Dental caries or tooth decay is a disease that results in the destruction of tooth structure. It arises from an overgrowth of specific bacteria that can metabolize fermentable carbohydrates and generate acids as waste products of their metabolism. Streptococci mutans and Lactobacillus are the two principal species of bacteria involved in dental caries and are found in the plaque biofilm on the tooth surface [i] [ii] [iii]. When these bacteria produce acids, the acids diffuse into tooth enamel, cementum or dentin and dissolve or partially dissolve the mineral from crystals below the surface of the tooth. If the mineral dissolution is not halted or reversed, the early subsurface lesion becomes a “cavity”.
The tooth surface undergoes demineralization (breakdown) and remineralization continuously, with some reversibility. When exposed to acids, the hydroxyapatite crystals dissolve to release calcium and phosphate into the solution between the crystals. These ions diffuse out of the tooth leading to the formation of the initial carious lesion. The reversal of this process is remineralization. Remineralization will occur if the acid in the plaque is buffered by saliva, allowing calcium and phosphate present primarily in saliva to flow back into the tooth and form new mineral on the partially dissolved subsurface crystal remnants[iv]. The new “veneer” on the surface of the crystal is much more resistant to subsequent acid attack, especially if it is formed in the presence of sufficient fluoride. The balance between demineralization and remineralization is determined by a number of factors. Featherstone describes this as the “Caries Balance”, or the balance between protective and pathological factors [v].
These early lesions (both enamel and root surface) typically have an intact hard outer surface with subsurface demineralization. The tooth surface remains intact because remineralization occurs preferentially at the surface due to increased levels of calcium and phosphate ions. The clinical characteristics of these early carious lesions include:
- Loss of normal translucency of the enamel resulting in a chalky white appearance particularly when dehydrated,
- Fragile surface layer susceptible to damage from probing, particularly in the pits and fissures,
- Increased porosity, particularly of the subsurface, with increased potential for uptake of stain,
- Reduced density of the subsurface, which may be detectable radiographically (depending upon mineral loss and location) or with transillumination (depending upon location and loss of mineral),
- Potential for remineralization with increased resistance to further acid challenge particularly with the use of enhanced remineralization treatments[viii].
[i] Van Houte, J., “Bacterial specificity in the etiology of dental caries”, Int. Dent. J., 1980; 30: 305 – 326
[ii] Van Houte, J., “Role of Microorganism in the caries etiology”, J. Dent. Res., 1994; 73: 672- 681
[iii] Featherstone, J. D. B., “The Caries Balance: Contributing Factors and Early Detection”, CDA Journal, 2003; 13 (2): 129 – 133
[iv] Melberg, J. R., “Remineralization: A status report for the American Journal of Dentistry, Part 1, Am J. Dent., 1988; 1 (1): 39 – 43
[v] Featherstone, J. D. B., “The Science and Practice of Caries Prevention”, JADA, 2000; 131: 887 – 899
[viii] Mount, G. J., “Defining, Classifying, and Placing Incipient Caries Lesions in Perspective”, Dent Clin N. Am, 2005, Volume 49, pages 701 – 723
