Plaque acid production effects

Gillman ES, Hayes JA, Green AK, Duckworth RM Effect of fluoride on plaque acid production using capillary electrophoresis. J Dent Res 2003 82(Spec Iss C) 557. 

Green AK, Horay CP, Lloyd AM, Abraham PJ, Cox TF The effect of a 2% zinc citrate, 0.3% tri-closan dentifrice on plaque acid production following consumption of a snack food. Int Dent J 2003 53 385-390. 

Fluorides. Most woddwide reductions in dental decay can be ascribed to fluoride incorporation into drinking water, dentifrices, and mouth rinses. Numerous mechanisms have been described by which fluoride exerts a beneficial effect. Fluoride either reacts with tooth enamel to reduce its susceptibihty to dissolution in bacterial acids or interferes with the production of acid by bacterial within dental plaque. The multiple modes of action with fluoride may account for its remarkable effectiveness at concentrations far below those necessary with most therapeutic materials. Fluoride release from restorative dental materials foUow the same basic pattern. Fluoride is released in an initial short burst after placement of the material, and decreases rapidly to a low level of constant release. The constant low level release has been postulated to provide tooth protection by incorporation into tooth mineral. 

In general, saliva (as well as plaque fluid) is supersaturated with respect to calcium-phosphate salts, and they prevent tendency to dissolve mineral crystals of teeth. Moreover, precipitation of calcium-phosphate salts that include hydroxyapatite may also occur (remineralization) in early lesions of tooth surfaces injured by acidic bacterial products (i.e., lactic acid). Salivary fluoride facilitates calcium-phosphate precipitation, and such crystals (i.e., fluorapatite) show lower acid solubility properties that lead to an increased caries preventive effect. The increase of pFI (i.e., buffer capacity and pH of saliva, as well as ureolysis in dental plaque) also facilitates crystal precipitation and remineralization (4, 13). 

A closer look at the system, however, does pique curiosity. The initial pH within the chamber is not 7 but 2-3, and the reactions are non-equilibrium, often irreversible, and involve other intermediates that can become important end products. The acidic pH represents a problem in that thiolates, not thiols, are the operative reductants, thus cannot reduce at pH values below their typical i.e. 8-9. This is resolved by proteins, including mfp-6, by sequence specific effects such as flanking cationic groups that reduce the Cys pK, e.g. redox active Cys-59 in DsB-A has a p Tg of 3.5. Several Cys residues in mfp-6 are acidic, but specific p Tg values have yet to be measured. The non-equilibrium, irreversible nature of the oxidation reactions is a particular problem with Dopa and other catechols. Indeed, the chemical fate of catechols in mussel byssus is highly dependent on their location. In the cuticle, the fate of Dopa appears to be tris catecholato-Fe complexes in the thread and plaque core, Dopa forms covalent cross-links after oxidation to quinones, whereas at the plaque-substratum interface, it is some combination of metal chelates and reduced H-bonded Dopa on metal oxide surfaces. The reducing capacity of mfp-6 plays a role in maximizing the latter and is astonishingly sustained, i.e. >21 days. ... 

In summary it may be said that the plaque which forms in the absence of dietary carbohydrate is relatively thin and has a matrix which is almost entirely derived from the salivary proteins. This provides a relatively porous structure into which oxygen and fluids, e.g. saliva, gingival fluid and dietary liquids, can penetrate. It is also permeable to the bacterial products that form within it, which are readily lost by diffusion. It is the thicker gelatinous anaerobic plaque, formed in the presence of dietary sugars, notably sucrose, which excludes saliva and hence is responsible for the formation and accumulation of acid, that is conducive to the development of caries (Chapter 35). The marked effect of plaque thickness on the diffusion times of plaque adds is shown in Figure 34.7. 

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