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Sympathetic Dental Hypersensitivity: An Alternative Etiology for Dental Cold

Hypersensitivity

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 Yiannios N, Piper M, Radke J, Coleman T. Sympathetic Dental Hypersensitivity: An
Alternative Etiology for Dental Cold Hypersensitivity. Adv Dent Tech. Published online
July 31, 2025:1-13.

Occlusion

Sympathetic Dental Hypersensitivity: An Alternative Etiology for

Dental Cold Hypersensitivity
Nick Yiannios, DDS1, Mark Piper, MD, DMD2, John Radke, BM, MBA3 , Thomas Coleman, DDS4
1Director, Center for Neural Occlusion, 2 Director, Piper Education and Research Center, 3 Chairman of the Board of Directors, BioResearch
Associates, Inc., 4 Retired, Private Practice, Brandon, VT
Keywords: Sympathetic Dental Hypersensitivity (SDH), Greater Auricular Nerve (GAN), Superficial Cervical Plexus, sympathetic neuroinflammation, c-
fibers, pulp, Dentinal Hypersensitivity (DH), pulpal hypoxia, anesthetic injection, dermatome

Advanced Dental Technologies & Techniques

Abstract
INTRODUCTION
Cold sensitivity in the dentition is a common complaint of patients presenting to dental
practices. Causation is typically attributed to the mechanical breakdown of dental and
periodontal structures, and the specific area of damage can be localized to a dermatomal
distribution of branches of the second or third division of the trigeminal nerve. Beyond
structural damage as an etiology, it is accepted that exposed dentinal tubules account for
Dental Cold Hypersensitivity (DCH), which may be a source of localized or more
generalized dermatomal pain. There is no proven etiology for intraoral non-dermatomal
or multi-dermatomal pain from cold exposure in patients with no evidence of mechanical
damage to dental structures or with previously failed treatment of DCH. Neurogenic
inflammation of sympathetic nociceptive C-fibers originating from outside the oral cavity
may account for some patients who have dental allodynia to ice-cooled cold water.

AIM
To evaluate the responses of patients with DCH to superficial anesthetic injection of the
great auricular nerve.

METHODS
Clinic records from a private practice (NY) were reviewed concerning routine injections of
the Great Auricular Nerve applied to temporarily reduce dental cold hypersensitivity. The
GAN is a sensory branch of the superficial cervical plexus that carries non-myelinated
sympathetic C-fibers. One hundred ninety-four records of patients with an allodynic pain
response to a cold-water swish were given local anesthetic injections bilaterally to their
greater auricular nerves (GAN) where they cross the sternocleidomastoid muscles. Before
the injection and at 10 minutes post-injection, patients reported their Verbally
Announced Scores (VAS = 0 to 10) response to a repeated ice-cold water swish. All
patients were fully informed and provided with written consent for this diagnostic
procedure in accordance with the World Medical Association Declaration of Helsinki. The
null hypothesis was that a GAN anesthetic injection would produce no reduction of group
mean VAS. Multiple statistical tests were employed with alpha level of 0.05.

RESULTS
Patient VAS values pre- and post-injection demonstrated three response groups, nearly
equally divided into non-responders (no change), partial responders (small change), and
complete responders (large change). Within both responder groups, significant reduction
of mean pain was experienced (p < 0.05) without the benefit of trigeminal anesthetic
blockade. Local anesthetic injection of the GAN reduced sensation of the skin at the
angle of the mandible, but there was no intraoral anesthesia. The generalized significant
pain reduction reported by 129 subjects was in a non-dermatomal distribution, like the
responses from sympathetic blocks elsewhere in the body. The results were consistent
with an extraoral contribution to DCH in many patients with allodynia from an intraoral
ice-cold water swish.
 Sympathetic Dental Hypersensitivity

CONCLUSIONS
It was concluded that neuroinflammation of sympathetic nerves originating outside the
oral cavity can add a layer of pain in some DCH patients. These findings may also have
implications for sympathetic neurogenic inflammation in other types of idiopathic pain.
It is proposed that the novel etiology of Sympathetic Dental Hypersensitivity (SDH) may
account for a subset of patients who experience confounding cold hypersensitivity of the
dentition within instances of both dermatomal and non-dermatomal distributions. The
null hypothesis was rejected.

