Vol.4 No.2 - May/June 2010
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Dentin Hypersensitivity

Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis & Management of Dentin Hypersensitivity

Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity

David H. Pashley, DMD, PhD, Franklin R. Tay, BDSc (Hons), PhD, Van B. Haywood, DMD, Marie A. Collins, RDH, EdD, Connie L. Drisko, DDS

Pain and discomfort have many causes in dentistry, and are typically one of the major reasons for unscheduled or emergency dental visits. As American dentistry has strived to bring the diseases of infectious origin, caries and periodontitis, under control, a new set of conditions is emerging—as a consequence of the 21st century lifestyle. Gingival recession may well be caused by overly enthusiastic oral hygiene, and acid wear may be becoming more prevalent in all ages due to the modern acid-containing diet. Both of these conditions lead to exposed dentin, which under the right circumstances, leads to the initiation of dentin hypersensitivity—their sole and common symptom. The final common path for dentin hypersensitivity is the activation of pulpal nerves. The successful use of potassium-containing products to treat both types of tooth sensitivity justifies the thorough treatment of the clinical condition. This consensus monograph purposes to help clinicians define, diagnose, and treat a condition that appears to be increasing in incidence. Furthermore, as all forms of vital bleaching—a treatment of ever-increasing commonality in the age of esthetic dentistry—are associated with some level of tooth sensitivity, that condition and its management are addressed as well.

Dentin hypersensitivity is best defined as 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 any other form of dental defect or pathology.”1 Dentin hypersensitivity is a common oral condition that affects as many as 57% of patients.2-8 It has been described as the “common cold of dentistry”9 by some and “toothbrush disease” by others, when it occurs in the presence of gingival recession.10

Dentin hypersensitivity is often episodic and the strategies for managing the condition are remarkably varied. Recognizing these issues, the Medical College of Georgia School of Dentistry, under the leadership of Dean Connie Drisko and her world-renowned team of category experts—Drs. Pashley, Tay, Haywood, and Collins—undertook to evaluate the condition and present a consensus statement regarding definition, etiology, diagnosis, and treatment. In August 2008, a consensus panel recommendation, peer-reviewed by the associate dean for research, Gerard Kugel, and assistant dean of international relations, Noshir Mehta, of Tufts University School of Dental Medicine, was produced.

The panel considered data from an extensive literature search and recognizes that dentin hypersensitivity is complex and is best diagnosed by a process of elimination by a thorough dental screening, examination, and dental history. Conditions that must be excluded include cracked-tooth syndrome, fractured restorations, chipped teeth, dental caries, gingival inflammation, post-restorative sensitivity, marginal leakage, pulpitis, and palatogingival grooves. The panel brought together all of its considerations to form a set of consensus recommendations to guide practitioners through diagnosis and case management. The consensus recommendations are supported by an algorithm (Figure 1 View Figure) for quick reference by the practitioner to the elements and critical steps required in making diagnostic decisions and the appropriate action based upon the findings.

Data Collection—Literature Search
An extensive computer (MEDLINE) and hand search of the literature identified original articles and reviews for the period 1966 to 2008.

Dentin hypersensitivity is characterized by short, sharp pain arising from exposed dentin in response to stimuli—typically thermal, evaporative, tactile, osmotic, or chemical—that cannot be attributed to any other dental defect or pathology.


  • The presence of tubules renders dentin permeable to fluid movement. The number of tubules per unit area varies depending on location, because of the decreasing area of the dentin surface in a pulpal direction. Dentinal tubules follow a sinuous course from the amelodentinal junction and from the cementodentinal junction and are conical, being wider at the pulpal end than at the periphery. These tubules are interconnected by an intricate and profuse system of canaliculi that branch off from the main tubules at different angles.
  • The three essential features required for dentin hypersensitivity to occur are:
    1. the presence of exposed dentin surfaces;
    2. open tubule orifices on the exposed dentin surface; and
    3. patent tubules leading to a vital pulp.
  • The short, sharp pain arising from exposed dentin in response to thermal, evaporative, tactile, or osmotic stimuli is a result of minute inward or outward movement of dentinal fluid inside tubules that activate pulpal nerve fibers.
  • Occlusion of dentin tubular orifices by a smear layer created during tooth brushing or by silica particles in a dentifrice result in reduction of fluid movements within the dentinal tubules. This physical blockade may partially account for the effectiveness of desensitizing dentifrices.
  • Changes occur in the dentin as a result of age or trauma. Secondary dentin is deposited throughout life, and the formation of peritubular dentin and/or deposition of intratubular whitlockite (ie, magnesium-substituted tricalcium phosphate) crystals may ultimately result in partial or complete obturation of the dentinal tubules, producing dead tracts and areas of sclerotic dentin. Traumatic injuries to the tooth may result in the deposition of an irregular layer of tertiary dentin that has fewer tubules. As these newly deposited tubules are not continuous with those in primary dentin, they provide an effective barrier to diffusion and rapid fluid movements and contribute to the reduction of dentin hypersensitivity.

