DENTIN SENSITIVITY:
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CAUSES AND INCIDENCEHypersensitivity of exposed root surfaces is a common dental problem for adults. Cementum is relatively soft and thin. Once this layer of covering cementum is worn away, the exposed dentin reacts to tactile, chemical and thermal irritants within the oral cavity. Tooth fractures and marginal leakage around restorations also expose dentin and can render teeth sensitive. There is no single cause for dentin sensitivity, but various predisposing factors have been suggested in the dental literature. Essentially, the tooth becomes sensitive after enamel is lost or the root surface is abraided. Enamel loss can occur because of either mechanical wear due to occlusal wear or cervical abrasion, or to chemical erosion caused by acidic foods or certain eating disorders that are accompanied by frequent stomach regurgitation. The causes of gingival recession include incorrect toothbrushing techniques, normal aging, abnormal tooth position, chronic periodontal disease, periodontal therapy and root preparation. All of these precipitating factors result in exposed root surfaces and open dentinal tubules, and thus create the necessary conditions for dentin sensitivity. Epidemological research suggests that one out of four adult patients in your practice will experience dentin sensitivity. One particularly common and troubling form of root sensitivity occurs for many patients following periodontal therapy. Removal of cementum, or a protective layer of organic and mineral debris (smear layer), from the root surface leaves dentin and its tubules exposed. A variety of materials have been applied topically as desensitizing agents to the exposed areas of the root. These therapeutic approaches have involved either physically occluding the dentin tubules through a mineralization process, or attempting to decrease the activation or excitability of the interdental nerve fibers. Clinical trials, designed to evaluate various therapeutic agents for use in treating dentin sensitivity, typically vary in their reported level of effectiveness. This is due primarily to the subjective nature of tooth pain, as well as to the documented natural remission or spontaneous resolution that occurs in some hypersensitive areas. In most cases, however, patients with mild to moderate pain can be successfully treated with a combination of professional and home-care desensitizing components. The failure of some surfaces to respond to a significantly effective therapeutic agent may suggest other undiagnosed dental problems; for example, occlusal trauma, pulpitis, and periodontal lesions may be responsible for certain false diagnoses of dentin sensitivity. CLINICAL CONSEQUENCESDentin hypersensitivity is one of the most painful, widespread, and least satisfactorily treated chronic problems of the teeth. Complaints of tooth sensitivity should not be taken lightly in clinical practice. Patients with sensitive teeth have difficulty complying with even simple oral hygiene procedures. Because of the discomfort associated with brushing these areas, patients tend to avoid them in their normal oral hygiene regimens. Exposed root surfaces that are not kept clean may become increasingly hypersensitive. Furthermore, when we consider that plaque is responsible for both caries and periodontal disease and that people with dentinal hypersensitivity often are unable to remove plaque by effective daily brushing, then the full extent of the problem can be appreciated. When plaque is left to build-up because of improper or inadequate home-care and professional treatment, the patient will likely experience additional problems with his or her dentition, including tooth loss and the need for extensive restorative procedures. Dentin sensitivity can lead to more than just dental problems. When a patient's dentition is very uncomfortable, they fear any pain that may result from touching or brushing their teeth, and worry about hypersensitivity caused by contact with cold, hot, sour and acidic foods and beverages. This can represent a major health care problem because the quality of a patient's life may suffer. Some individuals develop dietary deficiencies and emotional problems due to the pain experienced during normal eating. In certain situations, emotional distress and problems with interpersonal relations have been traced to psychological worry about dentin hypersensitivity and its consequences. Individuals with dentin sensitivity not only tend to avoid normal home hygiene regimens, but often are unwilling to visit a dentist. When they seek professional treatment, hypersensitivity can make the simplest office procedure difficult and time consuming. In many cases, a patient's complaint of pain can cause the practitioner to either alter the therapy to minimize the discomfort or to use techniques that require significant set-up time or that fail to offer long-term restorative solutions. Another potentially troubling situation can develop following periodontal therapy. Post-treatment sensitivity can cause patients to avoid home-care recommendations. Any resultant plaque accumulation, especially in areas already affected by periodontal disease, can exacerbate the situation and compromise the integrity of the affected teeth. Recent surveys of the U.S. population point to a growing number of older Americans. With people both living