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Tooth Hypersensitivity
32
 Introduction
 Definition
 Neurophysiology of Teeth
 Mechanism of Dentin Sensitivity
 Incidence and Distribution of Dentin
Hypersensitivity
INTRODUCTION
The term tooth hypersensitivity, dentinal sensitivity or
hypersensitivity often used intermittently to describe clinically
condition of an exaggerated response to an exogenous stimulus.
The exogenous stimuli may include thermal, tactile or
osmotic changes. While extreme stimuli can make all the teeth
hurt, the term hypersensitivity means painful response to stimuli
not normally associated with pain. The response to a stimulus
varies from person to person due to difference in pain tolerance,
environment factors and psychology of patient. Tooth
hypersensitivity can fit the criteria of several pain terms described
by Merskey (1979), for the International Association for the
study of pain (IASP). Pain is described “as an unpleasant sensory
and emotional experience associated with actual or potential
tissue damage”.
DEFINITION
Dentin hypersensitivity is defined as “sharp, short pain arising
from exposed dentin in response to stimuli typically thermal,
chemical, tactile or osmotic and which cannot be ascribed to
any other form of dental defect or pathology (Holland et al,
1997).”
Historic review
• Leeuwenhoek (1678) described “tooth canals in dentin”.
• JD White (1855) proposed that dentinal pain was caused by
movement of fluid in dentinal tubules.
• Lukomsky (1941) advocated sodium fluoride as a desensitizing
obtundent.
• Brannstrom (1962) described hydrodynamic theory of dentinal
pain.
• Kleinberg (1986) summarized different approaches that are used
to treat hypersensitivity.
 Etiology and Predisposing Factors
 Differential Diagnosis
 Diagnosis
 Treatment Strategies
Tooth hypersensitivity is not associated with actual tissue
damage in the acute sense but can involve potential tissue
damage with constant erosion of the enamel or cementum along
with the concomitant pulpal response.
NEUROPHYSIOLOGY OF TEETH
The dental pulp is richly innervated. According to conduction
velocities, the nerve units can be classified into A group—having
the conduction velocity more than 2 m/s and C group—with
conduction velocity less than 2 m/s.
The sharp, better localized pain is mediated by A delta fibers,
whereas C fibers activation seems to be connected with the
dull radiating pain sensation. Myelinated A fiber seems to be
responsible for dentin sensitivity.
MECHANISM OF DENTIN SENSITIVITY
Theories of dentin sensitivity
• Neural theory.
• Odontoblastic transduction theory.
• Hydrodynamic theory.
Theories of Dentin Sensitivity
Neural Theory
The neural theory attributes to activation of nerves ending lying
within the dentinal tubules. These nerve signals are then
conducted along the parent primary afferent nerve fibers in
the pulp, into the dental nerve branches and then into the brain
(Fig. 32.1). Neural theory considered that entire length of tubule
contains free nerve endings.
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Fig. 32.1: Theories of dentin hypersensitivity; (1) Neural theory: Stimulus
applied to dentin causes direct excitation of the nerve fibers;
(2) Odontoblastic transduction theory: Stimulus is transmitted along the
odontoblast and passes to the sensory nerve endings through synapse;
(3) Hydrodynamic theory: Stimulus causes displacement of fluid present
in dentinal tubules which further excite nerve fibers
Odontoblastic Transduction Theory
