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Understanding and managing dentin hypersensitivity. (American Dental Hygienists' Association Continuing Education).

Introduction

Understanding Dentin Hypersensitivity

Dental hygienists frequently encounter clients with sensitive teeth and recognize `the look' elicited when their sensitive teeth are stimulated. Many clients with sensitive teeth are clearly uncomfortable during dental hygiene procedures (Figure 1). In these instances, there is an added element of stress for the clinician who needs to provide a thorough debridement, yet seems to inflict pain with every stroke of the instrument. The client often looks to the dental hygienist to provide relief both during and after the procedure and is seeking information concerning the cause of the discomfort he or she is experiencing.

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As with any disease or painful condition, it is essential to understand the etiology of tooth sensitivity to plan for effectively managing client discomfort and preventing subsequent painful episodes. However, hypersensitivity is a confounding condition because its development and expression is influenced by modifying and predisposing factors as well as by individual susceptibility. Additionally, an individual's psychogenic pain response impacts the perception of the severity of the condition and the benefits of treatment.

Hypersensitivity has been referred to as an enigma (1,2) for a variety of reasons, including difficulty in determining the etiology, the numerous treatment approaches, variability in pain relief, and because in-vivo objective clinical trials are difficult to conduct. A prerequisite for the occurrence of hypersensitivity is gingival recession and subsequent dentin exposure as a result of loss of cementum or enamel. Reasons for cementum and enamel loss are often difficult to determine.

There is no consensus in the literature concerning terminology used to describe the condition. The terms dentin hypersensitivity and tooth hypersensitivity or hypersensitivity have been questioned because the pulp response that is elicited by the stimulation of exposed dentin would be expected as a normal rather than a hyper-reaction. (3) The terms dentinal, dentin, or tooth sensitivity frequently have been used. The condition has also been referred to as cervical dentin sensitivity (4,5) and as cervical tooth sensitivity, (6) adding a location-based descriptor to differentiate it from other types of tooth pain.

For this continuing education course, the terms dentin hypersensitivity or hypersensitivity will be used.

Definition

Dentin hypersensitivity has been defined as short or transient sharp pain of a rapid onset that arises from exposed dentin. It usually occurs in response to stimuli--typically thermal, evaporative, tactile, osmotic, or chemical--and cannot be ascribed to any other dental defects or pathology (3) This definition, with only minor variations, is found in recent literature on the topic, and was accepted by participants in an international workshop on dentin hypersensitivity. (7) It can also be described as a response from a non-noxious stimulus and characterized as a chronic condition with acute episodes. (8) This differs from dentinal pain which is a response from a noxious stimulus and often an acute condition. For example, tactile (i.e., instrumentation) and thermal (i.e., hot or cold water) stimuli are non-noxious, and are not generally expected to generate a pain response, except as seen in hypersensitivity. An example of a noxious stimulus would be the toxins of bacteria within a carious lesion leading to dentinal pain.

The Pain Experience

The pain experience varies for different individuals as a result of factors, such as age, gender, situation and context, previous experiences, present expectations, and a host of other psychological and physiological conditions which are difficult to characterize. Personality characteristics and emotive reactions play a major role in how an individual reacts to pain. Thus, perceived pain is not always proportional to the intensity of the tissue damage or the undesirable stimulus. Rather, the nociceptive system (a peripheral nerve, organ, or mechanism for the reception and transmission of painful or injurious stimuli) modulates the perception of pain from tissue injury for transmittal to the brain. (9) Hypersensitivity is a chronic condition with acute exacerbations. Acute pain often causes anxiety, while chronic pain is more likely to lead to depression. The pain of hypersensitivity may lead to the expression of both.

Oral health care professionals vary in their expression of compassion and degree of concern they show for their clients' pain. An appreciation for the impact of the pain on a client's quality of life and a more thorough understanding of hypersensitivity may lead clinicians to be more sympathetic. Probable causative factors should be identified, and various treatment options thoroughly explored and offered to these clients.

Measuring Tooth Hypersensitivity

Many of the same stimuli that cause hypersensitivity in the oral cavity are utilized to elicit tooth hypersensitivity in the experimental setting: tactile, thermal, osmotic, and electrical. Passing a sharp dental explorer over the sensitive area of a tooth and asking the client to grade the pain response on a numeric severity scale, such as 0-3, is the simplest tactile method used in research. Lack of standardization of pressure and location of the explorer on the tooth affects research findings. For these reasons, more sophisticated tactile stimulation methods have been developed to control for these factors. (10-12) Similar technology has been developed for standardizing thermal, osmotic, and electrical testing. (13-16)

Further standardization difficulties arise when attempts are made to quantify a subject's assessment of a change in pain sensation. Pain is a subjective phenomenon which defies objective measurement. Most clinical trials have employed either the Verbal Rating Scale (VRS) or the Visual Analog Scale (VAS). A VRS may have three to five descriptors that allow a person to verbally grade the degree of discomfort. The VAS approach provides a line, usually 10 cm in length, that represents a continuum from no pain to severe pain. Subjects place a mark at the location that best indicates their level of discomfort. The VAS has generally been found to be more reproducible, and therefore, more appropriate for hypersensitivity measurement than the VRS. (15) However, both approaches rely on an individual's subjective assessment of change in the intensity of pain. Examples of a VAS and VRS are shown in Table I.

Prevalence

It has been reported that 8 to 30% of adults are affected by hypersensitivity. (17) However, a large study of more than 3,500 subjects with gingival recession revealed only a 3.8% prevalence. (18) Part of the variability in findings results from data collection discrepancies. Three studies in Scotland, (17) Sweden, (19) and Brazil (20) that used self-reporting found 28%, 22%, and 25% of subjects described discomfort to daily life stimuli, respectively. When validated clinically, the prevalence was reported at only 14 to 18%. (17,21) Outcomes are dependent upon whether such data are gathered by subject report or by clinical examination or a combination of both.

Rates of tooth sensitivity among clients in periodontal practices have been reported as higher than among the general dental population. (4) The prevalence has been reported at 72 to 98% in periodontal patients compared to 3.8 to 57% in other populations. (22) Presumably this is due to the greater incidence of root exposure and accompanying loss of tooth structure resulting from periodontal disease and therapy.

Females have been reported to have a higher incidence of hypersensitivity than males, although the difference is not statistically significant. (17,20) The reported difference may be an artifact of the sampling methods used. Also, women may experience and report pain differently than men. (23)

With respect to the prevalence of hypersensitivity related to age, reports vary. The greatest incidence has been documented in the 20 to 40 year-old group, peaking in the third decade of life. (17,20) This parallels the age group most affected by periodontal disease, with associated gingival recession and loss of enamel and cementum.

The impact of aging on hypersensitivity prevalence is unclear. With the average human lifespan at 76.9 years, and more people keeping their teeth longer, it can be assumed that clinicians will see more people with hypersensitivity in their practices. This is based on the observation that gingival recession, and concomitant loss of enamel and cementum, is more prevalent in older people. (24) However, the paradox is that the incidence of hypersensitivity decreases after the fourth and fifth decades of life. (2) This may be explained by the decrease in dentin permeability and neural response that takes place with age. These changes occur from the natural desensitization process of sclerosis and secondary dentin deposition. Long-term use of a fluoride dentifrice can also add to the desensitization process as the abrasive particles can occlude the dentin tubule openings and the mineralizing capacity of fluoride can decrease the diameter of the tubules.

