Clinical Research
Expression of Transient Receptor Potential Ankyrin 1
in Human Dental Pulp
Yun Sook Kim, PhD,* Hoon Kap Jung, DDS,* Tae Kyung Kwon, DDS,† Chin Soo Kim, DDS, PhD,*
Jin Hyun Cho, DDS, PhD,* Dong Kuk Ahn, DDS, PhD,* and Yong Chul Bae, DDS, PhD*
Abstract
Introduction: Transient receptor potential ankyrin 1
(TRPA1) is activated by noxious cold (<17 C) and
contributes to cold and mechanical hypersensitivity after
inflammation and nerve injury. Methods: To investigate
whether TRPA1 is involved in the mediation of nocicep-
tion, including noxious cold and cold hypersensitivity in
teeth, we examined the expression of TRPA1 and sodium
channel Nav1.8 in human dental pulp using fluorescent
and electron microscopic immunocytochemistry. Results:
TRPA1 was expressed in a large number of axons branch-
ing extensively in the peripheral pulp and in a few axons
within the nerve bundles in the core of the coronal pulp
and in the radicular pulp. Under electron microscopy,
TRPA1 immunoreactivity was typically localized near
the plasma membrane of unmyelinated axons in the
peripheral pulp, suggesting that in these axons it may
act as a functional receptor. The proportion of axons ex-
pressing TRPA1 in neurofilament 200–positive axons
significantly increased in the painful pulp compared
with the normal pulp. TRPA1 was also densely expressed
in the processes and the cell body of odontoblasts. A large
number of axons coexpressed TRPA1 and Nav1.8.
Conclusions: These findings support the notion that
TRPA1 is involved in the perception of noxious cold and
cold hypersensitivity in human dental pulp and that
TRPA1-mediated nociception is primarily mediated by
axons and odontoblasts in the peripheral pulp. (J Endod
2012;38:1087–1092)
Key Words
Cold hypersensitivity, dental pulp, immunohistochem-
istry, inflammation, Nav1.8, nociception, TRPA1
From the *Department of Oral Anatomy and Neurobiology,
School of Dentistry, Kyungpook National University, Daegu,
Korea; and †Mir Dental Hospital, Daegu, Korea.
Supported by Basic Science Research Program through the
National Research Foundation of Korea funded by the Ministry
of Education, Science and Technology (2011-0028240).
Address requests for reprints to Dr Yong Chul Bae, Depart-
ment of Oral Anatomy and Neurobiology, School of Dentistry,
Kyungpook National University, 188-1, 2-Ga, Samdeok-Dong,
Jung-Gu, Daegu 700-412, South Korea. E-mail address:
ycbae@knu.ac.kr
0099-2399/$ - see front matter
Copyright ª 2012 American Association of Endodontists.
doi:10.1016/j.joen.2012.04.024
JOE — Volume 38, Number 8, August 2012
D ental cold hypersensitivity is one of the most frequently suffered symptoms in many
adult dental patients. Yet, our knowledge of the mechanisms of dental cold
nociception and cold hypersensitivity are just now beginning to be elucidated.
Recently, a family of nonselective cation channels (transient receptor potential
[TRP] channels) has been shown to render neurons and other cells that express
them on their plasma membrane thermosensitive in a fairly narrow and partially over-
lapping temperature range. Different TRP channels also mediate the action of a variety of
pungent compounds in plant extracts on sensory neurons that is perceived as ‘‘hot’’ (eg,
capsaicin via the transient receptor potential vanilloid 1) or ‘‘cold’’ (eg, menthol via the
transient receptor potential ankyrin 1 [TRPA1]).
TRPA1 is expressed primarily in nociceptive neurons and plays a crucial role in the
perception of noxious cold (1). It also mediates the hypersensitivity to cold after inflam-
mation and nerve injury (2–4). Recently, it has been shown that neurons in the rat
trigeminal ganglion (TG) that innervate the dental pulp express messenger RNA for
TRPA1 and that stimulation with noxious cold (<17 C) causes increased intracellular
calcium and evoked currents in these neurons (5, 6), implicating TRPA1 in the
