Treatment of Dentin Hypersensitivity

Dentinal hypersensitivity is exemplified by brief, sharp, well-localized pain in response to thermal, evaporative, tactile, osmotic, or chemical stimuli that cannot be ascribed to any other form of dental defect or pathology. Pulpal pain is usually more prolonged, dull, aching, and poorly localized and lasts longer than the applied stimulus. Up to 30% of adults have dentinal hypersensitivity at some time. Current techniques for treatment may be only transient in nature and results are not always predictable. Two methods of treatment of dentin hypersensitivity are tubular occlusion and blockage of nerve activity. A differential diagnosis needs to be accomplished before any treatment.

Dentin hypersensitivity is exemplified by brief, sharp, well-localized pain in response to thermal, evaporative, tactile, osmotic, or chemical stimuli that cannot be ascribed to any other form of dental defect or pathology. Pulpal pain is usually more prolonged, dull, aching, and poorly localized and usually lasts longer than the applied stimulus. Up to 30% of adults have dentin hypersensitivity at some period of their lives. Current techniques for treatment may be only transient in nature and results are not always predictable. Two chief methods of treatment of dentin hypersensitivity are tubular occlusion and blockage of nerve activity. A differential diagnosis needs to be accomplished before any treatment because many symptoms are common to a variety of causes. Items to be considered: the pain—sharp, dull, or throbbing; how many teeth and their location; which part of the tooth elicits the pain; and the intensity of the pain. Clinical and radiographic examination is necessary to elucidate the cause. The following questions need to be asked: Can the pain be localized to one tooth or area of the tooth? Is the area sensitive to a moderate flow of air from an air water syringe? Is the tooth sensitive to percussion? Is there sensitivity to biting pressure or on release? What is the extent of the pain after the stimuli is removed? Do radiographs demonstrate caries or periapical pathology? Is the dentin exposed as a result of recession and are there any cracked cusps, open margins, or occlusal hyperfunction?

Mechanism

There are regional differences in dentin sensitivity. Freshly exposed dentin in the coronal part of the tooth is more sensitive than cervical dentin. This may be due to the higher conduction velocity or structural differences in dentinal innervations and in the dentin structure itself. Hypersensitive dentin, however, is found most often in the cervical area. Chronic dentin exposure may affect mineralization and inflammatory reactions in the pulp. The sensitivity of dentin has a direct correlation with the size and patency of the dentinal tubules. Absi and colleagues discovered that hypersensitive teeth have an increased number of patent tubules and wider tubules than those of nonsensitive teeth. Even if the tubules are covered by a smear layer or pellicle, however, the teeth can be sensitive due to pulpal inflammation. Also, tubules that are patent at the surface may not be patent down to the pulp. Absi and colleagues demonstrated that the tubules may not be patent all the way. The tubules may be occluded by plaque, smeared dentin in the periphery, peritubular dentin, and closer to the pulp by secondary or reparative dentin. Intratubular is formed by a hypercalcified lining in the tubule that increases in width with age resulting in sclerotic dentin. Weber found physiologic sclerosis is greatest in the region equidistant from the dentin-enamel junction and the exterior of the pulp. Even when sclerotic dentin is present, less than 50% of the tubules are blocked.

The popular assumption has been that tubular occlusion is greater in areas of attrition or abrasion. Mendis and Darling found, however, peritubular dentin to be only 20% thicker in these areas compared with areas than are not subject to attrition. In addition, increased peritubular dentin formation may not eradicate dentin permeability but only reduce it. The classic hydrodynamic theory has proposed fluid movement in the tubules and increased nerve excitability as the mechanism eliciting dental sensitivity. A variety of stimuli can result in pressure change traverse the dentin, resulting in stimulation of intradental nerves. The reaction that occurs is proportional to the pressure and rate of fluid flow. Surprisingly, cold, which actually causes fluid movement away from the pulp, creates a swifter and more profound response than heat, which causes an inward flow. It is believed that pressure traverse the dentin results in activation of a mechanoreceptor response. The odontoblastic processes were thought to contribute to dentin sensitivity by a mechanism known as the odontoblast transducer mechanism. Because odontoblasts only protrude a short distance into the dentin tubules, however, they cannot contribute directly to stimulus transmission.