Mechanism of Action
By far, the most widely accepted theory for dentin hypersensitivity is the hydrodynamic theory. When dentinal tubules in vital teeth are exposed after cementum or enamel is lost due to erosion, abrasion, dental manipulation, or a tooth defect, fluid within the dentinal tubules may flow in either an inward or outward direction depending on pressure differences in the surrounding tissue. A cold stimulus causes the tissue fluid volume to shrink slightly, and heat causes it to expand. Strongly osmotic sugar or sour solutions cause fluid to be drawn out of the tubules. An air blast on the tooth dries a tiny portion of fluid at the distal end of the tubule, causing a significant outer flow of fluid in the tubule. Touching the tooth with a dental instrument or periodontal cleansing aid forces a small amount of fluid into the tubule. These intratubular fluid shifts, in turn, activate mechanoreceptors in intratubular nerves or in the superficial pulp, and are perceived as pain by the patient.


  • Differential diagnosis is essential in order to exclude other conditions with similar symptoms where dentin is exposed and sensitive, such as chipped teeth, fractured cusps, cracked teeth, caries, and restorations with marginal deficiencies/leakage. Arriving at a correct differential diagnosis requires careful clinical and radiographic examinations and a thorough dental history (Figure 1 View Figure).


  • The most important factor in the etiology of dentin hypersensitivity is exposed dentin as a result of gingival recession associated with exposure of root surfaces and/or as a result of loss of enamel associated with tooth wear or trauma; followed by opening of the dentinal tubules (ie, loss of cementum or removal of any smear layer).
  • Traumatic tooth brushing in an otherwise healthy dentition is often undiagnosed in adolescents and early adults. Subclinical soft and hard tissue abrasion lesions are most likely a precursor of gingival recession and tooth wear, and thus dentin hypersensitivity.
  • Tooth wear refers to the irreversible loss of tooth structure and includes conditions such as abrasion, erosion, attrition, and abfraction. Development of wedge-shaped cervical lesions is often associated with abrasion and occlusal hyperfunction. Some lesions may be located subgingivally, out of reach of a toothbrush, and have been referred to as abfraction to describe the mechanism associated with the cervical loss of enamel and dentin.
  • Although there are many causes of noncarious cervical lesions of dentin, improper brushing, especially in the presence of an acidic diet, is a major cause.


  • The prevalence of dentin hypersensitivity varies, but averages about 57% and peaks between 20 to 40 years of age.
  • The loss of enamel in the absence of gingival recession can involve any location on the tooth and is usually a result of the combined actions of attrition, abrasion, erosion, and abfraction.
  • The individual sites around the mouth with the highest prevalence of dentin hypersensitivity are associated with gingival recession and are located on the facial surfaces of canines > premolars > incisors > molars.
  • Use of a highly abrasive dentifrice may also cause additional soft tissue damage and tooth wear leading to hypersensitivity, although this phenomenon is not well-documented in the literature.
  • Dentin hypersensitivity peaks in the first few days after scaling and root planing or periodontal surgery and usually is substantially reduced by 8 weeks, but can vary from months to more than 30 years.

Clinical Trials

  • Clinical trials on dentin hypersensitivity should use randomized group assignments, be double-masked and contain a placebo product that is identical to the test product except that it does not contain the active ingredient.
  • It is critical to evaluate the placebo effect, which can be very strong in such studies.
  • Conclusions derived from early studies on dentin hypersensitivity using single-masked methods, or inappropriate stimuli, such as electric pulp testing, should be viewed with caution.
  • Limited evidence would indicate tooth brushing without dentifrice lowers hypersensitivity scores (promotes the formation of a smear layer) while brushing with a dentifrice increases dentin hypersensitivity scores (removes the smear layer) unless the dentifrice contains a potassium-containing desensitizing agent.
  • Although a recent meta-analysis of six clinical trials using potassium-containing desensitizing dentifrices demonstrated reductions in the patients’ perceived symptoms of dentin hypersensitivity compared to control dentifrices, the scientific evidence supporting the use of potassium salts to reduce nerve activity is based largely on in vivo animal studies and one recent human in vivo study.

