This article reviews the evidence regarding the effectiveness of various patient-applied interventions for dentinal hypersensitivity. Self-applied treatments are popular because they are both economical and easy to use. The disadvantages include compliance, difficulty to deliver to specific sites, slow onset of action, and the requirement for continuous use. Conflicting research findings make it difficult for the practitioner to determine which self-applied product to advise patients to use. There are a number of issues that have plagued research in this area, including the lack of standardization of stimulus testing and inadequate sample size. The evidence is insufficient to permit the development of evidence-based guidelines for the treatment of dentinal hypersensitivity.
Dentinal hypersensitivity (DH) is defined as an exaggerated response to nonnoxious and noxious stimuli. A more specific definition was provided by Holland and colleagues, who stated that DH is a “short, sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic, or chemical and which cannot be ascribed to another form of dental defect or pathology.” The etiology and diagnosis of this condition is discussed by Sabbagh, Brown, and Thomas elsewhere in this issue. The purpose of this article is to examine the evidence regarding the effectiveness of various patient-applied interventions for DH.
Treatment options for dentinal hypersensitivity
A variety of patient-applied products have been developed for the treatment of DH. The majority of products focus on blocking the mechanism of pain transmission, primarily by dentinal tubule obturation and increased pain threshold of sensory nerves. The goal of such therapies is to prevent the pain signal from being triggered. We will review the literature on various treatments for DH, both self-applied and in-office treatments.
The search strategy for this review included a MEDLINE search (through PubMed) to identify English-language articles published between 1960 to 2007. The search terms used are shown in Box 1 . Various combinations of these terms were used. The “related articles” feature of PubMed was also used to identify additional citations. The searches yielded a large number of citations, most of which consisted of low-level evidence (eg, small exploratory studies and in vitro experiments). These reports were examined by title and abstract to ascertain relevance. If the content was related to the research question and met the original inclusion criteria ( Box 2 ), then the full report was retrieved. Very few publications met even the most liberal interpretation of the inclusion criteria (see Box 2 ). The Cochrane Library was also searched for systematic reviews and reviews of effectiveness related to DH.
a Commonly used conversions when researching electronic databases.
Study type: randomized clinical trials, clinical trials, meta-analyses, systematic reviews, or evidence-based practice guidelines
A more focused search was then conducted, using the search terms “dentinal hypersensitivity” and using the “limits” tool to restrict the search to clinical trials, meta-analyses, practice guidelines, and randomized controlled trials. This search was also limited to English-language publications. Twenty-five citations were returned, of which none were systematic reviews of the topic. Only seven of the reports had been published since 2000. Most were small pilot or exploratory studies that tested only two interventions. The more inclusive search did yield a number of narrative reviews, but none were systematic reviews or meta-analyses. Thus, the level of evidence in support of any intervention is rather weak, according to the techniques of evidence-based health care. The remainder of this article describes and analyzes the results of this search as it applies to in-office interventions for DH, although it must be noted that the level of evidence is insufficient to permit definitive recommendations to be made regarding the management of this condition. Due to the paucity of high-level evidence, this review has, of necessity, been configured as a narrative review, since a systematic review of this topic is not possible at this time.
Self-Applied Desensitizing Agents
The ideal patient-applied desensitizing agent should be nonirritating to the pulp, leave no deposits on tooth surfaces or restorations, and should not be irritating to the soft tissues. To ensure compliance the product should be easily applied, have a rapid onset, produce long-lasting relief, and provide effective relief from DH.
There are two major sites of action for self-applied DH-treatment products. The majority of products reduce fluid movement through dentin by obturating the tubules. This concept is based on Brannstrom’s hydrodynamic theory of DH which asserted that fluid movement in the dentinal tubules can generate action potentials in associated afferent nerve fibers. A second therapeutic strategy targets these nerve fibers. These products act to decrease the activity of dentinal sensory nerves thereby preventing the pain signal from being transmitted to the central nervous system. The mechanism of action for DH products can include one or both of these mechanisms. Many of these agents are reviewed below.