Causes

There are many varieties of potential causes for dentin sensitivity. There is no principal cause. The loss of enamel and removal of cementum from the root with exposure of dentin, however, is a major contributing factor. Causes also include gingival recession due to root prominence and thin overlying mucosa, dehiscences and fenestrations, frenum pulls, and orthodontic movement, which causes a root to be moved outside its alveolar housing. Loss of enamel may be a consequence of attrition, erosion, abrasion, and abfraction. The loss of enamel, however, is usually a combination of two or more of these factors. Attrition is the wear that occurs when teeth are in direct contact and is usually associated with occlusal function. Excessive or parafunctional habits, such as bruxism, may result in extreme pathologic wear and increased sensitivity. Abrasion is the tooth wear caused by objects other than other teeth. Toothbrush/toothpaste abrasion is an example. Toothbrushing by itself, however, has minimal effect on enamel and even with toothpaste the effect is minimal on both enamel and dentin. The combination of toothbrushing and erosive agents results in loss of tooth structure. West and colleagues found, however, that toothbrushing with toothpaste was able to erode or abrade dentin in various amounts and cause tubule opening. Brushing dentin that has a smear layer with silica-based toothpaste opened the most tubules. Abrasion may cause gingival recession and, as a result of the recession, the softer root surface is exposed. Erosion is the loss of tooth structure by acids that are not of bacterial origin. Erosion can be caused by extrinsic or intrinsic acids. Intrinsic acid is a consequence of exposure to gastric acid (acid regurgitation or gastroesophogeal reflux disease) causing dissolution of teeth by the acid (periomolysis). Extrinsic acid can be a result of dietary or environmental factors. A variety of foods and drinks that may contain acid can contribute to the erosion by demineralization and chelation of calcium. Industrial erosion can occur by exposure to acid vapors produced in a battery factory and wine tasters. Swimmers are exposed to acid in pools maintained at a low pH of 2.7. The loss of tooth structure by erosion is an active process that consists of episodes of demineralization and remineralization. Acidified fluoride gel demonstrated a protective effect against abrasion in eroded enamel but fluoride does not seem to reduce dental erosion. A variety of studies have indicated the possibility of iron reducing enamel demineralization, but potential adverse problems, such as tooth staining, may prohibit its use. A recent study demonstrated iron in a gel increased enamel resistance to acids and helped minimize dental erosion.

Causes

There are many varieties of potential causes for dentin sensitivity. There is no principal cause. The loss of enamel and removal of cementum from the root with exposure of dentin, however, is a major contributing factor. Causes also include gingival recession due to root prominence and thin overlying mucosa, dehiscences and fenestrations, frenum pulls, and orthodontic movement, which causes a root to be moved outside its alveolar housing. Loss of enamel may be a consequence of attrition, erosion, abrasion, and abfraction. The loss of enamel, however, is usually a combination of two or more of these factors. Attrition is the wear that occurs when teeth are in direct contact and is usually associated with occlusal function. Excessive or parafunctional habits, such as bruxism, may result in extreme pathologic wear and increased sensitivity. Abrasion is the tooth wear caused by objects other than other teeth. Toothbrush/toothpaste abrasion is an example. Toothbrushing by itself, however, has minimal effect on enamel and even with toothpaste the effect is minimal on both enamel and dentin. The combination of toothbrushing and erosive agents results in loss of tooth structure. West and colleagues found, however, that toothbrushing with toothpaste was able to erode or abrade dentin in various amounts and cause tubule opening. Brushing dentin that has a smear layer with silica-based toothpaste opened the most tubules. Abrasion may cause gingival recession and, as a result of the recession, the softer root surface is exposed. Erosion is the loss of tooth structure by acids that are not of bacterial origin. Erosion can be caused by extrinsic or intrinsic acids. Intrinsic acid is a consequence of exposure to gastric acid (acid regurgitation or gastroesophogeal reflux disease) causing dissolution of teeth by the acid (periomolysis). Extrinsic acid can be a result of dietary or environmental factors. A variety of foods and drinks that may contain acid can contribute to the erosion by demineralization and chelation of calcium. Industrial erosion can occur by exposure to acid vapors produced in a battery factory and wine tasters. Swimmers are exposed to acid in pools maintained at a low pH of 2.7. The loss of tooth structure by erosion is an active process that consists of episodes of demineralization and remineralization. Acidified fluoride gel demonstrated a protective effect against abrasion in eroded enamel but fluoride does not seem to reduce dental erosion. A variety of studies have indicated the possibility of iron reducing enamel demineralization, but potential adverse problems, such as tooth staining, may prohibit its use. A recent study demonstrated iron in a gel increased enamel resistance to acids and helped minimize dental erosion.

Bleaching

The sensitivity that occurs with bleaching is a result of a reversible pulpitis that is caused by the flow of dentinal fluid from osmolarity changes in the pulp. These changes occur when the bleaching material rapidly penetrates enamel and dentin to the pulp. Hydrogen peroxide and urea penetrate through integral enamel, through the dentin, and into the pulp in 5 to 10 minutes. Most often, the sensitivity is generalized, but many times a sharp shooting pain may occur. This can be from the peroxide penetrating into the pulp or mechanical pressure due to an ill-fitting tray or occlusion on the tray. The estimates of tooth hypersensitivity caused by whitening are usually approximately 60% and the degree of discomfort can be minor to excruciating. Sensitivity usually stops on conclusion of the bleaching treatment and sometimes during treatment. Unfortunately, the patients who exhibit unendurable pain during the procedure do not comply with treatment and a poor result is the consequence. The components of whitening gels are usually carbamide peroxide or hydrogen peroxide; glycerin or propylene glycol is the carrier; and carbapol is used as a polymer-thickening agent. Phosphoric or citric acid is often added in slight amounts to increase the acidity and improve shelf life. The carbamide peroxide breaks down in saliva into hydrogen peroxide and urea. Subsequently, the urea breaks down into ammonia and carbon dioxide. Hydrogen peroxide enters the tooth and forms oxygen and water. The oxygen oxidizes the pigment molecule present in the enamel and dentin and creates a bleached effect.

