presence of a lesion, since many noncavitated lesions are arrested and tooth structure can be remineralized. It is important to determine whether a lesion is active prior to making a decision to restore or re-restore.

The first step in the decision-making process is to conduct a thorough analysis of the patient's health and dental history, based on (1) individual, family, and community health levels; (2) a clinical oral exam; and (3) risk factors, including previous dental experience (DMFS, DFS, DMFT, DFT), smoking, general health, manual dexterity, learning ability, sociodemographic data, behavioral factors, diet and nutrition, fluoride exposure, and dental health knowledge. The oral exam may require visual, tactile, radiographic, bacterial, and other diagnostic methods to record plaque levels and potentially high-risk areas of enamel demineralization. The exam should also identify high-risk tooth surfaces for caries initiation and progression, such as existing white spots or areas where plaque accumulation is likely. Caries risk may be defined as the probability that an initial lesion will develop or that an existing lesion will progress over a specified period of time. The exam must be sufficiently accurate to positively diagnose the presence of caries lesions, if present, and questionable lesions, if high sensitivity in diagnosis is not possible.

The second step is to describe the extent of all lesions, if possible, using a classification such as the following: E0 (no enamel lesion); E1 (lesion in the outer half of enamel); E2 (lesion in the inner half of enamel); D1 (outer third of dentin); D2 (middle third of dentin); and D3 (inner third of dentin). Such a classification will permit lesion activity over time to be determined and the success of caries arresting and remineralizing treatments to be assessed.

The third step is to list possible treatment options as a function of present and predicted risk levels. Treatment options for a nonrestored site (in the most general sense) include (1) no treatment except for oral prophylaxis and monitoring; (2) oral prophylaxis followed by chemotherapeutic management of infection (fluoride only, or chlorhexidine and fluoride) and monitoring; and (3) placement of a sealant, repair or sealing of a restoration, or placement/replacement of a restoration.

Optimizing the Decision-Making Process

The main objective of this review is to answer the following question: What are the appropriate treatment options for coronal caries in permanent teeth for patients at low-, moderate-, or high-risk for primary and secondary caries initiation and progression? One needs to know whether the lesion is slightly or well into enamel, or slightly or well into dentin. Furthermore, one must know whether the caries process is active or arrested. This can best be determined by monitoring the lesion over time. For a high-risk individual, one might choose to restore or monitor a lesion that extends slightly into dentin.

There is some evidence that supports the placement of a restoration when the lesion has progressed 0.5 mm or more into dentin. However, this recommendation may have been based on individuals at a moderate- to high-risk of caries progression. What threshold level is appropriate for low-risk patients is unknown. For the most minimally invasive strategy, actual observation of tooth surface cavitation can be considered the threshold for placement or replacement of a restoration. The long-term goal is to ensure that the best outcome is reached, based on the most reliable scientific evidence and practical experience.

To competently answer the question posed at the beginning of this section about treatment options, the following additional information is required:

  1. Probability of lesion progression as a function of caries risk level
  2. Probability of tooth surface cavitation over a specified period of time
  3. Best treatment methods to arrest active lesions and potentially to remineralize teeth with noncavitated lesions as a function of patient risk level
  4. Lesion depth at which a restoration should be placed (threshold for surgical intervention) for a patient's initial risk level and at recall exams.

Obviously, the optimal outcome for a high-risk patient with a D1 lesion would be based on a treatment decision to not restore the tooth with a D1 lesion but to monitor the lesion over time. For an approximal lesion, tooth separation would be required to ensure that cavitation of the approximal surface has not occurred. This may not be deemed practical by most dentists, and the next best option would be to use probability data based on the studies of Pitts and Rimmer (1992) and others.

Chemotherapeutic Agents for Reducing Caries Risk

Unfortunately, few randomized, controlled clinical trials have been conducted to answer questions related to management of caries as a chronic infectious disease. Thus, we may need to use data from studies that are based on populations rather than studies in which the caries risk of individual subjects was assessed.

