What is caries?

It is perhaps unfortunate that the word caries is used to describe both the caries process and the caries lesion. The caries process occurs in the biofilm, a community of microorganisms with a collective physiology that respond to the environment at the site. The biofilm is always metabolically active with minute fluctuations in pH. The result may be nothing to see or there may be a net loss of mineral, leading to a caries lesion that can be seen. Thus, caries the process occurs in the biofilm, and the interaction of the biofilm with the tooth surface may result in the formation of caries the lesion, the consequence or reflection of the process.

Caries control by nonoperative treatments

Wherever a patient can access and disturb the biofilm with a fluoride-containing dentifrice, a filling is not needed. This simple cleaning measure will control caries lesion progression. No fillings are required in the following circumstances:

• White spot lesions including those on occlusal surfaces

• Approximal caries lesions where the lesion is confined to the enamel, or just into dentin on bitewing radiograph. These lesions are unlikely to be cavitated in contemporary populations and should be given a chance to arrest with nonoperative treatments

• Root surface lesions accessible to cleaning, both cavitated and noncavitated

• Recurrent caries lesions adjacent to fillings, uncavitated or cavitated but cleansable, also do not require restorations. Amalgam fillings should not be replaced simply because of ditching and staining around them. Mild ditching, that a periodontal probe will not enter, and staining around a restoration are poor predictors of infected dentin beneath the restoration

• Large cavitated lesions where overhanging enamel has been removed by the dentist, or has fractured away, are also cleansable and can be arrested by cleaning alone. This is a clinical observation. The author does not know of a clinical study that has addressed this in a controlled manner.

Caries control by nonoperative treatments

Wherever a patient can access and disturb the biofilm with a fluoride-containing dentifrice, a filling is not needed. This simple cleaning measure will control caries lesion progression. No fillings are required in the following circumstances:

• White spot lesions including those on occlusal surfaces

• Approximal caries lesions where the lesion is confined to the enamel, or just into dentin on bitewing radiograph. These lesions are unlikely to be cavitated in contemporary populations and should be given a chance to arrest with nonoperative treatments

• Root surface lesions accessible to cleaning, both cavitated and noncavitated

• Recurrent caries lesions adjacent to fillings, uncavitated or cavitated but cleansable, also do not require restorations. Amalgam fillings should not be replaced simply because of ditching and staining around them. Mild ditching, that a periodontal probe will not enter, and staining around a restoration are poor predictors of infected dentin beneath the restoration

• Large cavitated lesions where overhanging enamel has been removed by the dentist, or has fractured away, are also cleansable and can be arrested by cleaning alone. This is a clinical observation. The author does not know of a clinical study that has addressed this in a controlled manner.

When is a filling needed to control caries?

A cavitated lesion, where the patient cannot access the biofilm with a toothbrush, is likely to progress and requires restoration as part of caries lesion control. Put simply, the filling restores the integrity of the tooth surface and allows the patient to clean again. Thus, from a cariological point of view, restoring the tooth is part of plaque control.

Fillings are required in the following circumstances:

• Cavitated occlusal lesions, (codes 3 or higher ICDAS II, see the article by Braga and colleagues elsewhere in this issue for further exploration of this topic); these are likely to be visible in dentine on a bitewing radiograph

• Cavitated approximal lesions; these are clearly into dentin on a bitewing radiograph.

Objectives of restoration from a cariological point of view

Caries removal and restoration should:

• Arrest caries lesion progression

• Provide an adequate base for the restorative material

• Produce a filling that the patient can clean.

The advent of adhesive restorative materials was particularly exciting, because whereas amalgam could be regarded as a plug in a hole, bonded adhesive materials might be capable of improving cavity seal and even giving back some strength to tooth tissue undermined by demineralization. Good cavity seal is thought to be of great import, because it is leakage of bacteria that potentially damages a vital pulp. Supporting tooth tissue undermined by demineralization may allow preparations to be much more conservative, preserving tissue that would have to be removed without the strengthening effect of the adhesive material.

An old argument

Discussions on how much demineralized tissue must be removed before restoration are hardly new. One can go back 150 years to Tomes writing in 1859:

“It is better that a layer of discoloured dentine should be allowed to remain for the protection of the pulp rather than run the risk of sacrificing the tooth.”