Variability is reported in the distribution among specific teeth or teeth types that are most affected by hypersensitivity. The research is not conclusive as to the specific teeth and types of teeth that are affected by hypersensitivity. There is agreement that the buccal or facial surfaces are more affected by both recession and sensitivity than are the lingual surfaces. Upper premolars have been identified as the teeth that are the most affected, followed by upper first molars and incisors. (18) The reported variation among tooth types may be the result of the use of different eliciting stimuli. In addition, it has been shown that heavy-handed brushing leads to more sensitivity on the opposite side. (27) For example, a right handed brusher would likely have more sensitive teeth on the left side of the mouth.

Pain Transmission Theory

Tooth pain is not a recent phenomenon, as historical records show that sensitive teeth have plagued mankind for thousands of years. (26) In the mid-19th century, a Philadelphia dentist conjectured that the hollow tubules of dentin were filled with a fluid secreted by the pulp, and that pressure on this fluid affected the pulp within. This information had been described earlier and was reiterated about 100 years later. (26,27) For a long time it was unclear how the stimulus information was transmitted to the pulp tissue and recognized as pain. Initially, it was believed that the nerve fibers or the odontoblasts in teeth were responsible. More sophisticated microscopy techniques revealed that neither the nerve fibers nor the odontoblasts reached from the pulp all the way through the dentin. (28) It wasn't until the 1960s that Brannstrom developed a theory, based upon two decades of research, that became known as the hydrodynamic theory. (29) Although his theory has not been unequivocally proven, it has not been disproved, and no other account has emerged to explain hypersensitivity. Brannstrom is credited with demonstrating the movement of fluid within the dentin tubules and the effects of various stimuli, including cold, heat, acids, pressure, chemicals, and high osmotic solutions in creating this movement. The theory suggests that a stimulus causes the fluid within the tubules to flow inward or outward, creating a mechanical disturbance or cellular perturbation. (8) This excites the nerves in the tooth, thereby transmitting the signal to the pulp where the sensation of pain is registered by the same depolarization neural discharge mechanism that characterizes all nerve activity (Figure 2). Interestingly, and in support of the hydrodynamic theory, it has been shown that individuals with sensitive teeth exhibit open dentinal tubules and lack the presence of a smear layer (Figure 3). (30,31)

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Current approaches to the treatment of hypersensitivity are designed to target the hydrodynamic process or to interfere with pain transmission. There are two main treatment approaches for the hydrodynamic theory: occlude the dentin tubule to prevent movement of the fluid, or decrease the lumen size of the tubules so that the movement of the fluid is reduced. Pain transmission is reduced by the action of potassium ions blocking repolarization of the nerves around the odontoblasts. (32)

Biology of Tooth Structures

Visualizing the interplay between the dentinal tubules and the pulp is helpful in understanding the development of hypersensitivity. The dentin layer that is surrounded by the enamel of the crown and cementum of the root is comprised of a succession of dentinal tubules reaching from the pulp to the dentin enamel junction (Figure 4). The tubular structure of dentin makes it porous with the tubules serving as the portal through which stimuli enter the pulp (Figure 3). The pulp is highly innervated, with fibers that enter the dentinal tubules. (28,33,34) The question for a very long time was how far the nerve fibers reach into the dentin. It is now known that nerve fibers are located only in the dentin that is closest to the pulp. (28) The question then becomes how stimuli to the outside of the tooth are received by these circumpulpal nerve fibers. Additionally, the odontoblasts, which are the dentin-producing cells, are located near the pulp with the odontoblastic processes being restricted to the inner one-third of the dentinal tubules. (35,36) Since neither the odontoblastic processes nor the nerve fibers extend throughout the dentin, one might question whether or not there is another yet unknown mechanism for transmission of the information provided by the stimulus to the pulp.

Natural Desensitization

There are several naturally occurring processes that can improve hypersensitivity over time, even without treatment intervention. These include sclerosis of dentin, deposition of secondary, and tertiary dentin, creation of a smear layer, and calculus formation on the surface of the dentin.

Sclerosis of dentin is the naturally occurring deposition of minerals within tubules that results in a thicker layer of peritubular dentin that is a highly mineralized dentin that is deposited inside the periphery of the tubules. This process eventually results in the tubule becoming smaller in diameter, making it less permeable and less able to transmit stimuli. Many desensitizing agents are intended to stimulate mineral deposition to reduce the circumference of the dentinal tubules. Secondary dentin develops after the tooth root is formed. It differs from the primary dentin, which is formed prior to tooth eruption. Both types are formed by odontoblasts, but secondary dentin is secreted more slowly than primary dentin. Secondary dentin also is formed on the floor and roof of the pulp chamber which causes the pulp chamber to eventually decrease in size. This, in effect, provides a barrier between the dentinal tubules and the pulp to protect the pulp from additional stimuli. Tertiary dentin, also known as reparative dentin, forms after exposed dentin has been traumatized by a stimulus. These natural processes affect dentin permeability and the neural responses of the pulp. (9,37)

The smear layer has been described as a combination of organic and inorganic microcrystalline debris of cementum and dentin which forms in response to instrumentation such as scaling and root planing, or can occur by burnishing the tooth with a toothbrush, toothpick or other device. (10,38) The smear layer plugs the dentinal tubule orifices with debris that consists of dentinal shavings, tissue debris, odontoblastic processes, and microbial elements. (39) Calculus formation also provides a protective coating to shield exposed dentin from stimuli. This is evidenced by the post-debridement sensitivity that clients report after removal of heavy calculus deposits.

Just two weeks after subgingival debridement, natural desensitization has been shown to occur. (11) Current hypersensitivity treatment modalities are aimed at stimulating these natural processes.

Gingival Recession

The occurrence of gingival recession is a precursor to the loss of cementum, the exposure of dentin, and the subsequent development of hypersensitivity (Figure 5). Recession can occur for a variety of reasons.

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Anatomically, some teeth may exhibit a narrow zone of attached gingiva. If this narrow zone of attached gingiva is further reduced by recession, little to no gingiva is left to cover and protect the cervical area of the tooth. Tooth apposition also may predispose a tooth to gingival tissue loss since the buccal alveolar plate may be thin.

Excessive and abrasive use of any oral hygiene device can lead to gingival recession, although toothbrush type and the technique used are the primary contributing factors. However, it is not believed that the toothbrush alone causes loss of enamel or cementum. (40,41)

Gingiva can be lost secondary to tissue destructive processes of periodontitis, necrotizing ulcerative gingivitis (NUG), and viral disorders, such as HIV. Surgical and nonsurgical periodontal treatment can result in gingival recession and root exposure. Certain other surgical and restorative procedures, such as crown preparations, may also contribute to gingival recession and root exposure.

There is some speculation that gingival recession is a natural sequela of aging. In a sample of more than 500 people over 65 years of age, 39% of the tooth surfaces had gingival recession. (42) There was not a significant increase across age groups, although there was a trend toward more recession in older groups. It is unclear whether recession occurs as a result of the aging process alone because it is difficult to eliminate the additive life-time effects of toothbrushing, the use of other oral hygiene devices, and oral habits.

