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JOURNAL OF ENDODONTICS Printed in U.S.A.
Copyright 9 1990 by The American AssOCiation of Endodontists VOL 16. NO. 2. FEBRUARY1990

SCIENTIFIC ARTICLES

Neurovascular Interactions in the Dental Pulp in

Health and Inflammation

Syngcuk Kim, DDS, PhD

The two key components in pulpal inflammation are and there is a lack of information on the neurovascular
microcirculation and sensory nerve activity. With relationship in the inflamed pulp. In this article the interre-
advancement of techniques they can be measured lationship between microcirculation and sensory nerve activ-
simultaneously in the same tooth. Excitation of A- ities in health and disease will be examined using current
basic research information.
delta fibers seems to have an insignificant effect on
The inflammatory processes in the pulp does not differ
puIpal blood flow (PBF), whereas C fiber activation
significantly from that in other tissues in most respects, with
causes an increase in PBF. This C fiber-induced PBF a notable exception, however, which is the physical environ-
increase is caused by neurokinins, especially sub- ment of the pulp. the low compliance environment, created by
stance P, which is released from the C fiber nerve dentin and enamel. Figure l represents a schematic illustra-
terminals. Manipulation of PBF has varying effects tion of events involving inflammation in general, in which
on sensory nerve activity. An increase in PBF causes noxious stimuli have profound effects on the tissue cells.
excitation of both A-delta and C fibers via an in- Mechanical stimuli, such as drilling or cutting tooth structure
crease in tissue pressure, whereas flow reduction generate noxious vibration or frictional heat; chemical com-
has an inhibitory effect on A-delta fibers, but no ponents of various dental materials and cavity washing agents
discernible effect on C fiber activity. Understanding and bacterial byproducts as a result of caries are considered
chemical and bacterial stimuli, respectively. When reaching
of this complex neurovascular relationship in the
the noxious range, the stimuli degranulate mast cells, disrupt
pulp, especially given the fact that the pulp is in a
important nutrient flow, damage cells, and in the process
low compliance system, is prerequisite to more com- lower the excitability threshold of sensory nerves. The attend-
prehensive characterization of pulpal inflammation. ant release of various inflammatory mediators, e.g. histamine,
5-hydroxytryptamine, kinins, prostaglandins, substance P,
and other neurokinins causes pain directly by lowering the
sensory, nerve excitability threshold. These substances also
Pulpal inflammation is a subject of interest not only to cause pain indirectly by vasodilating arterioles and by pro-
endodontists, but to all dental disciplines. We understand moting vascular leakage in venules, resulting in edema and
pulpal inflammation clinically as a toothache and histologi - subsequent elevation in tissue pressure, which is of critical
cally as an accumulation of polymorpholeukocytes around importance in pulpal inflammation. Finally, the mediators
the site of insult in a pulp section. In addition to this evidence, cause chemotaxis via leukocytes. Pulpal inflammation, if
however, are many complicated dynamic mechanisms, some unattended, eventually leads to pulpal necrosis, which in turn
of which are known and more which are as yet unknown. It causes periapical pathosis. An example of such a case is shown
is, however, generally well-accepted knowledge that the two in Fig. 2. a radiograph of fully crowned mandibular anterior
key components in pulpal inflammation are microcirculation teeth of a healthy female patient. There was no pulpal or
and sensory nerve activity. Sensory nerve activity and micro- periapical pathosis prior to the prosthodontic procedures, but
circulation in the pulp have been studied as separate entities as shown in the radiograph, periapical radiolucencies are
by many investigators (1-7) and special emphasis has been present on all of the treated anterior teeth. Since these teeth
given to the characterization of pulpal nerve activity, since had no history, of decay or trauma prior to the restoration,
pain is the more acute clinical problem in an inflamed tooth. the probable cause of the periapical pathosis was the restora-
With advancements in circulatory techniques and methods, tive procedure. The questions are "Why does tooth prepara-
microcirculatory contributions to pulpal inflammation have tion result in periapical pathosisT' and "What are the mech-
also been studied (8, 9). There is, however, a relative paucity anisms of this process?" This fundamental problem in clinical
of information generated from simultaneous measurements dentistry can be partially explained by the dynamic relation-
of microcirculatory and neural parameters in the same tooth, ship between blood vessels and sensory nerves in the pulp.
48
Vol. 16, No. 2, February 1990 Neurovascular Reactions in Pulp 49
Injurious Agents Before discussing this interrelationship, let us first look at
(McclumJeal / Chemac.tl / Bactenad) circulation and sensory nerve fimction independently of each
other.

