Professional Documents
Culture Documents
net/publication/319607678
CITATIONS READS
0 80
2 authors, including:
SEE PROFILE
All content following this page was uploaded by Joo Cheol Park on 28 June 2018.
Review
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
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
Table 1
Three hypotheses to explain dentin hypersensitivity.
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].
dentinal tubules should be restored by new bioactive materials [24] Hildebrand C, Fried K, Tuisku F, Johansson C. Teeth and tooth nerves. Prog
with adhesive treatments. Neurobiol 1995;45:165–222.
[25] Matthews B, Andrew D, Wanachantararak S. Biology of the dental pulp with
special reference to its vasculature and innervation. In: Embery G, Edgar WM,
Orchardson R, Addy M, editors. Tooth wear and sensitivity. London: Taylor and
Ethical approval Francis; 2000. p. 39–51.
[26] Nordenvall K-J, Brännström M. In vivo resin impregnation of dentinal tubules.
J Prosthet Dent 1980;44:630–7.
Document all ethical approvals and/or informed consents [27] Rapp R, Avery JK, Strachan DS. Possible role of the acetylcholinesterase in
obtained. neural conduction within the dental pulp. In: Finn SB, editor. Biology of dental
pulp organ. Birmingham: University of Alabama Press; 1968. p. 309.
[28] Allard B, Couble ML, Magloire H, Bleicher F. Characterization and gene ex-
pression of high conductance calcium-activated potassium channels display-
Conflicts of interest ing mechanosensitivity in human odontoblasts. J Biol Chem 2000;275:25556–
61.
[29] Lim J, Mitchell C. Inflammation, pain, and pressure – purinergic signaling in
The authors declare no conflicts of interest with respect to the oral tissues. J Dent Res 2012;91:1103–9.
authorship and/or publication of this article. [30] Magloire H, Maurin JC, Couble ML, Shibukawa Y, Tsumura M, Bleicher F. To-
pical review. Dental pain and odontoblasts: facts and hypotheses. J Orofac Pain
2010;24:335–49.
[31] Allard B, Magloire H, Couble ML, Maurin JC, Bleicher F. Voltage-gated sodium
Acknowledgments channels confer excitability to human odontoblasts possible role in tooth pain
transmission. J Biol Chem 2006;281:29002–10.
[32] Tokuda M, Tatsuyama S, Fujisawa M, Morimoto-Yamashita Y, Kawakami Y,
This work was supported by National Research Foundation of Shibukawa Y, Torii M. Dentin and pulp sense cold stimulus. Med Hypotheses
Korea grants NRF-2016R1A2B3006584 and NRF-2017R1E1A2A 2015;84:442–4.
02022384. [33] Hirvonen TJ, Närhi MV, Hakumäki MO. The excitability of dog pulp nerves in
relation to the condition of dentine surface. J Endod 1984;10:294–8.
[34] Xie H, Zhang F, Wu Y, Chen C, Liu W. Dentine bond strength and microleakage
of flowable composite, compomer and glass ionomer cement. Aust Dent J
References 2008;53:325–31.
[35] Geurtsen W. Biocompatibility of resin-modified filling materials. Crit Rev Oral
Biol Med 2000;11:333–55.
[1] Fischer C, Fischer R, Wennberg A. Prevalence and distribution of cervical [36] Bouillaguet S. Biological risks of resin-based materials to the dentin-pulp
dentine hypersensitivity in a population in Rio de Janeiro, Brazil. J Dent complex. Crit Rev Oral Biol Med 2004;15:47–60.
