Management of dentinal hypersensitivity
By Alessandra Helen Magacho Vieira, DDS, MS
Sergio Lima Santiago, DDS, MS, PhD
Featured in General Dentistry, March/April 2009
Pg. 120-126

Posted on Friday, March 06, 2009

Dentinal hypersensitivity is a complex condition that can cause considerable concern in the dental office. Despite the large number of available treatment modalities, no current desensitizing agent is considered ideal for managing this uncomfortable condition. Selecting the right therapy requires a complete understanding of how applying a stimulus to the exposed dentin surface can influence the nerve fibers and produce hyperesthesia. This article reviews the etiology and critically analyzes management of dentinal hypersensitivity by reviewing laboratory and clinical investigations.

Received: March 30, 2008

Accepted: June 16, 2008

Dentinal hypersensitivity is an exaggerated response of exposed dentin that makes contact with thermal, evaporative, tactile, osmotic, or chemical stimuli.1 It is characterized by a localized, transient, sharp sensation that may range from mild discomfort to extreme pain.1,2 Depending on its intensity, the hyperesthesia can affect eating, drinking, and breathing; hinder one’s ability to control dental plaque effectively; and may even result in emotional changes that alter a patient’s lifestyle.¹

Among reported cases of odontalgia, pain in the dentin is considered the most frequent complaint.3 Prevalence studies concerning dentinal hypersensitivity indicate that it affects 10–30% of the general population.^2,4-8 Moreover, as teeth are being retained for longer periods, the number of patients with this condition will increase.^1,2,4,9,10

Several theories have been proposed to explain the mechanism of dentinal hypersensitivity.^4,11-14 The hydrodynamic theory is considered the most widely accepted explanation for the presence of stimuli on the dentin surface and nerve activation.^11,12,14-20 According to this theory, dentin exposure to the oral environment and the patency of the dentinal tubules are the main factors associated with dentinal hypersensitivity.^2,11,18,21 Dentin exposure usually results from enamel loss by erosion, abrasion, abfraction, or denudation of root surfaces due to gingival recession or periodontal procedures.^{1,3,4,17,22,23}

A number of treatment modalities are available in the literature for managing dentinal hypersensitivity.^{3,4,9,10,14,16,17,19} The most common involves local application of desensitizing agents, either by a dental professional or by the patient at home.⁴ Nevertheless, no single product contains all of the qualities that would designate it as the ideal dentin desensitizer.^3,4

Critical analysis concerning the development of this hyperesthesia and the therapeutic approaches for treating it are indispensable to control its incidence and suggest an effective treatment. This article analyzes laboratory and clinical studies that relate to the etiology and management of dentinal hypersensitivity.

Mechanisms of dentinal pain

The mechanism of dentinal pain in response to a variety of stimuli is very complex and is not yet understood clearly.^15,17,24,25 Several theories have been proposed in recent years to explain this mechanism.^4,11-14,26

According to the transducer theory, the odontoblastic processes can be excited directly by a variety of sensorial stimuli, releasing neurotransmitters that conduct impulses to the nerve endings.^4,15,24 The neural theory is based on the hypothesis that an applied stimulus can directly influence the nerve terminals within the dentinal tubules through direct communication with nerve fibers from the dental pulp.^4,11,15,24 However, there was no solid evidence to support either of these theories.^4,11,14,24

The most widely accepted hypothesis about how the stimuli influence nerve fibers is the hydrodynamic theory, which states that pain from exposed dentin following stimulation results from rapid fluid movement inside the dentinal tubules.^11,12,14-20 The presence of tube-like structures in hypersensitive dentin is important in maintaining the patency of the dentinal tubules, as these structures may contain sulfur-rich, non-collagenous acidic phosphoproteins. These phospho-proteins have been implicated in the stabilization of the tube-like lamina limitans and may prevent the mineralization of hypersensitive dentin surfaces.²⁷ Yoshiyama et al observed biopsies of hypersensitive regions and noted that 75.8% of dentinal tubules displayed hollow, tube-like structures within the lumina. By comparison, biopsies in non-sensitive areas of the same teeth revealed these tube-like structures in only 20.4% of the dentinal tubules.²⁷