The theory assumed that odontoblasts extend to the periphery.
The stimuli initially excite the process or body of the
odontoblast. The membrane of odontoblasts may come into
close apposition with that of nerve endings in the pulp or in
the dentinal tubule and the odontoblast transmits the excitation
of these associated nerve endings. However, in the most recent
study; Thomas (1984) indicated that the odontoblastic process
is restricted to the inner third of the dentinal tubules.
Accordingly it seems that the outer part of the dentinal tubules
does not contain any cellular elements but is only filled with
dentinal fluid.
Hydrodynamic Theory
This theory proposes that a stimulus causes displacement of
the fluid that exists in the dentinal tubules. The displacement
occurs in either an outward or inward direction and this
mechanical disturbance activates the nerve endings present in
the dentin or pulp.
Brannstrom (1962) suggested that the displacement of the
tubule contents is rapid enough to deform nerve fiber in pulp
or predentin or damage odontoblast cell. Both of these effects
appear capable of producing pain.
Currently most investigators accept that dentin sensitivity
is due to the hydrodynamic fluid shift, which occurs across
exposed dentin with open tubules. This rapid fluid movement
in turn activates the mechanoreceptor nerves of A group in
the pulp (Fig. 32.2).
Mathews et al (1994) noted that stimuli such as cold causes
fluid flow away from the pulp, produces more rapid and greater
pulp nerve responses than those such as heat, which causes
an inward flow. This certainly would explain the rapid and severe
response to cold stimuli compared to the slow dull response
to heat.
Tooth Hypersensitivity
Fig. 32.2: Hydrodynamic theory; (A) Odontoblast; (B) Dentin;
(C) A-δ nerve fiber; (D) Odontoblastic process; (E) Stimulation of A-δ
nerve fiber from fluid movement
The dehydration of dentin by air blasts or absorbent paper
causes outward fluid movement and stimulates the mechano-
receptor of the odontoblast, causing pain. Prolonged air blast
causes formation of protein plug into the dentinal tubules,
reducing the fluid movement and thus decreasing pain
(Fig. 32.3A).
The pain produced when sugar or salt solutions are placed
in contact with exposed dentin can also be explained by dentinal
fluid movement. Dentinal fluid is of relatively low osmolarity,
which have tendency to flow towards solution of higher
osmolarity, i.e. salt or sugar solution (Fig. 32.3B).
INCIDENCE AND DISTRIBUTION
OF DENTIN HYPERSENSITIVITY
The prevalence studies for dentin hypersensitivity are limited
in number. The available prevalence data vary considerably and
dentin hypersensitivity has been stated to range from 8 to 30
percent of adult population.
• Most sufferers range from 20-40 years of age and a peak
occurrence is found at the end of the third decade.
• In general, a slightly higher incidence of dentin hyper-
sensitivity is reported in females than in males.
• The reduced incidence of dentin hypersensitivity in older
individuals reflects age changes in dentin and the dental pulp.
Sclerosis of dentin, the laying down of secondary dentin
and fibrosis of the pulp would all interfere with the
hydrodynamic transmission of stimuli through exposed
dentin.
Intraoral Distribution
• Hypersensitivity is most commonly noted on buccal cervical
zones of permanent teeth. Although all tooth type may be
affected, canines and premolars in either jaw are the most
frequently involved.
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Textbook of Endodontics

