This article provides a state-of-the-art overview of clinically relevant evidence regarding effective, noninvasive management strategies to prevent, arrest, and remineralize caries lesions. With the rapidly increasing knowledge about oral biofilms and the process of caries in itself, the profession is embarking on new strategies. This is an exciting time, with several promising new agents and novel treatment modalities at the horizon to prevent and manage caries lesions. Some are already available in clinical practice. Studies, however, have yet to show conclusive evidence of clinical efficacy. None have shown to be more effective than fluoride and protection by sealant.
Traditional management of a caries lesion primarily was focused on operative treatment. This often started an irreversible, restorative cycle, leading to several replacements over time with increasing restoration size and every so often iatrogenic damage. The last two decades have seen a growing insight about the process of lesion development and its causal and continual factors. This awareness changed the paradigm of Black’s “extension for prevention” into the motto “extension of prevention”. The effect of caries disease in the tissue sets off/prompts lesion formation. Once the first clinically visible signs have been discovered, the detection should be followed by diagnosis of severity and extent of the lesion and whether it is an active process or not. Presence of tissue damage alone is not sufficient for management decisions as the present lesion might be rather a scar than a sign of current activity.
Fortunately, recognition of caries as a multifactorial disease process involving the biofilm has received more and more attention. The first step in contemporary caries management is focused on the various options to cope with the locally out-of-balance oral biofilm and stop progression of the disease (see the articles by Philip D. Marsh; and Svante Twetman elsewhere in this issue for further exploration of this topic). After the caries process has been halted, causative factors need to be evaluated and individual treatment regimens installed that will prevent new occurrence of the caries disease. Caries lesions develop by dissolution of minerals from the tooth tissues, leaving behind a more porous structure. Therapies that focus on rebalancing the interplay between demineralization and remineralization (see the article by Young and Featherstone elsewhere in this issue for further exploration of this topic), tipping the balance toward an overriding mineral uptake in the tissue, not only result in repair of the damage done, but concurrently assist in preventing new lesions of forming.
This article focuses on the repair of affected hard tooth tissues using noninvasive management strategies. Such an approach takes into account the dynamic nature of the caries disease process (see the article by Hara and Zero elsewhere in this issue for further exploration of this topic). For successful noninvasive management, the lesions have to be detected early on, so they can be managed in a nonoperative way. This type of early caries management requires special clinical attention, detection, and diagnostic skills (see the article by Braga and colleagues elsewhere in this issue for further exploration of this topic). It is time-consuming, but reestablishing the integrity of the tooth surface early on in the caries process will bring great rewards for patients. Their tooth structures will be preserved, and costly, extensive restorative treatments in the future prevented.
The disease—a slow-paced process
The equilibrium that exists between plaque fluids and apatite crystals at the tooth surface is constantly overwhelmed by pH fluctuations at the plaque–tooth interface. In a healthy mouth, this is a normal physiologic process that takes place at a subclinical level numerous times a day. During periods of neutral pH, lost minerals are replaced by calcium and phosphates from saliva, forming a hard outer surface. A continual ion exchange, in both directions across the tooth surface interface, attempts to reestablish the mineral balance. The caries lesion is a result of loss of mineral from the dental tissues. Caries is not a disease process that develops rapidly, but it takes time for the effect (ie, lesion) to develop. Initial lesions undergo a constant daily battle between progression and regression. It may take 3 to 4 years to develop a cavitation. Not all initial lesions, however, develop to cavities at the same rate. The progression rates are not the same for each site, and they are independent of the patient’s decayed, missing or filled surfaces (DMFS).
In general, there is ample time—between lesion initiation in enamel and subsequent progression into dentin involvement—to interrupt this process using preventive and repair strategies. Preventive management strategies can effectively arrest and even completely reverse the caries process. It is therefore important to detect lesions in their early stage. Reasons for slower pace of lesion progression in the last three decades are not clearly defined, but increased use of fluoride may have attributed to lower progression rates of fissure caries for example. Some lesions may have become arrested. This will lead to clinically undetected carious dentin at the base of occlusal fissures. This phenomenon, reported since 1931, received renewed attention in the 1990s. When initial lesions are taken into account, however, the percentage of clinically undetected carious dentin lesions dropped dramatically to less than 2% and were in the same order of magnitude as pre-eruptive lesions.
A critical period for rapid caries development occurs when a tooth erupts in the oral environment and the enamel is not yet fully matured. Continuous exposure to saliva promotes full maturation. This maturation and the continuing demineralization/remineralization processes lead to a more acid-resistant outer enamel. The time during eruption and immediately after is the most vulnerable period for caries development. Caries initiation and progression rates of permanent molars are highest during this early posteruptive period. Additional fluoride during the first few years after eruption will encourage full maturation of the enamel. To counteract plaque stagnation and provide fluoride ions, it is crucially important to teach parents to brush erupting surfaces of first molars with special attention using fluoride toothpaste.
Another exception to the usually slow pace of lesion development occurs in high-risk patients (eg, those with compromised salivary flow). Patients who suffer from hyposalivation or a reduced quality of saliva are missing the protective clearance and buffering effects of saliva (see the article by Hara and Zero elsewhere in this issue for further exploration of this topic). This may lead to rapid and rampant lesion development. The calcium and phosphates from the saliva are the primary source for the recrystallizing minerals and thus for remineralization. Therefore, also in healthy individuals, stimulation of salivary flow by daily use of sugar-free chewing gum assists in caries management.
Changes in tooth structure
Teeth are composed of calcium phosphate minerals (hydroxyapatite) that dissolve when the pH drops below the critical value. The drop in pH necessary for demineralization in cementum and dentin (pH 6.2 to 6.7) is less than that required for enamel (pH 5.4 to 5.5). Therefore, given the proper environment, both the initiation and progression of root surface caries lesions will occur more rapidly than in an enamel surface. As the environmental pH recovers, the minerals precipitate on the remaining mineral crystals. Remineralization is slower than the dissolution process, but is still able to eliminate the damage done to tooth tissues by demineralization. If no or limited remineralization takes place, however, the demineralization will proceed, and a caries lesion will develop.
The dental caries process starts in the outer enamel and, as it proceeds, also involves and demineralizes dentin to a significant depth, even when the outer layer is still noncavitated. Low levels of fluoride are adequate for enamel remineralization but insufficient to facilitate dentin remineralization. The effect of the caries process in dentin is similar to that in enamel, except that dentin demineralizes at a higher pH and proceeds about twice as fast, because dentin has only half the mineral content of enamel. Even very deep lesions, extending through enamel into dentin, can be remineralized. Although this is a slow process, it enlarges the window for noninvasive management and postponement of operative intervention for lesions that have passed the enamel–dentino junction.
Both initiation and progression of root surface caries lesions occur more rapidly in dentin than in coronal enamel. Surface irregularities, collagen degradation, longer periods of acid challenge, and lower saliva clearance all aggravate the process of root caries. Taking the multitude of changes associated with aging into account, and the fact that root dentin is more prone to acid dissolution, it will be obvious that this will lead to differences in management strategy. Combating root caries may need greater fervor.