The movement of fluid inside the dentinal tubules that is elicited by hydrodynamic stimuli is thought to serve as a fluid transducer, signaling the presence of stimuli at the outer opening of the tubules.^25,26 Depending on the nature of the applied stimulus, the fluid within the dentinal tubules can be displaced easily in either an inward or outward direction; such movement alters the intrapulpal pressure and causes pain by stimulating nociceptive nerve fibers located on the pulpal side of the tubules (Fig. 1).^11,12

The pressure on the nerve endings of the subodontoblastic plexus produces deformations on the nerve membranes and opens the channels that are permeable to sodium.¹³ The concentration gradient and negative charge in extracellular fluid causes these ions to enter the fiber through these channels and depolarize the membrane.¹³ After nerve activation, nociceptive signals are transmitted to the trigeminal nuclear complex located in the medulla. This site processes and transfers these signals to higher brain regions. This is important, as it is believed that the perception of pain occurs primarily within the cerebral cortex.²⁶

Management of dentinal hypersensitivity

The management of dentinal hypersensitivity should be based on a correct diagnosis of both the condition and its causative factors.²⁸ In addition to the desensitizing approach, the treatment plan for dentinal hypersensitivity should identify and eliminate any predisposing etiologic factors (such as endogenous or exogenous acids and toothbrush trauma) to prevent or minimize additional damage to the exposed dentin surface; otherwise, the treatment is likely to provide only short-term success.^20,28,29

For years, an effective treatment for dentinal hypersensitivity has been a challenge for clinicians.⁴ Historically, several desensitizing agents have been used for treating this condition, including hot oil, arsenic, silver nitrate, and formaldehyde.²³ More recently, other types of treatment (including oxalates and calcium phosphate solutions) have shown significant effectiveness in reducing hyperesthesia.^{3,14,17,19,23,30-33}

Dentin desensitizers usually belong to one of three categories: anti-inflammatory, therapeutic occlusive, and nerve-fiber depolarization agents.¹⁹ Since the hydrodynamic mechanism is the most accepted explanation for dentinal pain, products that interfere with dentinal permeability appear to be more appropriate for desensitization.^3,6,23,24,26 The occlusion of dentinal tubules promotes reduction in dentinal permeability and decreases the degree of pain proportionally.^3,6,24,30,34 This occlusion can be obtained through protein precipitation, particle deposition, laser application, or restorative procedures.^18,19

The ideal therapeutic occlusive agent must meet several requirements.³⁵ It should have long-term effectiveness and it should be easy and practical to apply, well-tolerated by the patient, and not irritating to the pulp.^3,35 However, no currently available agent incorporates all of these requirements.^3,19,35 Products that obliterate dentinal tubules (including oxalates, fluorides, laser beams, and calcium phosphate solutions) have been tested intensely through laboratory and clinical studies (see Tables 1 and 2).^{3,10,14,17-19,23,24,31-33,36-44}

Laboratory investigations

Greenhill and Pashley evaluated dentin desensitizers in terms of their ability to reduce the rate of fluid flowing through dentin discs. Specimens treated with 30% potassium oxalate presented the largest reduction (98.4%) in the hydraulic conductance of dentin. This reduction probably resulted from the deposition of insoluble calcium oxalate crystals on the dentin surface; these crystals control the permeability of the exposed dentin.²⁴

Four years later, Pashley and Galloway applied 30% neutral dipotassium oxalate and acidic 3% monopotassium-monohydrogen oxalate in different experimental groups of dentin discs. The authors also reported a reduction in dentin permeability after dentin surface treatment with potassium oxalate.³⁶

A 2005 in vitro study by Pereira et al observed that potassium oxalate-based agents were able to reduce filtration values by approximately 83%, similar to filtration values for the smear layer. In this study, fluoride gel reduced hydraulic conductance from 41.47–77.47%.⁴³ According to a 2006 study by Santiago et al, various potassium oxalate formulations decreased dentin permeability by approximately 75%, indicating the effectiveness of these products.²³

A 1995 study by Suge et al examined dentin discs treated with the calcium phosphate precipitation method and those treated with potassium oxalate, sodium fluoride, and strontium chloride. The calcium phosphate precipitation method produced an immediate reduction in dentin permeability to 6%. This permeability remained low seven days after the discs were immersed in artificial saliva. The potassium oxalate treatment reduced dentin permeability to 8%; however, this permeability increased gradually as the immersion time increased.³⁹