The three basic classifications of bleaching, which include in office, tray, and over the counter, all incur some degree of sensitivity. Usually higher concentrations of peroxide results in a greater degree of sensitivity. The addition of low levels of potassium nitrate to tray bleaches has reduced but not eradicated sensitivity.

Periodontal treatment

Periodontal treatment is sometimes needed to preserve the dentition by eliminating inflammation, regenerating missing periodontium, maintaining esthetics, and stopping the progression of the disease. Unfortunately, patient discomfort often occurs while undergoing periodontal treatment. Postoperative pain and dentin hypersensitivity are often occurrences. Some patients find both the nonsurgical and surgical treatment painful. It has been reported that periodontal therapy can be an important source of dentin hypersensitivity. On conclusion of periodontal therapy, the gingival protective barrier is reduced as a result of the removal of tissue that covers the root surface. Scaling and root planing can remove 20 to 50 μm of cementum and expose the dentinal tubules to a variety of stimuli. von Troil and colleagues found 50% of patients undergoing scaling and root planing had dentin hypersensitivity after treatment. Wallace and Bissada felt that scaling and root planing did not produce hypersensitivity but periodontal surgery that resulted in extensive exposure of root surface did produce dentin hypersensitivity. Smokers also presented with increased pain level in dentin hypersensitivity.

Treatment—self-applied and office supplied

Self-applied treatments to reduce sensitivity consist of materials that occlude dentinal tubules, coagulate or precipitate tubular fluids, encourage secondary dentin formation, or obstruct pulpal neural response. Desensitizing toothpastes that contain potassium salts, either nitrates or chlorides, are believed to act by depolarizing the nerve surrounding the odontoblastic process, resulting in interference of transmission. Usually it takes 2 weeks with twice-a-day usage to get a reduction in sensitivity. Instead of having patients brush with the toothpaste, the paste could be placed in a soft tray to increase contact time. Haywood and colleagues recommended placing 5% potassium nitrate in bleaching trays to minimize sensitivity that may occur as a result of bleaching. Ten-minute to 30-minute applications seemed to assuage any sensitivity that may occur. Ideally, the desensitizing toothpaste should not have sodium lauryl sulfate because a large amount of this ingredient may cause tissue irritation.

Laser treatment

Laser treatment has also been recommended for the treatment of dentin hypersensitivity. The treatment seems to be only transient, however, and the sensitivity returns in time. In order for a laser to actually alter the dentin surface, it has to melt and resolidify the surface. This effectively closes the dentinal tubules. This does not occur. It is felt that laser treatment reduces sensitivity by coagulation of protein and without altering the surface of the dentin. Dicalcium phosphate-bioglass in combination with Nd:YAG laser treatment has sealed dentin tubules to a depth of 10 μm, and dicalcium phosphate-bioglass plus 30% phosphoric acid occluded exposed tubules up to 60 μm.

Fluoride treatment

Patients can apply stannous fluoride in a 0.4% gel or sodium fluoride in a 0.5% mouth rinse or a 1.1% gel. Fluorides reduce the permeability of dentin probably by precipitation of insoluble calcium fluoride inside the dentinal tubules and reduce sensitivity. Gel-Kam Dentin Block (Colgate Oral Pharmaceuticals, New York, NY, USA) consists of 1.09% sodium fluoride, 0.4% stannous fluoride, and 0.14% hydrogen fluoride that can be applied in a tray.

Pro-Argin

In 2002, Kleinberg developed a material to reduce sensitivity based on saliva’s natural role in reducing sensitivity. Saliva usually allows calcium and phosphate ions to migrate to open dentin tubules and form a precipitate of salivary glycoproteins and calcium phosphate that occludes the tubules. The material developed by Kleinberg consisted of arginine, which is an amino acid that has a positive charge at physiologic pH; bicarbonate as a pH buffer; and calcium carbonate, which provides a source of calcium. This material was able to plug and seal exposed dental tubules to decrease sensitivity. Confocal laser scanning microscopy has demonstrated the occlusion to be resistant to acid exposure and normal pulpal pressure. Kleinberg found that the application of arginine-calcium carbonate applied in a paste provided instantaneous relief that lasted for 28 days. Atomic-force microscopy also demonstrated that the normal helical fine structure of intertubular dentin, normally present, was not discernible, due to a surface coating, and the tubules were closed.

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Oct 29, 2016 | Posted by in General Dentistry | Comments Off on Treatment of Dentin Hypersensitivity
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