A PubMed search was conducted using the search term “strontium” in the title or abstract field (with limits set to dental journals only). Thirty-three citations were returned. Only three of these had been published since 2000. Strontium has been suggested to have several effects on teeth, including a cariostatic effect which is alleged to be most effective in the pre-eruptive phase of tooth formation. Additionally, there is some evidence that strontium may have an effect on cariogenic bacteria when used topically. Strontium can substitute for calcium in activating secretory mechanisms and can also possibly affect or modulate the pulpal cholinergic and adrenergic mechanisms involved in DH.
The manner in which strontium affects DH has not been elucidated, but it has been proposed that the ions occlude dentinal tubules by binding to the tooth substance and stimulating reparative dentin formation. It has also been suggested that strontium ions have the capacity to reduce sensory nerve activity, but less effectively than potassium ions. However, Kishore and colleagues reported that strontium chloride is more effective than potassium nitrate. These workers demonstrated that 10% and 2% strontium chloride significantly reduced DH, while a 5% solution of potassium nitrate did not show a significant reduction in DH.
Dentifrices containing 10% strontium chloride have been widely used as desensitizing agents and were one of the first agents to be marketed for that purpose. Cohen found that 67% of the subjects using a strontium chloride-containing toothpaste reported complete relief of DH within a 2 month period. Meffert and Hoskins reported that 78% of the subjects achieved almost complete relief of DH. In a double-blinded, placebo-controlled study (n = 62), Minkoff and Axelrod found that 10% strontium chloride is an effective treatment for DH. The effectiveness was evident within 2 weeks and lasted for the length of the 6-week study. Following periodontal surgery, Uchida and colleagues treated DH patients with a 10% strontium chloride dentifrice. The 10% strontium chloride dentifrice was more effective in treating DH following periodontal surgery than a placebo dentifrice.
Some reports suggest that strontium is less effective than other desensitizing agents. For example, potassium nitrate has replaced strontium chloride in the treatment of DH. Silverman and colleagues conducted a multicenter clinical trial that compared 5% potassium nitrate-containing dentifrices (with and without 0.243 percent sodium fluoride) with a 10% strontium chloride-containing dentifrice. The study sample consisted of 230 adults who were followed for 8 weeks. Both the potassium nitrate dentifrices were reported by subjects to be significantly superior to the negative placebo and strontium chloride dentifrices. Clinical evaluations gave similar results. The study was conducted in several private practices. This study was reasonably well-powered, but was of relatively brief duration. Other investigators have also reported the superiority potassium nitrate over strontium chloride.
In summary, there is some evidence supporting the effectiveness of patient-applied strontium chloride as a treatment for DH, although the evidence is generally of low quality. One of the trials was a multicenter, placebo-controlled trial with a reasonable sample size. This study did demonstrate the superiority of two potassium nitrate toothpastes to a strontium chloride-containing dentifrice and a negative placebo.
Potassium salts block neural transmission at the pulp and depolarize the nerve around the odontoblasts. Potassium nitrate has been incorporated into both toothpastes and mouthrinses for use as a treatment for DH. Kim reported for the first time that the potassium ion is the active portion of potassium nitrate. Greenhill and Pashley found potassium nitrate ineffective in decreasing dentinal fluid flow in vitro coated dentin, even at 30% concentration. This suggests a lack of effect on fluid flow.
Products containing potassium have been studied to evaluate the efficacy of potassium nitrate as a desensitizing agent. For example, Tarbet and colleagues found that a 5% potassium nitrate paste reduced DH effectively at 1 week and up to 4 weeks. Tarbet and colleagues also compared the abilities of strontium chloride, dibasic sodium citrate, formaldehyde and potassium nitrate to desensitize hypersensitive teeth and reported that 5% potassium nitrate was the most effective in reducing DH.
More recently, Nagata and colleagues compared the effectiveness of a 5% potassium nitrate dentifrice compared with placebo in a double-blind study and found a significant reduction in DH for subjects using potassium nitrate. Placebo subjects showed a 6% reduction in DH, while 67% of the potassium nitrate subjects reported complete relief throughout the 12 weeks of the study. As with many of the studies in this area, the sample size was small (N = 36).
