This article was published in Quintessence International, Vol. 29 No. 9 (September 1998).

I. How Should We Manage Initial and Secondary Caries?

Anders Thylstrup

Before we can begin to discuss whether the propositions we make about the world are true, we must be sure that they will be understood by others, that we are speaking the same language. This is why we apply the logical rules of linguistics, the science of language, to common speech. Scientists in particular operate with agreed norms of speech for specific situations, where everyone agrees to adopt the same criteria for language use, and propositions can then be debated. At least that is what we assume about the language of reason used in science, as opposed to the language of poetry or dreams, for example. However, when facing the evergrowing mountains of research on caries, let alone those aspects of the disease termed initial or secondary, one may wonder whether scientists are debating the same issue. Perhaps there is a tendency to believe that a little more research along the same lines will produce the answer based on the underlying, but not very scientific, argument that the future will sort out the problems. Addressing the issue of how to manage caries therefore requires a rapid but bold sweep across cariology to answer the question What is caries? and to define initial and secondary caries.

What is caries? Textbooks describe caries either as an infectious disease caused by bacteria adhering to tooth surfaces or, more often, as a multifactorial disease. The multifactorial model can be very elaborate but is most often portrayed as the familiar triad of host, microflora, and diet. Neither definition is entirely correct or incorrect, but what is more important is that neither is particularly useful to dentists, whose job is to care for patients seeking professional help, to determine the causes of caries, and to prevent the next attack. For example, extracting teeth to eliminate the host and thus prevent caries can hardly be recommended. The bacteria in the second circle of the multifactorial model are not invaders but members of the commensal oral flora and hence cannot be eradicated. Finally, diet is obviously an essential part of life, and while its omission most certainly will reduce body weight, the growth of oral bacteria will not be prevented because saliva is their main source of nutrients. Tooth surfaces, bacteria, saliva, diet, and anything we find in the oral cavity under normal conditions are therefore not to be considered factors that cause the onset of dental caries, for the simple reason that they are in themselves absolutely necessary conditions for life, and thus also for the occurrence of this disease.

It might therefore be appropriate to first propose that dental caries is a localized disease resulting from localized bacterial activities. The bacteria that cause caries are not foreign invaders of the oral cavity, but members of the indigenous microflora that are present not only in the oral cavity but also in the gastrointestinal tract and other parts of the body. Somehow scientists have estimated that the human body consists of about 1014 cells, of which only 10% are thought to be human cells.1 For this reason alone it may not be prudent to describe caries as an infectious disease in the classic sense.

How, then, do oral bacteria become cariogenic? To answer this question it is important to consider indigenous oral microflora as being continuously engaged in a struggle for survival in the harsh oral environment1 because the mouth is frequently exposed to environmental extremes of temperature, pH, viscosity, and chemical composition of ingested food. The most serious assaults, however, are generated by oral mechanical forces that operate during activities such as singing, eating, and toothbrushing, to mention just a few significant examples. Enormous numbers of micro-organisms are continually dislodged from the oral surfaces and removed from the oral cavity by frequent swallowing. The main source of salivary bacteria is the oral soft tissues, which continually shed oral mucosal cells. Therefore, from a bacterial survival point of view, the solid and nonshedding surfaces of the teeth are very attractive.

However, oral bacteria do not grow on all tooth surfaces with equal preference or intensity. The cuspal and incisal parts of the teeth are most often devoid of bacterial accumulation, in contrast to, for example, the enamel along the gingival margin. Areas without visible bacterial accumulation are continuously exposed to mechanical wear and shear during oral function. To look at it another way, oral bacteria colonize and grow more readily in areas of the dentition where they are protected against intraoral mechanical disturbance. Because these areas, in general, are associated with the most disease, it seems obvious to acknowledge that the degree of oral mechanical disturbance is an important intraoral factor that dictates the evolution of bacterial accumulation with cariogenic potential. This common clinical experience has been demonstrated in several clinical studies.2 In short, it can be concluded that variations in intraoral mechanical forces (or protection against mechanical wear) determine not only the formation of microbial accumulation on teeth but also the conditions for the evolution of microbial ecosystems with cariogenic potential?r the evolution of the cariogenic plaque that causes the first indications of enamel dissolution.3,4

