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JOURNAL OF ENDODONTICS
Copynght 9 1986 by The Amencan Assc~atPonof Endodonhsts
The Hydrodynamic Theory of Dentinal Pain: Sensation
in Preparations, Caries, and the Dentinal Crack
Syndrome
Martin Brannstrom, DDS, Dr. Odont.
The peculiar nature of dentin sensitivity is a source
of puzzlement to the dentist. Dentin is a good insu-
lator, but even small temperature changes that do
not reach the pulp may cause pain. A series of
studies are described that provide evidence that the
main cause of dentinal pain is a rapid outward flow
of fluid in the dentinal tubules that is initiated by
strong capillary forces.
The peculiar nature of dentin sensitivity is a source of
puzzlement to the dentist. How can the neck of a tooth
sometimes be so sensitive to the slightest touch? Why
may an air blast directed toward exposed dentin cause
so much pain while careful grinding of the same surface
using a water coolant may elicit only a slight response?
How can we explain tooth sensitivity associated with
temperature variations? Dentin is a good insulator, but
even small temperature changes that do not reach the
pulp may cause pain. This is particularly true in the
case of cold. How is it that dry absorbent paper (1) and
sugar can cause pain while many chemical agents that
are known to stimulate pain fibers do not produce a
response when applied to exposed dentin? I will try to
answer these questions by briefly reviewing a series of
experiments that we initiated in the late 1950's. These
studies provided evidence that the main cause of den-
tinal pain is a rapid outward flow of fluid in the dentinal
tubules that is initiated by strong capillary forces.
THE EFFECT OF REMOVING FLUID FROM THE
DENTIN AND ACTIVATION OF CAPILLARY
FORCES
In Vivo Experiments Utilizing Histological
Techniques
The first series of experiments I will discuss utilized
the following histological method. Cavities were cut into
intact human premolars that were scheduled for extrac-
tion for orthodontic purposes. The exposed dentin in
453
Printed m U S A.
VOL 12, NO. 10, OCTOBER1986
the cavities was then subjected to negative pressure
or desiccation. The teeth were subsequently extracted
and prepared for light and electron microscopic exam-
ination.
In my first experiment on pairs of human premolars,
reduced pressure using a vacuum pump was applied
for 20 s and 2 min to cavities randomly selected for
testing in one-half of the teeth. No suction was applied
to cavities in contralateral control teeth. Pain was elic-
ited instantly in the experimental teeth and continued
until the suction was removed. Histological evaluation
of these teeth revealed that odontoblast nuclei had
been displaced from the odontoblast layer into the
dentinal tubules beneath the area of dentin where the
suction had been applied. More than 100 nuclei could
be visualized in each histological section from the af-
fected area (Fig. 1). No aspirated nuclei were seen in
the control teeth. The extent of displacement of nuclei
varied from tubule to tubule. Some nuclei had moved
into the tubules only a few micrometers whereas others
had been displaced as much as 150 #m. Presumably,
the reduced pressure in the cavity caused excessive
evaporation of fluid from the dentinal tubules. The same
negative pressure that was used in these experiments
causes water to boil (2).
Similar results were obtained when an air blast or dry
heat was applied to test cavities (3, 4). A blast of air
may cause evaporation and severe pain in this situation.
This will occur regardless of whether the orifices of the
dentinal tubules are wide open or covered by a thin
smear layer, i.e. grinding debris produced by the bur
during cavity preparation. An air blast is capable of
causing rapid movement of fluid in the dentinal tubules
and this results in odontoblast displacement. A blast of
air lasting 10 to 20 s is capable of causing odontoblast
nuclei to move a distance of 20 to 50 #m outward in
the tubules.
In recent studies with transmission electron micros-
copy, we found that prolonged desiccation caused
nerve fibers as well as odontoblast nuclei to be drawn
up into the tubules (5). These nerve fibers were frag-
454 Brannstrom
. , . ,
., ,.
