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Dentin hypersensitivity and emerging concepts for treatments

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DOI: 10.1016/j.job.2017.09.001

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Journal of Oral Biosciences 59 (2017) 211–217

Contents lists available at ScienceDirect

Journal of Oral Biosciences


journal homepage: www.elsevier.com/locate/job

Review

Dentin hypersensitivity and emerging concepts for treatments


Ji won Kim, Joo-Cheol Park n
Department of Oral Histology, Developmental Biology, School of Dentistry and Dental Research Institute, Seoul National University, Gwanak-ro 1, Gwanak-gu,
Seoul 08826, Republic of Korea

art ic l e i nf o a b s t r a c t

Article history: Background: Dentin hypersensitivity is a relatively common pain symptom caused by evaporative, che-
Received 21 July 2017 mical, thermal, tactile, or osmotic stimuli. Despite its high prevalence, many aspects of dentin hy-
Received in revised form persensitivity remain unknown. Current treatments for dentin hypersensitivity include desensitizers and
24 August 2017
adhesive materials. Several factors that occur in the oral cavity, such as occlusal force and intrapulpal
Accepted 25 August 2017
pressure, cause microleakage, the primary defect of adhesive treatments.
Available online 8 September 2017
Highlight: (1) This review article explains the etiology and pain mechanisms of dentin hypersensitivity.
Keywords: (2) Microleakage, a primary cause of restoration failures, is emphasized. (3) Current and ideal treatments
Dentin hypersensitivity for dentin hypersensitivity are described.
Hydrodynamic theory Conclusion: The ideal treatment for dentin hypersensitivity should restore the original impermeability of
Desensitizing treatment
the dentinal tubules. A novel way to treat dentin hypersensitivity is the regeneration of tubular dentin to
Microleakage
overcome microleakage.
Tubular dentin
& 2017 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
2. Etiology and mechanisms of dentin hypersensitivity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
2.1. Etiology and diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
2.2. Pain mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
2.2.1. Direct innervation theory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
2.2.2. Hydrodynamic theory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
2.2.3. Odontoblastic transducer theory. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
3. Microleakage, a primary cause of restoration failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
3.1. External factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
3.2. Internal factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
4. Current and ideal treatments for dentin hypersensitivity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
4.1. Current treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
4.1.1. Desensitization of the pulpal nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
4.1.2. Tubule occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
4.2. Ideal treatments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
5. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
Ethical approval. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
Conflicts of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216

Abbreviations: CLTE, coefficient of linear thermal expansion; CPNE7, Copine7; TRPM, transient receptor potential cation channel subfamily M; TRPV, transient receptor
potential cation channel subfamily V
n
Corresponding author.
E-mail address: jcapark@snu.ac.kr (J.-C. Park).

http://dx.doi.org/10.1016/j.job.2017.09.001
1349-0079/& 2017 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.
212 J.w. Kim, J.-C. Park / Journal of Oral Biosciences 59 (2017) 211–217

1. Introduction

Dentin hypersensitivity is a short, sharp pain caused by ex-


posed dentin. Such pain is produced by evaporative, chemical,
thermal, tactile, or osmotic stimuli and is dependent on the
duration of the applied stimuli. Discomfort from dentin hy-
persensitivity occurs in 8–57% of the adult population [1], and the
prevalence of dentin hypersensitivity ranges from 72.5–98% in
periodontal patients [2]. The severity of dentin hypersensitivity
can increase because of gingival recession, cervical lesions, peri-
odontal disease, or erosion. Although three theories explaining the
mechanism of dentin hypersensitivity have been suggested, hy-
persensitive pain has not yet been fully explained by a specific
theory.
For dentin hypersensitivity to occur, the dentin surface must be
exposed so that the dentinal tubules are patent from the pulp to
the oral environment. As the numbers of wider tubules and open
tubules increase, hypersensitive pain becomes more severe [3].
Current treatments for dentin hypersensitivity either hinder the
neural response to pain stimuli or block the exposed tubules.
Desensitizing treatments include at-home and in-office treat-
ments, such as the use of desensitizing toothpastes. Adhesive
treatments are currently the most common occluding treatments;
however, external and internal tooth factors weaken the dentin-
resin bond strength and may lead to microleakage, allowing bac-
teria to spread into the dentinal tubules [4], which results in
secondary caries [5]. To prevent microleakage following adhesive
treatments, the original impermeability of the dentinal tubules
should be restored. This review presents the etiology, mechanism,
and treatments of dentin hypersensitivity and provides an ex-
planation of how both external and internal factors contribute to
microleakage.