When plaque bacteria are allowed to grow without mechanical disturbance, the shortage of oxygen gradually favors the growth of anaerobic bacteria at the expense of aerobic bacteria, whose survival depends on an adequate oxygen supply. In the absence of oxygen, glucose can be broken down only to lactic acid or ethanol, the end products of anaerobic glycolysis. In other words, the energy production of anaerobic bacteria, which are dominant in the protected, cariogenic plaque, results in production of acid that dissolves the underlying enamel. While additional glucose may be supplied from external sources (carbohydrates in food), saliva is the primary source of bacterial chemical energy. Also, since the velocity of the salivary film movement is lower in the natural stagnation areas?he protected areas?cids are less rapidly removed from these areas than from areas where the salivary film moves at a higher speed.5 These areas also happen to be the areas where plaque forms less readily. If no measures are taken to disturb or remove the cariogenic plaque, the condition becomes a self-perpetuated process that slowly may result in the visible destruction (a lesion) that is first detected years after its initiation.

What is initial caries? This question implies that we subconsciously have shifted our attention from the disease itself to the signs or symptoms of the disease. When we discuss whether patients have caries or not, we are most often discussing whether they present any visible signs of the disease, ie, a lesion or cavity, and usually not whether or where they have cariogenic or would-be cariogenic plaque. While in reality identifying cariogenic plaque is part of the process of diagnosing the disease, and thus central to the health of any regular patient, education and research have been devoted almost exclusively to identifying the signs of the disease. Whats worse, the relatively simple process of discriminating between advanced stages of destruction is now increasingly being examined, discussed, and critically evaluated by researchers. However, the simple diagnostic criteria, based solely on isolated observations and regularly used by researchers, has nothing in common with the far more complex art of using and applying knowledge to diagnose and treat caries in the individual patient.

Because the patient is central to this discussion, we must agree that by treatment we mean all professional measures to control or arrest ongoing disease. As professionals we are familiar with the health consequences of the advanced stages of destruction and with the procedures for treatment, conventionally known as operative dentistry. However, common clinical experience confirms that operative treatment is neither the beginning nor the end of caries treatment. Since this experience correlates well with the biologic nature of dental caries, there should be no problem in accepting a definition of nonoperative treatment as all procedures aiming to arrest disease without resorting to operative and restorative therapy. Likewise, nonoperative treatment is the natural extension of restorative treatment to avoid recurrence of the disease.

Early diagnosis of caries as a procedure has thus advanced far ahead of the epidemiologic search for cavities and the like, and the aim is now to institute early or nonoperative treatment after identifying cariogenic or would-be cariogenic plaque in areas of the dentition where protection against oral mechanical forces has favored the evolution of anaerobic bacteria. The first, albeit invisible, indication of the acid-producing and acid-tolerant bacteria is a microdissolution of the enamel surface beneath the protected bacterial accumulation. The initial surface dissolution obviously results in a physically firmer attachment between the cariogenic plaque and the underlying enamel. Thus a potential focus of destruction is established and professional intervention is required. If, however, the cariogenic focus remains undisturbed, dissolution of the underlying enamel will proceed, eventually forming the subsurface lesion, or the white spot lesion. This stage of destruction lies somewhere between the microdissolution of the surface and the very first localized microcavities. The white appearance is caused by a combination of surface dissolution, resulting in a diffuse back-scattering of the light, and altered enamel translucency due to the subsurface porosity.2

Arrest of the initial lesion. We have seen that initiation of the lesion is related to the local elimination of mechanical forces, and it is therefore logical that reexposure to mechanical wear and removal of cariogenic plaque ends further dissolution2 and leads to the arrest of further lesion progression. It is equally clear that professional plaque removal and regular toothbrushing combine to wear away or polish the partly dissolved enamel surface, reducing the clinical whiteness and restoring the surface luster and hardness of the arrested lesion. Unfortunately, the laboratory research on this topic has created a great deal of confusion because the word remineralization has often been used by researchers to indicate that progression has stopped because the lesion is remineralized. However, lesion arrest occurs in vivo only when the acid-producing plaque has been removed, and the lesion remains arrested when the evolution of new cariogenic plaque is hindered.

