NIH: Caries CDC: Abstracts: Kidd

Edwina Kidd, B.D.S, Ph.D., F.D.S., R.C.S.:

Diagnosis of Secondary Caries

The specific assignment is to address the findings of the Research Triangle Institute (RTI) report on the diagnosis of secondary caries and translate them into recommendations for research, clinical practice, and education. Since the report did not investigate the diagnosis of secondary caries, there are no findings. This is just as well, since:

There is minimal literature on the subject
The definition of secondary caries is in doubt
There is no appropriate way to validate the diagnosis.

Definitions of Dental Caries and Diagnosis

Before justifying these statements, it is sensible to define what is meant by dental caries and by diagnosis. "Dental caries" is a result of metabolic activities in the microbial deposits covering the tooth surface at any given site. These metabolic processes are a physiological phenomenon, and caries is ubiquitous and natural at the crystal level. Mineral loss and subsequent cavity formation are the result of an imbalance in the dynamic equilibrium between tooth mineral and plaque fluid. The carious lesion reflects the activity of the biofilm, and lesion progression can be controlled (Fejerskov, 1997). "Diagnosis" implies deciding whether a lesion is active, progressing rapidly or slowly, or already arrested. Without this information, a logical decision about treatment is impossible.

The report produced concerns the detection of demineralization (Featherstone, 1996); there is no mention of lesion activity. Perhaps this is inevitable in a report that sees histological validation as an appropriate "gold standard." It is difficult to judge lesion activity histologically and unwise to attempt diagnosis in a laboratory simulation of a clinical setting. Diagnosis requires a warm human being and a clinical nose.

Questions Relevant to Secondary Caries Diagnosis

The following questions are important:

What is secondary caries?
Why is it important?
Where does it occur, and why?
What does it look like?
What does it not look like?
What are the problems in validating the diagnosis?

What Is Secondary Caries?

Secondary caries is the lesion at the margin of an existing restoration. Primary caries is the lesion at the margin of an existing filling (Mj�r, Toffenetti, 2000). These definitions have been misunderstood for many years by those working only in the laboratory (Kidd, Toffenetti, Mj�r, 1992). In that setting, histological examination of artificial and natural lesions around restorations may show lines of demineralized tissue running along the cavity wall. These are called wall lesions, and they are the result of microleakage. They are very commonly seen around amalgam restorations and probably indicate initial leakage prior to sealing of the margin (Kidd, O�Hara, 1990).

It is also important to consider residual caries, which is residual demineralized tissue left in the tooth during cavity preparation. Our thoughts on how much demineralized tissue may be left during cavity preparation should have been profoundly shaken by the careful clinical studies of the Mertz-Fairhurst group (Mertz-Fairhurst, Curtis, Ergle, et al., 1998). This group removed the enamel lid from large occlusal lesions, leaving extensively demineralized dentine. The cavities were then sealed with acid-etch composite restorations. Ten-year results showed that these restorations were satisfactory�provided the patients did not escape to new dentists who took radiographs, noted the demineralization, and replaced the fillings. This work makes sense if it is accepted that dental caries is the tissue destruction caused by bacterial metabolism in the biofilm. If the process can be arrested by simply removing the biofilm, why does the symptom of the process (demineralized dentine) have to be removed at all? Why not just remove the biofilm and seal the hole in the tooth? This argument has profound implications for operative dentistry and for the validation of a diagnosis of secondary caries.

Why Is the Diagnosis of Secondary Caries Important?

This diagnosis is the main reason given by dentists for replacing fillings. Fifty to 60 percent of restorations are replaced because dentists diagnose secondary caries (Mj�r, Toffenetti, 2000). Are they correct? This high prevalence is not found in controlled clinical trials, where 1 to 4 percent of secondary caries has been reported. Incidentally, only these latter trials would survive the scrutiny of a systematic review on the causes of the failure of restorations. Why are there huge differences between a general practice setting and a clinical trial? Are general practitioners poorly trained, idiosyncratic, and ignorant about this diagnosis? That explanation seems dangerously facile.

Where Does Secondary Caries Occur and Why?

This is easy to answer. It occurs in areas of plaque stagnation, and therefore the cervical margins of restorations are commonly affected.

What Does It Look Like?

Again, this is easy to answer. If secondary caries is primary caries at the margin of a filling, it looks clinically and radiographically like primary caries (Kidd, 1999).

What Does It Not Look Like?

There is some evidence from combined clinical and microbiological studies that ditching and staining around amalgam fillings (Kidd, Joyston-Bechal, Beighton, 1995) and staining around tooth-colored restorations (Kidd, Beighton, 1996) are poor predictors of active secondary caries.

What Are the Problems in Validating the Diagnosis?