2. Etiology and mechanisms of dentin hypersensitivity

2.1. Etiology and diagnosis

Fig. 1. Cause of dentin hypersensitivity. Dentinal tubules may be open to the oral
Dentin hypersensitivity may be produced by the loss of enamel environment due to enamel loss or gingival recession.
or by gingival recession, which exposes the underlying dentin
(Fig. 1) [6]. Gingival recession, the most common cause of dentin
hypersensitivity, exposes the dentinal tubules [7]. Gingival reces- Dentin hypersensitivity is diagnosed by excluding other
sion is believed to be primarily due to excessive brushing [8]. The pathologies, such as gingival inflammation, dental caries, chipped
cementum layer on the root surface is thin and easily abolished. As or cracked teeth, fractured cusps, fractured restorations or re-
a result, gingival recession results in rapid and widespread dis- storations with deficient margins and marginal leakage, post-op-
closure of the dentinal tubules. Possible causes of gingival recession erative sensitivity, periodontal disease, pulpitis or other en-
are periodontitis, trauma, orthodontic treatment [9], frontolateral dodontic problems, and sensitivity due to bleaching. Pain arising
bruxism [10], prosthodontic treatment, traumatic tooth brushing, from dentin hypersensitivity cannot be ascribed to any other form
thin alveolar cortex, buccal or lingual dehiscence and fenestration of of dental defect or pathology [15]. There are two common meth-
the alveolar bone, oral piercing, and self-inflicted injury [11]. ods to determine the intensity of dentin hypersensitivity. One is by
Cervical lesions, which can be caused by incorrect tooth asking the patient questions; the other is through clinical
brushing, caries, or occlusal loading factors, expose dentinal tu- examination.
bules that have little or no enamel at the cervical margin [12].
Enamel loss from non-carious cervical lesions, which can result 2.2. Pain mechanisms
from attrition, abrasions, or erosion, exposes dentinal tubules
under the enamel and induces dentin hypersensitivity. Attrition, 2.2.1. Direct innervation theory
tooth wear from direct contact between teeth, is linked to occlusal Dentin hypersensitivity has received a considerable amount of
force and can be exacerbated by habits such as bruxism. Abrasion study; however, its exact mechanism is not yet fully understood.
is physical tooth wear caused by mechanical processes of foreign Most studies of dentin hypersensitivity are based on practical
objects such as a toothbrush or toothpaste. Erosion is chemical theories rather than scientific evidence [16]. One of the three
wear caused by extrinsic or intrinsic acid acting on plaque-free theories to explain dentin hypersensitivity is the direct innerva-
tooth surfaces. Biological, chemical, and behavioral factors change tion theory (Fig. 2A), which emphasizes the direct transduction of
the effects of acids on enamel differently [13]. Abfraction, which is external thermal or mechanical stimuli through the nerve endings
caused by microfractures in the enamel and dentin due to occlusal in the dentinal tubules. Nociceptive trigeminal ganglion neurons
loading stress on the cement-enamel region, has also been hy- that innervate the dental pulp must have receptors that transduce
pothesized to be an etiological factor in tooth wear [14]. a specific stimulus to electrical impulses [17].
J.w. Kim, J.-C. Park / Journal of Oral Biosciences 59 (2017) 211–217 213