,.- , 9 .
,~k'l-,t,t, l l I J l , ~ r ~ r , , ~,.. r"
J tip ' I ,x
FtG 1. Pulpal area correspondmg to cawty in whtch reduced pressure
was applied. Odontoblasts aspirated into dentinal tubules. The same
s~tuation was seen under cavities air-jet dried for 30 s or when dry
heat was apphed to the cavtty.
mented and remnants were found more than 200 #m
out in the tubules. After desiccation for more than 1
min, the dentin lost its sensitivity, presumably because
fluid stopped flowing in the tubules. This was because
fluid was removed from the tubules faster than it could
be replaced, so the outer part of the tubules was filled
with air (5, 6). Thus, fluid communication between the
pulp and the outer surface of the dentin was lost, so
the dentin failed to respond to stimulation. When water
was applied to the surface of the desiccated dentin,
sensitivity was restored (5, 7). These observations fur-
ther supported the hydrodynamic theory of dentin sen-
sitivity.
Since the movement of odontoblast nuclei into tu-
bules provides a means of assessing fluid movement
in the dentinal tubules, it was possible to use this
experimental model system to determine the effects of
pain-producing stimuli on fluid movement. We found
that at least three stimuli known to evoke pain also
produced a rapid outward movement of fluid in the
tubules. However, pain is not always associated with
displacement of odontoblast nuclei. Thus, careful drill-
ing in dentin using a water spray produced a slight
amount of pain but no displacement of odontoblast
nuclei. We also found that application of dry absorbent
paper to the dentin produced immediate pain without
causing displacement of odontoblasts (1). The same
was true for a hypertonic sucrose solution.
In Vitro Studies Involving Capillary Forces
Dentinal tubules provide an ideal model system for
the study of capillary forces. My colleagues and I con-
ducted several experiments with a variety of tissue
fluids in which we measured viscosity, surface tension,
density, angle of contact, etc. By using the Hagen-
Poiseuille Law, we calculated that the rate of flow in
the dentinal tubule could be as high as 2 mm per s
Joumal of Endodontics
,f
-~ A=Cov i,5mm
B=Cov 2,0 mm
r ,
0 60 sec
f j .
Sugar sot o.
1 minute
-, it i* ' 0 ,,
"-~ mm
k I .- r
Pu[po[
movement
FIG 2. Experimental arrangement for measuring the outward move-
ment of flutd in the dentin following application of sugar to a cavity.
The glass capillary connected to the pulp cavity contains saline and
has an inner diameter of 0.2 mm. Apphcation of dehydrating agents
move the meniscus in the capillary toward the pulp. The application
of an air blast for 1 rain resulted un a movement of 3.5 ram.
(8). Presumably, this rapid outward flow of fluid elicited
pain by deforming the plasma membrane of mechano-
receptors located at the pulpal ends of the tubules.
About this time we developed an alternative method
for demonstrating the outward flow of fluid that oc-
curred in response to pain-producing stimuli (Fig. 2).
With a glass capillary filled with saline and connected
to the pulp of freshly extracted teeth, we were able to
demonstrate that common pain-producing stimuli re-
move fluid from the dentinal tubules, thus activating
capillary forces. It should be pointed out that unlike
teeth with vital pulps, there was no pressure gradient
between the pulp and the exterior of the tooth in this
in vitro model system that would cause fluid to flow
outward through the dentin. This technique offered a
simple method for measuring the extent of fluid move-
ment in the tubules due to various pain-producing stim-
uli activating capillary forces.
There has been some confusion conceming pain
associated with hyperosmotic stimulation with agents
such as hypertonic solutions of sucrose and calcium
chloride. The effect of such agents seen in Fig. 2 seems
to be due to thermodynamic forces and the removal of
fluid from the dentin. Hyperosmotic stimulation pro-
duces the same effect as an air blast, although it is not
as extensive (9). In similar experiments we found that
filling materials, such as Cavit, which are known to
cause pain on application, had the same dehydrating
effect, thus activating capillary forces (10).