Fig. 32.3A: Effect of air blast on dentin

Fig. 32.4: Recession of gingiva

The recession may or may not be associated with bone loss.

If bone loss occurs, more dentinal tubules get exposed. When
gingival recession occurs, the outer protective layer of root
dentin, i.e. cementum gets abraded or eroded away (Fig. 32.5).
This leaves the exposed underlying dentin, which consists
of protoplasmic projections of odontoblasts within the pulp
chamber (Fig. 32.6). These cells contain nerve endings and when

Fig. 32.3B: Pain produced by different stimuli

• Regarding the side of mouth, in right handed tooth brushers,

the dentin hypersensitivity is greater on the left sided teeth
compared with the equivalent contralateral teeth.

ETIOLOGY AND PREDISPOSING FACTORS

The primary underlying cause for dentin hypersensitivity is
exposed dentin tubules. Dentin may become exposed by two
processes; either by loss of covering periodontal structures Fig. 32.5: Erosion of cementum
(gingival recession), or by loss of enamel.
The most common clinical cause for exposed dentinal
tubules is gingival recession (Fig. 32.4). Various factors which
can cause recession are inadequate attached gingiva, improper
brushing technique, periodontal surgery, overzealous tooth
cleansing habits, oral habits, etc.
Common reasons for gingival recession
• Inadequate attached gingiva.
• Prominent roots.
• Toothbrush abrasion.
• Oral habits resulting in gingival laceration, i.e. traumatic tooth
picking, eating hard foods.
• Excessive tooth cleaning.
• Excessive flossing.
• Gingival recession secondary to specific diseases, i.e. NUG,
periodontitis, herpetic gingivostomatitis.
• Crown preparation. Fig. 32.6: Exposure of dentinal tubules
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Fig. 32.7: Depolarization of nerve ending causing pain
disturbed, nerves depolarize and this is interpreted as pain
(Fig. 32.7).
Once the dentinal tubules are exposed, there are oral
processes which keep them exposed. These include poor plaque
control, enamel wear, improper oral hygiene technique, cervical
erosions, enamel wear and exposure to acids.
Reasons for continued dentinal tubular exposure
• Poor plaque control, i.e. acidic bacterial byproducts.
• Excess oral acids, i.e. soda, fruit juice, swimming pool chlorine,
bulimia.
• Cervical decay.
• Toothbrush abrasion.
• Tartar control toothpaste.
The other reason for exposure of dentinal tubules is due
to loss of enamel.
Causes of loss of enamel
• Attrition by exaggerated occlusal functions like bruxism.
• Abrasion from dietary components or improper brushing
technique.
• Erosion associated with environmental or dietary components
particularly acids.
Since dentinal tubules get sclerosed of their own and plug
themselves up in the oral environment, treatment should focus
on eliminating factors associated with continued dentinal
exposure.
DIFFERENTIAL DIAGNOSIS
Dentin hypersensitivity is perhaps a symptom complex rather
than a true disease and results from stimulus transmission across
exposed dentin. A number of dental conditions are associated
with dentin exposure and therefore, may produce the same
Tooth Hypersensitivity
symptoms.
Such conditions include:
• Chipped teeth.
• Fractured restoration.
• Restorative treatments.
• Dental caries.
• Cracked tooth syndrome.
• Other enamel invaginations.
DIAGNOSIS
• A careful history together with a thorough clinical and
radiographic examination is necessary before arriving at a
definitive diagnosis of dentin hypersensitivity. However, the
problem may be made difficult when two or more conditions
coexist.
• Tooth hypersensitivity differs from dentinal or pulpal pain.
In case of dentin hypersensitivity, patient’s ability to locate
the source of pain is very good, whereas in case of pulpal
pain, it is very poor.
• The character of the pain does not outlast the stimulus;
the pain is intensified by thermal changes, sweet and sour.
• Intensity of pain is usually mild to moderate.
• The pain can be duplicated by hot or cold application or
by scratching the dentin. The pulpal pain is explosive,
intermittent and throbbing and can be affected by hot or
cold.
TREATMENT STRATEGIES
Hypersensitivity can resolve without the treatment or may
require several weeks of desensitizing agents before
improvement is seen. Treatment of dentin hypersensitivity is
challenging for both patient and the clinician mainly for two
main reasons:
1. It is difficult to measure or compare pain among different
patients.
2. It is difficult for patient to change the habits that initially
caused the problem.
Management of Tooth Hypersensitivity
It is well known that hypersensitivity often resolves without
treatment. This is probably related to the fact that dentin
permeability decrease spontaneously because of occurrence of
natural processes in the oral cavity.
Natural Process Contributing to Desensitization
1. Formation of reparative dentin by the pulp.
2. Obturation of tubules by the formation of mineral deposits
(dental sclerosis).
3. Calculus formation on the surface of the dentin.
Two principal treatment options are:
1. Plug the dentinal tubules preventing the fluid flow.
2. Desensitize the nerve, making it less responsive to stimulation.
All the current modalities address these two options.
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Treatment of dentin hypersensitivity can be divided into: After professional diagnosis, dentinal hypersensitivity can
Textbook of Endodontics