2.2.2. Hydrodynamic theory


Tooth pain is provoked not only by thermal stimuli, but also by
stimuli such as water sprays, air blasts, and sweets. The hydro-
dynamic theory (Fig. 2B), which currently has the most support,
assumes that the fluid-filled dentinal tubules of sensitive dentin
are patent at the dentin surface and also within the pulp. Ac-
cording to the hydrodynamic theory, stimuli increase the dentinal
fluid flow, excite the nervous system, and activate pain nociception
in the pulp-dentin border area [23]. However, the absence of nerve
terminals at the dentino-enamel junction, the most sensitive zone
of the dentin, and the failure of pain-producing stimuli to directly
excite the intradentinal axons, contradict the hydrodynamic the-
ory [24].
In contrast, the presence of mechano-sensitive receptors ex-
pressed in afferent neurons reinforces the hydrodynamic theory
[18]. The short, sharp pain of dentin hypersensitivity causes me-
chanical deformation of A-δ nerves, in which myelinated A-β and
some A-δ fibers in dentin respond to stimuli that cause dentinal
fluid flow [25], which can occur at a rate as high as 2 mm
per second [26]. The inward movement of dentinal fluid due to hot
stimuli activates sensitized C-fibers in deep pulpal tissue and
causes dull pain [17].

2.2.3. Odontoblastic transducer theory


A growing body of evidence supports the odontoblastic trans-
ducer theory (Fig. 2C), which projects odontoblasts as sensory cells
that directly mediate tooth pain sensation via synaptic junctions
Fig. 2. Three supported theories of dentin hypersensitivity. (A) Direct innervation with nerves. The odontoblastic transducer theory primarily
theory: direct transduction of stimuli through the nerve endings in the dentinal emerged because odontoblasts are embryologically derived from
tubule. (B) Hydrodynamic theory: pain-producing stimuli increase dentinal fluid
mesenchymal cells of the neural crest [27]. The proximal location of
flow in the tubules, excite the nervous system, and activate pain nociception.
(C) Odontoblastic transducer theory: odontoblasts act as sensory cells and directly the odontoblasts relative to the dentinal nerve terminals suggests
mediate pain sensation via synaptic junctions with nerves. that odontoblasts may sense external stimuli, transform pain-
evoking fluid displacement within dentinal tubules into electrical
The functional expression of several thermo-TRP channels, signals, and transmit the signals to nearby nerve cells [28]. As a
transient receptor potential cation channel subfamily V (TRPV) signaling mechanism, ATP could mediate painful signaling between
1 and TRPV2, in the dental primary afferent neurons [18] supports odontoblasts and underlying dental primary neurons [29].
the conventional perspective that most dental afferent neurons are Thermosensitive transient receptor potential ion channels
nociceptors. The presence of unmyelinated nerve fibers in the (TRPV1, TRPV2, TRPV3, TRPV4, and TRPM3) and/or mechan-
osensitive K þ channels (Kca and TWIK-related K þ channel) [30],
outer layer of root dentin [19], and the presumed presence of
expressed in odontoblasts, may sense heat and/or cold or dentinal
neurogenic polypeptides [20], support the direct innervation the-
fluid movements and generate action potentials [31]. The cold
ory. However, results from histological staining experiments have
receptor TRPM8 was expressed in odontoblasts using im-
shown that the activation by stimuli was not entirely specific for munohistochemistry [32]. However, the odontoblastic transducer
nerve fibers [21]. Electron microscopy studies of nerve fibers in theory has been refuted by the absence of neurotransmitter ve-
some dentinal tubules showed that the fibers did not penetrate sicles in the odontoblast process to assist in synapse or synaptic
the dentinal tubules more than 100 μm, and were instead present specialization [30]. Electrophysiological and histological studies
primarily over the pulpal horns, which excludes the possibility have shown that dentin is still sensitive even in the presence of
that the nerves are present in dentin [22]. irritation-induced odontoblasts and nerve injury [33], suggesting

Table 1
Three hypotheses to explain dentin hypersensitivity.