~lll $t C~ll Dis;~ptJon Stimulation

l~grl~uhttlon Blood Vef~,,cls ~nsor 7 Nerves PULPAL MICROCIRCULATION

L__ i I J
Studies of pulpal microcirculation have greatly advanced
___ Histamine _~
in the last 15 yr due to the development of sophisticated
/ .... ~ ~ Kinlns etc. -- ~ - ~ techniques employing radioisotope tracers (1, 4, 6, 10), radi-
oisotope-labeled microspheres (7, 9), plethysmography (11),
and laser Doppler flowmetry (12). Many of these techniques
/-- ,/ , [ Nerves I ~ ~ , are noninvasive of the pulp (7, 9-12) and have facilitated a
quantitative and qualitative analysis of pulpal blood flow
! \ \ ,~rterlol.
~. Pain J/~ / --/ ;
(PBF) under various experimental conditions in animal and
--_ v.oo.a.o ..... human teeth. Basically three types of PBF responses to stimuli
have been established. In Type I PBF decreases markedly
t..eui,. .... -- .... Leakage .... ~-- .-.,
with the intraarterial (i.a.) administration of norepinephrine
......... ~_. Chemotaxis . - - -" (13) or 5-hydroxytryptamine (9), with electrical stimulation
of the cervical sympathetic nerve and reflex excitation of the
FIG 1. Schematic illustration of events involving inflammation in gen- sympathetic nervous system by hemorrhage and extreme
eral.
hematocrit variations (13, 14). This type of flow response is
due to activation of a-receptors located in pulpal resistance
vessels and the activation of sympathetic adrenergic vasocon-
strictor fibers (8, 13). In the Type II response, PBF decreases
gradually, as after the i.a. infusion of histamine. This gradual
flow reduction is most probably due to an increase in capillary
permeability and resultant increased tissue pressure in the low
compliance system of the dental pulp. Finally, the Type Ill
PBF respon.~ is biphasic; an initial increase is followed by a
rapid decrease. This unusual response is caused by the known
vasodilators substance P (SP), isoproterenol, prostaglandin E2,
and bradykinin (8, 15). The initial vasodilation in response
to isoproterenol indicates the presence of ~-adrenergic recep-
tors in the resistance vessels (13, 15). This biphasic flow
response to the vasodilators is a result of the low compliance
environment of the pulp, in which passive compression of
venules may result from active dilation of arterioles with an
attendant rise in pulpal tissue pressure, i.e. an inflammatory
process (13, 16). It seems clear, that the low compliance
environment of the tooth plays an important role in the
unusual reduction of PBF during inflammation, since media-
tors released in the pulp during inflammation, e.g. SP, pros-
taglandin E2, and bradykinin, etc., are powerful vasodilators.

P U L P A L SENSORY NERVE ACTIVITY

The physiological characterization of the pulpal sensory

fibers was made using two techniques: multiunit intradental
recording, in which electrodes measure nerve activity from
dentinal cavities in canine teeth (4, 17) and single fiber unit
recording, in which nerve activity is measured from the
dissected inferior alveolar nerve in dogs and cats (3, 18). In
these studies two types of nerve fibers were found in the pulp:
fast-conducting, low-threshold, myelinated A-delta fibers
(mean conduction velocity 13.4 m per s and 8.4 to 13.4 mA
mean threshold with 20-ms pulse) and slow-conducting, high-
threshold, unmyelinated C fibers (mean conduction velocity
FiG 2. A radiograph of mandibular anterior teeth of a patient with full- 1.0 m per s and 37.4 to 40.4/zA mean threshold with 10-ms
mouth reconstruction. Extensive periapieal radiolucencies occurred pulse) (19). Fast-conducting A-beta fibers have also been
following preparation of the teeth. identified, but their role in the pulp is still unclear. In addition
50 Kim Journal of Endodontics