No salivary repair mechanism contributes to the arrest of subsurface enamel lesions. While dissolved ions in the internal lesion may return to the solid phase (the crystals) by reprecipitation when acid production at the surface has ceased, most of the calcium and phosphates, which have left the enamel, will never return to the lesion under real-life conditions.2 Of course, owing to its extremely complicated composition, saliva has a great deal of influence on the events related to caries, but the function of saliva should be seen primarily as modifying or reducing the results of local acid production rather than as a belated mechanism of repair.

What is secondary caries? Available data indicate that visible gaps, marginal discrepancies, and marginal microleakage are poorly related to secondary caries and that secondary caries is a localized phenomenon caused by local conditions that contribute to the evolution of cariogenic plaque.6 Consequently, secondary caries is not a universal attack along the entire tooth-restoration interface, but should rather be considered a new lesion or reestablishment of caries on the surface.

Examination of extracted teeth with approximal amalgam restorations revealed most microbial accumulation, independent of gap size, to be in the stagnation area along the gingival margin. Accordingly, this part of the surface most often had dental caries along the restoration margin. Histologic analyses of the development of the gingival lesions showed that the lesions were initiated at the enamel surface without relation to either the marginal gap or the cavity wall.7 This explanation, which is in agreement with clinical experience, has several consequences, the most important being that the margins of the restoration should be placed in a way that makes it possible for both patient and dentist to keep the margins free of any disease-producing plaque. Black8 expressed this at the beginning of this century: Fillings do not remove the tendency to caries, and the curative effect of a filling is literally no broader than its outline. He continues, If the outlines are so laid that the microbic plaques cover it and lap over its margins, it will not protect the area of liability; decay will begin again close beside the filling. The enamel margin is the vulnerable line. In short, Extension for the prevention of the recurrence of decay after a filling has been made.8

It is evident that cavities should not be made larger than necessary, but it is equally clear that they should be large enough to enable fabrication of an adequate restoration and that self-performed cleaning should be possible under normal conditions.

Particularly in the case of approximal restorations, it is vital, for the service time of the restoration, that the interdental papilla recovers completely after operative treatment and that additional devices for interdental cleaning, if needed, are recommended. Conclusion. In this short communication, the focus of attention has been on the localized nature of caries. The purpose was not only to individualize patient examination and treatment but also to provide information that might help patients to become aware of the individual parts of their mouths so they can give more attention to the vulnerable zones than to the safer zones. To understand, to act, and to get feedback are key in the management of initial and secondary caries.

References

1. Marsh P, Martin M. Oral Microbiology, ed 3. London: Chapman, Hall, 1992.

2. Thylstrup A, Bruun C, Holmen L. In vivo caries models-mechanisms for caries initiation and arrestment. Adv Dent Res 1994;8:144?57.

3. Thylstrup A, Bruun C. The use of dentifrices in the treatment of dental caries. In: Embery G, Ra.lla G (eds). Clinical and Biological Aspects of Dentifrices. Oxford: Oxford University Press, 1992;131?43.

4. Thylstrup A, Fejerskov O. Clinical and pathological features of dental caries. In: Thylstrup A, Fejerskov O (eds). Textbook of Clinical Cariology, ed 2. Copenhagen: Munksgaard, 1994;111?57.

5. Dawes C. An analysis of factors influencing diffusion from dental plaque into a moving film of saliva and the implications for caries. J Dent Res 1989;68: 1483?488.

6.zer L, Thylstrup A. What is known about caries in relation to restorations as a reason for replacement? A review. Adv Dent Res 1995;9:394?02.

7.zer L. The relation between gap size, microbial accumulation and the structural features on natural caries in extracted teeth with Class II amalgam restorations [thesis]. Copenhagen: Department of Cariology and Endodontics, 1997.

8.Black GV. A Work on Operative Dentistry, vol 1, ed 2. Chicago: Medico-Dental, 1914:193?89.