Here, there is a major difficulty. There are few reliable validators of the diagnosis. It might be possible to use histology on freshly extracted teeth to relate lesions at the margins of fillings to the overlying plaque (Ozer, 1997). In any laboratory study, however, great care is needed not to confuse active secondary caries with old microleakage or residual caries (Merrett, Elderton, 1984).

Clinical study, where a diagnosis is made and the restoration dissected out to allow examination of the cavity beneath, may be similarly fraught with dangers (Kidd, Joyston-Bechal, Beighton, 1995; Kidd, Beighton, 1996). It would be all too easy to confuse residual caries with secondary caries. Imagine dissecting out a Mertz-Fairhurst type restoration (Mertz-Fairhurst, Curtis, Ergle, et al., 1998). Soft demineralized dentine would be present beneath the filling, but this is residual caries, not primary caries at the margin of the restoration.

Similarly, the clinical and microbiological studies referred to may oversimplify the problem (Kidd, Joyston-Bechal, Beighton, 1995; Kidd, Beighton, 1996). There are now many studies showing that the microbiological load in infected dentine is reduced when it is sealed off from the oral environment (Schouboe, MacDonald, 1962; King, Crawford, Lindahl, 1965; Mertz-Fairhurst, Schuster, Williams et al., 1979; Handelman, 1991; Bj�rndal, Larsen, Thylstrup, 1997; Weerheijm, Kreulen, de Soet, et al., 1999). However, it is not eliminated. The relevance of these residual organisms is not clear. If Mertz-Fairhurst�s work is to be believed (Mertz-Fairhurst, Curtis, Ergle, et al., 1998), they have no relevance.

The only valid test is the visual appearance of the lesions in patients. These appearances, however, are open to interpretation, and the authors of the RTI report would dismiss them as poor and insufficient evidence.

References

Bj�rndal L, Larsen T, Thylstrup A. A clinical and microbiological study of deep carious lesions during stepwise excavation using long treatment intervals. Caries Res 1997;31:411�7.

Featherstone JDB. Clinical implications: new strategies for caries prevention. In: Proceedings of the 1st Annual Indiana Conference: early detection of dental caries. Ed. Stookey, GK. Indiana University 1996: 287�95.

Fejerskov O. Concepts of dental caries and their consequences for understanding the disease. Community Dent Oral Epidemiol 1997;25:5�12.

Handelman SL. Therapeutic use of sealants for incipient or early carious lesions in young adults. Proc Finn Dent Soc 1991;87:467�475.

Kidd, EA. Caries management. Dent Clin North America 1999;43:743�764.

Kidd EA, O�Hara JW. The caries status of occlusal amalgam restorations with marginal defects. J Dent Res 1990;69:1275�7.

Kidd EA, Toffenetti F, Mj�r IA. Secondary caries. Int Dent J 1992;42:127�38.

Kidd EA, Joyston-Bechal S, Beighton D. Marginal ditching and staining as a predictor of secondary caries around amalgam restorations: a clinical and microbiological study. J Dent Res 1995;75:1206�11.

Kidd EA, Beighton D. Prediction of secondary caries around tooth-colored restorations: a clinical and microbiological study. J Dent Res 1996;75:1942�6.

King JB, Crawford JJ, Lindahl RL. Indirect pulp capping: a bacteriologic study of deep carious dentine in human teeth. Oral Surg Oral Med Oral Pathol 1965;20:663�9.

Merrett MCW, Elderton RJ. An in vitro study of restorative dental treatment decisions and dental caries. Br Dent J 1984;157:128�33.

Mertz-Fairhurst EJ, Schuster GS, Williams JE, Fairhurst CW. Clinical progress of sealed and unsealed caries. Part 1: Depth changes and bacterial counts. J Prosthet Dent 1979;42:521�6.

Mertz-Fairhurst EJ, Curtis JW, Ergle JW, Rueggeberg FA, et al. Ultra-conservative and cariostatic sealed restorations: results at year 10. J Am Dent Assoc 1998;129:55�66.

Mj�r IA, Toffenetti F. Secondary caries: a literature review with case reports. Quintessence Int 2000;31:165�79.

�zer L. The relationship between gap size, microbial accumulation and the structural features of natural caries in extracted teeth with Class II amalgam restorations (thesis). University of Copenhagen, 1997.

Schouboe T, MacDonald JB. Prolonged viability of organisms sealed in dentinal caries. Arch Oral Biol 1962;7:525�6.

Weerheijm KL, Kreulen CM, de Soet JJ, Groen HJ, van Amerongen WE. Bacterial counts in carious dentine under restorations; 2-year in vivo effects. Caries Res 1999;33:130�4.

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