Loss of Tooth Structure

Both enamel and cementum may be lost either gradually or suddenly from the tooth surface. The sudden exposure of dentin will elicit more acute hypersensitivity since gradual dentin exposure over time allows for the development of protective measures such as smear layer, sclerosis, and proliferation of secondary/reparative dentin.

Enamel is less susceptible than cementum to erosion or abrasion, since it is thicker and more highly mineralized. At the area of the cementoenamel junction there may be only a thin layer of enamel, making this area particularly susceptible to loss of tooth structure. Because the layer of cementum is thin and not highly mineralized, it easily can be abraded or eroded in this area. In approximately 10% of teeth, the enamel and cementum do not meet, leaving an area of exposed dentin. When gingival recession is also present, this is a mechanism by which sensitivity occurs. (43)

Tooth wear, leading to loss of enamel or root surface, may result from abrasion or attrition. Attrition is tooth-to-tooth contact, which results from occlusal function or para-function, such as bruxism, and can cause loss of tooth structure on the occlusal surfaces and incisal edges. Neither abrasion nor attrition usually results in hypersensitivity due to the force-created smear layer, which obturates dentin tubules. (44) Both of these gradual traumatic processes stimulate the development of natural protective measures, such as secondary dentin and sclerosis. This can be observed in older individuals who show more exposed dentin, but less sensitivity than their younger counterparts. (45)

Erosion is thought to be the major source of tooth wear, and has been defined as tooth dissolution by acids that are not of bacterial origin. (46) Erosion from dietary acids is thought to work in combination with abrasion from toothbrushing and toothpaste, leading to more loss of tooth structure than would be possible with either effect alone. (47,49) That is why brushing with toothpaste after consuming acidic food or drinks can be damaging. (1) The additive combined effects of abrasion and erosion may not always lead to hypersensitivity since protective measures may develop over time. Protective measures can be enhanced by the burnishing effects of the toothbrush or toothpick which may stimulate secondary dentin, and the toothpaste abrasives which may serve to obliterate dentinal tubules (Figure 6).

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Abfraction is another mechanism that can lead to loss of tooth structure. An association has been demonstrated between cervical dentin hypersensitivity and abfractive lesions, (50) These cervical lesions, caused by occlusal stresses, lead to weakening of the cervical tooth structure and can cause enamel, cementum, or dentin to chip away from the cervical aspect of the tooth (Figure 7). The appearance of the lesion is a V-shaped cervical notch (Figure 8). Abfraction is most likely a co-factor with abrasion or erosion in tooth structure loss, since abfraction has not been identified as a sole cause of hypersensitivity. (51) In fact, enamel loss rarely results from a single agent but rather from a combination of two or three contributing factors. (1,3)

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Management and Prevention of Dentin Hypersensitivity

Differential diagnosis

When clients present with complaints of sensitive teeth, the first consideration should be to determine the etiology of the pain, since it may be difficult to differentiate between dentinal hypersensitivity and a variety of other tooth and/or pulp-associated reasons for discomfort. Clients often have a difficult time describing the pain and may not be able to localize it to any specific tooth or teeth, although they are usually more accurate in localizing hypersensitivity (caused by a non-noxious agent) than dentinal or pulpal pain. The character of the pain is similar when comparing dentin pain to hypersensitivity pain from exposed dentin. Dentin pain (caused by a noxious agent, i.e. dental caries) can be intensified by thermal change, sweet, and sour, all of which could elicit a hypersensitivity reaction as well. Additionally, pain from both is usually within the mild to moderate range. Pulpal pain can be differentiated from dentin pain since it is often described as severe, intermittent, and throbbing. However, both can be elicited by hot and/or cold stimuli. Pulpal pain may also manifest during chewing, which would distinguish it from hypersensitivity.

Pulpal inflammation or pulpitis can be difficult to assess, since there is no way to be certain of the diagnosis, short of tooth extraction combined with histologic examination. A diagnosis of pulpitis is based upon a combination of clinical findings and symptomology. Diagnostic aids include history of pain, percussion and palpation tests, inspection of the teeth and surrounding tissues, thermal and electric pulp tests, and radiographic examination. The dental history should include chronology, nature, location, and aggravating and alleviating factors that influence pain. (43) The pain of pulpitis often occurs without provocation, and particularly after thermal tests, may persist after the stimulus has been removed. This would differentiate pulpitis from dentin hypersensitivity pain, which subsides after removal of the stimulus. Additional tests for pulpitis could include painful response to percussion and tooth mobility.

A differential diagnosis to rule out other conditions must be established before treating for hypersensitivity. Dentists vary in the techniques used to arrive at a differential diagnosis. Some of these include pain response upon the pressure of tapping teeth to indicate pulpitis; having the client bite on a stick to evoke pain that is suggestive of tooth fracture; use of lights or dyes to aid in the diagnosis of a fracture line in the tooth; fractured restorations visualized by careful examination of the restoration, perhaps aided by magnification; pain associated with a recent restoration as determined by dental history; and adjusting the occlusion to produce relief from the hyperfunction created by placement of a new restoration or crown.

Treatment Strategies and Interventions

There are numerous methods used to treat, eliminate or manage hypersensitivity. Long-term management is most successful when, in addition to pain control, treatment strategies include the elimination or reduction of contributing factors. Dentin sensitivity is managed best through self-care, professional care, or a combination of the two. Not all gingival recession and subsequent cementum or dentin exposure elicits a painful response. Exposed surfaces that do not elicit pain need only be monitored and treated as needed to reduce caries risk.

Communication between client and clinician is an initial and crucial step in the management of sensitivity. Listening to a client's description of the pain and the activities that elicit the pain response is an integral part of the diagnosis and subsequent treatment of hypersensitivity. By utilizing the trigger questions listed in Table II, the client can articulate the specifics of their discomfort. The client responses contribute to the development of an individualized management strategy. Counseling can be provided to encourage behavior changes aimed at preventing further gingival recession and subsequent loss of tooth structure that contribute to hypersensitivity.

Individual clients should be informed of the risk for increased sensitivity following various surgical and restoration treatment procedures before consenting to the treatment. Advance notice of the possibility of developing hypersensitivity would likely minimize client dissatisfaction and enhance the likelihood of compliance with the recommended treatment and follow-up care. Such information should be properly documented in the client's record. Evaluation and follow-up communication after use of various treatment modalities is an often overlooked aspect of treating sensitive teeth.

Once other causes for tooth pain have been ruled out, and hypersensitivity has become the established diagnosis, determining the level or intensity of a client's reported pain will help determine treatment recommendations. Current research does not indicate any one treatment approach that offers the greatest efficacy and duration with the least potential for adverse effects.

Self-Care Strategies

A thorough assessment and evaluation of each client's current oral hygiene self-care practices, parafunctional behaviors, and dietary habits is necessary prior to recommending the strategies to follow. The client's demonstration of his or her brushing and flossing technique also provides invaluable assessment information, as the simple alteration of these alone can positively impact the treatment and prevention of hypersensitive teeth (Figure 10). Sensitivity that is not responsive to self-care strategies should be reevaluated for professional management.

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Toothbrushing

Manual toothbrush--Use of a soft or ultra soft toothbrush with soft end rounded bristles lowers the risk of gingival recession and abrasion of exposed cementum and dentin.

Power toothbrush--Less force or pressure on the teeth is needed when brushing with a powered toothbrush, since they require a light grasp and a minimal amount of pressure to remove plaque. When dental hygienists encounter clients who are aggressive brushers, they should instruct them to grasp the power toothbrush lightly and apply minimal pressure.