1992;20:272–6. [37] Jang K, Chung D, Shin D, García-Godoy F. Effect of eccentric load cycling on
[2] Chabanski M, Gillam D, Bulman J, Newman H. Clinical evaluation of cervical microleakage of Class V flowable and packable composite resin restorations.
dentine sensitivity in a population of patients referred to a specialist period- Oper Dent 2000;26:603–8.
ontology department: a pilot study. J Oral Rehabil 1997;24:666–72. [38] Swanson K, Madison S. An evaluation of coronal microleakage in en-
[3] Addy E, Addy M, Adams D. Dentin hypersensitivity, a study of the patency of dodontically treated teeth. Part I time periods. J Endod 1987;13:56–9.
dentinal tubules in sensitive and non-sensitive cervical dentin. J Clin Period- [39] Kermanshahi S, Santerre J, Cvitkovitch D, Finer Y. Biodegradation of resin-dentin
ontol 1987;14:280–4. interfaces increases bacterial microleakage. J Dent Res 2010;89:996–1001.
[4] Bergenholtz G. Evidence for bacterial causation of adverse pulpal responses in [40] Asmussen E. Composite restorative resins: composition versus wall-to-wall
resin-based dental restorations. Crit Rev Oral Biol Med 2000;11:467–80. polymerization contraction. Acta Odontol Scand 1975;33:337–44.
[5] Sideridou I, Achilias DS, Kyrikou E. Thermal expansion characteristics of light- [41] Davidson CL, De Gee AJ. Light-curing units, polymerization, and clinical im-
cured dental resins and resin composites. Biomaterials 2004;25:3087–97. plications. J Adhes Dent 2000;2:167–73.
[6] Dababneh R, Khouri A, Addy M. Dentine hypersensitivity: dentine hy- [42] Feilzer A, De Gee A, Davidson C. Setting stress in composite resin in relation to
persensitivity—an enigma? A review of terminology, mechanisms, aetiology configuration of the restoration. J Dent Res 1987;66:1636–9.
and management Br Dent J 1999;187:606–11. [43] Rosin M, Urban A, Gärtner C, Bernhardt O, Splieth C, Meyer G. Polymerization
[7] Taani S, Awartani F. Clinical evaluation of cervical dentin sensitivity (CDS) in shrinkage-strain and microleakage in dentin-bordered cavities of chemically
patients attending general dental clinics (GDC) and periodontal specialty and light-cured restorative materials. Dent Mater 2002;18:521–8.
clinics (PSC). J Clin Periodontol 2002;29:118–22. [44] Leloup G, D'hoore W, Bouter D, Degrange M, Vreven J. Concise review bio-
[8] Drisko CH. Dentine hypersensitivity – dental hygiene and periodontal con- materials & bioengineering: meta-analytical review of factors involved in
siderations. Int Dent J 2002;52:385–93. dentin adherence. J Dent Res 2001;80:1605–14.
[9] Slutzkey S, Levin L. Gingival recession in young adults: occurrence, severity, [45] Prati C, Pashley DH, Montanari G. Hydrostatic intrapulpal pressure and bond
and relationship to past orthodontic treatment and oral piercing. Am J Orthod strength of bonding systems. Dent Mater 1991;7:54–8.
Dentofac Orthop 2008;134:652–6. [46] Pashely D. Dynamics of the pulp-dentinal complex. Crit Rev Oral Biol Med
[10] Abboud M, Grüner M, Koeck B. Anterior crowding – just an esthetic problem? J 1996;7:104–33.
Orofac Orthop 2002;63:264–73. [47] Pashley DH, Ciucchi B, Sano H, Carvalho R, Russell C. Bond strength versus
[11] Smith RG. Gingival recession reappraisal of an enigmatic condition and a new dentine structure: a modelling approach. Arch Oral Biol 1995;40:1109–18.
index for monitoring. J Clin Periodontol 1997;24:201–5. [48] Pereira P, Okuda M, Sano H, Yoshikawa T, Burrow M, Tagami J. Effect of in-
[12] Powell L, Gordon GE, Johnson GH. Clinical evaluation of direct esthetic re- trinsic wetness and regional difference on dentin bond strength. Dent Mater
storations in cervical abrasion/erosion lesions: one-year results. Quintessence 1999;15:46–53.