mediation of noxious cold within the dental pulp. Large numbers of TRPA1-positive
(+) axons also terminate in the dorsal part of the trigeminal sensory nuclei that receive
intraoral input (7), suggesting that the oral cavity may be densely innervated by TRPA1+
sensory neurons. In addition, a potential role for TRPA1 in human odontoblasts is now
beginning to be elucidated (8). However, evidence for a TRPA1-mediated nociception in
the dental pulp is still lacking.
Voltage-gated sodium channels (Navs) play a crucial role in the generation and
propagation of action potentials in neurons. Among the 9 subtypes of Navs in humans,
the tetrodotoxin-resistant Nav1.8 is expressed mainly in small-sized nociceptive
neurons in the TG (9, 10) and dorsal root ganglia (DRG) (11, 12). Nav1.8-null
mice show a negligible behavioral response to noxious cold (13, 14), and their DRG
neurons are also unexcitable in the cold (15), suggesting that Nav1.8 is important
for the generation and propagation of action potentials at low temperatures. Recently,
it has also been reported that rat TG neurons that innervate the dental pulp express
messenger RNA for both TRPA1 and Nav1.8 and respond to temperatures below
17 C (5, 6). However, whether Nav1.8 is involved in the transduction of
TRPA1-mediated nociception in human pulp is currently unknown. To address these
issues, we examined the expression of TRPA1 and Nav1.8 in human dental pulp using
fluorescent and electron microscopic immunohistochemistry.
Materials and Methods
Tissue Preparation
This study was approved by the Research and Ethics Committee of Kyungpook
National University, Daegu, Korea, and informed consent was obtained from all human
subjects who participated in the experimental investigation after the nature of the proce-
dure had been fully explained. Twelve pulps from healthy premolars extracted during
the course of orthodontic treatment (males, age range: 17–21 years old) and 3 pulps
from a painful premolar and molar diagnosed with irreversible pulpitis (males, age
range: 18–23 years old) at Kyungpook National University Hospital and Mir Dental
Hospital, Daegu, Korea, were used for this study. Four normal pulps were used for
immunofluorescent staining for TRPA1 and/or Nav1.8, 5 normal pulps and 3 painful
Expression of TRPA1 in Human Dental Pulp 1087
Clinical Research
pulps for immunofluorescent staining for TRPA1 and/or neurofilament
200 (NF200), and 3 normal pulps for electron microscopic (EM)
immunohistochemistry for TRPA1. Immediately after extraction, teeth
were stored in 0.1 mol/L phosphate buffer (PB) (pH = 7.4) at 4 C
for 1 to 4 hours. Then, the teeth were cut longitudinally with a water-
cooled high-speed diamond bur, and the pulps were fixed for 2 hours
in 4% (w/v) paraformaldehyde (PFA) in 0.1 mol/L PB (pH = 7.4) for
immunofluorescence or in a mixture of 4% PFA and 0.05% glutaralde-
hyde for EM immunohistochemistry. For immunofluorescence, the
pulps were cryoprotected in 30% sucrose in PB overnight at 4 C and
cut on a freezing microtome at 40 mm. For EM immunohistochemistry,
the pulps were cut on a vibratome at 60 mm and also cryoprotected in
30% sucrose in PB overnight at 4 C.
Immunofluorescence and Analysis
for Immunopositive Axons
For immunofluorescence, sections were permeabilized with 50%
ethanol for 30 minutes to enhance penetration, blocked with 10%
normal donkey serum (Jackson ImmunoResearch, West Grove, PA)
for 30 minutes to mask secondary antibody binding sites, and incubated
overnight in a mixture of rabbit anti-TRPA1 antiserum (1:1,000,
RA14135; Neuromics, Edina, MN) and mouse anti-Nav1.8 antiserum
(1:100, 75-166; NeuroMab, Davis, CA) or in a mixture of rabbit
anti-TRPA1 antiserum and mouse anti-NF200 antiserum (1:200,000,
N0142; Sigma-Aldrich, St Louis, MO) in phosphate-buffered saline
(PBS, 0.01 mol/L, pH = 7.4). After washing with PBS, the sections
were incubated with appropriate secondary antibodies (fluorescence