INTRODUCTION 90% of nerve fibers entering the dental pulp are myelinated
sensory afferents from the trigeminal nerve, another 10%
Pain of dental origin is most frequently related to structural are unmyelinated sympathetic fibers arising from the supe-
alteration of individual teeth or the associated periodon- rior cervical ganglion.3,21 Of note, parasympathetic fibers
tium. Depending upon the localization of damage to either have not been histologically identified within the dental
maxillary or mandibular structures, nociceptive sensory pulp.22‑24 It is widely accepted that sympathetic c-fibers
pain commonly follows the dermatomal distribution of the are a source of nociception and that the autonomic nervous
second or third divisions of the trigeminal nerve, but not to system aids in regulating pain.25 It is beyond the scope of
both. Exceptions arise when deviations occur concurrently this paper to detail all mechanisms of sympathetic-medi-
in the structures of both the upper and lower jaws. How- ated nociceptive, neuropathic, and inflammatory pain, but
ever, generalized maxillary and mandibular pain involv- these pathways are detailed elsewhere.26‑28 The sympa-
ing both divisions may exist without apparent structural thetic response to acute injury is vasodilatation; in chronic
damage, and dentists and pain specialists need more in- pain, there is sympathetic-maintained vasoconstriction.25
sight into this enigma of intraoral tooth sensitivity to cold Sympathetically maintained pain, aka SMP (defined as con-
that follows non-dermatomal or multi-dermatomal path- founding pain and hyperalgesia which is maintained by
ways and extends beyond a single division of the trigeminal efferent sympathetic activity and circulating cate-
nerve. cholamines), has been reported in the literature to occur
Dental Cold Hypersensitivity (DCH) is an accepted expla- throughout the body.29 Sympathetic nerve blocks are ef-
nation for generalized tooth sensitivity in the dermatomal fective in modulating neuropathic pain and other SMPs
distribution of both the second and third divisions of the elsewhere in the body, and this paper explores whether
trigeminal nerve. DCH affects both maxillary and mandibu- there may be analogous sympathetic nociception and al-
lar teeth in 25-30% of the global population. Exposed tered blood flow in DCH.
dentinal tubules that activate trigeminal nerve afferents A prior study supported a correlation between cervical
have been theorized as the cause of (DCH), also commonly spine innervation and confounding cases of DCH.30 In the
known as dentinal hypersensitivity (DH).1‑10 present retrospective clinical study, the authors sought fur-
In the 1990s, Pashley identified cervical dentin hyper- ther support for the role of cervical input into DCH by anes-
sensitivity (CDH), originating from the cervical root of thetizing the greater auricular nerve (GAN), a branch of the
teeth, as distinct from DH. In clinical practice, DH typically superficial cervical plexus. The Superior Cervical Ganglion
presents as a dull pain and often resolves by itself in a of the sympathetic trunk sends branches to the common
week or two. CDH is an acute, sharp pain associated with and external carotid vasculature, and it also supplies grey
cold exposure, which usually requires intervention, such as rami to cervical nerves C1 through C4, which in turn form
removing a biocorrosive agent or initiating occlusal ther- the cervical plexus.31‑33 VAS responses were recorded pre-
apy.11‑14 DH is further distinguished as exposed coronal block and post-block. A reduction in sensation was noted at
dentin presenting with a dull pain of presumed c-fiber ori- the angle of the mandible to confirm a positive GAN block,
gin, as distinguished from CDH occurring from exposed cer- but no branches of the trigeminal nerve were anesthetized.
vical dentinal tubules presenting with a sharp, fast pain at- Responses were consistent with a cervical source of pain
tributed to a-delta fibers.6,15 Though several theories exist in some cases of DCH. Given that there was no intraoral
regarding the etiology of DH and CDH, the classical hy- sensory anesthesia initiated throughout the patient pool in
drodynamic theory proffered by Brännström & Åström in this study, the positive responses are consistent with sym-
1964, involving fluid flow within dentinal tubules, is cur- pathetic c-fiber nociception of the cervical plexus as an al-
rently the most widely accepted etiology.3,16 Various chem- ternative source of DCH. These findings may be supportive
ical medicaments, laser treatments, occlusal therapies, and of exploring c-fiber nociception in other sources of facial
medical grade ozone exposure have been purported to ad- pain.
dress DCH, with mixed and often less than predictable re-
sults.17‑20 Due to the variability of treatment responses and MATERIALS & METHODS
the lack of improvement in some patients, practitioners
may encounter complex DCH unrelated to the trigeminal c- Informed written consent was obtained from the 194 par-
fiber-alpha-delta nociceptors. ticipants in the study in accordance with the World Medical
The presence of non-myelinated C-fibers in the dental Association Declaration of Helsinki, all of whom expressed
pulp provides an alternative pathway for DCH. Although DCH pain conditions, including a history of confounding