Int 1991;22:687–92. [49] Wang Y, Spencer P. Hybridization efficiency of the adhesive/dentin interface
[13] Lussi A. Erosive tooth wear – a multifactorial condition of growing concern with wet bonding. J Dent Res 2003;82:141–5.
and increasing knowledge. Monogr Oral Sci 2006;20:1–8. [50] Yiu CK, Pashley EL, Hiraishi N, King NM, Goracci C, Ferrari M, Carvalho RM,
[14] Grippo JO. Abfractions: a new classification of hard tissue lesions of teeth. J Pashley DH, Tay FR. Solvent and water retention in dental adhesive blends
Esthet Dent 1991;3:14–9. after evaporation. Biomaterials 2005;26:6863–72.
[15] Mantzourani M, Sharma D. Dentine sensitivity: past, present and future. J Dent [51] Jacobsen T, Söderholm K-J. Some effects of water on dentin bonding. Dent
2013;41:S3–17. Mater 1995;11:132–6.
[16] Addy M. Dentine hypersensitivity: new perspectives on an old problem. Int [52] Tønder KJ, Kvinnsland I. Micropuncture measurements of interstitial fluid
Dent J 2002;52:367–75. pressure in normal and inflamed dental pulp in cats. J Endod 1983;9:105–9.
[17] Chung G, Jung S, Oh S. Cellular and molecular mechanisms of dental noci- [53] Brown A, Beveridge E. The relation between tooth pulp pressure and systemic
ception. J Dent Res 2013;92:948–55. arterial pressure. Arch Oral Biol 1966;11:1181–93.
[18] Chung G, Oh SB. TRP channels in dental pain. Open Pain J 2013;6:31–6. [54] Ciucchi B, Bouillaguet S, Holz J, Pashley D. Dentinal fluid dynamics in human
[19] Frank R, Steuer P. Transmission electron microscopy of the human odontoblast teeth, in vivo. J Endod 1995;21:191–4.
process in peripheral root dentine. Arch Oral Biol 1988;33:91–8. [55] Johnson G, Olgart L, Brännström M. Outward fluid flow in dentin under a
[20] McGrath PA. The measurement of human pain. Endod Dent Traumatol physiologic pressure gradient: experiments in vitro. Oral Surg Oral Med Oral
1986;2:124–9. Pathol 1973;35:238–48.
[21] Rapp R, Avery J, Rector R. A study of the distribution of nerves in human teeth. [56] Sauro S, Pashley DH, Montanari M, Chersoni S, Carvalho RM, Toledano M,
J Can Dent Assoc 1957;23:447–53. Osorio R, Tay FR, Prati C. Effect of simulated pulpal pressure on dentin per-
[22] Brännström M. The hydrodynamic theory of dentinal pain: sensation in pre- meability and adhesion of self-etch adhesives. Dent Mater 2007;23:705–13.
parations, caries, and the dentinal crack syndrome. J Endod 1986;12:453–7. [57] Kim S, Schuessler G, Chien S. Measurement of blood flow in the dental pulp of
[23] Närhi M, Jyväsjärvi E, Virtanen A, Huopaniemi T, Ngassapa D, Hirvonen T. Role dogs with the 133xenon washout method. Arch Oral Biol 1983;28:501–5.
of intradental A-and C-type nerve fibres in dental pain mechanisms. Proc Finn [58] Greenhill JD, Pashley DH. The effects of desensitizing agents on the hydraulic
Dent Soc 1991;88:507–16. conductance of human dentin in vitro. J Dent Res 1981;60:686–98.
J.w. Kim, J.-C. Park / Journal of Oral Biosciences 59 (2017) 211–217 217
[59] Pashley DH. Dentin permeability, dentin sensitivity, and treatment through Albernaz PLM, Weckx LLM. Laser therapy in the treatment of dentine hy-
tubule occlusion. J Endod 1986;12:465–74. persensitivity. Braz Dent J 2004;15:144–50.
[60] Gillam D, Bulman J, Jackson R, Newman H. Efficacy of a potassium nitrate [71] Han L, Okiji T. Dentin tubule occluding ability of dentin desensitizers. Am J
mouthwash in alleviating cervical dentine sensitivity (CDS). J Clin Periodontol Dent 2015;28:90–4.