Before the early 1990s, desensitizing dentifrices with potassium nitrate were not combined with fluoride agents in the United States. This was inconvenient, as many patients who wished to use the desensitizing dentifrices had to also use another toothpaste if they wished to receive the effect of the fluoride. In 1992, the US Food and Drug Administration considered the combination of 5% potassium nitrate and fluoride dentifrice as a safe and effective combined treatment option. In a multi-center double-blind controlled study, Silverman and colleagues found that the combination of 5% potassium nitrate and 0.243% sodium fluoride in dentifrice is significantly more effective in the treatment of DH than a 10% strontium chloride-containing dentifrice. Additional clinical research has confirmed the effectiveness of the potassium nitrate–fluoride dentifrice in the treatment of DH.
While most of the research in this area has used potassium nitrate, some investigators have used potassium citrate. Hu and colleagues recently compared a dentifrice containing 5.5% potassium citrate to a commercially available dentifrice containing 3.75% potassium chloride, 0.32% sodium fluoride, and 0.3% triclosan in a silica base. There was no statistically significant difference between these formulations. This was an 8-week double-blinded study involving 80 subjects. Chesters and colleagues compared a potassium citrate–sodium monofluorophosphate (PC–SMFP) dentifrice to potassium nitrate-SMFP and control dentifrices containing only SMFP and reported that the PC–SMFP was significantly more effective in reducing DH.
Whereas many studies have found potassium nitrate toothpastes to have some effect in reducing DH, a recent systematic review published in the Cochrane Database found “no clear evidence is available for the support of potassium-containing toothpastes for DH.”
Dibasic sodium citrate
In an in vitro study by Greenhill and Pashley, a 19% reduction in dentinal fluid flow was thought to be attributable to dentinal tubule obturation. In a number of double-blind, placebo-controlled studies, dibasic sodium citrate was significantly superior to a placebo in reducing DH. However, in a 6 week trial, sodium citrate dentifrice was not significantly more effective than a 0.76% SMFP control.
Clinical trials have shown that some fluoride dentifrices or concentrated fluoride solutions are effective in producing favorable results in the treatment of DH. Tal and colleagues proposed that precipitated fluoride compounds may reduce DH by occlusion of the dentinal tubules. In a 3 month study, Kanouse and Ash reported that subjects using a monofluorophosphate (MFP) dentifrice had a statistically significant increased tolerance to cold and hot in comparison to subjects using a placebo dentifrice.
Stannous fluoride has also been proposed as a treatment for DH. Thrash and colleagues noted that topical application of 0.717% aqueous stannous fluoride (SnF 2 ) gave patients immediate relief from DH. Blong and colleagues found that application of 0.4% SnF 2 gel was also an effective treatment for DH. However, prolonged use of the SnF2 gel with a minimum of 4 weeks of treatment was necessary to achieve satisfactory results.
Schiff and colleagues recently examined the efficacy and safety of a toothpaste containing 0.454% stabilized SnF 2 and sodium hexametaphosphate (SHMP). The control dentifrice was a sodium fluoride dentifrice. The double-blind, parallel-group, randomized clinical trial had subjects using the SnF 2 and SHMP or the control dentifrice twice a day for 8 weeks. The SnF 2 and SHMP produced a significant reduction in DH and a mean desensitizing improvement of 71% greater than the sodium fluoride control group.
Orchardson and Gillam suggest that prevention of DH is not given enough emphasis by dental professionals. Reduction of risk factors should generally be considered when treating any condition. The identification and elimination of such factors should routinely be considered when developing a treatment plan. Risk factors allegedly associated with DH include exposure to erosive substances (eg, acidic beverages) and brushing with an abrasive paste. The effect of chemically erosive substances can be limited by treatment of gastroesophageal reflux disease, limiting consumption of acidic foods and beverages, and avoiding brushing for two to three hours after consumption of acidic substances (or following an episode of gastric reflux). Dietary analysis may be a useful tool in risk assessment.