1. Home care with dentifrices. be treated simply and inexpensively by home use of desensitizing
2. In-office treatment procedure. dentifrices. The habit of toothbrushing with a dentifrice for
3. Patient education. cosmetic reasons is well established in the population, thus
compliance with this regimen can be easily made.
Management of dentin hypersensitivity
Strontium Chloride Dentifrices
1. Home care with dentifrices:
a. Strontium chloride dentifrices. Ten percent strontium chloride desensitizing dentifrices have
b. Potassium nitrate dentifrices. been found to be effective in relieving the pain of tooth
c. Fluoride dentifrices. hypersensitivity.
2. In-office treatment procedure:
a. Varnishes. Potassium Nitrate Dentifrices
b. Corticosteroids.
c. Treatments that partially obturate dentinal tubules.
Five percent potassium nitrate dentifrices have been found to
• Burnishing of dentin alleviate pain related to tooth hypersensitivity.
• Silver nitrate
• Zinc chloride—potassium ferrocyanide Fluoride Dentifrices
• Formalin Sodium monofluorophosphates dentifrices are the effective
• Calcium compounds mode of treating tooth hypersensitivity.
– Calcium hydroxide
– Dibasic calcium phosphate
In-office Treatment Procedure
• Fluoride compounds
– Sodium fluoride Rationale of Therapy
– Sodium silicofluoride
According to hydrodynamic theory of hypersensitivity, a rapid
– Stannous fluoride
• Iontophoresis
movement of fluid in the dentinal tubules is capable of activating
• Strontium chloride intradental sensory nerves. Therefore, treatment of hyper-
• Potassium oxalate. sensitive teeth should be directed towards reducing the
d. Tubule sealant anatomical diameter of the tubules, obliteration of the tubules
• Restorative resins or to surgically cover the exposed dentinal tubules so as to limit
• Dentin bonding agents. fluid movement (Figs 32.9A to C).
e. Miscellaneous
• Laser. Criteria for selecting desensitizing agent
3. Patient education: • Provides immediate and lasting relief from pain.
a. Dietary counseling • Easy to apply.
b. Toothbrushing technique • Well tolerated by patients.
c. Plaque control. • Not injurious to the pulp.
• Does not stain the tooth.
Home Care with Dentifrices (Fig. 32.8) • Relatively inexpensive.
Dentifrice has been defined as a substance used with a
toothbrush to aid in cleaning the accessible surfaces of the teeth.
Dentifrice components include abrasive, surfactant, humectant,
thickener, flavor, sweetener, coloring agent and water.

