Caries is a disease of the teeth involving demineralization of enamel by organic acids produced by the fermentation of a dietary carbohydrate by plaque bacteria. This usually occurs on the tooth surface and is influenced by salivary effects. It involves demineralization of the enamel. Usually, the enamel natural surface is exposed to a demineralizing solution that diffuses inward stimulating caries but is not specific to the natural surface. Subsurface demineralization occurs although the surface layer is less pronounced. Demineralization rate increases with distance from the natural surface. Real demineralization occurs due to the acidic pH resulting from the bacterial breakdown of carbohydrates to release acids.
Similarities between Enamel and Calcium Hydroxyapatite
Calcium hydroxyapatite and enamel are made up of calcium and phosphates in their structures. Both have a similar density refractive index and birefringence, the difference in the refractive index for light vibrating parallel and perpendicular to the major crystal axis. Their X- ray and electron diffraction show identical lattice spacing of those lattice planes that are extensive i.e. those perpendicular to the axis of the elongated crystals. High-resolution images of enamel crystallites show details of the lattice that are indistinguishable from pure hydroxyapatite.
Differences in Structure of Calcium Hydroxyapatite and Enamel. Enamel is a cellular tissue made up of 80-90% by volume of crystals of carbonated calcium hydroxyapatite and the remaining 10-20% consists of fluid and organic, usually proteinaceous, material whereas Calcium Hydroxyapatite is a homogeneous inorganic compound made up mainly of apatite.
The enamel calcium hydroxyapatite crystals are mainly arranged with their long (c-) axes that parallel the long axes of the prisms. At the periphery of each prism, the crystals deviate from this orientation, producing an interface between prisms where there tends to be more intercrystalline space. (Robinson 2000). The spaces offer diffusion pathways within the tissue while natural crystal habits of apatite forms crystals more extensive in the b-axis than the C-axis direction. The crystals density throughout the enamel is not uniform. It decreases from the tissue surface toward the dentin, while porosity, fluid, and the organic material increase in this direction. However, in specific locations the porosity, protein, and crystal distribution are quite complex but in calcium hydroxyapatite crystal densities throughout its structure are uniform, and there is a random decrease in density.
The mineral component of enamel is a substituted calcium hydroxyapatite, the stoichiometric formula for hydroxyapatite being Ca10(PO4)6(OH)2. The structure is easily appreciated when the arrangement of ions around the central hydroxyl column is considered. It extends in the c-axis direction through the long axes of the crystals. Enamel exhibits many variations such as missing ions, particularly calcium and stoichiometric apatite but instead contains extraneous ions such as carbonate, fluoride, sodium, magnesium among others substitute either calcium or hydroxyl. These have a profound effect on the behaviour of apatite, concerning its solubility at low pH. The solubility product for enamel mineral is higher than that calculated for stoichiometric apatite.
Birefringence data are not identical, and the chemical data shows a non-stoichiometric ratio of Ca:P. Hydroxyapatite is ca10(po4)6 2H2o giving a ca:p ratio of 1.66 measured ratios are ~1.61. Biological apatite is nonstoichiometric for example, Ca/P molar ratio is less than 1.67 minor and trace inorganic elements are present with biological apatite that may be either substituent in the apatite lattice adsorbed on the apatite crystal surface or both or present in nonapathic phases.
Enamel apatite crystals are tightly bound to enamelin while the amelogenin component decreases with maturation.
Why Enamel Dissolves.The concept of critical pH plays a key role in the dissolution of minerals. It is applicable only to solutions that are in contact with a particular mineral. For this case, we have enamel in contact with saliva and plaque fluid. The fluids, for instance, are normally supersaturated with respect to enamel because the pH is higher than the critical pH and; therefore, our teeth do not dissolve in our saliva or under plaque. Conversely, if the pH of the plaque fluid is less than the critical pH, the solution is unsaturated, and enamel will tend to dissolve until the solution becomes saturated.
Enamel dissolves due to the lower crystal packing, permitting easier diffusion of acids and protons into the tissue and mineral ions out of it. (Dawes 2003). Subsequent dissolution then appears to track across the prisms at the cross striations, followed by dissolution of the prism bodies.
Enamel is neither structurally nor chemically homogeneous. Both structural and chemical gradients exist within the tissue, often extending from the surface to the dentin structure of enamel, especially its microporosity, no doubt affects the diffusion of materials boundaries. Changes in pore structure, which will increase as the mineral is removed and this will enhance entry and egress of materials. By the fact, that fluid within caries lesions was saturated with respect to hydroxyapatite.
Fluoride lowers lattice energy and effectively stabilize the crystal structure resulting in lowered solubility product. This renders it more difficult to dissolve fluoridated crystals and to make it easier to redeposit fluoridated crystals. This is of crucial importance to the role of fluoride in dental caries prevention/control.