Advanced Dental Technologies & Techniques 2

 Sympathetic Dental Hypersensitivity

cold sensitivity in their dentition. All subjects responded

with moderate to severe tooth pain during a diagnostic
5-second ice-cold water swish test.
The Verbally Announced Score (VAS) responses of the
patients (0 to 10) were assessed following uniform testing
procedures as follows:
• Water was cooled with ice for 5-6 minutes minimally
in a cup
• The patients were instructed to swish the cold water
for 5 seconds before expectorating or swallowing and
then asked to indicate the sensitivity of their teeth on
a scale of 0 to 10 (10 unbearable pain, zero no pain)
• The blocking GAN injections were given by one au-
thor (NY). Approximately 0.5 – 1.0 cc of Bupivicaine
w/ 1:200 epinephrine was injected superficial to each
sternocleidomastoid muscle using a 12.7mm needle
with 2-4mm of subcutaneous penetration. The effec-
tiveness of the GAN block was confirmed by subse-
quent anesthesia along the ipsilateral mandibular an-
gle, the inferior aspect of the auricle, and the mastoid
region
• Approximately 10-15 minutes after each GAN block, a
post-injection ice-cold water swish of approximately Figure 1. Regions of the head that are affected by the
5 seconds was once again initiated, and the second GAN block are shown in aqua.
VAS was recorded. A retrospective statistical analysis
was applied to the 194 patients in the study by an in-
dependent statistician (JR). INITIATING THE GAN BLOCK TO REDUCE EXCESSIVE
SYMPATHETIC TONE AND TEST FOR THE SDH
• A separate group of subjects with their VAS = 0 prior
ENDOTYPE
to injection of the GAN and with zero post-injection
response served as controls.
Following the preoperative cold-water swish, the patient’s
neck was disinfected with alcohol-saturated gauze on both
INCLUSION CRITERIA
sides where the GAN nerve tracks closest to the epidermis.
1. All subjects were older than 18 years of age This was at the postero-superior aspect of the superficial
2. All patients previously sought professional opinions fibers of the sternocleidomastoid (SCM) muscle at the level
on tooth hypersensitivity to cold where a line drawn parallel with the inferior aspect of the
3. Patients reported pain from cold drinks or foods af- mandibular angle intersects with the location of the GAN.
fected their everyday life Note: A line drawn parallel with the inferior aspect of the
4. Acceptance of the GAN injection procedure following mandibular angle should intersect with the location of the
informed consent GAN, just slightly superior to Erb’s point. See Figures 1 &
5. Patients with at least twenty vital permanent teeth 2. Using a ½-inch, ultra-short 30-gauge needle, the oper-
ator slowly injected 0.5 to 1.0 cc of bupivacaine with 1:200
EXCLUSION CRITERIA epinephrine on one side of the neck, fanning out to en-
sure GAN saturation, while aspirating to avoid the external
1. Allergy to Bupivicaine (Marcaine) carotid vasculature. One rule was to never drop below the
2. Evidence of active periodontal disease or pulpal SCM to avoid anesthetizing the phrenic nerve. The usage of
pathology the ultra-short needle essentially removed that possibility
3. Patients needing operative interventions due to den- from occurring.
tal pathology After injecting, the clinician looked for signs on the in-
4. Signs of profound and/or generalized gingival reces- jected side to confirm that the ipsilateral GAN had been
sion anesthetized (Figure 1). The inferior border/angle of the
5. Patients with anterior open bite mandible, the ventral pinna, the inferior preauricular re-
6. History of temporomandibular joint surgery gion and the mastoid region became anesthetized within
7. Evidence of failing restorations, cracked tooth syn- a few minutes following a successful block. After 10 to 15
drome, or retentive pins in dentin in either vital or minutes, the clinician again prompted another cold-water
non-vital teeth swish, queried the patient as to their response, and looked
8. Palato-gingival groove or other enamel invaginations for any change regarding their cold hypersensitivity. A de-
9. Patients with four or more endodontically treated crease in the VAS response to the cold-water swish signi-
teeth fied sympathetic inputs as likely contributory, and hence
the presence of the SDH endotype. The patients were also