The Effect of Mechanical Stimulation on Dentin
It remained to be demonstrated that probing and
drilling also produce an outward displacement of fluid
in the tubules. When we used the electron microscope
Vol. 12, No. 10, October 1986
to examine dentin that had been probed or drilled, we
found that thousands of tubules were involved and
many small cracks had formed. It is possible that by
exerting pressure on the dentin a small amount of fluid
can be removed from the tubules. In addition, drilling
produces frictional heat which increases evaporation of
fluid from the dentin.
We used the histological technique described above
rather than the glass capillary method to demonstrate
the outward flow of fluid produced by probing of dentin.
The enamel was carefully removed and thereafter the
dentin was scraped with a chisel rather than a probe in
order to increase the area of dentin that would be
affected and thus increase the amount of pulp tissue
that might be altered. Slow and careful chiseling under
dry conditions caused aspiration of numerous cells into
the tubules. Chiseling under moist conditions caused
less injury to the odontoblast layer, but a few odonto-
blast nuclei were aspirated into the tubules in the
predentin. In this in vivo study we also found that when
the exposed dentin was kept dry evaporation occurred,
and after a few seconds the patient experienced pain
that lasted for at least 4 min. The pain stopped as soon
as water was applied to the surface of the dentin.
Histological examination of the pulp revealed extensive
displacement of odontoblasts.
Displaced Odontoblast Nuclei not Associated
with Pain
The intrapulpal pressure of teeth with vital pulps
varies from 15 to 30 mm Hg. In experiments in vitro we
found that this outward pressure gradient could empty
an open tubule about 10 times per day (12). Slow
outward flow of fluid does not produce pain but may
result in the movement of odontoblasts into the dentinal
tubules beneath a leaky filling or exposed dentin left
unprotected. Occasionally, when the pulp has been
injured, odontoblast displacement may occur even
though the dentin is still covered by intact enamel (4),
as fluid flows slowly outward through minute pores in
the enamel. The following experiment illustrates the
effect of intrapulpal pressure on fluid movement in
exposed dentin. Freshly extracted teeth with exposed
cuspal dentin were placed into Eagle's solution for
either 12 h or 1 wk. A glass capillary tube was con-
nected to the roots of all teeth, and a pressure of 30
mm Hg was applied to the pulp of each tooth in the
experimental group. Contralateral teeth served as con-
trois, and no pressure was applied to their pulps. Nuclei
in the dentinal tubules beneath the exposed dentin were
found only in the teeth in which hydrostatic pressure
was applied to the pulp (unpublished observations).
The Effect of Temperature Variations and Pressure
By using the glass capillary technique, it was easy to
demonstrate that application of cold to the tooth pro-
Hydrodynamic Theory of Dentinal Pain 455
duced a rapid outward flow of fluid in the dentinal
tubules (13). As the tooth is cooled the dentinal fluid
contracts, but it is held in position at the outer aperature
of the tubule by capillary forces. This results in a rapid
outward movement of fluid in the pulpal ends of the
tubules. In other words, the reduction of volume of fluid
due to cold has the same effect as removal of fluid by
evaporation, probing the dentin, or a short blast of air.
Calculations revealed that a temperature reduction of
20 to 30~ (as might be produced by ice cream) results
in an outward movement of fluid of 3 to 4 pm (14, 15).
While this small but rapid outward movement of fluid
does not cause displacement of odontoblasts into the
tubules, it is sufficient to activate the sensory nerve
fibers in the underlying pulp dentin border zone. It
should be remembered that probing and application of
hypertonic sucrose may produce an outward flow of
fluid of the same order of magnitude. It is important to
point out that application of cold or heat to the tooth
affects hundreds of thousands of dentinal tubules, so
the impact on the pulp can be quite extensive (13).