to conduction and threshold differences, there are other func-

tional differences between the A and C fibers. C fibers are BloodFlowMeasurement
activated by noxious heat or application of bradykinin and 3~ 1. 133Xenon washout method
histamine (20, 21). A-della fiber activity, on the other hand,
2. Radioisotope labeled microsphere method
is evoked by stimulation of the exposed superficial dentin by
3. Laser Doppler flowmetry
mild thermal, mechanical, and osmotic means (saturated
CaCI2); this is most plausibly explained by the hydrodynamic
theory (22). However, some hyperosmotic agents (e.g. 3 M 2L~ SensoryNerveRecording
NaCI) did not elicit intradental neural activity when applied 4. Intradental
in shallow cavities, but did cause excitation of A-delta fibers --.- ~ 5. Single fiber unit
when applied in deep dentinal cavities; the most probable
mechanism being direct ionic diffusion (23, 24). Thus, con- FiG 3. Schematic representation of a simultaneous recording of blood
trary to current thinking, recent experimental evidence sup- flow and sensory nerve activity in the pulp. The simultaneous record-
ports two mechanisms for pulpal pain, the hydrodynamic and ing of blood flow and sensory nerve activities can be made using any
direct ionic diffusion theories. In addition to the differences combination of methods shown in the diagram. The most widely used
between A and C libers, there are significant differences in combination is laser Doppler flowmetry for PBF and intradental re-
the character of tooth pain associated with A or C fibers. For cording technique for sensory nerve activity measurement.
instance, in response to heat stimulation, immediate, sharp
pain can be attributed to A-delta fibers, while a delayed, dull
pain is indicative of C fiber activity. The theory, that the Saline I 3M NaCI 5 secs
initial phase of pulpal inflammation, often accompanied by
sharp pain, involves A-delta fibers and that the latter phase,
more often characterized by dull pain, involves C fibers, has
been advanced (21, 25).

S I M U L T A N E O U S RECORDING OF P U L P A L
B L O O D FI,OW AND S E N S O R Y NERVE
ACI'IVITIES

When studying inflammation in the pulp, the simultaneous It

recording of blood flow and sensory nerve activity from the
same tooth has provided most useful insights into the mech-
anisms. A schematic representation of the way in which the
two parameters can be recorded simultaneously is presented
in Fig. 3. The first attempt at this was made in 1970 by a
group in Sweden (1). They used the radioactive iodine desat-
uration technique for measuring pulpal blood flow and the FIG 4. A polygraph tracing of simultaneous recordings of PBF and
intradental recording technique for measuring the sensory INA in response to application of 3 M NaCI into a dentinal cavity in a
nerve activities in feline teeth. More recently, a modified cat canine tooth. The top racing represents PBF measured with laser
Doppler flowmetry and the bottom tracing represents INA recorded
intradental recording technique and laser Doppler flowmetry
with the intradental recording technique.
have facilitated the in-depth examination of the neurovascular
interactions (26). Shown in Fig. 4 are simultaneous recordings
of PBF and intradental sensory nerve activity (INA) in re- tissue pressure rises to about 16 mm Hg (28). This tissue
sponse to osmotic stimulation with 3 M NaCI applied to a pressure increase would be insignificant in other tissues, but
deep dentin cavity. NaCI applied in dentinal cavities caused in the low compliance environment of the pulp, even a small
increases in both PBF and 1NA, with PBF increases preceding rise can a have significant impact on local circulation as well
the INA increases. This sequence suggests that PBF changes as sensory nerve activities. Nfirhi (18), recording from the
have an effect on INA. single nerve fiber, has found that an increase in the tissue
pressure increases sensory nerve activity.
ROLE OF PULPAI. TISSUE P R E S S U R E IN
PULPAL INFLAMMATION EFFECTS OF C I I A N G E S IN PUI,PAL B L O O D
F L O W ON P U L P A L SENSORY NERVE
Pulpal tissue pressure measurements, like PBF and sensory ACrlVITIES
nerve recordings, have benefited from technological advance-
ments in research equipment and increased sophistication in A number of separate studies on microcirculation and
research methods and can now be measured very precisely. sensory nerve activity in the dental pulp have shown that an
Using a micropipettc with a 2- to 4-~,m tip diameter, con- interrelationship exists and several investigators state that
trolled by a servo-nulling counter-pressure system, precise local microcirculatory changes may have profound effects on
pulpal tissue and intravascular pressures were recorded (27). sensory nerve functions in the pulp (1, 4, 30, 31). A severe
The normal resting tissue pressure has been recorded at 6 to reduction in PBF in feline teeth, caused by the apical injection
10 mm Hg, but when the pulp is locally inflamed, the local of adrenaline or electrical stimulation of the sympathetic
Vol. 16, No. 2, February 1990 Neurovescular Reactions in Pulp 51