We can justify delaying the restorative treatment of enamel lesions in the inner half of enamel (and even slightly into dentin) on the basis that caries progression through enamel in moderate-risk and high-risk patients is slow (Shwartz, Pliskin, Grondahl, et al., 1984; Berkey, Douglass, Valachovic, et al., 1988). Caries progression has been decreasing over recent decades (Ekanayake, Sheiham, 1987) and is slower in patients who have received regular fluoride treatment or who consume fluoridated water (Pitts, 1983; Shwartz, Pliskin, Grondahl, et al., 1984a; Schwartz, Grondahl, Pliskin, 1984b). Progression time through enamel may take from 6 to 8 years. Since many enamel lesions remain unchanged or progress very slowly over long periods, and because progression rates through dentin may also be comparably slow (Emslie, 1959; Kolehmainen, Ryt'maa, 1977), there is adequate time to apply infection control and monitoring procedures to assess caries risk and lesion activity. Furthermore, the percentage of radiographically visible approximal lesions in the outer half of dentin that are cavitated has declined over the past several decades to approximately 41 percent.

Preservative dentistry is based on a refined model of decision-making consisting of accurate caries diagnosis, classification of caries severity using radiographs, assessment of patient's caries risk (high, moderate, or low), placement of restorations in teeth with cavitated lesions, arresting of active lesions, remineralizing of noncavitated arrested lesions, monitoring of noncavitated lesions over time, and assessing of management outcomes (change in DMFS, DFS, D/DMFS, D/DFS, and D/DFS) at predetermined intervals. The bacterial infection which causes the production of demineralizing acids should be controlled to ensure the arrest of demineralization and, potentially, the initiation of remineralization. Once a decision has been made to monitor rather than restore primary or secondary lesions, the next decision is to decide whether caries risk can be reduced through the use of fluoride agents alone or in combination with antimicrobial therapy.

The effectiveness and sustantivity (sustaining power) of chlorhexidine in reducing the levels of S. mutans and potentially to enhance remineralization of demineralized enamel for high-risk patients provide renewed optimism for reducing caries risk and increasing the probability that a restoration decision may never need to be made (Schitt, Briner, Le, 1976; Schitt, Briner, Kirkland, et al., 1976; Emilson, 1977; Emilson, Lindquist, Wennerholm, 1987; Katz, 1982; Zickert, Emilson, Ekbloom, et al., 1987; Schaeken, DeHaan, 1989; Schaeken, Keltjens, Van Der Hoeven, 1991; Persson, Truelove, LeResche, et al., 1991; Joyston-Bechal, Hayes, Davenport, et al., 1992; Sorvari, Spets-Happonen, Luoma, 1994; Tenovuo, Hakkinen, Paunio, et al., 1992; Ullsfoss, gaard, Arends, et al., 1994; Pienihkkinen, Soderling, Ostela, et al., 1985; Anusavice, 1998; Petersson, Magnusson, Andersson, et al., 1988). However, only limited data are available on the optimum strategy for treatment of individual patients. Thus, data obtained in private practice from combined chemotherapeutic and fluoride treatment will be required in addition to published clinical trial data to further develop our ability to manage caries.


Anusavice KJ. Chlorhexidine, fluoride varnish, and xylitol chewing gum: underutilized preventive therapies? Gen Dent 1998;46:34-8, 40.

Berkey CS, Douglass CW, Valachovic RW, Chauncey HH. Longitudinal radiographic analysis of carious lesion progression. Comm Dent Oral Epidemiol 1988;16:83-90.

Ekanayake LS, Sheiham A. Reducing rates of progression of dental caries in British schoolchildren. A study using bitewing radiographs. Br Dent J 1987;163:265-9.

Emilson CG. Susceptibility of various microorganisms to chlorhexidine. Scand J Dent Res 1977;85:255-65.

Emilson CG, Lindquist B, Wennerholm K. Recolonization of human tooth surfaces by Streptococcus mutans after suppression by chlorhexidine treatment. J Dent Res 1987;66:1503-8.

Emslie RD. Radiographic assessment of approximal caries. J Dent Res 1959;38:1225-6.

Grondahl HG, Hollender L, Malmcrona E, Sundquist B. Dental caries and restorations in teenagers. II. A longitudinal radiographic study of the caries increment of proximal surfaces among urban teenagers in Sweden. Swed Dent J 1977;1:51-7.

