Routine questioning of the patient and his accompanying parent revealed no contributing medical history, and that two of the restorations (teeth nos. 3 and 14) had been placed within the last year. The parent reported that the boy drank fluoridated water and had received regular dental care beginning at age 3 years, including six-month recall appointments. The patient demonstrated adequate oral hygiene practices, and his parent confirmed that he brushed regularly at home and always at bedtime. However, the patient revealed that he ate sugary snacks after school and dinner without brushing his teeth immediately afterward.

The most reliable predictor of high caries risk to the permanent dentition is the caries experience in the primary dentition.

Prevention strategy. I initiated the following caries preventive strategy: tertiary treatment of carious teeth nos. I and J, consisting of placement of amalgam restorations; primary treatment of teeth nos. 19 and 30, involving the placement of occlusal sealants; modification of the patient’s diet to include fruit snacks after school and dinner; toothbrushing with fluoridated toothpaste immediately after breakfast and dinner; and rinsing with fluoridated mouthrinse after brushing before bedtime.

Three months after I placed the sealants, the patient had a recall appointment. Because his compliance was good and there was no clinical evidence of new or recurrent carious lesions, I instructed the patient to come back for six-month recall visits. I also referred him to an orthodontist because of an angle Class I malocclusion with bilateral posterior crossbite, constricted palate and anterior open bite resulting from a thumb-sucking habit.

Recall visits. From 1984 through 1987, the patient had six-month recall appointments, and he received orthodontic therapy from 1985 through 1987. During the period in which he received orthodontic treatment, I prescribed topical fluoride brush-on gel for use after brushing in the morning and before bedtime. I obtained bitewing radiographs in February 1985, January 1986, August 1986 and August 1987. At this last visit, the patient was aged 12 years and his second molars were erupted fully. I placed occlusal sealants at this visit. Throughout this period, no new carious activity was evident.

However, the patient did not keep his recall appointments throughout 1988, and a clinical examination in March 1989 revealed a disappointing clinical picture. Bitewing radiographs (Figure 2) indicated demineralization of the following teeth: 2, 3, 4, 5, 12, 13, 14, 18, 19, 20, 29, 30 and 31. Because caries is a dynamic process, the progress of individual lesions is an important factor in the diagnosis and prognosis.³ Clinical carious activity needs to be measured over time, and changes in disease activity indicate the need for strict periodic monitoring of high-risk patients.

View larger version (23K): [in this window] [in a new window]   Figure 2. Radiographs obtained in March 1989. The initial demineralization is seen interproximally on teeth nos. 2, 3, 4, 5, 12, 13, 14, 18, 19, 20, 29, 30 and 31. The lesions on the distal surface of teeth nos. 20 and 29 had advanced into the dentinoenamel junction.

In-office tests to measure S. mutans levels are not practical for every patient, because they measure only one component of the disease process, and a single microbiological examination is of little value on its own.⁵ In addition, these tests are not sensitive (that is, a negative result is equally likely to be a false-negative or true-negative result), and the tests are not good at predicting the onset of disease activity. However, salivary determination of S. mutans levels is highly specific (that is, a positive test result is almost always a true positive result), and high counts likely correlate with caries activity.⁶ Thus, a patient identified as being at high risk of developing caries on the basis of caries experience and whose radiographs reveal changes that reflect carious activity is most likely to test positive for S. mutans.

It may seem unnecessary to test patients bacteriologically while carious lesions, the nidi of infection, are left unrestored. However, a caries risk assessment can be used to motivate the patient (and, in this case, the parents) to intercept the disease process. For the moderate-to-high-risk patient, caries risk assessment allows for a custom-made prevention program.⁷ In this case, the microbiological method was a valuable adjunct to taking a medical history and conducting a careful clinical examination, as well as an aid in diagnosing and explaining the disease activity.

After March 1989, the caries prevention strategy for this patient was as follows: because most of the lesions were noncavitated, the primary objective was to alter the oral environment to promote remineralization. Hence, I reinforced oral hygiene techniques and prescribed a fluoride gel (5,000 parts per million) to be applied in trays twice daily for 15 minutes each.