1996;23:993–7. [72] Bartold P. Dentinal hypersensitivity: a review. Aust Dent J 2006;51:212–8.
[61] Yates R, West N, Addy M, Marlow I. The effects of a potassium citrate, ce- [73] Garberoglio R, Brännström M. Scanning electron microscopic investigation of
tylpyridinium chloride, sodium fluoride mouthrinse on dentine hypersensi- human dentinal tubules. Arch Oral Biol 1976;21:355–62.
tivity, plaque and gingivitis. J Clin Periodontol 1998;25:813–20. [74] West N, Lussi A, Seong J, Hellwig E. Dentin hypersensitivity: pain mechanisms
[62] Low SB, Allen EP, Kontogiorgos ED. Reduction in dental hypersensitivity with and aetiology of exposed cervical dentin. Clin Oral Investig 2013;17:9–19.
nano-hydroxyapatite, potassium nitrate, sodium monoflurophosphate and [75] Kim SG. Biological molecules for the regeneration of the pulp-dentin complex.
antioxidants. Open Dent J 2015;9:92–7. Dent Clin North Am 2017;61:127–41.
[63] Mjör IA. Dentin permeability: the basis for understanding pulp reactions and [76] Pulver W, Taubman M, Smith D. Immune components in normal and inflamed
adhesive technology. Braz Dent J 2009;20:3–16. human dental pulp. Arch Oral Biol 1977;22:103–11.
[64] Hiatt WH, Johansen E. Root preparation I. Obturation of dentinal tubules in [77] Hahn CL, Overton B. The effects of immunoglobulins on the convective per-
treatment of root hypersensitivity. J Periodontol 1972;43:373–80.
meability of human dentine in vitro. Arch Oral Biol 1997;42:835–43.
[65] Johnson G, Brännström M. The sensitivity of dentin changes in relation to
[78] Love R. The effect of tissue molecules on bacterial invasion of dentine. Oral
conditions at exposed tubule apertures. Acta Odontol Scand 1974;32:29–38.
Microbiol Immunol 2002;17:32–7.
[66] Pashley D, Michelich V, Kehl T. Dentin permeability: effects of smear layer
[79] Pashley DH. The influence of dentin permeability and pulpal blood flow on
removal. J Prosthet Dent 1981;46:531–7.
pulpal solute concentrations. J Endod 1979;5:355–61.
[67] Brännström M, Johnson G. Effects of various conditioners and cleaning agents
[80] Byers M, Narhi M. Dental injury models: experimental tools for understanding
on prepared dentin surfaces: a scanning electron microscopic investigation. J
Prosthet Dent 1974;31:422–30. neuroinflammatory interactions and polymodal nociceptor functions. Crit Rev
[68] Mehta D, Gowda V, Finger WJ, Sasaki K. Randomized, placebo-controlled Oral Biol Med 1999;10:4–39.
study of the efficacy of a calcium phosphate containing paste on dentin hy- [81] Oh HJ, Choung HW, Lee HK, Park SJ, Lee JH, Lee DS, Seo BM, Park JC. CPNE7, a
persensitivity. Dent Mater 2015;31:1298–303. preameloblast-derived factor, regulates odontoblastic differentiation of me-
[69] Earl J, Leary R, Muller K, Langford R, Greenspan D. Physical and chemical senchymal stem cells. Biomaterials 2015;37:208–17.
characterization of dentin surface following treatment with NovaMin tech- [82] Choung H, Lee D, Lee J-H, Shon W, Lee J-H, Ku Y, Park J. Tertiary dentin for-
nology. J Clin Dent 2011;22:62–7. mation after indirect pulp capping using protein CPNE7. J Dent Res
[70] Ladalardo TCCGP, Pinheiro A, Campos RAdC, Brugnera Júnior A, Zanin F, 2016;95:906–12.