isothiocyanate or Cy3-conjugated antibodies raised in donkey, 1:200
in PBS, Jackson ImmunoResearch) for 2 hours.
The sections were mounted on slides and examined under
a fluorescent microscope (Zeiss Axioplan 2; Carl Zeiss Inc, Jena,
Germany) or a laser confocal microscope (LSM 510 META, Carl Zeiss
Inc). The quantitative analysis of TRPA1 expression within
NF200-immunopositive axons was performed on 3 to 4 sections from
each of the 5 healthy pulps and from each of the 3 painful pulps with
irreversible pulpitis. Three to 4 images from each section were captured
from similar regions in the central and peripheral portions of the
coronal pulp with an Exi digital camera (Q-Imaging Inc, Surrey, CA)
using 20 objectives (1,360  1,036 pixels) and analyzed using
NIH ImageJ software (available at http://rsb.info.nih.gov/ij/). The
threshold level for classifying pixels as immunopositive for TRPA1
and NF200 was set between 100 and 120 gray levels from images
with 256 gray levels. The area fraction (%) of immunopositive axons
(TRPA1/NF200) was presented as the mean  the standard error.
Figure 1. Immunofluorescent staining for (A) TRPA1 in normal human dental pulp is completely abolished by (B) preadsorption with a control peptide, proving
the specificity of the TRPA1 antiserum (200, scale bars = 50 mm).
1088 Kim et al.
Data of the normal pulp and the painful pulp with irreversible pulpitis
were compared using an unpaired Student’s t test. Quantitative assess-
ment of colocalization of TRPA1 with Nav1.8 was performed on 3
images from each of the 16 sections of 4 healthy coronal pulps. The
omission of the primary or secondary antibodies or preadsorption of
the TRPA1 antibody with a blocking peptide at a final concentration
of 100 mg/mL completely abolished the specific immunostaining
(Fig. 1).
EM Immunohistochemistry
The procedure for pre-embedding immunohistochemistry was
performed as described elsewhere (7, 16). Briefly, cryoprotected
sections were frozen on dry ice for 20 minutes, thawed in PBS, and
treated with 1% sodium borohydride in PBS for 30 minutes. To
suppress endogenous peroxidase, sections were incubated with 3%
H2O2 for 10 minutes and blocked with 10% normal donkey serum
for 30 minutes. After overnight incubation with rabbit anti-TRPA1 anti-
serum (1:1,000, Neuromics), sections were incubated in biotinylated
donkey antirabbit antiserum (1:200, Jackson ImmunoResearch) for
2 hours, rinsed, incubated with ExtrAvidin peroxidase (1:5,000,
Sigma-Aldrich) for 1 hour, and visualized with nickel-intensified diami-
nobenzidine. Sections were then osmicated (1% osmium tetroxide in
PB), dehydrated in graded alcohols, and embedded in Durcupan
ACM (Fluka, Buchs, Switzerland). Thin sections were cut, mounted
on formvar-coated single-slot nickel grids, counterstained with Sato’s
lead, and examined on a Hitachi H 7500 electron microscope (Hitachi,
Tokyo, Japan).
Results
Strong immunofluorescent staining for TRPA1 was observed in
axons and axon collaterals in human dental pulp (Fig. 2). A small
number of axons within nerve bundles wrapped with connective tissue
were TRPA1 positive (+) in the radicular pulp and in the core of the
coronal pulp (Fig. 2A and B). In contrast, in the peripheral pulp,
TRPA1+ axons branched extensively and formed a network in the
vicinity of the cell-rich zone corresponding to the plexus of Raschow
in the occlusal and the cervical regions (Fig. 2C and D). TRPA1+ axons
ascending toward the dentin between odontoblasts were rarely
observed. The proportion of NF200+ axons expressing TRPA1 signifi-
cantly increased in the painful pulp compared with the normal pulp (P
< .05). Immunoreactivity for TRPA1 was more intense in the painful
pulp than in the normal pulp (Figs. 3 and 4). Immunoreactivity for
TRPA1 was also observed in the odontoblasts and their processes
(Fig. 5A–D). A large number of TRPA1+ axons were immunostained
JOE — Volume 38, Number 8, August 2012