and keeping their teeth longer, treating hypersensitivity is expected to remain a major area of concern for dentists. The goal of dental professionals should be to maintain appearance, function and comfort of dentitions for the lifetime of the patient; this objective can be accomplished only through better management of dentin hypersensitivity. MECHANISMS OF PAINExposed superficial dentin is free of nerve endings, yet this tissue can be sensitive. Experimental evidence suggests that certain stimuli, such as tactile pressure on the dentin surface and air blasts, induce fluid movements in the dentinal tubules. Most experts today believe that this movement of fluid within the dentin stimulate nerve fibers found at the dentin-pulp border. The prevailing thought is that pain occurs when the intradental sensory nerves are activated by hydrodynamic forces generated as a result of these fluid movements. Odontoblasts are the cells that lay down dentin during tooth development. Odontoblasts or the odontoblastic fibril can extend from the pulp/dentin interface to about one third the thickness of dentin. mature dentin is riddled with thin tubules that extend from the pulp to the enamel or cementum layer and occupy 20 to 30 percent of the dentin volume. Some nerve fibers actually extend into the dentin tubules to a distance of perhaps 10 to 15 percent from the pulpal side. Small changes in fluid movement within the dentinal tubules may deform the odontoblastic fibrils, causing the closely associated nerve endings to transmit pain. It has been shown that, by using very accurate impression techniques, it is possible to construct a replica of the dentin surface of intact teeth. In clinical studies, when replicas of sensitive and nonsensitive teeth were compared, some significant differences were readily apparent. Sensitive teeth were reported to have unoccluded dentinal tubules clearly visible on the exposed root surface. In nonsensitive teeth the surface was often covered with a smear layer so that either the dentin failed to show exposed tubules or had small, slit-like orifices partially occluded by the smear layer. This observation would support the "hydrodynamic" theory of pain transmission since occluded tubules would effectively block fluid movement through dentin tissue. The formation of dentin smear layer may also help to explain why natural remission of dentin sensitivity occurs, and suggests possible methods and agents for use in treating this condition. Exposed dentin, over time, can become covered by organic and inorganic debris, primarily derived from saliva. Following certain dental procedures such as root planing, it has been demonstrated that a smear layer is formed on the exposed root surface which effectively covers the orifices of the dentinal tubules. Because this smear layer is labile, such factors as dietary acids, or even brushing with an abrasive dentifrice, can cause the layer to be lost and sensitivity to return. In fact, it has been demonstrated clinically that the removal of the smear layer increases the patient's pain response to dentinal stimulation. With this new understanding of how pain is transmitted through dentinal tubules, and how the physical blocking of the tubules can decrease sensitivity, we can begin to appreciate why this condition is such a common, typically intermittent, and chronic problem for so many adult patients. PROFESSIONAL MANAGEMENT OF SENSITIVITYTreatment modalities for dentin hypersensitivity fall into two main categories: agents that occlude the dentinal tubules and chemicals that are capable of blocking intradental nerve response. All available professional treatments work to differing degrees depending on the treatment and the severity of the patient's hypersensitivity. However, initial treatment for dentin sensitivity should include a thorough examination to eliminate other sources of tooth pain such as active decay, occlusal interferences, and non-vital dental pulp or sinusitis. After these are eliminated, then therapy using chemical agents can be pursued. There is hierarchy of treatment options available to dental professionals. The clinician should try the most conservative treatment first. If that procedure doesn't work, then the next level of treatment can be tried. Initial therapy should involve the application of one of the commercially available oxalate compounds or a high potency fluoride formulation. As a next step, iontophoresis with fluoride has been found to be reasonably effective, provided the equipment is available. If the problem still doesn't resolve, then the dentist may try one of the physical barrier agents that seal the tubules, such as dentin bonding agents and glass ionomer cements. Desensitizing agents must have certain properties in addition to an ability to provide rapid and long lasting pain relief. The agent should be easily applied, be relatively painless during application, and should not discolor or somehow adversely affect the tooth or mucosa. Sodium fluoride, in the form of a 33 percent paste or a 2 percent solution, was the earliest compound professionally applied to alleviate dentinal pain. More recently, potassium and ferric oxalates have been marketed for in-office treatment. These compounds appear to work by depositing oxalate salts within the dentinal tubules. Fluoride containing preparations similarly occlude the tubules, but exhibit and additional anticaries