Restorative treatment. Dental practitioners generally recognize that surgical treatment is not indicated for lesions confined to the inner one-half of enamel and even for those that extend into dentin.⁸ However, the presence of caries in the distal triangular fossa and in the distal surface of tooth no. 20 undermined the marginal ridge (Figure 2). Thus, in June 1989, I restored this tooth with resin-based composite using a minimally invasive tooth preparation,⁹ such that buccal and lingual triangular ridges were not invaded by the restoration and distal contact was not broken (tunnel preparation). At this time, I also placed a preventive-resin restoration on the occlusal surface of tooth no. 19 and an occlusal amalgam restoration in tooth no. 2. I did not treat the other lesions surgically.

According to Anusavice,⁸ radiographic evidence of carious activity is not sufficient to warrant placing a restoration; rather, each tooth must be monitored over time to determine if the lesions can be arrested. My patient had recall visits every three months for the remainder of 1989. In September 1989, I used an in-office test to again record S. mutans levels, which were low ( 10⁵ CFU/mL).

The patient continued the at-home oral hygiene regimen until December 1989. He then stopped using the fluoride trays and began using over-the counter (OTC) mouthrinses (0.05 percent sodium fluoride) after brushing, because the clinical examination findings and bitewing radiographs revealed no advancement of the interproximal lesions. The patient’s therapy from March until December 1989 was consistent with the recommendation of Anderson and colleagues,⁶ who advised that caries be treated as a bacterial infection and, hence, be treated intensively on a short-term basis to a therapeutic endpoint.

I saw the patient at periodic six-month recall visits throughout the 1990s and found no change in caries activity. Every 18 months I obtained bitewing radiographs. Dental treatment was unremarkable throughout this period, with the exception of the extraction of the patient’s third molars in March 1991. Bitewing radiographs obtained in February 2000 revealed a change in caries activity; lesions had advanced in teeth nos. 13 and 18 (Figure 3). Although a review of the patient’s medical history revealed that he had been diagnosed with esophageal reflux in September 1999 (for which he was treated with omeprazole), his salivary buffering capacity was normal in February 2000. The enlarged lesions in teeth nos. 13 and 18 illustrate the episodic and site-specific nature of the caries process, with rapid demineralization occurring as a result of bacterial proliferation in protected cavitated areas.

View larger version (22K): [in this window] [in a new window]   Figure 3. Radiographs obtained in February 2000. The lesions in teeth nos. 13 and 18 were treated surgically, but the other interproximal lesions (for example, the distal surface of teeth nos. 19 and 29) were treated medically.

In September 2000, I found no progression in carious activity and again instructed the patient to have six-month recall appointments. To date, his long-term home care regimen includes brushing with a fluoridated toothpaste three times a day, flossing, rinsing with an OTC mouthrinse (0.05 percent sodium fluoride) and chewing xylitol gum. Figure 4 shows his most recent radiographs, obtained in December 2004.

View larger version (21K): [in this window] [in a new window]   Figure 4. The patient’s most recent radiographs were obtained in December 2004, when he was aged 29 years. Many lesions that had been observed in March 1989 (for example, tooth no. 29) were treated without operative intervention.

	DISCUSSION

TOP ABSTRACT CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
This case is based on the medical paradigm of treating dental caries by addressing the bacterial cause of the disease and emphasizing disease control. However, the case still involved the surgical paradigm, but it consisted of a minimally invasive approach in which surgical intervention was deferred until it could no longer be avoided. In addition, the patient was involved in treating the disease. Patient compliance is essential. Lesions confined to enamel and those extending slightly into dentin were arrested; only those with cavitation were treated surgically.

	CONCLUSION

TOP ABSTRACT CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
This case documents the use of a treatment regimen for dental caries proposed by Anderson and colleagues,⁶ Anusavice⁸ and others that integrates clinical experience, professional judgment and patient preference in the development of an individualized treatment plan. It is, however, only one case, and stringent, controlled, double-blind, longitudinal clinical trials are needed to validate the efficacy of the therapy for the population at large.