Direct Innervation theory Hydrodynamic theory Odontoblastic Transducer theory

Yes ● Functional expression of several thermo-TRP channels ● Normally innocuous stimuli such as water sprays, ● Odontoblasts constitute a cell layer at the out-
in dental primary afferent neurons air puffs, and sweets can elicit tooth pain. Thermo- ermost part of dental pulp; strategic location
● Presence of unmyelinated nerve fibers in the outer TRP channels alone cannot explain these. ● Expression of several channels involved in sig-
layer of root dentin; presence of putative neurogenic ● Expression of mechano-sensitive receptors in af- nal transduction in odontoblasts
polypeptides ferent neurons
No ● Nerves in the dentinal tubules are not commonly seen; ● Physical stimulation is difficult to explain with this ● No neurotransmitter vesicles in the odonto-
if they are, it is for a very short distance (no more than theory (mechanical abrasion of the exposed dentin blast process to facilitate the synapse or sy-
100 μm into the inner dentin) and primarily over the surface may be sufficient to induce unwanted fluid naptic specialization
pulpal horns flow) ● Tooth cavity preparation would destroy or dis-
● Topical application of local anesthetics does not abol- rupt the odontoblast layer, yet pain can still
ish sensitivity. emanate without a local anesthetic
● The excitability of the odontoblast remains
unknown
214 J.w. Kim, J.-C. Park / Journal of Oral Biosciences 59 (2017) 211–217

that odontoblasts may not initiate tooth pain sensation. There is dentin [48]. The permeability and increased wetness of deep
variation in dentin sensitivity to different stimuli, and the three dentin within the enlarged tubule openings, even without in-
aforementioned theories reflect the difficulty in pinpointing the trapulpal pressure, prevent the sufficient lateral bonding of the
mechanism of dentin hypersensitivity. Three hypotheses to ex- resin, resulting in an exceedingly wet environment, which weak-
plain dentin hypersensitivity are compared in Table 1. ens the bond strength by preventing adhesive resins from pene-
trating into the surface for an ideal bond. The excess water in
dentin impacts the resin-dentin bond by promoting the physical
3. Microleakage, a primary cause of restoration failure separation of adhesives into hydrophobic and hydrophilic phases
[49], diminishing solvent evaporation [50], restricting monomer-
Microleakage, a primary cause of restoration failure, allows to-polymer conversion [51], and provoking an excessively wet
fluids, bacteria, and molecules or ions to flow between the cavity environment.
wall and the applied restorative material. Primary factors that Pulpal pressure, the tissue pressure within the pulp, is the re-
contribute to microleakage can be divided into external factors, sult of vascular pressure [36]. Dental pulp exhibits a relatively high
which happen on the tooth surface or externally relative to the fluid pressure within its interstitial tissue, meaning that a pressure
tooth, and internal factors, which happen inside the tooth. gradient exists in dentinal tubules under normal conditions. Po-
sitive hydrostatic pressure within vital pulps has been reported to
3.1. External factors
range from 7 cm H2O (0.7 kPa) [52] to 40 cm H2O (3.9 kPa) [53];
normal pulpal pressure is approximately 15 cm H2O (1.5 kPa) [54].
Both occlusal force and thermal changes accelerate bond fail-
The outward pressure gradient could empty an open tubule ap-
ures and induce gap formation as well as dye penetration [34].
proximately 10 times per day [55]. Positive intrapulpal pressure
Thermal, mechanical, or chemical stimuli cause resin degradation
also negatively interferes with the bonding process by weakening
and erosion, promoting several factors from resin-based materials
the bonding of adhesives that require removal of the smear layer
to leach into the oral environment [35]. Oral conditions such as
[44,45]. Intrapulpal pressure beneath a leaky filling or exposed
occlusal force or hydrolytic degradation weaken the primary
dentin does not produce pain, but results in the movement of
bonds between the dentin and resin [36]. Due to occlusal force, the
odontoblasts into the dentinal tubules [22]. Lower bond strengths
restoration material contracts, and the cavity deforms under the
have been consistently produced under positive intrapulpal pres-
stresses at the restoration margins, eliciting bond failure and re-
sulting in microleakage as fluids flow around the restoration [37]. sure due to the increase in water outflow to the dentin surface
Saliva is another factor in the oral cavity that induces micro- [48]. In the absence of pulpal pressure, all adhesives showed
leakage. All experimental teeth exposed to saliva showed leakage higher bond strengths [56]. Pulpal blood flow was augmented by
from 79% to 85% of the root, whereas teeth not exposed to saliva increased tooth surface temperature [57]. Therefore, an increase in
showed no leakage [38]. Exposing resin-composite restorations to temperature may lead not only to thermal cycling, but also to in-
saliva-like esterase activities stimulates marginal bacterial micro- creased intrapulpal pressure, which promotes microleakage.
leakage [39].
Volumetric shrinkage that occurs with the polymerization of
resin materials is a significant factor that contributes to micro- 4. Current and ideal treatments for dentin hypersensitivity
leakage. The polymerization shrinkage of resin weakens the resin-
dentin bond, which may lead to microleakage [40] and allow 4.1. Current treatments
bacteria, fluids, molecules, ions, and air to pass through the in-
terface. All composites shrink linearly from 0.6% to 1.4% depending There are two mechanisms for dentin hypersensitivity treat-
on the amount and nature of the material, the type and cure rate ments: 1) pulpal nerve activity is blocked by a modification of the
of the composite [41], the shape of the cavity preparation, and the excitability of the sensory nerves (Fig. 3A), or 2) fluid movements
ratio of bonded to unbonded surfaces [42]. are prevented by the occlusion of the dentinal tubules (Fig. 3B).
Among the different factors that affect bond failure, the dif-
ference in the coefficient of linear thermal expansion (CLTE) be-
tween the tooth structure and the restoration was found to be the
primary cause of microleakage [5]. Continuous expansions and
contractions at the tooth-restorative interface, caused by the dif-
ference in the thermal expansion of fluids between the dentinal
tissues and the restorative material, develop stresses and may lead
to microleakage at the restoration margin [43].