Advanced Dental Technologies & Techniques 3

 Sympathetic Dental Hypersensitivity

Figure 2. (A) Injection of a patients’ left GAN using an ultra-short, ½ inch, 30-gauge needle using bupivacaine
(Marcaine) 0.5% with 1:200K EPI local anesthetic. (B) Anatomy of the left Greater Auricular Nerve displayed in
yellow on a cadaver specimen. Local anesthetic target injection point highlighted within the green circle. Notice
that the GAN reaches the angle of the mandible, the mastoid region, and the inferior aspect of the auricle.

queried as to any other profound changes that might have lar Nerve. The Sign Test was used when too many tied val-
experienced due to the temporary blockage of excessive ues were reported because no change occurred in the VAS.
sympathetic tone. Student’s Paired T test and the Wilcoxon Signed-Rank test
The clinician then repeated the procedure on the con- cannot handle many tied values.
tralateral side by injecting the other GAN, and once again
began looking for signs of anesthetization and any subse- STATISTICAL ANALYSIS
quent changes from yet another ice-cold water swish chal-
lenge, as well as any other changes that they might have The means and standard deviations of the pre-injection
experienced in and around their head and neck region. A and post-injection VAS sensitivities to ice-cold water swish
change in the intensity of the response to the cold-water were calculated for; a) the whole group, b) for a subgroup of
swish on one side likely indicated that the SDH endotype all responders, and c) for those that responded maximally.
was in play. The patients were informed that within 6-8 Due to the subjective nature of the VAS data, the pre-in-
hours, any reduction in symptoms they may have experi- jection and post-injection means were compared using the
enced in sensitivity to cold would likely return to pre-injec- Wilcoxon Signed-Rank test to detect any significant dif-
tion levels after the local anesthetic wore off. Interestingly, ferences. Alpha was selected at 0.05. The comparisons be-
in several cases the GAN block proved effective against tween groups pre and post injection were tested using the
other symptoms such as acute muscular trismus; however, Wilcoxon Rank-Sum test.
the DCH levels in all 194 studied patients returned to base-
line after the local anesthetic wore off. RESULTS
The 194 subjects were divided into three similar sized
groups as follows: Before the GAN block injections, each subject was tested
Group 1 – Subjects with zero VAS change in cold sensi- for cold sensitivity. The pre-injection mean VAS sensitivity
tivity after GAN block (n = 65). levels were compared between the three groups, including
Group 2 – Subjects with limited VAS reductions, post means between 6.1 and 6.7, and were found not to be sig-
GAN block injection levels > 3.0 (n = 71). nificantly different (p > 0.05). See Table 1.
Group 3 – Subjects with significant VAS reductions, post Ten minutes after the injections, all subjects were re-
GAN block injection levels ≤ 3.0 (n= 58). tested looking for any significant change in mean VAS lev-
To identify any significant differences in the initial sta- els. A significant reduction in patient-reported ice-cold wa-
tus of the three groups prior to the GAN block injections, ter swish VAS responses was observed among the entire
the non-parametric Wilcoxon Rank-Sum Test was used to group of subjects (n =194) (p < 0.00001). See Table 2.
compare the pre-block VAS data, which was determined to Based upon the subjects’ post-injection verbally an-
be non-normal. Subsequently, the Sign Test was chosen to nounced scores, they were then categorized based upon
evaluate the within-subject changes in each group as re- their response levels into three groups: 1) no response, 2) a
ported from pre-block to post-block of the Great Auricu- limited response and, 3) a maximal response.

Advanced Dental Technologies & Techniques 4

 Sympathetic Dental Hypersensitivity

Table 1. Comparison of the sensitivity levels of the three groups prior to the GAN-block injections. All three are
equivalent.

