Caries, lesion formation

Clarkson BH, Hall DL, Heilman JR and Wefel JS (1986) Effect of proteolytic enzymes on caries lesion formation in vitro. J Oral Pathol 15, 423-429. 

Another excellent example was also seen in studies of caries lesion formation. Enamel surfaces remain undissolved in water (pH = 5.5-5.8), in spite of any undersaturation consequently, caries (dissolution) will only be induced at localized sites where the bacteria have produced strong acidic conditions. The mineral crystallites can be stabilized in the fluctuating physiological fluids. Such nanodissolution behavior of nanoparticles may also be significant with regards to solvent stability and reactivity in working nanoparticle-based structures and sensors. 

LeGeros, R.Z., Silverstone, L.M., Daculsi, G. and Kerebel, L.M. (1983) In vitro caries-like lesion formation in F-containing tooth enamel. Journal of Dental Research, 62, 138-144. 

Klont B and Ten Cate JM (1991b) Susceptibility of the collagenous matrix from bovine incisor roots to proteolysis after in vitro lesion formation. Caries Res 25, 46-50. 

Aside from the Maillard reaction, other covalent modifications of amino acids and proteins are possible within the caries lesion, which merit future investigation. For example, certain oral microorganisms excrete y-glutamyl transferases. These enzymes catalyse the formation of cross-links between glutamic acid and lysine residues of proteins. In addition, N-acyl amino acids are present in plaque, which adsorb to mineral surfaces. 

From a mechanistic viewpoint it is reasonable to anticipate an inverse clinical relationship between calculus and caries. Calculus formation is essentially a mineralisation process. The development of a caries lesion is the result of the net demineralisation of tooth enamel by plaque acid. These processes both involve crystalline calcium phosphate phases in contact with liquid, saliva and/or plaque fluid, containing their constituent ions. The oral environment also contains other salivary constituents and bacteria, which either inhibit or promote crystal growth or dissolution. 

Dextrans are reported to interact with salivary proteins, " certain oral bacteria, and phosphate ions. It may be envisaged that each of these components could be actively incorporated into the matrix of a plaque that contains a dextran-gel network. The incorporation of proteins and phosphate ions, moreover, would impart a charge to this network thus, in addition to preventing the free exchange of macromolecules between saliva and the tooth surface, the dextran gel would have the capacity to control the rate at which calcium and phosphate ions leave the tooth surface, and this appears to be an important factor in the formation of natural, subsurface, caries lesions. In contrast, the diffusion of small, neutral molecules into plaque does not appear to be prevented by the dextran gel, as electron micrographs of plaques differentially stained for carbohydrates indicated that both endocellular and exocellular reserve-carbohydrates depleted by bacterial metabolism are rapidly re-formed in the presence of dietary sucrose. ... 

Although chlorhexidine affects virtually all bacteria, gram-positive bacteria are more susceptible than are gram-negative organisms. Furthermore, Streptococcus mutans and Antinomies viscosus seem to be particularly sensitive. S. mutans has been associated with the formation of carious lesions in fissures and on interproximal tooth surfaces and has been identified in large numbers in plaque and saliva samples of subjects with high caries activity. 

One of the limitations of the PRS method is that it is not trivial to determine the incipient lesion depth. This parameter is clinically relevant as it can guide the clinician in the treatment decision-making process. Furthermore, one additional challenge facing the use of the depolarization ratio of the Vi POJ3 mode as a marker for early caries formation is the speed required to complete a full... 

White spot lesions vary from person to person, from tooth to tooth and from surface to surface, as well as with age of the lesion. Their nonstandard nature makes analysis of the lesion incredibly difficult. In order to increase the level of control over experiments with lesions, a standard method of producing in vitro lesions has been used in this study. Many of the features of white spot lesions can be mimicked by in vitro lesions, though no method completely replicates the development of the natural lesion. The lesions produced are usually referred to as caries-like lesions indicating that they are not a natural white spot lesion, but an artificially produced lesion for experimental analysis. These artificial lesions provide invaluable information about the formation, the processes of demineralization and remineralization, and the composition of the lesion at different stages, in addition to being the basis for the understanding of possible treatments of the lesion. 

There are a certain number of options to control and reduce dental caries, the biggest problem in tooth care. The use of fluoride salts is one of the most effective methods to prevent or slow down demineralization that causes tooth decay [16,17]. The action of fluoride can be explained by its antimicrobial action, its interaction with enamel to form a fluorinated hydroxyapatite compound (hydroxyfluorapa-tite or fluorapatite Ca5(P04)3F) by substitution of an hydroxyl ion in hydroxyapatite Ca5(P04)3(0H), which is more resistant to add than enamel on its own, and its repairing effect by formation of calcium and phosphate, which ranineralize the tiny lesions in which caries begin. 

---