Fig. 32.8: Commonly used home care products Figs 32.9A to C: In-office treatment procedures
for dentin hypersensitivity for dentin hypersensitivity
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Treatment options to reduce the diameter of dentinal tubules
can be:
1. Formation of a smear layer by burnishing the exposed root
surface (smear layer consists of small amorphous particles of
dentin, minerals and organic matrix—denatured collagen).
2. Application of agents that form insoluble precipitates within
the tubules.
3. Impregnation of tubules with plastic resins.
4. Application of dental bonding agents to seal off the tubules.
5. Covering the exposed dentinal tubules by surgical means.
It must be recognized that single procedure may not be
consistently effective in the treatment of hypersensitivity;
therefore, the dentist must be familiar with alternative methods
of treatment. Prior to treating sensitive root surfaces, hard/
soft deposits should be removed from the teeth. Root planning
on sensitive dentin may cause considerable discomfort, in this
case, teeth should be anesthetized prior to treatment and teeth
should be isolated and dried with warm air.
Varnishes
Open tubules can be covered with a thin film of varnish,
providing a temporary relief; varnish such as copalite can be
used for this purpose. For more sustained relief a fluoride
containing varnish Duraflor can be applied.
Corticosteroids
Corticosteroids containing l percent prednisolone in
combination with 25 percent parachorophenol, 25 percent
methacresylacetate and 50 percent gum camphor was found
to be effective in preventing postoperative thermal sensitivity.
The use of corticosteroids is based, on the assumption that
hypersensitivity is linked to pulpal inflammation; hence, more
information is needed regarding the relationship between these
two conditions.
Partial Obliteration of Dentinal Tubules
Burnishing of dentin: Burnishing of dentin with a toothpick
or orange wood stick results in the formation of a smear layer
which, partially occludes the dentinal tubules and thus resulting
in decreased hypersensitivity.
Formation of insoluble precipitates to block tubules: Certain
soluble salts react with ions in tooth structure to form crystals
on the surface of the dentin. To be effective, crystallization
should occur in 1-2 minutes and the crystals should be small
enough to enter the tubules and must also be large enough to
partially obturate the tubules.
• Calcium oxalate dihydrate crystals are formed when
potassium oxalate is applied to dentin; these crystals are
very effective in reducing permeability.
• Silver nitrate (AgNO3) has ability to precipitate protein
constituents of odontoblast processes, thereby partially
blocking the tubules.
• Zinc chloride—potassium ferrocyanide: When applied
forms precipitate, which is highly crystalline and covers the
dentin surface.
• Formalin 40 percent is topically applied by means of cotton
Tooth Hypersensitivity
pellets or orangewood sticks on teeth. It had been proposed
by Grossman in 1935 as the desensitizing agent of choice
in treating anterior tooth because, unlike AgNO3, it does
not produce stain.
• Calcium compounds have been popular agent for
many years for the treatment of hypersensitivity. The
exact mechanism of action is unknown but evidence
suggests that:
a. It may block dentinal tubules.
b. May promote peritubular dentin formation.
c. On increasing the concentration of calcium ions around
nerve fibers, may results in decreased nerve excitability.
So, calcium hydroxide might be capable of suppressing
nerve activity.
– A paste of Ca(OH)2 and sterile distilled water applied
on exposed root surface and allowed to remain for
3-5 minutes, can give immediate relief in 75 percent
of cases.
– Dibasic calcium phosphate when burnished with
round toothpick forms mineral deposits near the
surface of the tubules and found to be effective in
93 percent of patients.
• Fluoride compounds: Lukomsky (1941) was the first to
propose sodium fluoride as desensitizing agent, because
dentinal fluid is saturated with respect to calcium and
phosphate ions. Application of NaF leads to precipitation
of calcium fluoride crystals, thus, reducing the functional
radius of the dentinal tubules.
– Acidulated sodium fluoride: Concentration of fluoride
in dentin treated with acidulated sodium fluoride is found
to be significantly higher than dentin treated with sodium
fluoride.
– Sodium silicofluoride: Silicic acid forms a gel with the
calcium of the tooth and produces an insulating barrier.
Thus application of 0.6 percent sodium silicofluoride
is much more potent than 2 percent solution of sodium
fluoride as desensitizing agent.
– Stannous fluoride: Ten percent solution of stannous
fluoride forms dense layer of tin and fluoride containing
globular particles blocking the dentinal tubules. 0.4
percent stannous fluoride is also an effective agent,
however, requires prolonged use (up to 4 weeks) to
achieve satisfactory results.
• Fluoride Iontophoresis: Iontophoresis is a term applied