Three Groups Compared Prior to the Injections Pre-Block Cold Sensitivity (1 - 10)
Mean (n = 65) 6.10
Non-Responders
Standard Deviation 2.24
Wilcoxon Rank-Sum test p > 0.2763
Mean (n = 71) 6.44
Limited Responders
Standard Deviation 2.59
Wilcoxon Rank-Sum test p < 0.6585
Mean (n = 58) 6.69
Maximal Responders
Standard Deviation 2.39
Wilcoxon Rank-Sum test p > 0.1482
Mean (n = 65) 6.10
Non-Responders
Standard Deviation 2.24

Table 2. Significant mean reduction of all 194 subjects with painful VAS responses to cold-water swish comparing
pre-GAN injections and 10 minutes post GAN injections.

Whole Mouth Cold Sensitivity Pre-Injection Whole Mouth Cold Sensitivity Post-Injection
GAN VAS Scores
(1 - 10) (1 - 10)
Mean 6.4 4.02
Std Dev 2.41 2.64
Wilcoxon Signed-Rank
p < 0.00001 n = 194
test

Table 3. Non-responder subjects (65) with no change in tooth sensitivity to cold-water.

Non-Responder Whole Mouth Cold Sensitivity Whole Mouth Cold Sensitivity Change in Cold
Subjects Pre-Op VAS (1 - 10) Post-Op VAS (1 - 10) Sensitivity VAS (1 - 10)
Means 6.10 6.14 -0.04
Standard
2.24 2.25 0.22
Deviations
95% C. I. 5.56 - 6.64 5.59 - 6.68 -0.09 - 0.02
Minimum 1.0 1.0 -1.5
Maximum 9.0 9.0 0.0
Sign Test p > 0.1573 n = 65

C. I. = Confidence Interval, VAS = Verbally Announced Score

The no response group, 65 of the 194 study participants, Among the remaining 129 subjects, 71 showed a limited
did not respond at all, with no significant change in their but significant reduction (p < 0.00001). See Table 4. This
ice-cold water swish VAS after the GAN block. These non- second group showed a significant, but limited response
responders did not possess the theoretical SDH endotype, (Limited Responders) with a mean reduction from 6.44 to
at least not via the GAN anatomical pathway. There were 4.14.
two patients (1 %) who reported slight increases in their The remaining subgroup (n = 58) included those who re-
VAS numbers post-injection, which accounted for the ported their post-injection symptoms reduced their mean
slightly negative mean value of -0.04 for the mean change VAS (0 to 10) from a mean of 6.69 to 1.47. See Table 5.
in sensitivity within the non-responding group. See Table Within this maximal responder group, the reduction was
3. However, considering that VAS is a subjective patient re- found to be statistically significant (p < 0.00000). This third
port with low resolution, it is possible that those two mini- group showed a maximal response (Maximal Responders).
mal changes were not real. No subject complained that the Focusing on the most sensitive patients, the 4th quartile
GAN block itself was very uncomfortable. subjects from each group were compared between pre-in-
jection and post-injection. See Table 6. These were all the

Advanced Dental Technologies & Techniques 5

 Sympathetic Dental Hypersensitivity

Table 4. Partial responders with reduced sensitivity, but still with discomfort.

Limited
Whole Mouth Cold Sensitivity Whole Mouth Cold Sensitivity Reduction in Cold
Responder
Pre-Op VAS (1 - 10) Post-Op VAS (1 - 10) Sensitivity VAS (0 - 10)
Subjects
Mean 6.44 4.14 2.30
Std. Dev. 2.59 2.02 1.36
95% C. I. 5.84 - 7.05 3.67 - 4.61 1.99 - 2.62
Minimum 1.0 0.0 0.5
Maximum 10.0 8.0 5.5
Sign test p < 0.00001 n = 71

Table 5. Complete responders with dramatically reduced sensitivity.