Other laboratory studies have used scanning electron microscopy (SEM) to verify the morphology of dentin treated with different desensitizing agents.^16,18,38,41 Oda et al evaluated the formation of an impermeable layer on the dentin surface when glutaraldehyde, potassium oxalate, and fluoride were applied to dentin discs after acid etching.¹⁶ No uniform impermeable layer was formed when glutaraldehyde and oxalate were used; however, this layer could be observed when the treatment with sodium fluoride was performed, although it was fragile and could be removed easily by washing the dentin surface. It must be noted that the specimens in this study were not fractured; as a result, the effects of the desensitizing agents were analyzed only at the dentin surface. In addition, the desensitizing agents were applied after acid etching removed calcium and phosphate, leaving fewer ions on the surface with which these agents might react.¹⁶

A 2004 study by Arrais et al verified the occurrence of intratubular precipitation and subsuperficial tubule occlusion by analyzing the effects of three desensitizing agents on fractured specimens. SEM examination demonstrated the precipitation of crystal-like deposits extending up to 15 µm inside the tubules of dentin treated with potassium oxalate, a 1 µm thick layer that covered the surface and infiltrated the tubules of dentin discs after the application of glutaraldehyde, and precipitates that occluded the dentin surface with no attachment to the tubule walls after phosphate fluoride treatment.⁴¹

Ishikawa et al observed longitudinally sectioned specimens that were treated using an acidic solution that contained both calcium and phosphate. Following treatment with the solution, the dentin discs showed tubules occluded by a calcium phosphate precipitate up to approximately 15 µm from the surface.³⁸ These findings are consistent with a 2002 in vitro study by Pereira et al in which impressions and resin replicas of three dentin discs (treated with potassium oxalate, calcium phosphate, or glutaraldehyde) were submitted to SEM analysis.¹⁸ The dentin disc treated with potassium oxalate revealed partial occlusion of dentinal tubules by crystal precipitation, usually below the surface. The disc treated with the calcium phosphate solution produced a thick smear of precipitated amorphous calcium phosphate that covered most of the tubules. The impressions of both of these discs presented short silicone tags, indicating that very little of the impression material penetrated into the tubules. The treatment with glutaraldehyde also partially obliterated the dentinal tubules; however, the corresponding impression showed that the impression material penetrated deeply into some open tubules.¹⁸

Clinical studies

Clinical trials are necessary for generating evidence regarding practical applications to manage dentinal hypersensitivity.^{3,10,14,17,19,31-33,36,40,42,45} However, the lack of standardized methods for clinical treatment can yield contradictory findings and produce results that make comparison difficult.⁴⁶ In addition, the physiologic and emotional aspects are important factors that influence these studies; that is, the patient’s response is subjective and depends largely on the individual’s pain threshold.^4,45

A controlled clinical study by Pillon et al verified that a single application of 3% potassium oxalate gel immediately after subgingival scaling and root planing produced greater reduction in dentinal hypersensitivity 7, 14, and 21 days after treatment, compared to a placebo gel applied to the homologous contralateral teeth. The greatest reduction for both the test (81%) and control (34.7%) groups was observed 21 days after the gel was applied.¹⁴

Kishore et al evaluated the effectiveness of strontium chloride, potassium nitrate, sodium fluoride, and formalin solutions for treating dentinal hypersensitivity. The authors verified that the strontium chloride, sodium fluoride, and formalin solutions significantly reduced the symptoms.³¹

Using a split-mouth design, Pereira et al applied one of three different potassium oxalate-based formulations (three individual experimental groups) and a placebo gel (control group) to hypersensitive teeth. The degree of sensitivity was assessed before application, after four applications (made at seven-day intervals), after six months, and after one year. All of the substances applied (including the placebo) produced an immediate reduction in dentinal hypersensitivity at all times of assessment, including six months and one year.¹⁷

The advent of laser technology and its growing use in dentistry offer an additional therapeutic option for the treatment of dentinal hypersensitivity.^3,9 Lasers used for this purpose may be divided into two groups: the low output power (low-level) lasers and the middle output power lasers.^19,35

The photobiomodulating effect of low-level laser therapy (LLLT) may increase tertiary dentin production by increasing the odontoblasts’ cellular metabolic activity, obliterating dentinal tubules as a result.⁴⁷ On the other hand, the middle output power laser application melts the dentin structure, which promotes occlusion of these tubules.³³