Brushing technique and sequence--The brushing sequence is best started in a nonsensitive quadrant and ended within the most sensitive quadrant. Brushing strokes that are focused on one to two teeth should be used instead of long horizontal strokes reaching across several teeth.

Use of nondominant hand--Use of the nondominant hand by an aggressive brusher forces attention to the toothbrushing task and increases awareness of the need to reduce the amount of pressure employed.

Change grasp--It takes a conscious effort for a client to change from using a palm grasp when using the toothbrush. By increasing the awareness of brushing technique the individual can focus on brushing thoroughly but gently.

Dentifrice

Fluoride--Although toothbrushing is a factor in gingival recession, in vitro research evidence suggests that it is the dentifrice rather than the toothbrush that abrades the enamel or dentin and leads to hypersensitivity. (40,41) Use of a standard fluoridated dentifrice can cause abrasive particles to be deposited at dentinal tubule openings and encourage their closure. (60) Anecdotal reports indicate that some individuals experience hypersensitivity as a result of using tartar control dentifrices, possibly due to the pyrophosphate content. (6) An initial pilot study reported a tartar control dentifrice containing pyrophosphates resulted in significantly greater dentin sensitivity than the control dentifrice. (61) Further long-term studies are needed to answer questions related to such products and hypersensitivity.

Desensitizing dentifrice--This is appropriate for mild to moderate hypersensitivity. Currently, the active agent in commercial dentifrices is 5% potassium nitrate in gel or paste. The action of potassium nitrate (5%) is thought to penetrate through the dentinal tubules towards the pulp, depolarizing the nerve and preventing repolarization, thereby blocking pain transmission. Several desensitizing dentifrices contain both potassium nitrate alone or with fluoride which promotes tooth remineralization. An in vitro study showed that the abrasive agent in a desensitizing dentifrice can occlude dentinal tubules and remain resistant to removal. (62) Desensitizing dentifrices generally require two to four weeks before sensitivity is reduced and discontinuation frequently results in a return of the sensitivity. Continued use is recommend to maintain desensitization benefits.

Mouthrinses

Inquiring about mouthrinse use can be an important assessment component. Some mouthrinses have an acidic pH and can dissolve the smear layer. Consequently, use of these products could present a risk factor for hypersensitivity, particularly for those with gingival recession and loss of tooth structure. (63) It has been suggested that mouthwash use followed by brushing would enhance dissolution of the smear layer, exposing dentinal tubules. (64)

Mouthrinses have been suggested as a vehicle for applying a desensitizing agent. A reduction in sensitivity has been demonstrated using a combined sequential rinse of chlorhexidine (0.12%) followed by a sodium fluoride (0.2%) rinse. (65) Additionally, a 3% potassium nitrate/0.2% sodium fluoride mouthrinse appears to have a therapeutic effectiveness in alleviating dentin hypersensitivity. (65) Further studies are recommended to determine the prolonged effect of these combined mouthrinse therapies.

Burnishing

Repeated daily applications of a desensitizing dentifrice, regular dentifrice, or concentrated fluoride product into the sensitive area with a toothpick can provide relief. This burnishing process causes particles of the dentifrice to fill in the openings of the tubules, and the fluoride remineralizes the enamel crystal. However, burnishing with a toothpick and water alone or with sodium fluoride have both been shown to reduce hypersensitivity. (10,67) The fact that burnishing with a toothbrush and water alone decreased sensitivity is likely a result of the burnishing producing secondary or reparative dentin and a smear layer (Figure 11). (43)

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Dietary modifications

The consumption of acidic foods and drinks, such as citrus fruits and juices, pickled foods, wine, ciders, fruit yogurt, and carbonated beverages should be controlled, since they can contribute to erosion of the enamel or cementum and expose underlying dentin. (52) Brushing immediately after ingesting acidic foods should also be avoided as it may accelerate the combined effects of abrasion and erosion. (47-49) Additionally, acidic food and drink, especially fruits and fruit drinks, dissolve the smear layer in a few minutes. (52) Erosion also causes dissolution of the smear layer increasing the patency of the tubules. (31) Extreme dentin loss from combined erosive and abrasive behaviors as seen in purging and acid reflux has been demonstrated. (48) In managing hypersensitivity, brushing before eating acid containing or generating foods is recommended, although this is counter to recommendations for caries prevention. Additional recommendations can include sipping acidic beverages through a straw, reducing the quantity and frequency of acid intake, drinking something neutral or alkaline--such as milk or water--after consuming dietary acids, and avoiding foods that have sharp flavors, spices, or are extremely hot or cold. An approach as simple as making dietary changes could provide pain relief. Having the client complete a diet history might reveal a daily acidic exposure such as a morning glass of grapefruit juice that could precipitate an entire day of hypersensitivity. If the client reports brushing after drinking the juice, the condition could be exacerbated by the combination of acid erosion setting the stage for abrasion. Also, the possibility of eating disorders that include purging behaviors should not be overlooked. Appropriate treatment and referral of such clients is essential.

Reduce or eliminate para-functional habits

Para-functional habits, such as teeth clenching and grinding, may be a factor in eccentric occlusal loading that leads to tooth flexure potentially resulting in an abfraction lesion (Figure 7). (12,68) The microscopic loss of enamel at the cervical portion of the tooth may contribute to dentin hypersensitivity as the tubules become exposed leaving them vulnerable to erosion. Initiating stress reduction methods can reduce these behaviors. Professionally fabricated occlusal night guards can also reduce the effects of unconscious habits such as these.

Professional Interventions

Professional treatment methods are aimed at occluding or sclerosing the dentinal tubules. These methods include physically covering the dentinal tubules with varnishes and liners, precipitating ions into the tubules causing intratubular crystal formation, and placing glass ionomer or bonding agent restorations to physically block stimuli.

A variety of products and procedures are currently in use to seal the dentin tubules and are successful to varying degrees.

Fluorides--These are believed to act by precipitating fluoride ions at low concentrations to be available simultaneously with calcium and phosphate to produce fluorapitate or fluoridate hydroxyapatite. Fluoride actively enhances remineralization while fluoride precipitates are thought to occlude the dentin tubules. (69) Although fluoride varnishes and burnishing fluoride into the tooth frequently result in reduced sensitivity, long term benefits have not been demonstrated because of the on-going tooth wear and daily occurring changes. (70) Topical applications of stannous fluoride applied in a tray or burnished into the tooth surface have been shown to control dentin hypersensitivity. (71) It can also be prescribed for home use utilizing a brush-on or tray technique.

