J Conserv Dent. 2010 Oct-Dec; 13(4): 218224.

Dentin hypersensitivity: Recent trends in management

Sanjay Miglani, Vivek Aggarwal, and Bhoomika Ahuja
Abstract
Dentinal hypersensitivity (DH) is a common clinical condition usually associated
with exposed dentinal surfaces. It can affect patients of any age group and
most commonly affects the canines and premolars of both the arches. This
article concisely reviews the patho-physiology, mechanism and clinical
management of the DH. Treatment of DH should start with an accurate
diagnosis. Differential diagnosis should be made and all other probable causes
should be excluded. An often neglected phase of clinical management of DH is
the identification and treatment of the causative factors of DH. By removing
the etiological factors, the condition can be even prevented from occurring or
recurring. There are various treatment modalities available which can be used
at home or may be professionally applied. The at home desensitizing agents
include toothpastes, mouthwashes or chewing gums and they act by either
occluding the dentinal tubules or blocking the neural transmission. This article
also discusses the recent treatment options like bioglass, Portland cement,
lasers and casein phosphopeptide.

Keywords: Casein phosphopeptide - amorphous calcium phosphate, dentinal

hypersensitivity, desensitizing agents, fluorides
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INTRODUCTION
Dentine sensitivity (DS) or dentinal hypersensitivity (DH) is one of the most
commonly encountered clinical problems. It is clinically described as an
exaggerated response to application of a stimulus to exposed dentine,
regardless of its location.[1,2] The terms DS or DH have been used
interchangeably to describe the same clinical condition. True hypersensitivity
can develop due to pulpal inflammation and can present the clinical features of
irreversible pulpitis, i.e., severe and persistent pain, as compared with typical
short sharp pain of DH.[3] Majority of literature reviews dealing with this clinical
condition have suggested the use of term DS and consider that the sharp pain
is actually the normal pulpal response to the exposed dentine.[4,5] But it is well
known that all exposed dentine are not sensitive and the term DH has been
used over the decades by the clinicians.[6,7] Therefore, both the terminologies
can be used to describe the clinical condition. The condition has been defined
by an international workshop on DH as follows:[8] Dentine hypersensitivity is

characterized by short, sharp pain arising from exposed dentine in response to

stimuli, typically thermal, evaporative, tactile, osmotic or chemical and which
cannot be ascribed to any other dental defect or pathology. Some authors
have substituted the word dentine and added the site, such as cervical or
root, resulting in various other terminologies (e.g., cervical
sensitivity/hypersensitivity) to describe the same clinical condition.[9]

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PREVALENCE AND EPIDEMIOLOGY
DH is a painful clinical condition with an incidence ranging from 4 to 74%.[10
14] The variations in the reports may be because of difference in populations
and different methods of investigations. The methods employed are usually
patient questionnaires or clinical examinations. Interestingly, the incidence of
DH is much higher in patient questionnaires studies than in clinical studies
which quote an incidence of mere 15%.[11,12]

A slightly higher incidence of DH is reported in females than in males. While DH

can affect the patient of any age, most affected patients are in the age group
of 2050 years, with a peak between 30 and 40 years of age.[11] Regarding the
type of teeth involved, canines and premolars of both the arches are the most
affected teeth. Buccal aspect of cervical area is the commonly affected site.
[15]

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ETIOPATHOGENESIS
Anatomy of dentine pulp complex

Dentine is covered and protected by hard tissues such as enamel or

cementum. Dentin itself is a vital tissue, consisting of dentinal tubules, and is
naturally sensitive because of extensions of odontoblasts and formation of
dentinepulp complex.[16] Although dentin and pulp are histologically different,
their origin is embryologically from the same precursor, i.e., the
ectomesenchyme.[16] Pulp is integrally connected to dentine, i.e., physiologic
and/or pathologic reactions in one of the tissues will also affect the other.
Dentin consists of small canal like spaces, dentinal tubules. These tubules
occupied by odontoblastic processes.[16] The odontoblastic processes may

extend through the entire thickness of dentin from pulp to dentino-enamel

junction. The odontoblastic processes are actually the extensions of
odontoblasts, which are the major cells of pulpdentin complex.[16] The
odontoblastic processes are surrounded by dentinal fluid inside the tubules.
The dentinal fluid forms around 22% of total volume of dentin.[16] It is an
ultrafiltrate of blood from the pulp via dentinal tubules and forms a
communication medium between the pulp (via the odontoblastic layer) and
outer regions of the dentin.

