Tooth hypersensitivity is a common problem which affects about 40 million adults in the United States, 10 million of which can be considered chronically affected (Kanapka, Dent. Clin. North Am., 34:54 (1990)). It is estimated that some 14% of adults in the U.S. have at least one or more sensitive teeth. The teeth may be sensitive to cold, heat, air or sugary foods.
The incidence of tooth hypersensitivity increases with age. The increased incidence is believed to be related to the general increase in exposed root surfaces of teeth as a result of periodontal disease, tooth brush abrasion or cyclic loading fatigue of the thin enamel near the dento-enamel junction.
The currently accepted theory for tooth hypersensitivity is called the hydrodynamic theory. This theory is based on the belief that open dentinal tubules allow fluid flow through the tubules. This flow excites the nerve endings in the dental pulp. Clinical replicas of sensitive teeth viewed in the scanning electron microscope (SEM) reveal varying numbers of open or partially open dentinal tubules.
Tubules generally are not seen at the tooth root surface because of the cementum covering the tooth root, or because of a smear layer of dentinal debris 2-5 microns in thickness that covers the tooth surface and masks the tubules. When the smear layer is present on the dentin, the fluid flow that can occur through the dentin is only a few percent of that possible following acid removal of the smear layer, which "opens" or uncovers the tubules.
There is a growing body of evidence that occlusion of the dentinal tubules of a sensitive tooth, whether by resin infiltration, varnish coat or more recently by crystallite precipitation, results in reduction or elimination of the hypersensitivity. The duration of relief, however, is highly variable. Hypersensitivity usually reappears because of tooth brush abrasion, presence of acid challenges in the mouth or aging of the coating material.
Various agents have been used to reduce tooth hypersensitivity, including potassium nitrate (Hodosh, J. Am. Dent. Assoc., 88:831 (1974), which is the active ingredient in the dentifrice AQUAFRESH SENSITIVE.TM.; strontium chloride, which is the active ingredient in the dentifrice SENSODYNE.TM.; and other reagents, such as sodium fluoride, which dentists may apply directly to the dentin to reduce sensitivity.
A two-step procedure involving application of a calcium nitrate solution and a potassium phosphate solution to the tooth has been found to produce numerous calcium phosphate crystals (Kaminske et al, J. Dent. Res., 69:68 (1990)).
Increasing concentrations of oxalic acid in the food bolus derived from dietary sources, up to 1.14 g/l, have also been found to yield precipitation of a deposit at the tooth surface. A maximal response was found to be obtained at a level of 0.1% (w/v) oxalic acid equivalents. Greater levels of oxalic acid did not yield greater protection of teeth. It has been postulated that the deposited material is calcium oxalate, resulting from interaction of the oxalic acid with calcium in the saliva (Gortner et al, J. Nutr., 32:121 (1946)). However, it is well-known that the level of calcium in saliva is very low, and thus the proposed mechanism may be incorrect.
Solutions of alkali metal or ammonium oxalates have also been used to reduce tooth hypersensitivity. The low pH of these solutions is believed to mobilize calcium and phosphate from the hard tissues (U.S. Pat. No. 4,057,621).
In addition, a 3.0% (w/v) monohydrogen monopotassium oxalate solution has been found to occlude dentinal tubules (Pashley et al, Arch. Oral. Biol., 23:1127 (1978)).
A variety of protein precipitants and tubule occluding agents have been evaluated by measuring the effect thereof on hydraulic conductance of human dentin. Potassium oxalate has been reported to yield a large reduction in conductance (Greenhill et al, J. Dent. Res., 60:686 (1981)).
Over-the-counter desensitizing dentifrices and an experimental 2.0% (w/v) potassium oxalate dentifrice for tubule occlusion have been found to be superior to the other known formulations (Pashley et al, J. Periodont., 55:522 (1984)). Potassium oxalate is thought to react with the smear layer, and is believed to reduce the permeability thereof, as well as increase resistance of the layer to acid attack. It is believed that the crystals produced when employing potassium oxalate are calcium oxalate crystals (Pashley et al, Arch. Oral Biol., 30:731 (1985)).
A two-component kit comprising a 1.0-30% (w/v) neutral oxalate solution, such as dipotassium oxalate, and a 0.5-3.0% (w/v) acidic oxalate solution, such as monopotassium-monohydrogen oxalate, has been described. It is asserted that the neutral oxalate forms large crystals all over the dentinal surface, and the acidic oxalate forms smaller crystals around and about the previously formed larger crystals, so as to form a combined uniform layer of microscopic crystals (U.S. Pat. No. 4,538,990).
The benefits of two potassium oxalate formulations, one comprising 30% (w/v) dipotassium oxalate, and the other 3.0% (w/v) monohydrogen-monopotassium oxalate have been evaluated. The results were varied, purportedly due to variations in the size and number of crystals generated by the two solutions, which in turn may depend on various factors, such as the pH of the solutions. The rate of crystal formation also was believed to be relevant. For example, the 30% (w/v) dipotassium oxalate reacts with ionized calcium in the dentinal fluid, and the acidic 3.0% (w/v) monohydrogen-monopotassium oxalate solution is reported to generate an extremely high local calcium ion concentration by etching the tooth, which results in greatly accelerated formation of abundant crystals to yield the desired reduction in hypersensitivity (Muzzin et al, J. Periodont., 60:151 (1989)). However, there has been no explanation as to the source of ionized calcium within the dentinal fluid; further, no definition has been provided as to what is meant by the phrase "extremely high local calcium ion concentration". In this context, it should be noted that dissolution of dentinal hydroxyapatite by the acidic oxalate solution, which releases Ca.sup.2+ ions, is limited by the amount of solution present on the dentin and by the pH at the dentin/solution interface. As the pH rises due to reaction between the acidic solution and the hydroxyapatite, the rate of hydroxyapatite dissolution will decrease, and there is an accompanying reduction in Ca.sup.2+ ion release. These physicochemical considerations clearly limit the amount of crystal formation on the dentin surface.
A commercial product, PROTECT.TM. (J. O. Butler Co., Chicago, Ill.) that is marketed for occluding dentinal tubules, utilizes an acidic potassium oxalate solution which is applied to the tooth surface. However, PROTECT.TM. has limited effectiveness as it leaves many tubules open (Kaminske et al, J. Dent. Res., 69:68 (1990)).
Accordingly, there has still been a need in the art to develop an effective treatment which will result is occlusion of substantially all of the tubules.
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