Fluoride varnishes have been approved by the U.S. Food and Drag Administration (FDA) for use as a cavity liner and for the treatment of hypersensitive teeth. (72) A 5% sodium fluoride varnish is an effective, convenient, and noninvasive method for desensitization. (73-74) An advantage of this method is that teeth do not need to be dried prior to application and use of the air syringe, which can be painful, is not necessary. The varnish can be applied directly to the tooth with a brush or cotton pellet and sets on contact with the moisture of the oral cavity. The taste is not objectionable, and varnishes cause no interruption to the individual's lifestyle or habits other than delaying the next brushing. The varnish acts as a reservoir for the fluoride, which is slowly released for remineralization to occur into the dentinal tubules, thereby blocking dentinal fluid flow. (72)

A new fluoride delivery method, an intraoral fluoride releasing device (IFRD), has been suggested and initially investigated. The device is bonded to the buccal surface of a maxillary molar and releases 0.04% mg of sodium fluoride per day. Although more comprehensive evaluation is indicated, in initial testing a significant reduction in sensitivity was reported to be evident at four weeks. (69)

Oxalates--These compounds are composed of ions that react with calcium to form an insoluble calcium oxalate crystal that occludes the dentinal tubules. Ferric and potassium oxalate compounds when professionally applied can reduce hypersensitivity. (75) Oxalates, although insoluble, do not penetrate far into the dentin tubules and may be readily dissolved or removed. (76) Although, short term relief has been reported, long-term results are limited because of the ongoing mechanical wear of the affected tooth surface and changes in the oral environment. (70)

Gluteraldehyde and hydroxyethylmethacrylate--This bonding agent system should be carefully applied to the tooth surface with a cotton tip applicator. Special precautions should be exercised to prevent the agent contacting gingival tissues.

Iontophoresis--Iontophoresis typically employs a low voltage charged electric current to drive a 2% sodium fluoride ion into the affected dentin. Use of iontophoresis has been shown to result in dentin incorporating two to six times more fluoride than dentin receiving only topically applied sodium fluoride. (77)

Composite resin or glass ionomer restorations--These resolve dentin sensitivity by sealing the surface and occluding the dentinal tubules. This long lasting, yet more invasive, procedure requires tooth surface preparation and is indicated when there is significant loss of tooth structure or the tooth doesn't respond to other less invasive desensitizing treatment.

Periodontal surgery--A tissue grafting procedure can be used to cover the sensitive surface and protect the dentinal tubules from the oral environment. The outcomes of this procedure to relieve sensitivity is unpredictable.

Lasers--The Nd:YAG laser has been used in conjunction with sodium fluoride varnish with encouraging results. One study found that over 90% of the dentinal tubule openings were occluded through use of this combined therapy. (78)

In one long-term in vivo study utilizing CO2 laser irradiation and stannous fluoride gel, the tubule closure was observed by SEM for four to six months after treatment. (79) Additionally tin ions were also seen, demonstrating integration of the fluoride into the dentin surface. Further in vivo studies are needed before long-term pain reduction with laser therapy can be confirmed. To date neither of these treatments has been approved by the FDA.

Bleaching considerations

Bleaching agents can potentially cause or increase dentin sensitivity. (80) An average of 25% of those who bleach their teeth develop hypersensitivity. (81) Improper use of tray-applied bleaching agents can erode enamel and dentin, a risk factor for the development of hypersensitivity. (82)

It has been suggested that protecting dentinal tubules (as with fluoride) prior to bleaching is not appropriate because bleaching is effective when it penetrates into dentin tubules to decolorize (oxidize) the nonfunctional staining proteins and materials present. (80) Recommendations to reduce sensitivity resulting from bleaching include using a desensitizing dentifrice that contains potassium nitrate or a more concentrated application using a tray delivery method, and reducing bleaching time and using fluoride after bleaching. (83,84) In addition, a lower concentration of carbamide peroxide (10 to 15%) can be used for bleaching. Although it may take longer to achieve the same level of whiteness as higher concentrations, it could reduce the incidence of sensitivity. (85) The majority of hypersensitivity that arises from bleaching dissipates within a few weeks. Those with existing dentin hypersensitivity are cautioned against bleaching until the condition has been resolved.

Clinical research issues

To date, research evidence that supports an ideal intervention for dentinal sensitivity that works 100% of the time with all patients, for all teeth, even within the same mouth, regardless of whether the strategy is self or professional care has not been reported. Well-designed clinical trials to compare treatment approaches are difficult to formulate because it is hard to standardize stimuli and pain reactions. Consequently, the evidence demonstrating superiority of any desensitizing agent over any other is not available. It is readily apparent that study design must be carefully considered when claims are made that improvements in hypersensitivity resulted from either therapeutic or natural resolution.

Designing studies to evaluate treatment approaches to relieve the pain of hypersensitivity is complicated for a variety of reasons. Pain, a subjective phenomenon, is difficult to quantify and measure. Lack of standardization in applying the stimulus agent can also lead to inconclusive or contradictory results. As a result of faulty research designs, many early studies do not provide reliable findings. (7) These studies often did not include necessary controls or use an adequate sample size, and lacked reliable evaluation methods. Additionally, some reports in the literature resemble testimonials provided by the clients of the operator who developed the treatment. Because the scientific method was not used in these studies, the results are inconclusive. Because of questionable early clinical trials, the ADA formed an ad hoc Advisory Committee on Dentinal Hypersensitivity in 1986. This group was asked to quantify the variables associated with pain perceptions and to assist in standardizing study protocols?

It has been suggested that a well designed hypersensitivity study should include three groups: a control group that receives no treatment, a group that receives a placebo, and a group that is treated with the agent or procedure being tested. (43) This design would address the placebo effect that has proven problematic in hypersensitivity research. (56-58) The literature now provides guidance for designing a hypersensitivity clinical trial. (7,59)

Continued research is needed to compare various therapeutic interventions. When selecting treatment options, clinicians will want to utilize an evidence-based approach that incorporates careful scrutiny of the available scientific literature, clinician judgment, and client preferences. A systematic approach will encourage individualized treatment (Figure 9).

[FIGURE 9 OMITTED]

Conclusion

Sensitive teeth present a challenge for clients and for the professionals who care for them. Initial completion of a differential diagnosis to rule out other causes of tooth pain followed by a determination of the presence of the contributing factors of hypersensitivity (whenever possible) allows the clinician to manage the condition in ways that prevent further sensitivity. Additionally, it may be necessary to sequentially try a variety of treatment approaches to relieve the client's pain.

Dental hygienists are often the first to encounter a client's tooth sensitivity since dental hygiene care can elicit the hypersensitivity response from the tactile stimulus of instruments or the thermal stimulus of a cold water spray. Dental hygienists who have a complete understanding of the etiology of hypersensitivity, including management and preventive approaches, will be able to provide appropriate palliative and preventive care.
Table I. Subjective Pain Assessment Tools

VAS--Visual Analog Scale

No Pain/Discomfort   Severe
                     Pain/Discomfort

VRS--Verbal Rating Scale

0 = No discomfort/pain, but aware of stimulus
1 = Mild discomfort/pain
2 = Marked discomfort/pain
3 = Marked discomfort/pain that lasted more than 10 seconds

Table II. Trigger questions for assessment of
hypersensitive teeth

* Where does the pain occur, on which tooth or teeth?

* How much does it hurt on a scale of 1-10, with 10 being the most
  painful?

* How long does the pain last?

* Is the pain sharp, dull, shooting, throbbing, persistent, constant,
  pressure, burning, intermittent?

* Do certain foods stimulate the pain response?

* Does sensitivity result from hot or cold beverages?

* Does discomfort stop immediately upon removal of the painful


Suggested Review Readings

(1.) Dababneh RH, Khouri AT, Addy M. Dentine hypersensitivity--an enigma? A review of terminology, epidemiology, mechanisms, aetiology, and management. Brit Dent J 1999;187:606-611.