Heat causes an inward movement of fluid in the
tubules due to expansion of the fluid, especially if the
tubules are covered by enamel. Less frequently the
tooth with an intact pulp is sensitive to heat that is
applied under normal conditions. The stimulus that
produces this sensitivity is evidently a very pronounced
inward movement of fluid, or else the pulp may be
inflamed and therefore unusually sensitive. It seems
that heat applied to an intact tooth may activate mainly
C-fibers (16). On the other hand, dry heat applied to
exposed dentin will result in an extensive outward flow
of fluid and activate A-fibers.
In two series of experiments, we tried to simulate the
inward flow of fluid that is produced by heat (17, 18).
We did this by applying pressure to the exposed dentin.
When fluid pressure was applied to the cavity, a de-
layed, dull pain was reported at certain levels of pres-
sure ranging from 0.5 to 3 kg per cm 2, depending on
the distance between the cavity and the pulp. After the
tooth was extracted the experiment was repeated with
a fluid-filled glass capillary tube connected to the root
pulp. An extensive inward movement of fluid was pro-
duced by the same level of pressure that had produced
pain in vivo. If exposed dentin is not deformed by the
application of pressure, pressure alone does not seem
to produce pain. The same should be true for filling
materials.
DISPLACEMENT OF NERVES AND
ODONTOBLASTS INTO DENTINAL TUBULES
In 1962 Declan Anderson and I independently failed
to produce pain when we applied potassium chloride
(KCI), an algogenic agent, to exposed dentin in cavities.
Pain was evoked only when KCI was applied to the
exposed pulp (19, 20). We repeated this experiment by
456 Brannstrom
applying KCI to deep cuspal fractures and obtained the
same result (unpublished data). This rules out the pos-
sibility that there are nerves in the main bulk of dentin.
In electron microscopic studies, nerves have been ob-
served in some dentinal tubules, but they do not extend
more than 100 #m into the tubules (21).
We have examined parallel fractured dentinal tubules
using the scanning electron microscope (22). After ex-
traction, premolar teeth were freeze-fixed and then
fractured and freeze-dried. This technique prevents
odontoblast processes from collapsing during histogical
processing. We were unable to find odontoblast proc-
esses extending more than about 0.7 mm into the
tubules. Similar results were obtained using transmis-
sion electron microscopy (23-25).
In many of our studies, including those utilizing elec-
tron microscopy, we have found that dentin can be
highly sensitive despite the absence of both odonto-
blasts and nerve fibers within the tubules (1, 5). Even
when there is an abscess or necrosis in the underlying
pulp, the dentin can be highly sensitive. Obviously the
outward flow of fluid in thousands of tubules must be
transmitted to nerve endings located in areas of the
pulp adjacent to the pathological lesions.
To conclude, in numerous in vivo and in vitro exper-
iments on human teeth we have found support for the
hydrodynamic theory. Semiquantitative measurements
of fluid movements in human dentin in connection with
pain-producing stimuli have demonstrated that it is not
a simple mechanism of fluid filtration through the dentin,
but rather the question of a rapid outward flow due to
the mobilization of capillary forces.
SENSATION ASSOCIATED WITH CAVITY
PREPARATION
It is important to realize that when dentin is sensitive,
the dentinal tubules must be open all the way to the
pulp. Thus, they are accessible not only to stimuli that
evoke pain but also to toxins and bacteria. Products of
both living and dead bacteria may diffuse to the pulp
and produce inflammation and hyperalgesia.
