Dental Caries Dental caries is a sugar-dependent infectious disease.1 Acid is produced as a by-product of the metabolism of dietary carbohydrate by plaque bacteria, which results in a drop in pH at the tooth surface. In response, calcium and phosphate ions diffuse out of enamel, resulting in demineralization. This process is reversed when the pH rises again. Caries is ∴ a dynamic process characterized by episodic demineralization and remineralization occurring over time. If destruction predominates, disintegration of the mineral component will occur, leading to cavitation. Enamel caries The initial lesion is visible as a white spot. This appearance is due to demineralization of the prisms in a subsurface layer, with the surface enamel remaining more mineralized. With continued acid attack the surface changes from being smooth to rough, and may become stained. As the lesion progresses, pitting and eventually cavitation occur. The carious process favors repair, as remineralized enamel concentrates fluoride and has larger crystals, with a ↓ surface area. Fissure caries often starts as two white spot lesions on opposing walls, which coalesce. Dentin caries comprises demineralization followed by bacterial invasion, but differs from enamel caries in the production of secondary dentine and the proximity of the pulp. Once bacteria reach the dentinoenamel junction (DEJ), lateral spread occurs, undermining the overlying enamel. Rate of progression of caries Although it has been suggested that the mean time that lesions remain confined radiographically to the enamel is 3–4 years,2 there is a great deal of individual variation and lesions may even regress.3 The rate of progression through dentine is unknown; however, it is likely to be faster than through enamel. Progression of fissure caries is usually rapid due to the morphology of the area. Arrested caries Under favorable conditions a lesion may become inactive and even regress. Clinically, arrested dentine caries has a hard or leathery consistency and is darker in color than soft, yellow active decay. Arrested enamel caries can be stained dark brown. Susceptible sites The sites on a tooth that are particularly prone to decay are those where plaque accumulation can occur unhindered, e.g., interproximal enamel surfaces, cervical margins, and pits and fissures. Host factors, e.g., the volume and composition of the saliva, can also affect susceptibility. Saliva and caries Saliva acts as an intraoral antacid, due to its alkali pH at high flow-rates and buffering capacity. In addition, saliva ↓ plaque accumulation and aids clearance of foodstuffs; acts as a reservoir of calcium, phosphate, and fluoride ions, thereby favoring remineralization; and has an antibacterial action because of its IgA, lysozyme, lactoferritin, and lactoperoxidase content. An appreciation of the importance of saliva can be gained by examining a patient with a dry mouth. Some manufacturers are now promoting the remineralizing potential of chewing gum, effected by an increase in salivary production. Chewing sugar-free gum (Xylitol) regularly after meals does appear to ↓ caries, but the reduction is small.1 Root caries With gingival recession, root dentine is exposed to carious attack. Rx requires first control of the etiological factors, and for most patients this involves dietary advice and OHI. Topical fluoride may aid remineralization and prevent new lesions from developing. However, active lesions will require restoration with glass ionomer (GI) cement (see section).
Posted on: Fri, 21 Jun 2013 03:58:28 +0000
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