(2.) Addy M, Pearce N. Aetiological, predisposing and environmental factors in dentine hypersensitivity. Archs Oral Biol 1994;39 (suppl):335-385.

(3.) Dental Clinics of North America, Volume # 34, 1990. Entire volume is devoted to hypersensitivity.

(4.) Jacobsen, PL, Bruce G. Clnicai Dentin Hypersensitivity: Understanding the causes and prescribing a treatment. J Contemp Dental Practice, 2001;2:1-12. (On-line journal www.dentalcare.com)

(5.) Orchardson R, Gangrasa LP, Holland GR, Pashley DH, Trowbridge HO, Ashley FP, Kleinberg I, Zappa U. Dentine hypersensitivity--in to the 21st century. Archs Oral Biol 1994;39:1135-1195.

References

(1.) Dababneh RH, Khouri AT, Addy M: Dentine hypersensitivity--an enigma? A review of terminology, epidemiology, mechanisms, aetiology, and management. Brit Dent J 1999;187:606-11.

(2.) Addy M, Pearce N: Aetiological, predisposing and environmental factors in dentine hypersensitivity. Archs Oral Biol 1994;39 (suppl):335-85.

(3.) Addy M: Etiology and clinical implications of dentine hypersensitivity. Dent Clin No Amer 1990;34:503-14.

(4.) Taari Q, Awartani F: Clinical evaluation of cervical dentin sensitivity (CDS) in patients attending general dental clinics and periodontal specialty clinics (PSC). J Clin Perio 2002;28:16-22.

(5.) Ide M, Wilson RF, Ashley FP: The reproducibility of methods of assessment for cervical dentine hypersensitivity. J Clin Perio 2001;28:16-22.

(6.) Christenson GJ: Desensitization of cervical tooth structure. J Amer Dent Assoc 1998;129:765-66.

(7.) Holland GR, Narhi MN, Addy M, Gangarosa L, Orchardson R: Guidelines for design and conduct of clinical trials on dentine hypersensitivity. J Clin Perio 1997;24:808-13.

(8.) Curro FA. Tooth hypersensitivity in the spectrum of pain: Dent Clin No Am 1990;34:429-37.

(9.) Seltzer S, Bender IB: The Dental Pulp 4th ed. Hardgreaves KM, Goodis HE. (Ed). Quintessence, Chicago 2002: p. 73, 75, 181.

(10.) Pashley DH, Leibach JG, Homer JA: The effects of burnishing F/kaolin/glycerin paste on dentin permeability. J Periodontol 1987;58:19-23.

(11.) Fischer C, Wennberg A, Fisher RG, Attstrom R: Clinical evaluation of pulp and dentine sensitivity after supragingival and subgingival scaling. End of Dent Tramatol 1991;7:259-65.

(12.) Coleman TA, Kinderknecht KE: Cervical dentin hypersensitivity. Part I: The air indexing method. Quint Int 2000;31:461-65.

(13.) Smith BA, Ash MM Jr: Evaluation of a desensitizing dentifrice and cervical hypersensitivity. J Amer Dent Assoc 1964;68:639-47.

(14.) Minkoff S, Azelrod S: Efficacy of strontium chloride in dental hypersensitivity. J Periodontol 1987;58:470.

(15.) Stark MM, Pelzner RB, Leung RL: Rationalization of electric pulp-testing methods. Oral Surg 1977;43:598-606.

(16.) Thrash WJ, Dorman HL, Smith FD: A method to measure pain associated with hypersensitive dentin. J Periodontol 1983;54:160-62.

(17.) Flynn J, Galloway R, Orchardson R: The incidence of hypersensitive teeth in the West of Scotland. J Dent 1985;13:230-36.

(18.) Rees JS. The prevalence of dentin hypersensitivity in general dental practice in the UK: J Clin Periodontol. 2000;27:860-65.

(19.) Collaert B, Fischer C: Dentin hypersensitivity--a review. Endod Dent Traumatol 1991;7:145-52.

(20.) Fischer C, Fischer RG, Wennberg A: Prevalence and distribution of cervical dentine hypersensitivity in a population in Rio de Janeiro, Brazil. J Dent 1992;20:272-76.

(21.) Graf H, Galasse R: Morbidity, prevalence and intra-oral distribution of hypersensitive teeth. J Dent Res 1977; 162 (Sp Issue A):56.

(22.) Chabanski MB, Gillam DG, Bulman JS, Newman HN: Clinical sensitivity in a population of patients referred to a specialist periodontal department: A pilot study. J Oral Rehabil 1997;24:666-72.

(23.) Fillingham RB: Sex, gender and pain: women and men really are different. Curr Rev Pain 2000;4(1):24-30.

(24.) Woofter C: The prevalence and aetiology of gingival recession. Perio Abstr 1969;17:45-50.

(25.) Addy M, Mostafa P, Newcombe RG: The distribution of recession, sensitivity and plaque. J Dent 1987;15:242-48.

(26.) Blandy AA. On the sensibility of teeth: Am J Dent Sci 1850-1851;1:22-8.

(27.) Kramer IRH: The relationship between dentine sensitivity and movement in the contents of the dentinal tubules. Br Dent J 1955;98:391-92.

(28.) Fearnhead RW: Innervation of dental tissues. In Miles AEW (ed): Structure and Chemical Organization of Teeth, Vol 1. Academic Press, NY 1967, p. 247-81.

(29.) Brannstrom M: The hydrodynamics of the dentinal tubule and of pulp fluid. Caries Res 1967;1:310-17.

(30.) Absi EG, Addy M, Adams D: Dentine hypersensitivity: The development & evaluation of a replica technique to study sensitive and non-sensitive cervical dentine. J Clin Periodontol 1989;16:190-95.

(31.) Addy M, Mostafa P, Absi Eg, et al.: Cervical dentin hypersensitivity: Etiology and management with particular reference to dentifrices. In Rowe NH (ed). Hypersensitive Dentin: Origin and Management. University of Michigan 1985, p 43.

(32.) Syngcuk K: Hypersensitive teeth: Desensitization of pulpal sensory nerves. J Endond 1986;12:482-485.

(33.) Arwill T: Studies on the ultrastructure of dental tissues II. The predentine-pulpal border zone. Odontol Revy 1967;18:191-208.

(34.) Frank RM: Attachment sites between odontoblast process and the intradental nerve fibers. Arch Oral Biol 1968;13:833-34.

(35.) Thomas HF: The lamina limitations of human dentinal tubules. J Dent Res 1984;63:1064-66.

(36.) Thomas HF, Cavrella P: Correlation of scanning and transmission electron microscopy of human dentinal tubules. Arch Oral Biol 1984;29:641-46.

(37.) Rushton MA, Cooke BED: Oral Histopathology. E & S Livingstone, London 1963; p94.

(38.) Cohen S, Burns RC, Eds: Pathways of the Pulp, 8th ed. Mosby, St. Louis, 2002.

(39.) McComb D, Smith DC: A preliminary scanning electron microscopic study of root canals after endodontic procedures. J Endond 1975;7:238.

(40.) Absi EG, Addy M, Adams D: Dentine hypersensitivity. The effect of toothbrushing and dietary compounds on dentine in vitro. J Oral Rehab 1992;19:101-10.

(41.) Davis WB: The cleansing, polishing and abrasion of teeth by dental products. Cosmetic Sci 1978;1:39-81.