Pathogenesis

It has been stated in the literature that DH develops in two phases: lesion
localization and lesion initiation.[17] Lesion localization occurs by loss of
protective covering over the dentin, thereby exposing it to external
environment. It includes loss of enamel via attrition, abrasion, erosion or
abfraction. Another cause for lesion localization is gingival recession which can
be due to toothbrush abrasion, pocket reduction surgery, tooth preparation for
crown, excessive flossing or secondary to periodontal diseases.[18] As stated
earlier, not all exposed dentine is sensitive. For DH to occur, the lesion
localization has to be initiated. It occurs after the protective covering of smear
layer is removed, leading to exposure and opening of dentinal tubules.

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MECHANISM
Three major mechanisms of dentinal sensitivity have been proposed in the
literature:

Direct innervation theory

Odontoblast receptor
Fluid movement/hydrodynamic theory
According to direct innervation theory, nerve endings penetrate dentine and
extend to the dentino-enamel junction.[19] Direct mechanical stimulation of
these nerves will initiate an action potential. There are many shortcomings of
this theory. There is lack of evidence that outer dentin, which is usually the
most sensitive part, is innervated. Developmental studies have shown that the

plexus of Rashkow and intratubular nerves do not establish themselves until

the tooth has erupted; yet, newly erupted tooth is sensitive.[16] Moreover, pain
inducers such as bradykinin fail to induce pain when applied to dentine, and
bathing dentine with local anesthetic solutions does not prevent pain, which
does so when applied to skin.

Odontoblast receptor theory states that odontoblasts acts as receptors by

themselves and relay the signal to a nerve terminal.[20] But majority of studies
have shown that odontoblasts are matrix forming cells and hence they are not
considered to be excitable cells, and no synapses have been demonstrated
between odontoblasts and nerve terminals.[21]

Brannstrom (1964) has proposed that dentinal pain is due to hydrodynamic

mechanism, i.e., fluid force.[22] Scanning electron microscopic (SEM) analysis
of hypersensitive dentin shows the presence of widely open dentinal tubules.
[6] The presence of wide tubules in hypersensitive dentin is consistent with the
hydrodynamic theory. This theory is based on the presence and movement of
fluid inside the dentinal tubules. This centrifugal fluid movement, in turn,
activates the nerve endings at the end of dentinal tubules or at the pulp
dentine complex.[21] This is similar to the activation of nerve fibers
surrounding the hair by touching or applying pressure to the hair. The response
of pulpal nerves, mainly A intradentinal afferent fibers, depends upon the
pressure applied, i.e., intensity of stimuli.[21] It has been noted that stimuli
which tend to move the fluid away from the pulpdentine complex produce
more pain. These stimuli include cooling, drying, evaporation and application of
hypertonic chemical substances.[23] Approximately, 75% of patients with DH
complain of pain with application of cold stimuli.[23] In spite of the fact that
fluid movement inside the dentinal tubules produces pain, it should be noted
that not all exposed dentine is sensitive. As stated before, the hypersensitive
dentin has more widely open tubules and thin/under calcified smear layer as
compared with non-sensitive dentine. The wider tubules increase the fluid
movement and thus the pain response.[6,7]

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CLINICAL MANAGEMENT OF DH
Diagnosis

As like any other clinical condition, an accurate diagnosis is important before

starting the management of DH. DH has features which are similar to other
conditions like caries, fractured or chipped enamel/dentine, pain due to
reversible pulpitis, and post dental bleaching sensitivity.[15,24] Diagnosis of DH
starts with a thorough clinical history and examination. The other causes of
dental pain should be excluded before a definite diagnosis of DH is made.
Some of these techniques include pain response upon the pressure of tapping
teeth (to indicate pulpitis/periodontal involvement), pain on biting a stick
(suggests fracture), use of transilluminating light or dyes (to diagnose
fractures), and pain associated with recent restorations.[25] A simple clinical
method of diagnosing DH includes a jet of air or using an exploratory probe on
the exposed dentin, in a mesio-distal direction, examining all the teeth in the
area in which the patient complains of pain.[26] The severity or degree of pain
can be quantified either according to categorical scale (i.e., slight, moderate or
severe pain) or using a visual analogue scale.[17]

