| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
LETTER TO THE EDITOR |
1 Department of Biomedical Engineering
2 Department of Dentistry and Dental Hygiene, Faculty of Medical Sciences, University of Groningen, PO Box 196, 9700 AD Groningen, The Netherlands
The call for caries diagnosis by caries lesion activity assessment is growing. Lesion progression monitoring is difficult and requires careful and time-consuming record-keeping, whereas a single time-point activity assessment makes immediate treatment decisions, mainly involving preventive care, possible. Nyvad and co-workers presented a formal visual/tactile scoring system for lesion activity (1999). They also recently presented a clinical validation of this method for non-cavitated enamel lesions (2003), an excellent effort. Using their data, we would like to extend their analysis.
Nyvad and co-workers analyzed the results from a previous study involving two groups: a group that received daily supervised toothbrushing with a fluoride-containing toothpaste, and a control group that received neither supervised brushing nor fluoride. Baseline and three-year lesion assessments were available. The authors present their case as involving both construct validity and predictive validity. Most important is the case the authors present for the predictive validity of the assessment. The ‘proof of the pudding’ of caries activity measurement must surely lie in the validation through observed caries progression. The authors conclude that, in the control group, lesions diagnosed at baseline as active, non-cavitated (ANC) have a relative risk (RR) of 1.24 to progress in a three-year period to a cavity or filling or be extracted (CFE) as compared with lesions that, at baseline, were diagnosed as inactive, non-cavitated (INC). For the fluoride group, this RR was 1.04.
We were interested in what happened to the non-cavitated lesions that did not progress. Therefore, we transformed the percentages in Table 1
of Nyvad et al.(2003) to numbers, using the totals given. The results may deviate from the original ones by a few units. From these results, we calculated the numbers and fractions of ANC and INC lesions that progressed to CFE, that remained non-cavitated, and that regressed to sound. From those, we determined the relative risks of ANC lesions compared with INC lesions. These calculations are presented in the Table.
|
of Nyvad and co-workers (2003), where, in the fluoride group, 53% of INC lesions remained INC, while only 19% of ANC lesions remained ANC. For the control group, these numbers were 42% and 28%, respectively. The factors that cause this difference in susceptibility are as yet unknown. They may, for instance, involve the ‘openness’ of the lesion surface, the age of the lesion, or its progression stage. At this moment, we therefore suggest only that the terminology be changed to unstable vs. stable lesions.
REFERENCES
Nyvad B, Machiulskiene V, Baelum V (1999). Reliability of a new caries diagnostic system differentiating between active and inactive caries lesions. Caries Res 33:252–260.[ISI][Medline]
Nyvad B, Machiulskiene V, Baelum V (2003). Construct and predictive validity of clinical caries diagnostic criteria assessing lesion activity. J Dent Res 82:117–122.
a Royal Dental College, Faculty of Health Sciences, Aarhus University, Vennelyst Boulevard 9, DK-8000 Aarhus C, Denmark
b Faculty of Stomatology, Kaunas University of Medicine, Eiveniu 2, LT-3007 Kaunas, Lithuania
In their letter, which we have read with great interest, ten Bosch and Huysmans observe that in our Control group (Nyvad et al., 2003), the RR for progression of active non-cavitated (ANC) lesions vs. inactive non-cavitated (INC) lesions is as large as the RR for regression (RRprogression = 1.25 vs. RRregression = 1.24). They furthermore note that, as concerns our Fluoride group, the RRregression (1.45) is even greater than the RRprogression, which they have calculated as 1.01. Based on an assumption that an active caries lesion cannot, by virtue of the definition of activity, regress, ten Bosch and Huysmans therefore suggest that the "active" vs. "inactive" caries lesion terminology be changed to one using "unstable" vs. "stable" lesions.
We are in concert with neither the argument used nor the conclusions drawn, for the following reasons: First, it seems to escape ten Bosch and Huysmans that there is a three-year lapse between the baseline recordings and the follow-up data. While we might agree with their premise that an active lesion cannot regress over a very short period, we find it difficult to accept that an initially active non-cavitated lesion should not be able to turn sound (regress) at some time during a three-year follow-up period. Similarly, we see no reason to expect that an initially inactive lesion should remain unchanged forever. In fact, lesion regression has been shown to be a commonly occurring phenomenon in longitudinal caries studies, even when there is no fluoride available in the lesion environment (Backer Dirks, 1966; Pot et al., 1977). We have recently identified some biological factors that may influence the dynamic balance of lesion transitions in caries (Baelum et al., 2003).
Second, in our understanding, the argumentation put forward by ten Bosch and Huysmans is clearly contradictory to well-known facts about the mode of action of fluoride in caries lesion control. Hence, fluoride is believed to exert its cariostatic effect mainly on the ongoing caries process (active lesion) (Fejerskov et al., 1981) by inhibiting demineralization and promoting remineralization (ten Cate and Featherstone, 1996). During such processes, lesions may lose the clinical characteristics that warrant the diagnosis of active caries.
Even if the premise put forward by ten Bosch and Huysmans is accepted, we have difficulties in understanding how the proposed terminology could contribute to an improved understanding of the caries lesion transition dynamics, or just be better. If "unstable" is better than "active" because the term "unstable" allows for progression as well as regression, then "stable" is worse than "inactive" because it allows for neither progression nor regression.
On a methodological note, we find it relevant to point out that the RR results presented by ten Bosch and Huysmans could have been obtained more easily—and perhaps more accurately—directly from our Table 1. Hence, RRregression, fluoride = 1.44 (ten Bosch and Huysmans report 1.45) can be obtained directly from Table 1 as the ratio of 36% to 25%. Similarly, RRregression, control = 1.22 (ten Bosch and Huysmans report 1.25) is obtained as the ratio of 22% to 18%. The progression RRs may similarly be calculated as: RRprogression, fluoride = 16%/16% = 1.00, and RRprogression, control = 27%/22% = 1.23.
REFERENCES
Backer Dirks O (1966). Posteruptive changes in dental enamel. J Dent Res 45:503–511.
Baelum V, Machiulskiene V, Nyvad B, Richards A, Væth M (2003). Application of survival analysis to carious lesion transitions in intervention trials. Community Dent Oral Epidemiol 31:252–260.[ISI][Medline]
Fejerskov O, Thylstrup A, Larsen MJ (1981). Rational use of fluorides in caries prevention. A concept based on possible cariostatic mechanisms. Acta Odontol Scand 39:241–249.[ISI][Medline]
Nyvad B, Machiulskiene V, Baelum V (2003). Construct and predictive validity of clinical caries diagnostic criteria assessing lesion activity. J Dent Res 82:117–122.
Pot TJ, Groeneveld A, Purdell-Lewis DJ (1977). The origin and behaviour of white spot enamel lesions. Ned Tijdsch Tandheelkd 85:6–18.
ten Cate JM, Featherstone JDB (1996). Physicochemical aspects of fluoride-enamel interactions. In: Fluoride in dentistry. Fejerskov O, Ekstrand J, Burt B, editors. Copenhagen: Munksgaard, pp. 252-272.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| IADR Journals | Advances in Dental Research ® |
| Journal of Dental Research ® | Critical Reviews (1990-2004) |