For reprints contact:

Prof Anders Thylstrup

Department of Cariology and Endodontics School of Dentistry, Faculty of Health Sciences

University of Copenhagen

N/Alle 20

DK-2200 Copenhagen N, Denmark

E-mail: ATH@odont.ku.dk

II. When Should We Restore Lesions of Initial Caries and with What Materials?

F. J. T. Burke/N. H. F. Wilson

Correct diagnosis and treatment of caries is central to clinical dental practice, and accordingly, the majority of dental practitioners spend much of their time (1) deciding whether lesions of caries are present, (2) accumulating information for each particular patient to make a judgment on how to treat such lesions, (3) deciding whether (and how) to treat the caries or replace restorations. Such decisions are of particular relevance to developed countries, where caries is under control and where the clinicians dilemma is often restoration versus prevention or the surgical versus nonsurgical approach. The challenge of treating caries may be less philosophical in less developed countries, given that extraction may be the only treatment suggested by the overriding economic and social conditions and given that extraction may be expected by the patient.

Given that approximately 70% of restorations are replacements of existing restorations,1 deciding whether to treat initial caries is of paramount importance, because the cutting of tooth substance and its ultimate restoration commits the tooth to a program of restorative treatment for its lifetime. It is important to remember that the caries process commences as a small subclinical, subsurface demineralization that, following periods of remineralization and demineralization, may progress or arrest.2

It is the aim of this paper to assess how the initial lesion of caries should be treated and, if restoration is indicated, with what material(s).

Diagnosis. Many factors are involved. First, a diagnosis has to be made-is caries present? To recognize initial caries, the tooth surface must be clean and dry. On a smooth surface the initial lesion appears as a white spot, while older lesions absorb stains and become brown. Fiber-optic transillumination and bitewing radiographs may help diagnose proximal caries, and tooth separation techniques have been shown to be of value, albeit with the disadvantage that these techniques require two visits approximately 1 week apart. More recently introduced methods such as electronic caries detectors and variable frequency AC impedance spectroscopy have shown promise.3 Radiographic evidence of caries will underestimate the extent of the histologic lesion.

Second, a decision has to be made on whether the caries is active. The crucial decisions are: Has the caries progressed into dentin, what distance has it traveled into dentin, and is the lesion cavitated? Generally, if the extent of caries is accurately diagnosed, for noncavitated lesions in enamel extending up to one third of the dentin width, remineralization should be attempted, provided that this can be justified in light of the patients caries risk status. Indeed, it has been considered that about 60% of teeth with proximal radiolucencies in the outer half of dentin are likely to be noncavitated.4 While accurate diagnosis is fundamental, the calculation of the patients caries risk status is the second most important consideration. This is not to be confused with caries activity, which may be defined as occurring when a plaque deposition on a tooth surface is causing demineralization.5 Important factors in risk assessment for caries (RAC) are shown in Table 1.

Risk assessment. Risk assessment for caries has been considered a developing science because most risk factors, individually, have low predictive value. However, it could be anticipated from Table 1 that a patient who has low fluoride availability at the time and site of demineralization, high dietary sucrose intake, poor compliance with dietary and oral hygiene advice, who has reduced salivary flow, is an irregular dental attender, has a high mutans streptococci (MS) count, and who already has active caries, would be at high risk for further caries. Reducing the number of risk factors may reduce the risk, but the influence of each factor may vary with each patient.

Table 1

Risk assessment for caries

An expert system for caries risk assessment has been developed and tested by Suddick and Dodds.5 This system considers that the following factors contribute to increasing risk of developing new lesions:

1. Prior caries incidence

2. Frequent intake of sugary foods or snacks

3. Not living in a fluoridated community and not using fluoride dentifrice

4. Age (ie, child, adolescent)

5. Low unstimulated salivary flow

6. High salivary MS count

When the above list is considered, the relevant evaluations, with the possible exception of the quantitative assessment of MS, may be readily available to the dental practitioner in the dental office. Accordingly, it should be possible to identify the at-risk patient with reasonable accuracy, and consequently, to make a decision on the need to restore a lesion. The decision not to restore should signal the commencement of preventive therapy, ultimately followed by the assessment of whether a particular lesion is active or not at a time determined by the RAC. Accompanying the decision to restore is the choice of the most appropriate restorative material.