Prevention of DH/removal of etiological factors

An often, neglected phase of clinical management of DH is the identification

and treatment of the causative factors of DH. By removing the etiological
factors, the condition can be even prevented from occurring or recurring. The
etiological factors include faulty tooth brushing, poor oral hygiene [Figure 1],
premature contacts, gingival recession because of periodontal therapy or
physiological reasons, and exogenous/endogenous non-bacterial acids.[17]

Figure 1
Figure 1
(1) Patient with poor oral hygiene, generalized attrition and deposition of
calculus, (2) Excessive scrubbing at cervical areas, leading to abrasion cavities
and gingival recession, (3) Generalized attrition, (4) Erosion defects on the
palatal surfaces ...
Faulty tooth brushing includes hard brushes, excessive forces, excessive
scrubbing at the cervical areas or even lack of brushing which causes plaque
accumulation and gingival recession [Figures [Figures22 and and33].[27] The
patient should be taught the correct method of tooth brushing with the help of
a model. Highly abrasive tooth powder or pastes should be avoided.[17] Also,
the patients should be instructed to avoid brushing for at least 2 hours after
acidic drinks to prevent agonist effect of acidic erosion on tooth brush abrasion.

Erosive agents are also important agents in initiation and progression of DH

[Figure 4]. They tend to remove the enamel or open up the dentinal tubules.
[28,29] The erosive agents can be either exogenous dietary acids or
endogenous acids. The exogenous dietary acids include carbonated drinks,
citrus fruits, wines, yogurt, and professional hazards (workers in battery
manufacturing, wine tasters).[28,29] A detailed dietary history should be taken.
The quantity and frequency of the foods containing acids should be reduced.
Patient should be advised to take something alkaline (milk) or at least neutral
(water) after acidic drinks and to use a straw to sip the drink and avoid
swishing it around the teeth. The endogenous acid comes from
gastroesophageal reflux or regurgitation. It is also common in patients with
eating disorders. The condition is characterized by generalized erosion of the
palatal surfaces of maxillary anterior teeth.[30] Such a patient should be
referred to the medical practitioner for expert management of the underlying
disease. An occlusal splint can be fabricated to cover the affected areas, to
prevent their contact with the acids.

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CLASSIFICATION OF DESENSITIZING AGENTS
Mode of administration
At home desensitizing agents
In-office treatment
On the basis of mechanism of action
Nerve desensitization
Potassium nitrate
Protein precipitation
Gluteraldehyde
Silver nitrate
Zinc chloride
Strontium chloride hexahydrate
Plugging dentinal tubules

Sodium fluoride
Stannous fluoride
Strontium chloride
Potassium oxalate
Calcium phosphate
Calcium carbonate
Bio active glasses (SiO2P2O5CaONa2O)
Dentine adhesive sealers
Fluoride varnishes
Oxalic acid and resin
Glass ionomer cements
Composites
Dentin bonding agents
Lasers
Neodymium:yttrium aluminum garnet (Nd-YAG) laser
GaAlAs (galium-aluminium-arsenide laser)
Erbium-YAG laser
Homeopathic medication
Propolis
At home desensitizing therapy

Grossman[31] listed the requirements for an ideal dentine desensitizing agent

as: rapidly acting with long-term effects, non-irritant to pulp, painless and easy
to apply, and should not stain the tooth. Traditionally, the therapy for
management of DH is primarily aimed at occluding the dentinal tubules or
making coagulates inside the tubules.[17] Patients are often prescribed overthe-counter desensitizing agents. These at home desensitizing agents include
toothpastes, mouthwashes and chewing gums.[17] Majority of the toothpastes
contain potassium salts (potassium nitrate, potassium chloride or potassium
citrate), sodium fluoride, strontium chloride, dibasic sodium citrate,