3.2. Internal factors

Internal factors include dentin permeability and intrapulpal


pressure [44]. Dentin permeability reduces the dentin-adhesive
bond strength and the durability of the restoration [45]. The
number of tubules per unit area increases from the enamel-ce-
mental junction (  20,000 per mm2) to the pulp (  45,000 per
mm2), as does the radius of the tubules, with the dentin wetness in
patent tubules increasing 20-fold from superficial to deep dentin
[46]. Theoretically, bond strength should be higher in deep dentin, Fig. 3. Summary of the mechanisms of treatments for dentin hypersensitivity.
because resins can be tightly hybridized to demineralized dentinal (A) Treatment by desensitization of the pulpal nerve, such as desensitizers con-
taining potassium salts, does not decrease fluid flow but reduces nerve sensitivity
tubule walls [47]. However, the reduced area of the solid inter- to fluid shifts produced by stimuli. (B) Treatment by tubule occlusion, such as ad-
tubular dentin and the increased amount of water make bonding hesive treatments, prevents fluid movement and decreases pain, acting as an ar-
to deep dentin more challenging than bonding to superficial tificial smear layer.
J.w. Kim, J.-C. Park / Journal of Oral Biosciences 59 (2017) 211–217 215

4.1.1. Desensitization of the pulpal nerve


Desensitizers contain 5% KNO3, which cannot entirely block
fluid flow across the dentin [58] by tubule occlusion, but can re-
duce the sensitivity of mechanoreceptor nerves to the fluid shifts
produced by normally painful stimuli [59]. Desensitizing treat-
ments include desensitizing toothpastes and mouthwashes; most
contain potassium salt (potassium nitrate [60], potassium chloride,
or potassium citrate [61]). When desensitizing treatment is ap-
plied, fluid flow due to stimuli still exists, but the nerves are either
unexcitable or are blocked from responding to the stimuli [59].
Recently, it was reported that daily use of a toothpaste containing
potassium nitrate significantly decreased tooth pain due to dentin
hypersensitivity within a two-week period [62]. Nevertheless,
desensitizing agents only provide partial relief, and recurrence is
common [6].