Vital Bleaching Sensitivity

  • All forms of vital bleaching are associated with some level of sensitivity.
  • The history of sensitive teeth as well as the patient’s response during examination to explorer touch or air can be a reasonable predictor that sensitivity will occur during bleaching.
  • Tooth sensitivity is the single most significant factor in non-compliance with, or failure to complete, a bleaching regimen, and must be understood to be able to manage treatment.
  • Tooth sensitivity is the most common side effect of bleaching, and may be caused primarily by the peroxide penetration to the pulp.
  • Treatment of bleaching sensitivity involves many possible options. Twice daily use of a potassium nitrate-containing toothpaste for 2 weeks before and during the regimen can reduce or avoid sensitivity from bleaching.
  • Further alleviation of bleaching sensitivity can be achieved by using bleaching materials containing potassium nitrate, or by applying a dentifrice or professional product containing potassium nitrate in a well-fitted tray.

Quality of Life

  • Early identification of risk factors and appropriate intervention, including changing destructive habits, are essential in preventing the onset of dentin sensitivity and ensuring long-term success in managing dentin hypersensitivity.
  • Quality of life, esthetic concerns, and chronic pain are strong motivators for patients to seek treatment for their dentin hypersensitivity.
  • Quality of life is significantly affected by the symptoms of hypersensitivity. Sufferers may no longer enjoy their favorite foods and beverages, allowing hot drinks to cool and putting less or no ice in cold drinks, using a straw to deflect cold drinks away from certain teeth. Many sufferers are only ‘somewhat bothered’ and about one third are ‘very bothered’.
  • The two conditions, gingival recession and tooth wear, most commonly leading to dentin hypersensitivity alter the appearance and visual appeal of the mouth, and thus facial expression and perceived beauty.

Treatment (Figure 1 View Figure)

  • Prevention is the most cost-effective treatment option.
  • The first recommendation by the dentist or dental hygienist should include cessation of predisposing destructive habits and the twice-daily use of a desensitizing dentifrice.
  • Tray application of potassium nitrate can be an effective episodic treatment for sensitivity according to limited practice-based evidence.
  • Clinical trials have shown that twice-daily use of desensitizing dentifrices improves hypersensitivity and increases in effectiveness over time.
  • If, after using a desensitizing dentifrice, the patient’s dentin hypersensitivity remains a problem, clinicians should re-evaluate the differential diagnosis and consider in-office treatments beginning with topically applied desensitizing agents. After the diagnosis is reconfirmed, including the elimination of other causative factors such as undiagnosed caries or cracked teeth, other methods of treatment including gingival grafting may need to be considered.
  • A periodontist should be consulted before placement of restorative materials on the roots to assess the potential for future use of gingival grafts for root coverage, as placement of any bonded restoration prior to grafting may diminish the success rate of such procedures.


  • Clinicians should take careful histories of their patients’ dietary habits and make patients aware of the importance of erosive influences.
  • Current in-office treatment modalities include use of professionally applied desensitizing agents (see Table and Figure 2 View Figure; Figure 3 View Figure; Figure 4 View Figure; Figure 5 View Figure in “Dentin Hypersensitivity: Current State of the Art and Science”).
  • Evidence-based recommendations regarding consumer products for management of dentin hypersensitivity should be communicated to patients, including use of potassium nitrate-containing, low-abrasivity dentifrice and soft toothbrushes.
  • Patients should demonstrate their tooth brushing technique to the dental hygienist or dentist at every appointment until they have mastered proper brushing techniques.
  • At-risk patients should avoid whitening toothpastes, and other dentifrices with high abrasivity values as these tend to contribute to removal of the smear layer and further tooth wear.

1. Ajcharanukul O, Kraivaphan P, Wanachantararak S, Vongsavan N, Matthews B. Effects of potassium ions on dentine sensitivity in man. Arch Oral Biol. 2007;52(7):632-639.