formaldehyde, sodium monofluorphosphate and stannous fluoride. Potassium

salts act by diffusion along the dentinal tubules and decreasing the excitability
of the intradental nerve fibers by blocking the axonic action.[32,33] Various
clinical studies have shown the efficacy of potassium salts in controlling the
DH.[34,35] It has been shown that toothpastes containing 5% potassium nitrate
and 0.454% stannous significantly reduced the DH. Also, toothpastes
containing potassium nitrate and fluorides have been shown to reduce postbleaching sensitivity.[36,37] The desensitizing toothpastes should be used with
the help of a toothbrush with soft bristles. Patients should be advised to use
minimal amount of water to prevent the dilution of the active agent. Along with
the desensitizing toothpastes, mouthwashes and chewing gums containing
potassium nitrate, sodium fluoride or potassium citrate are also recommended.
[17] The results of at-home desensitizing therapy should be reviewed after
every 34 weeks. If there is no relief in DH, in-office therapy should be
initiated.

In-office desensitizing agents

Theoretically, the in-office desensitizing therapy should provide an immediate

relief from the symptoms of DH. The in-office desensitizing agents can be
classified as the materials which undergo a setting reaction (glass ionomer
cement, composites) and which do not undergo a setting reaction (varnishes,
oxalates).

Fluorides

Traditionally, fluorides have been used as a caries preventive material which

can help in remineralization of enamel/dentin.[38] Also, various clinical trials
have shown that application of fluoride solution can decrease the DH.[39,40]
Fluorides decrease the dentinal permeability by precipitation of calcium
fluoride crystals inside the dentinal tubules.[17] These crystals are partially
insoluble in saliva. SEM revealed granular precipitates in the peritubular dentin
after application of fluorides.[41] Various fluoride formulations are used to treat
DH. These include sodium fluoride, stannous fluoride, sodium
monofluorophosphate, fluorosilicates and fluoride combined with iontophoresis.
[17] Sodium fluoride has been used in dentifrices or may be professional
applied in a concentration of 2%. The precipitates formed by sodium fluoride
can be mechanically removed by the action of saliva or mechanical action.

Therefore, an addition of acid formulation is recommended. The acidulated

sodium fluoride can form precipitates deep inside the tubules. Also, some
authors have recommended the use of ionotophoresis along with sodium
fluoride.[41,42] The electric current is supposed to increase the ion diffusion. A
clinical study has shown that 0.4% stannous fluoride along with 0.717% of
fluoride can provide an immediate affect after a 5 minute professional
application.[43] Stannous fluoride acts in a similar fashion as that of sodium
fluoride, i.e., formation of calcium fluoride precipitates inside tubules. Also, SEM
studies have shown that stannous fluoride itself can form insoluble precipitates
over the exposed dentine.[44] Fluorosilicates act by formation of precipitates of
calcium phosphates from saliva. Ammonium hexafluorosilicate has been used
as a desensitizing agent. It can present a continuous effect of dentinal tubule
occlusion via precipitation of a mixture of calcium fluoride and fluoridated
apatite.[45,46] If the precipitate is predominantly composed of fluoridated
apatite, it can form stable crystals deposited deep inside the dentinal tubules.
[45,46] These crystals are resistant to removal from the action of saliva,
brushing or action of dietary substances.

Oxalates

Oxalates can reduce dentinal permeability and occlude dentinal tubules. Thirty
percent potassium oxalate had shown a 98% reduction in dentinal permeability.
[47] Also, topical application of 3% potassium oxalate reduced DH after
periodontal therapy.[47] The oxalate reacts with the calcium ions of dentine
and forms calcium oxalate crystals inside the dentinal tubules as well as on the
dentinal surface. This results in a better sealing as compared with an intact
smear layer.[17] It has been shown that the effect of oxalates on DH diminishes
over a period of time. This can be attributed to the removal of the calcium
oxalate crystals by brushing or dietary acids. The condition can be improved by
acid etching of the dentinal surface, thus increasing the penetration of calcium
oxalate crystals deep into the dentinal tubules.[48] Many vegetables like
rhubarb, spinach and mint contain oxalates. It has been shown that
phytocomplexes obtained from these natural products can reduce the dentinal
permeability. This can also be followed by covering the exposed surface with a
dental adhesive.[49] Potassium oxalate can lead to gastric irritation. Therefore,
it should not be used with a tray with prolonged placement.