to the use of an electrical potential to transfer ions into
the body for therapeutic purposes. The objective of fluoride
iontophoresis is to drive fluoride ions more deeply into the
dentinal tubules that cannot be achieved with topical
application of fluoride alone.
• Strontium chloride: Studies have shown that topical
application of concentrated strontium chloride on an
abraded dentin surface produces a deposit of strontium that
penetrates dentin to a depth of approximately 10-20 μm
and extend into the dentinal tubules.
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• Oxalates: Oxalates are relatively inexpensive, easy to apply
Textbook of Endodontics
and well tolerated by patients. Potassium oxalate and ferric
oxalate solution make available oxalate ions that can react
with calcium ions in the dentin fluid to form insoluble
calcium oxalate crystals that are deposited in the apertures
of the dentinal tubules.
Dental Resins and Adhesives
The objective in employing resins and adhesives is to seal the
dentinal tubules to prevent pain producing stimuli from
reaching the pulp. Several investigators have demonstrated
immediate and enduring relief of pain for periods of up to
18 months following treatment. Although not intended for
treatment of generalized areas of root sensitivity, this can be
an effective method of treatment when other forms of therapy
have failed.
GLUMA is a dentin bonding system that includes
glutaraldehyde primer and 35 percent HEMA (hydroxyethyl
methacrylate). It provides an attachment to dentin that is
immediate and strong. GLUMA has been found to be highly
effective when other methods of treatment failed to provide
relief (Fig. 32.10).
Lasers
Treatment of Dentin Hypersensitivity by Lasers
Kimura Y et al (2000) reviewed treatment of dentin
hypersensitivity by lasers. The lasers used for the treatment of
dentin hypersensitivity are divided into two groups:
1. Low output power (low level) lasers: Helium-neon [He-Ne]
and gallium/aluminum/arsenide (GaAlAs) [diode] lasers.
2. Middle output power lasers: Nd:YAG and CO 2 lasers.
Laser effects are considered to be due to the effects of sealing
of dentinal tubules, nerve analgesia or placebo effect. The sealing
effect is considered to be durable, whereas nerve analgesia or
a placebo effects are not.
Fig. 32.10: GLUMA desensitizing solution
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Patient Education
Dietary Counseling
Dietary acids are capable of causing erosive loss of tooth
structure, thereby removing cementum and resulting in opening
of the dentinal tubules. Consequently, dietary counseling should
focus on the quantity and frequency of acid intake and intake
occurring in relation to toothbrushing. Any treatment may fail
if these factors are not controlled. A written diet history should
be obtained on patients with dentinal hypersensitivity in order
to advise those concerning eating habits.
Because of the presence of a smear layer on dentin, teeth
are not usually sensitive immediately following scaling and root
planning. However, removal of the smear layer may result from
exposure to certain components of the diet. Studies have shown
that citrus fruit juices, apple juice and yoghurt are capable of
dissolving the smear layer.
Because loss of dentin is greatly increased when brushing
is performed immediately after exposure of the tooth surface
to dietary acids. Patients should be cautioned against brushing
their teeth soon after ingestion of citrus food.
Toothbrushing Technique
Because incorrect toothbrushing appears to be an etiologic
factor in dentin hypersensitivity, instruction about proper
brushing techniques can prevent further loss of dentin and the
hypersensitivity.
Plaque Control
Saliva contains calcium and phosphate ions and is therefore
able to contribute to the formation of mineral deposits within
exposed dentinal tubules. The presence of plaque may interfere
with this process, as plaque bacteria, by producing acid, are
capable of dissolving any mineral precipitates that form, thus
opening tubules.
Professional interest in the causes and treatment of dentinal
hypersensitivity has been evident in the dental literature for
approximately 150 years or more. Dentinal hypersensitivity
satisfies all the criteria to be classified as a true pain syndrome.
Myelinated A fibers mostly A-delta type seems to be responsible
for the sensitivity of dentin. Of the various theories proposed,
the hydrodynamic theory is the most accepted explanation for
the mechanism of dentin hypersensitivity. Management of the
condition requires determination of etiologic factors and
predisposing influences. Desensitizing toothpastes containing
potassium nitrate, strontium chloride and sodium monofluoro-
phosphate have proven to be effective in the management of
hypersensitivity. Partial obturation of open tubules is the most
widely practiced in office treatment of dentinal hypersensitivity.
QUESTIONS
Q. Define dentin hypersensitivity?
Q. How will you manage a case of dentin hyper-
sensitivity?