Maximal
Whole Mouth Cold Sensitivity Whole Mouth Cold Sensitivity Reduction in Cold
Responder
Pre-Op VAS (1 - 10) Post-Op VAS (1 - 10) Sensitivity VAS (1 - 10)
Subjects
Means 6.69 1.47 5.23
Std Deviations 2.39 1.10 2.26
95 % C. I. 6.05 - 7.33 1.19 - 1.178 4.66 - 5.84
Minimums 3.0 0.0 1.5
Maximums 10.0 3.0 9.0
Wilcoxon Signed-
p < 0.00000 n =58
Rank

C. I. = Confidence Interval, VAS = Verbally Announced Score

patients, n = 89 (45.9 %), who were initially reported VAS or only a GAN sympathetic nerve input, as their response
≥ 7.5. The distribution of those in the 4th percentile among was more complete. Since there was no significant differ-
the three groups was non-responders = 16 (18 %), limited ence between the pre-GAN injection VAS means for these
responders = 48 (53.9 %) and maximal responders = 25 (28.1 three groups (p > 0.05), the significant differences in their
%). The non-responders had a significantly lower pre-GAN post-injection means were more likely etiological.
injection than the maximal responders (p < 0.0386). Other- Since it is well accepted that tooth sensitivity to cold in-
wise, the significance levels were comparable to the whole cludes multiple etiologies, it would be reasonable to expect
group. that within this group of subjects, some might have a single
The comparison of the limited responders and the max- etiology while others could have multiple etiologies. That
imal responders is shown in Table 7. The latter group’s re- could account for the fact that the GAN injections had no
sponse was significantly greater (p < 0.00000) than the for- effect on some, a partial effect on some, and a complete
mer group. The mean VAS post-GAN-block injection for the resolution of others.
latter group was 1.48 (+/- 1.11), which is widely considered
a successful resolution of sensitivity. However, for the lim- THE SYMPATHETIC EFFECT UPON DCH WHEN THE SDH
ited responders, their mean post-GAN-block injection VAS ENDOTYPE WAS IN PLAY
was 4.14 (+/-2.02), commonly considered only a partial re-
sponse or improvement. Importantly, the sympathetic fibers are efferent, not affer-
ent, as their neighboring trigeminal sensory cohorts are.
This is an important distinction, as the efferent sympa-
DISCUSSION
thetic nerves induce changes in the smooth muscle arte-
riole endothelium, leading to contraction, which in turn
The separation of Group 1 is quite clearly justified, as the
causes vasoconstriction. Additionally, the sympathetic
members did not respond to the GAN-block injection at all,
fibers can also cause a localized inflammatory response,
which suggests no GAN sympathetic nerve contribution to
leading to leakage of blood vessels within the affected pul-
the symptom. The division of Groups 2 and 3 is somewhat
pal arterioles. The concomitant release of biologically ac-
less precise, as it has a degree of arbitrariness with the de-
tive sensory neuropeptides in the dental pulp causes va-
cision to consider a VAS score of 3 as mild, although it is a
sodilation, leading to increased local tissue pressure and
common practice. The rationale was that those in Group 2
consequently, increased capillary permeability, resulting in
were responders, but more likely had at least one additional
plasma extravasation and edema formation.3 This leakage
factor besides a GAN sympathetic nerve input contributing
of fluids out of the arterioles and the subsequent edema
to their VAS reports. Those in Group 3 may have had mostly
substantially reduces blood flow distal to the affected re-

Advanced Dental Technologies & Techniques 6

 Sympathetic Dental Hypersensitivity

Table 6. 4th Quartile Comparison

4th Quartile n =
89 Whole Mouth Cold Sensitivity Pre- Whole Mouth Cold Sensitivity Post- Change in Sensitivity
Non- Block (0 - 10) Block (0 - 10) (0 - 10)
Responders
Mean 8.44 8.53 0.0
Standard
0.44 0.46 0.0
Deviation
Median 8.5 8.5 0.0
Partial
Responders* p < 0.0615 p < 0.0000 p < 0.0000
Mean 8.85 5.68 3.13
Standard
0.78 1.53 1.43
Deviation
Median 9.0 5.0 3.0
Maximal
Responders* p < 0.5696 p < 0.0000 p < 0.0000
Mean 9.02 1.96 7.06
Standard
0.76 0.46
Deviation
Median 9.0 2.0 7.3
Non-
p < 0.0386 p < 0.0000 p < 0.0000
responders*
Mean 8.44 8.53 0.0
Standard
0.44 0.46
Deviation
Median 8.5 8.5 0.0

* Wilcoxon Rank-Sum test

Table 7. Comparison between the limited responders and the significantly more complete responders.