Due to a poorer fit of carbonate in the lattice, it generates a less stable and more acid-soluble apatite phase. In combination with ion valences, carbonate a major reason for the much higher solubility product of enamel as compared to that of stoichiometric apatite.
Impurities such as Carbonate, magnesium and fluoride also influence the solubility of enamel. They have a positive synergistic effect and incorporation of both in hydroxyapatite lattice increase the acid solubility of enamel. Since they have an effect on the primary component of enamel, it thus leaves it unspared.
Real and in vitro demineralization. This occurs in the subsurface, and it doesnt progress into the dentine while in vitro demineralization attacks the tooth from any direction of exposure and there is no remineralization. During the real demineralization process, the enamel apatite crystals are dissolved by acid produced by bacteria. Real demineralization is controlled by surface processes rather than by diffusion of ions from the crystalline surfaces, and the rate is dependent on the sum of activities of the acidic species and the degree of saturation of the saliva.
Several calcium phosphates phases may precipitate during this process DCPD, OCP, (F, OH) apatite Beta TCMP. In vitro, the demineralizing agent is an acidified gel or organic acid buffer solution. Demineralization rate in vitro and its pattern is more influenced by the degree of saturation on hydroxyapatite than the pH of the demineralizing solution. The formation of DCPD on enamel surfaces in vitro results from the dissolution of enamel apatite in an acid solution containing phosphate and precipitation of DCPD the stable calcium phosphate phase under favorable conditions.
It has been suggested that diffusion might be rate-limiting. On the other hand, in vitro studies showing a nearly linear increase of lesion depth with time contradicted this view. By the fact that pore reduction, by deposition in positively birefringent and surface zones, together with the chemical changes described below, is likely to hinder demineralization. (Robinson 2000).
Analysis of these kinds of data suggests that demineralization may, to a large extent, be surface-controlled. The large variations in enamel composition, including local concentration gradients of specific mineral ions as well as endogenous organic material and organic acids. A discussion on chemical changes during caries, we have therefore endeavoured to relate the micro-architectural to the chemical structures of both intact tissue and the caries lesion. In dental caries, the mineral content of the surface zone is similar to that of sound enamel. It is either protected from dissolution compared to underlying tissue or that it forms/reforms during the caries process.
It occurs by redepositing of material dissolved from deeper layers, with perhaps some contribution from plaque fluid. This renders it less susceptible to acid attack. It contains, for example, high concentrations of fluoride, which stabilizes apatite and low carbonate (Robinson et al., 1983) and low magnesium, which have a reverse, destabilizing effect. This would favor a lower acid solubility for the mineral in this tissue region, effectively protecting it from dissolution.
It is stated that:
Penetration of acid into the deeper, more soluble, layers would remove interior mineral in preference to the outer tissue. The outer tissue could then continue to accumulate fluoride and become even more acid-resistant. Moving inward away from the surface, gradients of fluoride decrease, while carbonate and magnesium gradients increase together with increasing porosity. As the caries process tracks inward toward the dentin, the chemistry of dissolution will change, with the tissue showing evidence of increasing solubility. (Robinson et al., 1983)
Chemical gradients were interpreted as gradients in enamel solubility product, likely rate constants for enamel dissolution and increase in porosity. In a consideration of porosity, penetration of undissociated acid and protons into the complex micro-particulate enamel microstructure may also play a role in generating subsurface demineralization. The close packing of crystals during dissolution may affect the kinetics of mineral loss, leading to the formation of a surface zone. Dissolution of ions into the very small intercrystalline volume will tend to produce high solution concentrations and thus generate a high concentration gradient away from the lesion front. (Dawes 2003).
The development progression and reversal of dental caries are influenced by the degree of saturation of saliva on the different Ca-P phases and the presence of inhibitors. The degree of saliva saturation on the different types of Ca-P is affected by changes in the salivary pH and flow rate. The presence of inhibitors in saliva such us acidic proteins and pyrophosphates prevents spontaneous precipitation of Ca-P from supersaturated saliva under normal conditions.
In vitro, there is a preferential formation of CO3-substituted apatite (type B) when calcium containing solution was added to unstimulated human saliva at pH 7.
The water component plays a role the dissolution and remineralization of biological apatites by allowing the diffusion and storage of ions involved in these process. A small amount of HA dissolves, releasing calcium, phosphate and hydroxyl ions. This process continues until the water is saturated on HA. (Dawes 2003). At that point, the rate of the forward reaction (mineral dissolution) is equal to the rate of the backward reaction (mineral precipitation).
In an experiment
When a tooth is placed in distilled water of pH 7, a small amount will slowly dissolve (about 30 mg in 1 L of water).2 The Ip for HA in distilled water is zero, because although the water contains hydroxyl ions, it contains no...
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