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
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.
PRESENTING SIGNS AND SYMPTOMS
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:
the presence of exposed dentin surfaces;
open tubule orifices on the exposed
dentin surface; and
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
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
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
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
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
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.
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
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
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
Prevention is the most cost-effective treatment
recommendation by the dentist or dental hygienist should include cessation
of predisposing destructive habits and the twice-daily use of a
Tray application of potassium nitrate can be an
effective episodic treatment for sensitivity according to limited
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
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
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.
demonstrate their tooth brushing technique to the dental hygienist or
dentist at every appointment until they have mastered proper brushing
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.
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Figure 1 Flowchart showing the clinical management of dentin hypersensitivity.
Figure 2 through
Figure 5 in “Dentin Hypersensitivity: Current State of the Art and
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
Professor, Department of Oral Biology, Medical College of Georgia School of
Dentistry, Augusta, Georgia
Franklin R. Tay, BDSc (Hons), PhD
Professor, Department of Endodontics, Medical College of Georgia School of
Dentistry, Augusta, Georgia
Van B. Haywood, DMD
Department of Oral Rehabilitation, Medical College of Georgia School of
Dentistry, Augusta, Georgia
Marie A. Collins, RDH, EdD
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,