Joyston-Bechal S, Hayes K, Davenport ES, Hardie JM. Caries incidence, mutans streptococci and lactobacilli in irradiated patients during a 12-month preventive programme using chlorhexidine and fluoride. Caries Res 1992;26:384-90.

Katz S. The use of fluoride and chlorhexidine for the prevention of radiation caries. J Am Dent Assoc 1982;104:164-70.

Kolehmainen L, Ryt'maa I. Increment of dental caries among Finnish dental students over a period of 2 years. Comm Dent Oral Epidemiol 1977;5:140-4.

Persson RE, Truelove EL, LeResche L, Robinovitch MR. Therapeutic effects of daily or weekly chlorhexidine rinsing on oral health of a geriatric population. Oral Surg Oral Med Oral Pathol 1991;72:184-91.

Petersson LG, Magnusson K, Andersson H, Deierborg G, Twetman S. Effect of semi-annual applications of a chlorhexidine/fluoride varnish mixture on approximal caries incidence in schoolchildren. A three-year radiographic study. Eur J Oral Sci 1998;106(2 Pt 1):623-7.

Pienihkkinen K, Sderling E, Ostela I, Leskel I, Tenovuo J. Comparison of the efficacy of 40% chlorhexidine varnish and 1% chlorhexidine-fluoride gel in decreasing the level of salivary mutans streptococci. Caries Res 1995;29:62-7.

Pitts NB. Monitoring of caries progression in permanent and primary posterior approximal enamel by bitewing radiography. Comm Dent Oral Epidemiol 1983;11:228-35.

Pitts NB, Rimmer PA. An in vivo comparison of radiographic and directly assessed clinical caries status of posterior approximal surfaces in primary and permanent teeth. Caries Res 1992;26:146-52.

Schaeken MJ, Keltjens HM, Van Der Hoeven JS. Effects of fluoride and chlorhexidine on the microflora of dental root surfaces and progression of root-surface caries. J Dent Res 1991;70:150-3.

Schaeken MJM, De Haan P. Effects of sustained-release chlorhexidine acetate on the human dental plaque flora. J Dent Res 1989;68:119-23.

Schitt CR, Briner WW, Le H. Two year oral use of chlorhexidine in man. II. The effect on the salivary bacterial flora. J Periodont Res 1976;11:145-52.

Schitt CR, Le H, Briner WW. Two year clinical use of chlorhexidine in man. IV. Effect on various medical parameters. J Periodontal Res 1976;11(3):158-64.

Schitt CR, Briner WW, Kirkland JJ, Le H. Two years oral use of chlorhexidine in man. III. Changes in sensitivity of the salivary flora. J Periodont Res 1976;11:153-7.

Shwartz M, Pliskin J, Grndahl H, Boffa J. Study design to reduce biases in estimating the percentage of carious lesions that do not progress within a time period. Comm Dent Oral Epidemiol 1984;12:109-13.

Shwartz M, Grondahl HG, Pliskin JS, Boffa J. A longitudinal analysis from bite-wing radiographs of the rate of progression of approximal carious lesions through human dental enamel. Arch Oral Biol 1984;29:529-36.

Sorvari R, Spets-Happonen S, Luoma H. Efficacy of chlorhexidine solution with fluoride varnishing in preventing enamel softening by Streptococcus mutans in an artificial mouth. Scand J Dent Res 1994;102:206-9.

Tenovuo J, Hkkinen P, Paunio P, Emilson CG. Effects of chlorhexidine-fluoride gel treatments in mothers on the establishment of mutans streptococci in primary teeth and development of dental caries in children. Caries Res 1992;26:275-80.

Ullsfoss BN, gaard B, Arends J, Ruben J, Rlla G, Afseth J. Effect of a combined chlorhexidine and NaF mouthrinse: an in vivo human caries model study. Scand J Dent Res 1994;102:109-12.

Zamir T, Fisher D, Fishel D, Sharav Y. A longitudinal radiographic study of the rate of spread of human approximal dental caries. Arch Oral Biol 1976;21:523-6.

Zickert I, Emilson CG, Ekblom K, Krasse B. Prolonged oral reduction of Streptococcus mutans in humans after chlorhexidine disinfection followed by fluoride treatment. Scand J Dent Res 1987;95:315-9.

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