Sensitive dentin is often encountered in cavities,
especially in the cervical wall. The pulpal and axial walls
can be less sensitive or not sensitive at all. One reason
for this difference in sensitivity is that the pulpal wall of
proximal and buccal cavities may have considerably
fewer tubules per unit area available for stimulation
than the cervical wall (26). In the pulpal wall of the
cavity, the tubules may run oblique or even parallel to
the cavity wall. Another reason for insensitive dentin
walls is the presence of irregular dentin blocking the
pulpal end of the tubules. Irregular dentin is often
deposited beneath a carious lesion, and in this case
insensitive dentin does not mean that the pulp is dis-
eased. In such situations the pulpal wall may be the
one at least risk, and obviously this has clinical rele-
Joumal of Endodontics
vance with regard to the need for lining and sealing. If
we want to reduce the risk of secondary caries, hyper-
sensitivity, and pulpal injury, a thin lining is needed to
cover the cervical and lateral walls and sensitive areas
of the pulpal walls in order to seal the tubules and
protect the pulp from the ingress of toxic bacterial
products.
CARIES AND THE SENSATION OF PAIN
Occasionally under deep carious lesions no irregular
dentin forms, or it is present only in a limited area. In
such cases bacteria may already be present within a
necrotic area of the pulp. We should not be surprised
if such a tooth has sensitive dentin when the carious
dentin is excavated, since fluid in the underlying tubules
is in communication with the nerve fibers deeper in the
pulp. In early caries in which the dentin has been
invaded, as in root caries or secondary caries involving
the cervical wall, pain may occur in response to touch,
sugar, and temperature variations. This is because
irregular dentin has not yet been formed beneath the
carious lesion. Usually, the tubules are open and wid-
ened at the surface and there has been bacterial inva-
sion. In early caries cold may occasionally produce pain
before dentin has been exposed. This is apt to occur
when bacteria have penetrated deep beneath an en-
amel lesion, and, as a result, primary odontoblasts as
well as cells in the cell-rich zone of the pulp have been
injured so that no irregular dentin has formed. Instead
there may be a persistent inflammatory reaction. More-
over, we have observed that a fluid gap filled with
bacteria develops at the dentinoenamel junction be-
neath an early enamel lesion, sometimes preventing the
formation of irregular dentin. This gap may extend a
great distance laterally from the center of the lesion
(27, 28). If cold is applied to the corresponding enamel
surface, pain may be experienced because of the con-
traction of fluid in the gap, and this will result in a rapid
outward flow of fluid from the pulpal ends of the tubules.
The presence of pain indicates that there is pulpal
inflammation and hyperalgesia, and it can be assumed
that no irregular dentin has formed. Thus, the situation
may be similar to the cracked tooth syndrome or fluid-
filled contraction gaps beneath restorations.
THE DENTINAL CRACK SYNDROME
Finally, let us consider the dentinal crack syndrome
commonly seen in posterior teeth that have been ex-
tensively restored. A crack may develop because of
expansion of amalgam which results from continuous
corrosion, trauma, or pressure associated with bruxism
and stress. Patients suffering from this syndrome seek
help because of poorly localized tooth sensitivity (par-
ticularly to cold) in one quadrant. Sometimes biting
pressure evokes pain. By applying ice to each tooth in
Vol. 12, No. 10, October 1986
the affected quadrant, it is possible to locate the tooth
with the cracked cusp that is responsible for the sen-
sitivity. Application of ice to the surface of the tooth
usually triggers immediate, intense pain. Pressure be-
tween the cusps may also cause fluid movement and
pain, especially when the pressure is released. In a
histological examination of such cracks, I have found
them filled not only with fluid but also with bacteria that
have entered the gap at the amalgam filling. Contraction
of the fluid in the peripheral tubules due to the appli-
cation of ice results in rapid outward movement of fluid
in the crack and in the adjacent tubules. Bacterial
products diffusing to the pulp elicit an inflammatory
response which in turn results in hyperalgesia. When,
during chewing, the fractured cusp is broken off, the
sensitivity is often greatly reduced.
Presented at the F~rst World Conference on Dental and Pulpal Pain, New
York, NY, October 25-27, 1985.
Dr. Brannstrom is affiliated with the Department of Oral Pathology, Karolm-
ska Institute, Huddmge, Sweden
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Hydrodynamic Theory of Dentinal Pain 457
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