benefit. In this category, a low pH solution containing 0.717% fluoride, derived from a combination of sodium and stannous fluoride, is commercially available and has been shown to provide a virtually immediate and significant reduction in pain for most cases of hypersensitivity. Furthermore, the benefits of this treatment seem to continue for several months. The probable mechanism of action is likely the occlusion of tubules with tin fluoride rich mineral deposits. Fluoride iontophoresis, using a 2 percent sodium fluoride solution, can also occlude the dentin tubules. Although there is clinical support for the effectiveness of this treatment in reducing hypersensitivity, iontophoresis is a relatively expensive in-office procedure, involves special equipment, and often requires more than one application. If conservative chemical procedures are not effective in eliminating a patient's sensitivity, certain techniques that physically block dentin tubules can be employed. The most common agents in this treatment category are composite resins, varnishes, sealants, soft tissue grafts and glass ionomer cements. Treatment with these types of agents, however, can be time consuming and typically require tooth preparation before application. Except for the soft tissue grafts, these techniques are all tubule sealants. Copal varnishes and cyanoacrylate sealants have been reported to provide almost immediate relief, but erode or abrade quickly and must be reapplied. Recent breakthroughs in the development of more hydrophilic dentin sealants and bonding agents offer the promise of more permanent relief, especially for severe and chronic cases of hypersensitivity. To date, however, no long term studies exist to document the efficacy of these new in-office techniques for controlling sensitive teeth. HOME TREATMENT OF HYPERSENSITIVITYHome treatment should be recommended as an adjunct to chairside therapy for dentin sensitivity. Exposed root surfaces that are not kept clean may become increasingly hypersensitive, and so without effective home care, any relief obtained in the dental office is likely to be transitory. Many agents have shown varying degrees of effectiveness on dentinal pain. Included in this home care group are compositions containing sodium and stannous fluorides, strontium chloride, sodium and stannous fluorides, strontium chloride, sodium citrate, potassium nitrate, oxalates and pyrophosphate, primarily delivered in dentifrice formulations. It is difficult to critically compare the effectiveness of different desensitizing agents because of the small patient sample sizes, variable study duration, and the lack of controls that are typical of these kinds of clinical trials. Furthermore, pain is extremely subjective so that therapeutic effectiveness can often depend on the type of stimuli employed in the study (e.g., thermal, tactile or electrical) and on the individual's pain threshold. Finally, because of the natural remission of some hypersensitive areas, placebo treatments frequently elicit a favorable response and mask the magnitude of the active ingredient's effect. Nevertheless, published studies, on the whole, support the clinical impression that home-care desensitizing formulations do reduce cervical hypersensitivity. Home desensitizing agents produce their benefits more gradually than processional therapies and generally require 1-2 weeks of use for full effectiveness. Due to the gradual nature of the effect, patients may not readily notice the benefit and can become discouraged regarding product use. Patients, however, should be advised to continue treatment throughout the recommended duration. It has also been suggested that daily brushing using abrasive dentifrices may occasionally cause dentin sensitivity in the cervical regions. Studies demonstrate that the brushing action removes protective deposits (smear layer) and opens the tubules to fluid movement. Several commercial toothpastes, based on strontium chloride or potassium nitrate, have been clinically demonstrated to effectively control mild to moderate hypersensitivity, but without fluoride, they lack any anticaries or antiplaque benefit. Potassium nitrate was first studied as a treatment for cervical hypersensitivity in the late 1960s. Currently there are over a dozen different toothpastes containing potassium nitrate. This compound appears to work by decreasing the excitability of interdental nerve fibers in a manner comparable to a local anesthetic. In order to be effective, potassium nitrate must have access to the sensory nerve fibers. For this reason, the agent may not provide and added benefit if the dentinal tubules have been occluded, especially following professional treatment. Fluoride containing dentifrices have been the subject of multiple sensitivity studies, as reported in the literature. In addition to conventional dentifrices, abrasive-free formulations containing 1.1% neutral sodium fluoride and nonaqueous 0.4% stannous fluoride have been recommended for use in treating recurrent sensitivity. These formulations, in fact, should be particularly efficacious oral therapeutic agents in that they not only control pain associated with dentin sensitivity, but are effective in protecting exposed root surfaces against decay, and exert an antibacterial effect on microorganisms associated with periodontal disease.
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