(42.) Beck JD, Hunt RJ, Hand JS, Field HM: Prevalence of root and coronal caries in a non-institutionalized older population. J Amer Dent Assoc 1985;111:964-67.

(43.) Trowbridge HO, Silver DR: A review of current approaches and in-office management of tooth hypersensitivity. Dent Clin No Am 1990;34:561-87.

(44.) Shortall AC: Cavity cleansers in restorative dentistry. Br Dent J 1981;150:243-47.

(45.) Bissada NF: Symptomology & clinical features of hypersensitive teeth. Archs Oral Biol 1994;39:315-25.

(46.) Pindborg JJ: Pathology of the hard dental tissues. Munksgaard, Copenhagen 1970, p 312-21.

(47.) Davis WB, Winter PJ: The effect of abrasion on enamel and dentine after exposure to dietary acid. Br Dent J 1980;148:253-56.

(48.) West N, Addy M: The in vitro effects of toothbrushing, toothpaste and dietary acids on dentine. J Dent Res 1993;72:728(Abstr 336).

(49.) Absi EG, Addy M, Adams D: Dentine hypersensitivity. The effect of toothbrushing and dietary compounds on dentine in vitro. J Oral Rehabil 1992;19:101-10.

(50.) Coleman TA, Grippo JO, Kinderknecht JE: Cervical dentin hypersensitivity. Part II: Associations with abfractive lesions. Quint Intl 2000;31:466-73.

(51.) Milosevic A: Toothwear aetiology and presentation. Dent Update 1998;25:6-11.

(52.) Addy M, Absi EG, Adams D: Dental hypersensitivity: the effects in vitro of acids and dietary substances on root planed and burred dentine. J Clin Periodontol 1987;14:274-79.

(53.) Pashley DH: Smear layer: Physiological considerations. Oper Dent 1984;3(suppl): 13-16.

(54.) Pashley DH, O'Meara JA, Kepler EE, Galloway SE, Stewart FP: Dentine permeability: Effects of desensitizing dentrifices in vitro. J Periodontol 1984;55:522-25.

(55.) Ad Hoc Advisory Committee on Dentinal Hypersensitivity. Council on Dental Therapeutics: Recommendations for evaluating agents for the reduction of dentinal hypersensitivity. J Amer Dent Assoc 1986;112:709.

(56.) Yates R, West N, Addy M, Marlow I: The effects of a potassium citrate, cetylpyridinium chloride, sodium fluoride mouthrinse on dentine hypersensitivity, plaque and gingivitis. A placebo controlled study. J Clin Perio 1998;25:813-20.

(57.) Overman PR: Calcium hydrophosphate as a root densensitizing agent. Dent Hyg 1983;57:35.

(58.) Green BL, Green ML, McFall WT: Calcium hydroxide and potassium nitrate as densensitizing agents for hypersensitive root surfaces. J Periodontol 1977;48:667.

(59.) Gillam DG: Clinical trial designs for testing of products for dentine hypersensitivity-A Review. Perio Abst 1997;45:37-46.

(60.) Kuroiwa M, Kodaka T, Kuroiwa M, Abe M: Dentine hypersensitivity occlusion of dentinal tubules by brushing with and without an abrasive dentifrice. J Periodontol 1994;65:291-96.

(61.) Lavigne SE, Gutenkunst LS, Williams KB: Effects of tartar control dentifrice on tooth sensitivity: a pilot study. J Dent Hyg 1997;71(3):105-11.

(62.) Absi EG, Addy M, Adam D: Dentin hypersensitivity: uptake of toothpastes onto dentin and effect of brushing, washing and dietary acid, SEM in vitro study. J Oral Rehabil 1995;22:175-82.

(63.) Bhati SA, Walsh TF, Douglas CIW: Ethanol and pH levels of proprietary mouthrinses. Comm Dent Health 1994;11:71-74.

(64.) Addy M, Loyn T, Adams D: Dentine hypersensitivity--effects of some proprietary mouthwashes on the dentine smear layer: a SEM study. J Dent 1991;19:148-52.

(65.) Lawson K, Gross KB, Overman P, Anderson D: Effectiveness of chlorhexidine and sodium fluoride in reducing dentin hypersensitivity. J Dent Hyg 1991;65:340-43.

(66.) Pereira R, Chava V: Efficacy of a 3% potassium nitrate desensitizing

mouthwash in the treatment of dentinal hypersensitivity. J Periodontol 2001;72:1720-25.

(67.) Cooley RL, Sandoval VA: Effectiveness of potassium oxalate treatment on dentin hypersensitivity. Gen Dent 1989;37(4):330-33.

(68.) Spranger H: Investigation into the genesis of angular lesions at the cervical region. Quint Int 1995;26:149-54.

(69.) Marini I, Luigi C, Vicchiet F, Spiazzi L: Intraoral fluoride releasing device: a new clinical therapy for dentine sensitivity. J Periodontol 2000;71:90-95.

(70.) Scherman A, Jacobsen PL: Managing dentin hypersensitivity: what treatment to recommend to patients. J Am Dent Assoc 1992;123(4):57-61.

(71.) Miller JT, Shannon IL, Kilgore WG, Bookman JE: Use of water-free stannous fluoride-containing gel in the control of dental hypersensitivity. J Periodont 1969;40:490-91.

(72.) Gaffar A: Treating hypersensitivity with fluoride varnishes. Compendium 1998;19(1):1088-97.

(73.) Peterson LG: Fluoride mouthrinses and fluoride varnishes. Caries Res 1993;27(supple1):35-42.

(74.) Clark DC, Hanley JA, Geoghegan S, Vinet D: The effectiveness of fluoride varnish and a desensitizing toothpaste in treating dentin hypersensitivity. J Period Res 1985;20:212-19.

(75.) Johnson R, Muzzin KB: Effects of potassium oxalate on dentin hypersensitivity in vivo. J Periodontol 1989;60(3):151-8.

(76.) Wichgers MAJ, Emert LTC: Dentin hypersensitivity. General Dent 1996;44(3):225-30.

(77.) McBride M, Gilpatrick R, Fowler, W: The effectiveness of sodium fluoride iontophoresis in patients with sensitive teeth. Quint Int. 1991;22:637-40.

(78.) Wan-Hong Lan, et al: The combined occluding effect of sodium fluoride varnish and Nd: YAG laser irradiation on human dentinal tubules. J Endodontics. 1999;25(6):424-26.

(79.) Moritz A, et. al. Long-term effects of CO2 laser irradiation on treatment of hypersensitive dental necks: results of an in vivo study. J Clin Laser Med & Surg. 1998;16(4):211-15.

(80.) Jacobsen PL, Bruce G: Clinical dentin hypersensitivity: understanding the causes and prescribing a treatment. J Contemporary Dent Practice 2001;2(1):1-8. (online publication)

(81.) Frazier KB, Haywood VB: Teaching nightguard bleaching and other tooth-whitening procedures in North American dental schools. J Dent Educ 2000;64(5):357-64.

(82.) Leonard RH Jr, Haywood VB, Phillips C: isk factors for developing tooth sensitivity and gingival irritation associated with nightguard vital bleaching. Quint Int 1997;28:527-34.

(83.) Haywood VB, Caughman WF, Frazier KB, Myers ML: Tray delivery of potassium nitrate-fluoride to reduce bleaching sensitivity. Quint Int 2001;32(2):105-9.