Ladalardo et al compared the therapeutic effects of a red diode laser (660 nm) and an infrared diode laser (830 nm) for treating adults with dentinal hypersensitivity. The authors observed that the 660 nm red diode laser produced a higher level of desensitization.³

Corona et al evaluated both LLLT and sodium fluoride varnish application for the treatment of dentinal hypersensitivity. Both treatments were effective in decreasing the painful condition, although laser therapy was significantly more effective than sodium fluoride varnish, mainly at reducing sensitivity, according to an adopted verbal rating scale.¹⁹

Schwarz et al observed how an erbium:yttrium-aluminum-garnet (Er:YAG) laser and an aqueous solution (22.5% polyurethane-
isocyanate; 77.5% methylenechloride) affected hypersensitive dentin.³² Both therapies caused significant reduction in discomfort, both immediately and one-week post-treatment. After two months, the discomfort in the group treated with the desensitizing solution increased up to 65% from the immediate post-treatment level (and up to 90% after six months), while patients treated with the laser noted no change during that period. Compared to an untreated control group, both types of treatment caused a significant reduction in hyperesthesia at each follow-up examination.³²

To evaluate the morphologic changes of hypersensitive dentin after irradiation by a neodynium: YAG (Nd:YAG) laser, Lan et al took an impression of the dentin surface before and after laser treatment and examined both surfaces using SEM. The presence of protrusive rods on the impression indicated that the material had penetrated the dentin structure and thus was a measure of open dentinal tubules. The impression obtained after laser treatment showed no protrusive rods, despite the presence of numerous rods prior to irradiation. The presence of protrusive rods on the impression material is related to open tubules in hypersensitive areas; as a result, this study supported the hypothesis that the Nd:YAG laser can be used to seal exposed dentinal tubules of hypersensitive teeth.³³

Some clinical studies have reported that the placebo effect influences how dentinal hypersensitivity is treated.^{10,17,37,40,42} This effect is described as a complex physiological and psychological interaction that depends to a large extent on the relationship between the patient and the professional.^10,35 A positive attitude toward treatment may activate the central system pain inhibition, which controls the painful stimulus of the periphery by releasing endorphins. Based on the literature, trust in one’s dentist and the desire for relief contribute to this effect.¹⁷

The Hawthorne effect also can occur in clinical trials.^10,45 This effect is related to non-intervention procedures, such as frequent examinations, improved oral hygiene, or compliance with the treatment regimen. In clinical studies, better oral hygiene may improve saliva’s access to patent dentinal tubules and thus may enhance tubule occlusion through the deposition of salivary calcium, phosphate, and proteins.¹⁰ In addition, clinical investigations that evaluated different desensitizing agents have noted that saliva could dissolve and carry the agents in question, causing the desensitization of non-treated teeth (known as the carryover effect).⁴⁵

Lier et al verified that a placebo produced a positive response.⁴⁰ In this 2002 study, a test group treated with an Nd:YAG laser was compared to a control group in which the laser device was positioned but not activated. Both groups reported a similar reduction in pain.⁴⁰

A 2004 study by Gentile et al distributed 32 patients into two groups: one exposed to six applications of a gallium-aluminum-arsenide (GaAlAs) diode laser and a control group treated with a photocuring light as a placebo. According to the authors, no statistically significant difference in pain reduction was noted between treated and control groups over the course of treatment.⁴² Similar results were obtained in the split-mouth study by Pereira et al.¹⁷

In a 1989 study, Cooley and Sandoval examined 28 individuals who had hypersensitive teeth in two different areas of the mouth. One area was treated with distilled water; the other with potassium oxalate. Initially, both groups reported a decrease in sensitivity; however, the sensitivity of the teeth treated with water remained approximately the same for three months, while the sensitivity of the oxalate-treated teeth increased progressively over the same period.³⁷

Summary

Dentinal hypersensitivity is a complex condition. The literature indicates several treatment modalities ranging from simple procedures that can be performed by the patient to complex procedures that involve combination therapy. To perform an effective treatment, dentists must be aware of the available desensitizing products and the factors involved in dentinal hypersensitivity.

Author information

Dr. Santiago is a professor, Department of Restorative Dentistry, School of Dentistry, Federal University of Ceara, Ceara, Brazil, where Dr. Vieira is a Master’s student, Department of Clinical Dentistry.

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