Arrested caries and remineralization
Pre-Cavitation, or “white spot” caries lesions, can stop when the balance between demineralization and remineralization is changed in favor of remineralization. This could follow the restriction of sucrose, the application of fluoride, or the loss of an adjacent tooth to a proximal caries. This loss of tooth uncovers the area of stagnation and allows proper oral hygiene procedures. The source of the calcium and phosphate for remineralization of the lesion is saliva and plaque. The caries progresses slowly, and even under natural conditions, about 50% of proximal enamel lesions may show no radiographic evidence of progression for 3 years, showing that a small change may be needed to encourage reversal of the process. Although remineralization can bring the mineral content of an enamel lesion closer to that of the original enamel, the deposition is irregular and disorganized at the single crystal level, and the structure of the original enamel cannot be recovered. Despite this, remineralized lesions that have incorporated fluoride may be less prone to caries attack than intact enamel. Arrested enamel cavities can remain dull and white or more often discolored due to the incorporation of an extrinsic dye. This is known as inactive lesion or brown spot.
Clinical illustration of arrested caries. The dentin is hard, darkly discolored, dry looking and plaque free. [2]
Dentinal caries can also stop. This can follow a preventive intervention or after the collapse of the overlying enamel, exposing the dentin to saliva and cleaning. Dentin under a fully sealed restoration also stops and remineralizes using mineral ions from the pulp. Remineralization of dentin does not produce hard material. Regrowth of crystals is less than that of enamel, and the stopping process includes stopping demineralization on the advancing front, stopping proteolysis of dentin by death or inhibition of bacteria in dentin and deposit of new minerals. Arrested remineralized dentin caries does not give a feel of normal dentin when touched by a probe, but feels leathery, hard and dry, and not soft and wet like active caries.
The increased porosity allows the extrinsic stains to be incorporated into the arrested caries. This, the bacterial products, and the reactions between the acids and the matrix produce a dark brown color for the arrested dentin. If the pulp is viable, stopping the caries allows defense reactions in the pulp to produce peritubular dentin and translucent areas. This process increases the mineral density of the dentin under the lesion to slow its progression in the event of reactivation of the caries. Even the largest caries lesions can stop if they are deprived of sucrose and exposed to saliva. That is why a tooth caries under leaky restorations usually does not arrest. A preventive treatment to stop and remineralize tooth caries has become the paradigm of modern caries management, both for untreated caries and for the insertion of restorations.
Caries of deciduous teeth
In adults, tooth caries usually progresses slowly and a small cavity can take several months to develop and several years to penetrate the enamel. Conversely, tooth caries in children progresses rapidly. Much of this can be explained by poor nutrition, but compared to permanent teeth, deciduous teeth have thinner enamel and dentin, wider, flatter contact areas that produce larger proximal lesions, and wider dentinal tubules that allow earlier bacterial penetration.
Hidden Caries
Hidden caries describes the situation where caries begins in an occlusal fissure and forms a very large lesion, often enough to destroy much of the coronal dentin and involve the pulp, despite the enamel remained clinically reasonably intact and patient had few or no symptoms. The permanent lower molars are the most commonly affected teeth, and the presentation is normally seen in children or young adults.
The absence of superficial changes means that these lesions are often discovered by x-ray, otherwise true extension may not be revealed until the fissure is opened for exploration or to place a preventive resin restoration. However, these lesions are not really hidden and on close examination, and transillumination generally reveals crack staining or subtle discoloration.
Occult caries processes are no different from typical caries. The presentation has only become common all over in the past 20-30 years and may reflect the increase in the use of fluoride. This produces harder, more resilient enamel which is less likely to collapse under occlusal stress, and also more likely to remineralize using calcium and phosphate released from underlying dentinal caries.
Root surface caries
The incidence of root surface caries is increasing as the aging population retains more teeth. After the recession, the gingival margin, the cementum and the root dentine are accessible to plaque. Cementum is easily decalcified and puts very few barriers to infection. Root caries does not develop below the gingival margin in pockets.
Cervical cementum is very skinny and invaded alongside the direction of Sharpey’s fibers. Infection spreads between the lamellae alongside the incremental lines, and underlying dentin is involved almost immediately. The causative microbial flora includes S. mutans, Lactobacilli and several species of Actinomyces. Organisms such as Actinomyces that are unable to cause enamel caries in animal models are capable of inflicting root caries, but the plaque over root surface lesions is very mixed and consists of many putative anaerobic periodontal pathogens too. Once the caries has invaded into dentine, the flora possibly matures to one equal to coronal dentine caries.
Root surface caries causes reactionary dentine on the pulp surface apical to the lesion because of the curvature of the dentinal tubules. This permits slowly progressing lesions to eventually penetrate to the coronal pulp without devitalizing the apical pulp, which turns closed off by way of the reactionary dentine. Once the caries has invaded the dentin, the flora probably matures to become a caries identical to the coronal dentin.
Like enamel caries, root caries has an area of superficial remineralization, but it is porous and bacteria enter the tissues earlier than enamel caries. Root surface caries causes dentin reaction on the pulpal apical surface of the lesion due to the curvature of the dentinal tubules. This allows slowly evolving lesions up to eventually penetrate the coronal pulp without devitalizing the apical pulp, which closes with the reactive dentin. Root surface caries is particularly noticeable in those with dry mouth and in those with poor oral hygiene.
Clinical aspects of caries reactions
The pathology of dental caries may seem complex and largely irrelevant to clinical dentistry, but it forms the basis for effective prevention and restoration strategies. The mechanistic methods of dental restoration used in the 20th century could be applied without reference to the underlying biology of the disease, but modern minimal intervention or minimally invasive dentistry is based entirely on a good understanding of the pathology of caries.
MCQs
Ref:
1. Cawson’s Essentials of Oral Pathology and Oral Medicine 9th Ed.
2. https://www.researchgate.net/publication/26237790/figure/fig16/AS:309986006716420@1450917831485/Clinical-illustration-of-arrested-caries-The-dentin-is-hard-darkly-discolored-dry.png