Black, however, did not agree for he wrote in 1908

“…it will often be a question of whether or not the pulp will be exposed when all decayed dentin overlaying it is removed….it is better to expose the pulp of a tooth than to leave it covered only with softened dentin.”

This article now focuses on the biologic arguments for and against vigorous caries removal before examining the research evidence on the consequences of incomplete caries removal.

Pulpo–dentinal reactions to dental caries

Dentin is a vital, cellular tissue, containing the cellular processes of the odontoblasts. Thus dentin and pulp must be considered together. The ecological catastrophe in the biofilm, which is the caries disease process, is an assault on this vital tissue that is capable of defending itself. In 1967, Massler distilled current scientific knowledge on this matter including describing his own research performed over a period of 11 years on more than 800 human teeth. His sense of frustration at some of his colleagues jumps from the page:

“It is somewhat disturbing to the biologically orientated clinical teacher to witness the overly focused attention of some dentists upon the operative and restorative phases of dentistry, the ‘drilling and filling’ of teeth, to the neglect of the disease process which caused the lesion (cariology) and the preoperative treatment of the wounded tooth–bone.”

A combination of defense and degenerative reactions characterizes the caries lesion in the pulpo–dentinal complex. Massler’s particular contribution was to point out how essential it is to differentiate active from arrested lesions if one is to make any sense of the biologic reactions. From this, a logical management follows. This seeks to convert an active lesion into an inactive or arrested lesion, thus aiding the defense and healing processes in dentin and pulp before restorative procedures are attempted.

Massler showed that under an active lesion, the dentinal tubules were permeable, whereas under arrested lesions, there were sclerotic zones in the dentin that were impermeable to dyes and isotopes. He pointed out that the plugging of the tubules forms a very effective barrier against further penetration of toxic materials toward the pulp. Thus it would be biologically crazy to damage this area by attacking it with a bur.

Massler described an active lesion as one characterized by an active bacterial colony on the surface (the infected layer) and a very wide layer of demineralized dentin beneath, containing few pathogenic microorganisms (the affected dentin). Massler subsequently pointed out that most lesions found clinically were a combination of active and arrested lesions. At the periphery of the lesion, an active lesion is often spreading under the overhanging enamel, along the enamel–dentin junction, while the central, more easily cleaned area is hard and partially remineralized. Thus, as stated at the beginning of this article, the lesion reflects the activity in the overlying biofilm.

Can and should infected dentin be removed?

If the biofilm at the tooth surface drives the caries lesion, all that must be removed to arrest the lesion is the biofilm. Supposing a clinician disagrees with this interpretation and wishes to remove all the infected dentin, can this be achieved? The answer is to this question is that it is not possible. Shovelton’s review of 1968 showed that softening of dentin generally precedes the organisms responsible for it, but a few organisms will remain even if all the soft dentin is removed.

Conventional caries removal

The most commonly used criterion for the removal of infected dentin is to scoop out all the soft stuff with an excavator. At the enamel–dentin junction, some schools teach the area should be made stain-free as well as hard; others just say hard and ignore the stain. Because staining is an unreliable guide to the level of infection of the dentin, and because a few bacteria will remain whatever approach is adopted, leaving stain seems more conservative.

Over the pulpal surface, stained dentin should remain so long as it is reasonably hard. Provided a tooth is symptomless and responds as vital to pulp testing, vigorous excavation over the pulpal surface seems positively contraindicated once the cavity floor is reasonably firm. The student, however, will find that teachers do not agree on what constitutes reasonably firm. The subjectivity of these assessments led to the development by Fusayama of red dyes to be used clinically to differentiate infected from affected dentin. Infected dentin was shown to be an irreversibly damaged layer, while affected dentin was the inner, remineralizable zone. The same author tentatively suggested the dye staining front coincided with the bacterial invasion front.

Thus, in theory, this dye could be used to identify the carious tissue that is infected with bacteria and thus needs to be excavated. Subsequently, several studies showed the dye does not necessarily discriminate infected tissue and use of the dye could lead to overpreparation of cavities, encouraging removal of excess tissue at the enamel–dentin junction and removal of sclerotic and reparative dentin over the pulpal surface.