2. Graf HE, Galasse R. Morbidity, prevalence and intraoral distribution of hypersensitive teeth. J Dent Res. 1977;56(Spec Iss A):Abst.#479.

3. Flynn J, Galloway R, Orchardson R. The incidence of “hypersensitive” teeth in the West of Scotland. J Dent. 1985;13(3):230-236.

4. Liu HC, Lan WH, Hsieh CC. Prevalence and distribution of cervical dentin hypersensitivity in a population in Taipei, Taiwan. J Endod. 1998;24(1):45-47.

5. Irwin CR, McCusker P. Prevalence of dentine hypersensitivity in a general dental population. J Irish Dent Assoc. 1997;43(1):7-9.

6. Rees JS. The prevalence of dentine hypersensitivity in general dental practice in the UK. J Clinical Periodontol. 2000;27(11):860-865.

7. Rees JS, Addy M. A cross-sectional study of dentine hypersensitivity. J Clinical Periodontol. 2002;29(11):997-1003.

8. Al-Wahadni A, Linden GJ. Dentine hypersensitivity in Jordanian dental attenders: a case control study. J Clin Periodontol. 2002;29(8): 688-693.

9. Strassler HE, Drisko CL, Alexander DC. Dentin hypersensivity: its inter-relationship to gingival recession and acid erosion. Compend Contin Educ Dent. 2008;29(5 Special Issue):1-9.

10. Bamise CT, Olusile AO, Oginni AO. An analysis of the etiological and predisposing factors related to dentin hypersensitivity. J Contemp Dent Pract. 2008;9(5):52-59.

Figure 1 Flowchart showing the clinical management of dentin hypersensitivity.

Figure 2 through Figure 5 in “Dentin Hypersensitivity: Current State of the Art and Science”
Figure 2 Scanning electron micrograph showing occlusion of dentinal tubules with calcium oxalate crystals (arrow) after the application of a slightly acidic potassium oxalate solution to acid-etched dentin.
Figure 3 (A) Two-step, two-bottle type calcium precipitating solutions have been developed to occlude open dentinal tubules during in-office treatment. (B) Topical application of a phosphate-containing Solution A. (C) This was followed by the topical application of a calcium-ion containing Solution B. (D) Formation of a white calcium-phosphate precipitate could not be identified clinically from the dentin surface, but was apparent along the adjacent buccal gingivae. (E) Transmission electron micrograph showing the occlusion of a patent dentinal tubule (T) with needle-shaped apatite crystals (pointer). P: peritubular dentin; D: intertubular dentin.
Figure 4 Fluorescence microscopy (A) and scanning electron microscopy (B) showing precipitations of plasma proteins derived from the dentinal fluid as intratubular septa (arrow) after the topical application of an aqueous solution of 35% hydroxyethyl methacrylate and 5% glutaraldehyde. These intra-tubular septa reduce the permeability of dentinal tubules to fluid movement and contribute to the reduction of dentin hypersensitivity (reprinted from Schüpbach et al, 2007, with permission from the publisher). Figure 5 (A) Attempts to seal open dentinal tubules with adhesive resins can fail if the resin film is too thin and becomes saturated with atmospheric oxygen that consumes all of the free radicals generated during light-curing. The co-monomers never polymerize and the film is incomplete, leaving many tubules open. (B) Even thicker films can be displaced by water seeping from dentin during bonding. These water blisters represent unbonded areas that can be removed by toothbrushing (Courtesy of Dr. Stephan Paul).
About the Authors

David H. Pashley, DMD, PhD
Regents’ Professor, Department of Oral Biology, Medical College of Georgia School of Dentistry, Augusta, Georgia

Franklin R. Tay, BDSc (Hons), PhD
Associate Professor, Department of Endodontics, Medical College of Georgia School of Dentistry, Augusta, Georgia

Van B. Haywood, DMD
Professor, Department of Oral Rehabilitation, Medical College of Georgia School of Dentistry, Augusta, Georgia

Marie A. Collins, RDH, EdD
Chair and Associate Professor, Department of Dental Hygiene, Associate Professor, Department of Periodontics, Medical College of Georgia School of Allied Health and School of Dentistry, Augusta, Georgia

Connie L. Drisko, DDS
Merritt Professor and Dean, Medical College of Georgia School of Dentistry, Augusta, Georgia