nerve, resulted in concomitant decreases in INA (1, 32); the changes depend on the degree of neural stimulation. For
excitability of intradental sensory, units seems thus modulated instance, weak orthodromic stimulation of the tooth surface,
by sympathetic vasoconstrictor fibers. This linear relationship which excites only A-delta fibers, causes no changes in PBF,
between the reduction of pulpal blood flow and ofintradental suggesting that excitation of the A-delta fibers has no signifi-
nerve activity has not been duplicated in our laboratory. cant effect on PBF (Fig. 6). However, strong orthodromic
Careful examinations reveal that pulpal blood flow must be stimulation of the tooth surface causes erratic changes in PBF,
reduced significantly (approximately 90%) for a substantial most likely by C fiber excitation (Fig. 6). Antidromic stimu-
duration of more than 10 min, in order to have an effect on lation of the inferior alveolar nerve in cats, pretreated with an
intradental nerve activities. It has been hypothesized that the a-adrenergic blocker, caused an increase in PBF and biphasic
fast-conducting A fibers lose their function rapidly as a result neural activity; an increase followed by a prolonged depres-
of ischemia, to which the slow-conducting C fibers are less sion (31). This neurogenic vasodilation is mediated by the
sensitive (28). [his suggests that C fibers may maintain their neurokinin SP, which is released from unmyelinated C fiber
functional capacity longer than A-delta fibers during inflam- endings when antidromic stimulation is applied (35, 36).
mation, in which PBF and therefore O2 content are reduced Recent evidence suggests that this neurogenic vasodilation is
as a result of the low compliance system of the pulp (30, 33). mediated not only by SP, but also by neurokinin A, B, and
A systematic study of the possible modulating effect of ische- especially by calcitonin gene-related peptides. The biphasic
mia on nerve fiber activity should provide important insights neural response following the antidromic stimulation may be
into dentinal pain mechanisms, especially during inflamma- related to the biphasic PBF response after i.a. infusion of SP
tion. Changes in pulpal blood flow may not have a direct (16), since SP effects are both vascular and neural. Another
effect on pulpal C fiber activities; however, increases in pulpal explanation for the biphasic neural response is that SP triggers
tissue pressure by flow elevation cause excitation of the sen- the release of histamine, which causes an elevation of pulpal
sory nerves. Increased tissue pressure is a function of an tissue pressure via an increase in vascular permeability (31).
increase in blood flow accompanied by an increase in vascular Thus, an increase in PBF by vasoactive substances, released
permeability. Thus, we could conclude that changes in blood either from the sensory nerve endings or from other cellular
flow have a direct effect on pulpal A fiber activities but components, may have profound effects on both circulatory
minimum effect on C fibers. However, tissue pressure eleva- and neural behavior.
tion excites all sensory nerves (Fig. 5).
'9
EFFECI" OF C H A N G E S IN PULPAL S E N S O R Y
NERVE ACI'IVITIES ON P U L P A L B L O O D F L O W
Evidence that excitation of pulpal sensory fibers has a
profound effect on pulpal microcirculation has been provided
by a number of researchers (26, 34). However, the flow
PBF
AS|

l | (low flow)

NEUROPEPTIDES
SP, CGRP etc. )