(84.) Tam L: Effect of potassium nitrate and fluoride on carbamide peroxide bleaching. Quint Int 2001;32(10):766-70.

(85.) Mokhlis GR, Matis BA, Cochran MA, Eckert GJ: A clinical evaluation of carbamide peroxide and hydrogen peroxide whitening agents during daytime use. J Am Dent Assoc 2000;131:1269-77.

(86.) Newman P, Addy M: Comparison of hypertonic saline and chlorhexidine mouthrinse after the inverse bevel flap procedure. J Periodontol 1982;53:315-18.

(87.) Kawasaki A, Ishikawa K, Suge T, Shimizu H, Suzuki K, Matsuo T, Ebisy S: Effects of plaque control on the patency and occlusion of dentine tubules in situ. J Oral Rehabil 2001;28:439-49.

(88.) Lundy T., Stanley HR: Correlation of pulpal histopathology and clinical symptoms in human teeth subjected to experimental irritation. Oral Surg 1969;76:187.

RELATED ARTICLE: Course instructions.

This is a continuing education home-study course. It comes in two parts--the course and the post-test. Most state dental boards will accept the course for fulfillment of CE requirements toward licensure renewal. However, the course is not valid unless you take the post-test and send it in for grading. If you pass the course, you will receive a certificate of completion for submission to your state dental board or to keep on file in the event of an audit, depending on the roles in your area.

Please consult the chart on page 314 to verify if this course is approved for CE in your state and to learn if there are special requirements. Please note that the chart contains general information valid as of the date of publication. If you have specific questions about your license renewal requirements, or if you're not sure if the course will be accepted, please consult your state dental board.

After you have finished studying the course, please take the post-test beginning on page 312, complete the answer sheet on page 313, and send it to ADHA, along with the processing fee, for grading.

RELATED ARTICLE: CREDITS: 2 hours.

COURSE GOALS: The purpose of this continuing education course is to review the scientific and clinical evidence pertaining to dentin hypersensitivity. The pain experience associated with hypersensitivity, the prevalence of the condition, relevant tooth/root biology, pain transmission theory, etiology of dentin exposure, clinical assessment considerations, clinical research issues, treatment approaches, and therapeutic agents and options will be discussed.

LEARNING OUTCOMES:

Upon completion of this course, the participant will be able to:

1. Describe the pain sensation of sensitive teeth.

2. Discuss prevalence features related to periodontal status, age, gender, and tooth type and surface.

3. Describe the orientation and the role of the enamel, cementum, dentin, dentinal tubules, tubular fluid, pulp, nerve fibers, and odontoblasts in hypersensitivity.

4. Identify the stimuli that lead to nerve depolarization.

5. Explain the hydrodynamic theory.

6. Identify common causes of gingival recession and loss of tooth structure, as well as the role of each in the development of hypersensitivity.

7. Identify other conditions that manifest as tooth pain and describe the process of differential diagnosis.

8. Discuss factors related to hypersensitivity, including the role of plaque, bleaching, oral habits, and diet.

9. Discuss the challenges that are inherent in clinical hypersensitivity research.

10. Describe how treatment strategies impact hypersensitivity.

11. Explain the process of natural remission of hypersensitivity.

12. Evaluate treatment and management options including self- and professionally applied desensitizing agents.

ASSESSMENT METHOD: Post-test only

RELATED ARTICLE: Predisposing factors to gingival recession.

* Anatomic narrow zone of attached gingiva

* Tooth malposition/thin buccal plate of bone or tissue

* Excessive use/pressure with oral hygiene devices

* Periodontal diseases, including NUG

* Oral viral infections

* Tooth preparation for restorations

* Post-periodontal non-surgical or surgical treatment

RELATED ARTICLE: Loss of tooth structure.

Predisposing Factors:

* Erosion

* Abrasion

* Attrition

* Anatomic zone of exposed dentin at CEJ

* Abfraction

* Crown preparation

* Combined effects

RELATED ARTICLE: Ideal desensitizing agents.

* Minimum application time

* Does not endanger the soft tissues

* Minimum expense

* Minimum number of dental appointments

* Does not cause pulpal irritation or pain in general

* Easy application procedure

* Rapid and effective for long time

* Causes no staining

* Consistently effective

(Adapted from Grossman, L.I. A systemic method for the treatment of hypersensitive dentin, J Amer Dent Assoc1935;22:592.)

RELATED ARTICLE: Role of plaque.

The effectiveness of clients' plaque removal should be assessed when evaluating causes of tooth sensitivity. However, the role of plaque in the initiation and/or persistence of cervical hypersensitivity is controversial. Logic would suggest that plaque deposits would likely demineralize tooth structure and perhaps lead to gingival/periodontal pathology, and initiate gingival recession as a precursor to hypersensitivity. The clinical reality is that the teeth with the most extensive recession and hypersensitivity usually have been subjected to excessive buccal tooth cleaning, and therefore exhibit little to no plaque.

Further evidence against the role of plaque in hypersensitivity comes from reports of sensitivity following periodontal surgery where chemical agents such as chlorhexidine have rendered the teeth nearly plaque free. (86) Additionally, some people with periodontal disease often harbor copious amounts of plaque on their teeth and report no sensitivity. Following periodontal therapy, they demonstrate relatively plaque-free tooth surfaces, yet report experiencing hypersensitivity. This post-surgical sensitivity frequently occurs several days after surgery rather than immediately. (44,52)

However, plaque has been shown to play a role in the patency of dental tubule orifices. One study found that when plaque was not removed from teeth the diameter of the tubule orifices increased to three times their original size within three. (87) With plaque control, the orifices became less than 20% of their original diameter within one week, suggesting that plaque control can occlude tubules. These investigators concluded that plaque removal does play a key role in the patency versus occlusion of dentinal tubules and thus the process of hypersensitivity. (87)

Bacteria have been shown to diffuse into open dentin tubules and may diffuse into the pulp resulting in hypersensitivity. (88) However, the diffusion would be against the outward flow of dentinal fluid. Such bacterial penetration could occur as a result of marginal leakage or secondary decay around restorations. The deleterious effect of the bacterial toxins would be inflammation of the pulp. If hypersensitivity is defined as a reaction to a non-noxious stimulus, then plaque-induced dentin sensitivity would not be as true hypersensitivity.

RELATED ARTICLE: Research challenges.

* Placebo effect

* Standardization of stimulus

* Objective pain measurement

* Natural spontaneous remission

RELATED ARTICLE: Topics for future research.

* Role of CNS in hypersensitive teeth

* Prevalence studies to more clearly identify individuals at risk

* Role of plaque bacteria and biofilms

* Effects of demineralization and remineralization * Role of salivary buffers

* Is inflammation involved in dentinal hypersensitivity?

* Role of abfraction lesions

Terri S.I. Tilliss, RDH, MS, MA, is a professor in the Dental Hygiene Department at the University of Colorado School of Dentistry. She is a PhD candidate in the Health and Behavioral Sciences program at the University of Colorado. Janis G. Keating, RDH, MA, is an associate professor in the Dental Hygiene Department at the University of Colorado School of Dentistry.
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Author:Tilliss, Terri S.I.; Keating, Janis G.
Publication:Journal of Dental Hygiene
Geographic Code:1USA
Date:Sep 22, 2002
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