Varnishes are commonly used useful in-office measures to treat DH. Copal
varnish can be applied to cover the exposed dentinal surface. But its effect is
for short term and is not recommended for long term management of DH.[50]

To improve its efficacy, removal of smear layer is advocated. Also, the

varnishes can act as a vehicle for fluoride. The fluoride varnishes can be
acidulated to increase the penetration of ions.[50]

Adhesive materials

Resin-based dental adhesive systems can provide a more durable and long
lasting dentine desensitizing effect. The adhesive resins can seal the dentinal
tubules effectively by forming a hybrid layer.[17] Various clinical studies have
demonstrated the effectiveness of adhesives in management of DH.[5153]
Traditionally, resin composites or dentin bonding agents are used as
desensitizing agents. The conventional dentin bonding agents (DBA) removes
the smear layer, etches the dentinal surface and forms deep dentinal resin tags
inside the dentinal tubules. The combined dentinresin layer (consisting of
penetrating resinous tags) has been termed as hybrid layer. It effectively seals
the dentinal tubules and prevents DH.[5153] Newer bonding agents modify
the smear layer and incorporate it in into the hybrid layer.[54] Recently, some
dentin bonding agents have been introduced in the market with the sole
purpose of treating DH. Gluma Desensitizer (Heraeus Kulzer, Hanau, Germany)
contains hydroxyethyl methacrylate (HEMA), benzalkonium chloride,
gluteraldehyde and fluoride. Gluteraldehyde causes coagulation of the proteins
inside the dentinal tubules.[54] It reacts with the serum albumin in the dentinal
fluid, causing its precipitation. HEMA forms deep resinous tags and occludes
the dentinal tubules.[54] Gluma has shown promising results in the clinical
trials.[54,55]

Bioglass

Bioglass was developed to stimulate the formation of new bone.[56] It is used

in orthopedics to cover the implants to promote union between implant and
bone.[56,57] It has been used in dentistry to fill up the osseous defects during
periodontal surgery.[58] It has been reported that a formulation of bioglass can
promote infiltration and remineralization of dentinal tubules.[59] The basic
component is silica, which acts as a nucleation site for precipitation of calcium
and phosphate. SEM analysis has shown that bioglass application forms an
apatite layer, which occludes the dentinal tubules.[59] The use of bioglass in
management of DH has been shown by some products such as NovaMin
(NovaMin Technology Inc., FL, USA).

Portland cement

Some authors have shown that calcium silicate cement derived from Portland
cement can help in the management of DH.[17] It helps to occlude the dentinal
tubules by remineralization.

Laser

Laser is an acronym for light amplification by stimulated emission of radiations.

It has been shown in various studies that lasers can be used in the effective
management of DH.[6063] The mechanism of action of lasers in treating DH is
not very clear. Some authors have shown that NdYAG laser application
occluded the dentinal tubules.[61,62] GaAlA laser is thought to act by affecting
the neural transmission in the dentinal tubules.[63] It has also been proposed
that lasers coagulate the proteins inside the dentinal tubules and block the
movement of fluid.[61]

Casein phosphopeptideamorphous calcium phosphate

Recently, milk protein casein has been used to develop a remineralizing agent
(GC Tooth Mousse). The casein phosphopeptide (CPP) contains phosphoseryl
sequences which get attached and stabilized with amorphous calcium
phosphate (ACP).[64] The stabilized CPPACP prevents the dissolution of
calcium and phosphate ions and maintains a supersaturated solution of
bioavailable calcium and phosphates.[64] Various studies have shown that
CPPACP can effectively remineralize the enamel subsurface lesions.[65,66] By
virtue of its remineralizing capacity, it has also been proposed by the
manufacturers that it can also help in prevention and treatment of DH.

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MANAGEMENT STRATEGY
Take a detailed clinical and dietary history.

Differentially diagnose the condition from other dental pain conditions.

Identify and manage etiological and predisposing factors.
In case of mild-to-moderate sensitivity, advice at-home desensitizing therapy.
If there is no relief or in case of severe sensitivity, initiate in-office treatment.
In extreme cases, if patient does not respond to the therapy and there are
individual teeth exhibiting the symptoms, then endodontic therapy can be
initiated.
A regular review should be made with an emphasis on prevention of the
condition.
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Footnotes
Source of Support: Nil

Conflict of Interest: None declared

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