Restoration of initial caries. The increasing availability of adhesive materials and techniques has improved the capability of the restorative dentist to treat initial caries in a conservative manner. While amalgam continues to be used as a restorative material worldwide, its lack of innate bonding capability makes it generally unsuitable for the restoration of the minimal lesion because the achievement of adequate resistance and retention form for such an amalgam restoration may require removal of considerable amounts of sound tooth substance. The use of materials that may be bonded to tooth substance is therefore encouraged for treatment of initial caries.

For the minimal Class I cavity, the preventive resin restoration, first described in 1978,7 has demonstrated high rates of success8 and would appear to be the treatment of choice for initial caries on an occlusal surface. The use of magnification during the preparation for the preventive resin restoration is highly recommended.

For treatment of the proximal lesion, adhesive materials such as resin composite, used in conjunction with dentin bonding systems, glass-ionomer materials, and compomer, may be appropriate. However, data on the wear resistance of these materials are scant, with the exception of resin composite, which has been rated favorably in a meta-analysis.9 Variants of conventional glass-ionomer cements, such as resin-modified glass-ionomers, metal-modified glass-ionomers, and the recently introduced heavily filled materials, may have improved physical properties, particularly in resisting tensile and bending forces when compared to conventional glass-ionomer cements; but the wear resistance of these materials requires further investigation.10 However, given that a first stage in the restoration of initial caries should be an assessment of the potential occlusal contacts on the restoration, derivatives of conventional glass-ionomer cements may perform adequately in situations where occlusal contact was found to be light or nonexistent. These comments may also apply to compomers.

Glass-ionomer cements may have the benefit of fluoride release, although the effect of this on reduction of secondary caries is presently the subject of debate.11-13 Glass-ionomer and compomer materials may have the benefit of less technique-sensitive placement as compared to resin composite, but more research is needed to fully evaluate the clinical performance of these materials in load-bearing situations. The tunnel preparation, first described by Jinks14 in 1963 as a conservative alternative to the conventional Class II preparation in primary molar teeth, employs a Class I preparation in an occlusal fossa, following which a small round bur is used to prepare a tunnel in a diagonal direction under the marginal ridge and into the caries. The technique originally used sodium silicofluoride cement, but current proponents of the technique use a glass-ionomer cement for the proximal part of the restoration.

Glass-ionomer and compomer materials may be indicated for the following situations: (1) patients who request a tooth-colored restoration and wish to accept a long-term provisional restoration, which may be placed at reduced cost as compared to other tooth-colored restorations such as direct-placement resin composite; (2) nervous, phobic patients in whom the use of materials that are more time-consuming or technique sensitive to place may be precluded; and (3) in situations where an easy-to-place restoration is required, for example, the Atraumatic Restorative Treatment.

Summary. Treatment of initial caries, albeit an everyday occurrence for the dental practitioner, presents considerable demands of patient assessment and diagnosis. Whatever decisions are made?o restore caries or to attempt to arrest its progress?he adoption of a maintenance program is of paramount importance. Patient motivation, in respect to dietary control and satisfactory oral hygiene, is central to a successful outcome, and in the future, practice management programs may include RAC as a diagnostic aid. New methods of caries management are more dynamic than traditional methods and place restoration of the lesion toward the bottom of the list of possible treatments, with the biologic rather than the mechanistic approach being a priority. However, the teaching of RAC in dental schools and the third-party funding of diagnostic tests and diagnosis are also required to reflect the increasing complexity of management of initial caries. If restorative intervention is indicated following diagnosis and RAC, treatment of initial caries should involve a minimal-intervention adhesive technique.

References

1. Mjör IA. Amalgam and composite restorations: Longevity and reasons for replacement. In: Anusavice K (ed). Quality Evaluation of Dental Restorations. Chicago: Quintessence, 1989:61?8.

2. Kidd EAM. The diagnosis and management of the early carious lesion in permanent teeth. Dent Update 1984;11:69?0.

3. Pitts NB. Patient caries status in the context of practical, evidence-based management of the initial caries lesion. J Dent Educ 1997;61:861?65.

4. Anusavice KJ. Efficacy of nonsurgical management of the initial caries lesion. J Dent Educ 1997;61:895?05.

5. Suddick RP, Dodds MWJ. Caries activity estimates and implications: Insights into risk versus activity. J Dent Educ 1997;61:876?83.