Comparison of Group 2 & Limited Responders Sensitivity Post-Block Maximum Responders Sensitivity Post-Block
Group 3 (1 - 10) (1 - 10)
Mean 4.14 1.48
Standard Dev. 2.02 1.11
95% C. I. 3.67 - 4.61 1.19 - 1.78
Minimum 0 0
Maximum 8 3.0
Wilcoxon Rank-Sum p < 0.00000

C. I. = Confidence Interval

gion, potentially creating a hypoxic event given that the ber that the sources of the sympathetic nerve fibers present
dental pulp is encased in a non-compliant, hard outer shell in the dental pulp are third-order, efferent, unmyelinated
and has no room for volumetric expansion; a classic com- postganglionic sympathetic nerve fibers originating in the
partment syndrome.3,30 superior cervical ganglion of the neck.
Reducing sympathetic nervous input via a local anes- For a description of the sympathetic nervous system as it
thetic block of the pathway whereby 3rd-order neurons that relates to the sympathetic anatomical pathways to the lat-
accompany the GAN may temporarily reverse the vasocon- eral face & ultimately the dentition.33 See Figure 8.
striction/inflammatory response leading to edema cascade,
resulting in almost instantaneously better perfusion of CONCLUSION
blood and reduction of the hypoxia within distal vessels
of the pulpal arteriole system. This volumetric increase in The significant temporary reduction in posterior tooth hy-
blood flow and loss of hypoxia may be directly responsible persensitivity to ice-cold water swishes within 129 of 194
for the instantaneous loss of cold hypersensitivity in indi- subjects after local anesthetic injection of the Great Auricu-
viduals with the SDH endotype. One must always remem-

Advanced Dental Technologies & Techniques 7

 Sympathetic Dental Hypersensitivity

Figure 4. A description of the sympathetic nervous

system with respect to the face and dentition.

• CDH = Cervical Dentin Hypersensitivity

Figure 3. (A) The 30 gauge, ½ inch, ultrashort needle • SDH = Sympathetic Dental Hypersensitivity
used by the authors for the GAN block. Ultrashort • SCG = Superior Cervical Ganglion
decreases the chance of hitting the deeper phrenic • VAS = Verbal Analog Scale
nerve. (B) Marcaine (bupivacaine) 0.5 % with 1:200K • SCM = Sternocleidomastoid Muscle
EPI anesthetic is typically used. Half of a carpule is • SCP = Superficial Cervical Plexus
usually more than sufficient per side. The block using
approximately 1.0 cc or less per side of this anesthetic
will typically last between 6-8 hours.
FUNDING

lar Nerve branch of the Superficial Cervical Plexus supports No funding was provided from any source for this activity.
a possible sympathetic neural system etiology enhancing
sensitivity to cold. While 2/3 of the subjects (129) exhib- SPECIAL THANKS
ited a sympathetic nerve contribution to their cold sensi-
tivity, for nearly 1 in 5 it was their only factor leading to To Mrs. Kennedy McDowell for searching the first author’s
cold hypersensitivity. The third of this subject group not database and compiling the excel data from that patient
responding likely suffered from a different mechanism, or pool in this retrospective study.
more likely, from involvement of the trigeminal nerve in-
stead. The null hypothesis was rejected. It was concluded DISCLOSURE STATEMENT
that, two out of three times, there may be a sympathetic
etiologic component in the clinical manifestation of DCH John Radke who provided the statistical analyses is the
and that Sympathetic Dental Hypersensitivity (SDH) can be Chairman of the Board of Directors of BioResearch Associ-
a term applied in such instances. ates, Inc. The remaining authors declared no conflict of in-
terest.
PUBLICATION ABBREVIATIONS
Submitted: May 05, 2025 CDT. Accepted: July 25, 2025 CDT.
• DCH = Dental Cold Hypersensitivity Published: July 31, 2025 CDT.
• SMP = Sympathetically Maintained Pain
• DCA = Dental Cold Allodynia
• DH = Dentin Hypersensitivity

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Advanced Dental Technologies & Techniques 8

 Sympathetic Dental Hypersensitivity

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