Figure 2. Immunofluorescent staining for TRPA1 in (A) the radicular portion, (B) the core of the coronal portion, and (C and D) the peripheral portion (C,
occlusal region; D, cervical region) of normal human dental pulp. (A and B) Relatively sparse TRPA1+ axons in the nerve bundle issue few axon collaterals in the
radicular pulp and the core of the coronal pulp. (C and D) TRPA1+ axons branch extensively and form a network in the (C) occlusal and (D) cervical regions of the
peripheral pulp (200, scale bars = 50 mm).
for Nav1.8. Of the 450 TRPA1+ axons examined in the coronal pulp in
16 sections from 4 pulps, 177 (39.3%) were Nav1.8+ (Fig. 6A–C).
At the electron microscopic level, TRPA1 immunoreactivity was
observed in the form of an electron-dense amorphous product in the
axoplasm of both myelinated and unmyelinated axons in the radicular
pulp and the central portion of the coronal pulp. However, it was usually
Figure 3. The area fraction (%) of TRPA1+ axons in NF200+ nerve fibers in
the normal and painful (irreversible pulpitis) pulp samples. *A significant
difference between normal and painful pulp samples (P < .05).
JOE — Volume 38, Number 8, August 2012
Clinical Research
observed near the axolemma of unmyelinated axons in the peripheral
pulp (Fig. 7).
Discussion
The main findings of this study are that TRPA1 is densely expressed
in the axons and odontoblasts in the peripheral portion of human dental
pulp and the expression of TRPA1 is increased in the pulpal axons after
pulpal inflammation. In addition, approximately 40% of TRPA1+ axons
coexpress the sodium channel Nav1.8.
TRPA1 is selectively expressed by small- and medium-sized, noci-
ceptive neurons in the DRG and TG and has been implicated in the medi-
ation of noxious cold (1, 7, 17) and the cold and mechanical
hypersensitivity after inflammation (18). Recently, Park et al (5)
showed that rat TG neurons innervating the dental pulp express
messenger RNA for TRPA1 and that the application of icilin or noxious
cold to these neurons increases their intracellular calcium and evoked
cationic currents, suggesting that TRPA1 may contribute to dental pain
evoked by noxious cold. The fact that a large number of pulpal axons in
the present study expressed TRPA1 is consistent with a TRPA1-mediated
cold nociception within human dental pulp.
TRPA1 was densely expressed in a large number of axons that
branched extensively outside the connective tissue sheath in the periph-
eral pulp and in a few axons within nerve bundles in the core of the
coronal pulp and in the radicular pulp. Electron microscopy revealed
that TRPA1 is expressed mostly in unmyelinated peripheral axons, in
which it was typically localized at the axonal membrane where it could
act as a functional receptor. In contrast, in myelinated axons in the core
of the coronal pulp and in the radicular pulp, TRPA1 was localized in the
axoplasm away from the membrane, possibly representing a pool of
receptors that is being transported to the peripheral pulp. These find-
ings suggest that the TRPA1-mediated sensitivity to noxious cold is
Expression of TRPA1 in Human Dental Pulp 1089
Clinical Research