4.1.2. Tubule occlusion


Whereas exposed non-sensitive dentin is impermeable, hy-
persensitive dentin is permeable because the dentinal tubules are
open and not occluded by mineral deposits [63]. Non-sensitive
Fig. 4. Ideal treatment for dentin hypersensitivity. Tertiary dentin formation and
dentin is hypermineralized, and the increased mineral content is
intratubular mineralization provide a tight seal to reduce dentin permeability and
due to tubule occlusion by crystalline material. Patients with non- restore the original impermeability of the dentinal tubules.
sensitive exposed root surfaces had dentinal tubules that were
completely occluded near the surface by a smear layer, salivary and speed of the reparative processes of the tooth that results in
minerals, minerals from dentinal fluid, or exogenously applied tubule occlusion [74]. Patients with chronic dentin hypersensitivity
mineral salts [64]. The removal of the smear layer increased sen- may be unable to differentiate new odontoblasts or produce tertiary
sitivity in unanesthetized patients [65]. Dentin permeability, the dentin because of destruction of progenitor cells due to constant
ability of a fluid to shift across the dentin, increased five- to 10-fold
inflammatory events, or because of damaged pulp leading to de-
when the smear layer was removed [66]. Therefore, reocclusion of
creased nutrient and blood flow near the open tubules [59].
the dentinal tubules has been used for many years to manage
The structure of tubular dentin contributes to the defense
dentin hypersensitivity [67].
mechanism of the dentin-pulp complex. The tubular structure of
Calcium phosphate and silicate phosphate, presumed hydro-
dentin results from odontoblastic differentiation of the outer cells
xyapatite, precipitated upon exposure to saliva and were able to
of the dental papilla, and the subsequent deposition and miner-
occlude open dentinal tubules to some extent [68,69]. Although
alization of the dentin matrix during tooth development [75].
the exact mechanism of action of lasers in dentin hypersensitivity
Immunoglobulins amassed in dentinal tubules could protect the
is not clearly understood, lasers or laser-combined applications
dentin by slowing bacterial invasion [76], by non-specifically de-
have been recently proposed for in-office treatment. Lasers may
creasing the inward diffusion of bacterial antigens or toxins [77],
increase the deposition of tertiary dentin and obliterate dentinal
or by binding to specific antibodies [78]. The outward flow of
tubules [70]. Recently, it was also reported that the dentin tubule-
dentinal fluid also restricts foreign substances, such as bacteria
occluding ability of fluoroaluminocalciumsilicate-based dentin
and bacterial by-products, from diffusing inward into the dentinal
desensitizers was significantly higher than that of diamine silver
tubules [79]. Sensory nerve endings in dentinal tubules can detect
fluoride dentin desensitizers [71].
temperature changes, mechanical stimuli, and nociception, and
Topically applied desensitizing agents or adhesives, including
thus protect the pulp from injuries [80]. Therefore, it is important
varnishes, bonding agents, and restorative materials, are thought
to maintain the tubular structure of dentin to protect the dentin
to form insoluble precipitates in dentinal tubules [26] and are
therefore used to block fluid movement in dentinal tubules via and pulp.
tubule occlusion. However, adhesive treatments for dentin hy- Recently, the tubular nature of dentin was regenerated with
persensitivity break away with time and re-expose the tubules; Copine 7 (CPNE7) [81]. CPNE7 stimulates odontoblasts to generate
the pain is decreased for only 3 to 6 months and microleakage is reactionary dentin in the pulp, protecting against painful stimuli
induced [72]. To overcome the microleakage of restorative mate- and reduces dentin permeability in the dentinal tubules. The for-
rials, physiologic dentin regeneration (occluded tubular dentin mation of tertiary dentin by bioactive molecules such as CPNE7
formation) including intratubular and tertiary dentin under the may be used as an alternative to prevent dentin hypersensitivity
restorative materials is an important prerequisite. pain by restoring the original impermeability of dentinal tubules
[82], which could eliminate microleakage, the largest disadvantage
4.2. Ideal treatments of resin adhesives.

Dentin is normally covered by enamel or cementum, and under


these conditions, it is impermeable. However, in a hypersensitive 5. Conclusions
state, the dentinal tubules are open and permeable. Therefore, an
ideal treatment for dentin sensitivity should restore the original im- The most common treatment for dentin hypersensitivity is
permeability of the dentinal tubules [59]. Tertiary dentin formation currently adhesive materials. However, due to different external
and increased intratubular mineralization (Fig. 4) influence dentin and internal tooth factors, the strength of the dentin-resin bond
permeability and thus act as a defense mechanism of the pulp-dentin weakens, leading to microleakage. Microleakage may greatly in-
complex in response to physiological or pathological causes [73]. crease the permeation of acids and microorganisms [4] and lead to
Important factors that determine an individual's risk of experi- sensitivity [59]. In order to prevent microleakage from inducing
encing hypersensitive pain are the age of the pulp and the capability sensitivity and secondary caries, the original impermeability of the
216 J.w. Kim, J.-C. Park / Journal of Oral Biosciences 59 (2017) 211–217

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