C PBF

C| = tPBF TISSUE PRESSURE

FiG 6. Relationship of pulpal blood flow and A-delta (A-d) and C fiber
FIG 5. Relationship of pulpal tissue pressure and A-delta and C fiber nerve activities. Excitation of A-~, has little effect on PBF. while a
nerve activities. + represents excitation or an increase in nerve decrease in flow has an inhibitory effect on A-~ fiber excitability.
activity. An increase in pulpal tissue pressure as a consequence of Excitation of C fibers increases PBF via neuropeptides, namely, SP
an increase in PBF has an excitatory effect on both A-delta (A-d) and and calcitonin gene-related peptide (CGRP). An increase in PBF per
C fibers. An excitation of C fibers in turn causes pulpal flow increase se has little effect on C fiber activity, but an increase in tissue pressure
via neurokinins released from the C fiber nerve endings. excites the nerve.
 52 Kim Journal of Endodontics

The important question "What are the roles of these pep- Tooth Preparation
(noxious stimulation)
tides in pulpal inflammation and under what circumstances
are these peptides released?" remains. It is known that a simple
tooth preparation can cause the release of a significant amount
Release of M e d l a t c r s Release of N e u r o p e p t i d e s
of SP-like or bradykinin-like substances (37). Also, noxious (BK. 5.HT, Histamine, PG,) {SP. CGRP}
stimuli of mechanical, thermal, and chemical characters,
which excite C fibers, can trigger the release of neuropeptides.
These, in turn, have an effect on pulpal blood flow and
subsequently on pulpal tissue pressure. Shown in Fig. 7 are
the key mediators involved in pulpal inflammation. Inflam-
9 Hyperexcltatlon
I=, 9 V a s o d l l a t l o n
, 9 Vascular leakage
[ ....
14
J
matory mediators prostaglandins and bradykinin are released
from the tissue components, and various kinins and SP are I Pulpal Tissue P r e s s u r e
I
released in response to sensory nerve excitation. The neuro-
kinins have a direct effect on the vasculature causing vasodi- I Pulpal Blood Flow
lation and leakage, while the simultaneous release of 5-hy- (low c o m p l i a n c e system)
droxytryptamine and kinins from vascular components cause
mast cells to release histamine which in turn causes further
A c c u m u l a t i o n of Mediators
vascular leakage.
To return to the initial question about the periapical pa-
thosis shown in the radiograph in Fig. 2, a hypothetical Vessel Damage
mechanism of pulpal necrosis can be constructed (Fig. 8). As I
a result of noxious stimulation, i.e. the mechanical, thermal.
Pulpal I n f l a m m a t i o n
and chemical stimulation caused by tooth preparation, in-
flammatory mediators and neuropeptides are released. These
mediators alter normal neural and vascular functions, which Pulpal Death
results in an increase in tissue pressure. Tissue pressure ele-
vation in the low compliance environment of the pulp quickly F=~ 8. Hypothetical mechanism of pulpal necrosis as a consequence
leads to a decrease in pulpal blood flow instead of an increase of tooth preparation for a full crown placement. See text for expla-
as in other tissues. Increased blood flow facilitates the removal nation.
of the inflammatory mediators and thereby helps heal the
tissue, but in the pulp the decreased flow results in an accu- primarily neurogenic in nature, our understanding of the
mulation of mediators, which in turn causes varying degrees neurovascular interrelationship in the pulp in health and
of vessel damage. This vicious cycle, once begun, leads to disease is of paramount importance.
successive areas of inflammation and eventual pulp necrosis.
The discovery of the neuropeptide involvement in pulpal
This work was supported by NIH/NIDR Grants DEO-05605 and DEO-O121.
inflammation revolutionized our thinking. It is now clear that
neuropeptides play an important role in the progression of The author wo~Jld like to acknowledge his co-workers, Drs. M. Liu, K.
Markowdz, J Bilotto, and Ms. J. Dorscher-Kim, for their contributions to this
pulpal inflammation by linking the actions of the sensory article.
nerves and blood vessels. The term neurogenic inflammation
describes a pathological change in the neurovascular relation- Or Kim is chairman, Department of Endodontics, and director, Laboratory
of Oral Physiology, Columl~a University, School of Dental and Oral Surgery,
ship, resulting in inflammation. Since pulpal inflammation is New York, NY.

InSUltS
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