Figure 4. Double immunofluorescent staining for (A and D) TRPA1 and (B and E) NF200 in the peripheral region of (A–C) normal human pulps and (D–F) painful
pulps. Numbers of axons showing TRPA1 expression in NF200+ axons increase in the painful pulp compared with the normal pulp (200, scale bars = 50 mm).

Figure 5. Immunofluorescent staining for TRPA1 in the (A–C) occlusal and (D) cervical regions of normal human dental pulp. Odontoblasts show intense immu-
noreactivity for TRPA1 in their cell bodies and in their processes (arrowheads). An arrow in C points to a TRPA1+ axon beneath the odontoblast layer (400,
scale bars = 50 mm).

1090 Kim et al. JOE — Volume 38, Number 8, August 2012

 Clinical Research

Figure 6. Double immunofluorescent staining for (A) TRPA1 and (B) Nav1.8 in normal human dental pulp. (C) Many TRPA1+ axons are Nav1.8-positive
(arrowheads) (200, scale bar = 20 mm).

mediated primarily by axons in the peripheral pulp rather than in the
core of the coronal pulp or in the radicular pulp. In addition, very
few axons passing between odontoblasts and entering dentinal tubules
were TRPA1 positive, suggesting that axons in the dentinal tubules either
express another TRP receptor or are insensitive to cold. In the
present study, the proportion of axons expressing TRPA1 within
NF200+ axons significantly increased, suggesting that TRPA1 is involved
in cold and mechanical allodynia and/or hyperalgesia after dental pulp
inflammation.
Several previous studies have proposed that odontoblasts may act
as sensory cells because they express mechanosensitive K+ channels
(19, 20), L-type Ca2+ channels (21), and thermosensitive TRP channels
including TRPA1 and the transient receptor potential vanilloid 1
(22, 23). They also express voltage-gated sodium channels (24, 25)
and may thus be electrically excitable and able to generate action
potentials (26). TRPA1 is functionally expressed in other non-
neuronal cells, including keratinocytes (27), fibroblasts (28), and syn-
oviocytes (29), which may act in concert with sensory afferents to
monitor the thermal environment.
In agreement with 1 recent report (8), in this study we showed that
TRPA1 is expressed by odontoblasts, thus providing morphologic
evidence that human odontoblasts may be involved in sensing and
transducing noxious cold information. TRPA1 immunoreactivity was
strong in the processes and in the cell bodies of the odontoblasts.
Because, as described previously, TRPA1+ axons were rarely seen
ascending toward the dentinal tubule between odontoblasts, we specu-
late that noxious cold may be sensed primarily by odontoblast processes
rather than by axons in the dentinal tubule.
About 40% of TRPA1+ axons coexpressed Nav1.8 in this study,
corroborating previous reports that TG neurons that innervate the
dental pulp express messenger RNA for both TRPA1 and Nav1.8
(5, 6) and that DRG neurons of Nav1.8-null mice have significantly
attenuated the expression of TRPA1 (15). Considering that among
the 9 subtypes of Nav channels in humans, Nav1.8 can generate
an electrical impulse and is involved in the transmission of nocicep-
tive information under cold conditions and plays a crucial role in
pain perception at a low temperature (14), our finding supports
the notion that Nav1.8 is involved in the conduction of TRPA1-
mediated cold nociception in human dental pulp. The TRPA1+
axons in the dental pulp that do not express Nav1.8 may express
other Navs, possibly Nav1.7 or Nav1.9, both of which have been
shown to be overexpressed after pulpal inflammation and have
been implicated in the perception of pain after inflammation and
nerve injury (30–32).

Figure 7. Electron micrographs showing immunoperoxidase staining for TRPA1 in normal human dental pulp. (A) As shown for an example, the TRPA1 immu-
noreactivity, indicated by patches of an electron-dense reaction product (arrow), is localized in the central regions of the axoplasm of myelinated axons in the
radicular pulp and (B) adjacent to the axonal membrane of unmyelinated axons in the peripheral pulp. Scale bars = 500 nm.

JOE — Volume 38, Number 8, August 2012 Expression of TRPA1 in Human Dental Pulp 1091
Clinical Research
Acknowledgments
The authors thank Dr Juli Valtschanoff for helpful discussion
and careful reading of the manuscript.
The authors deny any conflicts of interest related to this study.
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