6. Brown JP. Indicators for caries management from the patient history. J Dent Educ 1997;61:855?60.

7. Simonsen RJ. Preventive resin restoration. I. Quintessence Int 1978;9(1):69?6.

8. Simonsen RJ. Preventive resin restorations: Three-year results. J Am Dent Assoc 1980;100:535?39.

9. El-Mowafy OM, Lewis DW, Benmergui C, Levinton C. Meta-analysis on long-term clinical performance of posterior composite restorations. J Dent 1994;22:33?3.

10. Naasan MA, Watson TF. Conventional glass ionomers as posterior restorations. A status report for the American Journal of Dentistry. Am J Dent 1998;11:36?5.

11. Randall R, Wilson NHF. Glass ionomers: Systematic review of a secondary caries treatment effect [abstract 378]. J Dent Res 1997;76:1066.

12. Mjör IA. Glass-ionomer cement restorations and secondary caries: A preliminary report. Quintessence Int 1996;27:171?74.

13. Wilson NHF, Burke FJT, Mjs? Reasons for placement and replacement of restorations of direct restorative materials by a selected group of practitioners in the United Kingdom. Quintessence Int 1997;28:245?48.

14. Jinks GM. Fluoride-impregnated cements and their effect on the activity of interproximal caries. J Dent Child 1963;30:87?2.

For reprints contact:

Dr F. J. T. Burke

University of Glasgow Dental School

378 Sauchiehall Street

Glasgow G2 3JZ, United Kingdom

E-mail: f.j.t.burke@ dental.gla.ac.uk

III. When Should We Restore Lesions of Secondary Caries and with What Materials?

Nairn H. F. Wilson/F. J. Trevor Burke

Treatment decisions in respect to secondary (recurrent) caries are complex.1 Variables to be considered in such decisions include signs and symptoms of pulpal disease; the location, extent, and activity of the caries; the qualities of the associated restoration; the prognosis and value of the tooth; the patients caries susceptibility, motivation, and preferences; and esthetic considerations; not to mention the need to manage individual teeth as part of a comprehensive patient-specific oral health strategy. Further confounding variables to be considered encompass cost-benefit and risk-benefit considerations, the influence of the patients pattern of attendance and presentation, and the clinicians knowledge of the patient and the affected restoration.2 Above all else, treatment decisions in respect to secondary caries should not be reduced to the inappropriate application of flawed associations, notably the widely held but hopefully now waning view that all but the smallest of marginal deficiencies and discrete forms of discoloration around restorations are indicative of secondary caries warranting operative intervention.3

Notwithstanding the above, patients and health care agencies expect clinicians to make reliable, consistent decisions about secondary caries as a central element of everyday clinical practice. To this end it remains an urgent priority to describe and validate new suitably sensitive and specific methods of diagnosing secondary caries that can be readily and widely applied in many diverse situations.2 In the meantime, however, clinicians must work with justifiable criteria for treatment. It is suggested that existing knowledge and understanding support the application of certain criteria for the operative management of secondary caries: (1) pain and discomfort attributed to the lesion, (2) frank cavitation with the exposure of dentin, (3) the presence of a marginal gap wide enough to accommodate the tip of a blunt explorer (0.25 to 0.4 mm) with or without marginal and subjacent discoloration, and (4) radiographic or fiber-optic transillumination evidence of caries progression into dentin.1,2 These signs and symptoms are not considered to be mutually exclusive, and decisions to intervene should tend to be made on the basis of more than one significant finding. When findings of marginal deficiencies, discoloration, radiographic progression, etc, are not considered to justify operative intervention, a preventive/reparative approach, rather than a wait and see approach, should be adopted as part of the ongoing care of the patient.5

In situations in which operative intervention is indicated, the treatment options are now many and varied. Increasingly, in contemporary clinical practice, management of secondary caries involves the extension, repair, or resurfacing of the failing restoration rather than total restoration replacement,6 albeit that this poses technical difficulties, given that 80% to 90% of clinically diagnosed secondary caries have been reported to be located gingivally, irrespective of the type of restoration and restorative material employed.6 This shift in procedure is supported by evidence that indicates that in many cases the total restoration replacement approach may be excessively aggressive, with the unnecessary loss of sound tooth tissue and acceleration of the restoration cycle.7 H