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JOURNAL OF ENDODONTICS
Copyright 9 1990 by The American AssOCiation of Endodontists
SCIENTIFIC ARTICLES
Neurovascular Interactions in the Dental Pulp in
Health and Inflammation
Syngcuk Kim, DDS, PhD
The two key components in pulpal inflammation are
microcirculation and sensory nerve activity. With
advancement of techniques they can be measured
simultaneously in the same tooth. Excitation of A-
delta fibers seems to have an insignificant effect on
puIpal blood flow (PBF), whereas C fiber activation
causes an increase in PBF. This C fiber-induced PBF
increase is caused by neurokinins, especially sub-
stance P, which is released from the C fiber nerve
terminals. Manipulation of PBF has varying effects
on sensory nerve activity. An increase in PBF causes
excitation of both A-delta and C fibers via an in-
crease in tissue pressure, whereas flow reduction
has an inhibitory effect on A-delta fibers, but no
discernible effect on C fiber activity. Understanding
of this complex neurovascular relationship in the
pulp, especially given the fact that the pulp is in a
low compliance system, is prerequisite to more com-
prehensive characterization of pulpal inflammation.
Pulpal inflammation is a subject of interest not only to
endodontists, but to all dental disciplines. We understand
pulpal inflammation clinically as a toothache and histologi -
cally as an accumulation of polymorpholeukocytes around
the site of insult in a pulp section. In addition to this evidence,
however, are many complicated dynamic mechanisms, some
of which are known and more which are as yet unknown. It
is, however, generally well-accepted knowledge that the two
key components in pulpal inflammation are microcirculation
and sensory nerve activity. Sensory nerve activity and micro-
circulation in the pulp have been studied as separate entities
by many investigators (1-7) and special emphasis has been
given to the characterization of pulpal nerve activity, since
pain is the more acute clinical problem in an inflamed tooth.
With advancements in circulatory techniques and methods,
microcirculatory contributions to pulpal inflammation have
also been studied (8, 9). There is, however, a relative paucity
of information generated from simultaneous measurements
of microcirculatory and neural parameters in the same tooth,
48
Printed in U.S.A.
VOL 16. NO. 2. FEBRUARY1990
and there is a lack of information on the neurovascular
relationship in the inflamed pulp. In this article the interre-
lationship between microcirculation and sensory nerve activ-
ities in health and disease will be examined using current
basic research information.
The inflammatory processes in the pulp does not differ
significantly from that in other tissues in most respects, with
a notable exception, however, which is the physical environ-
ment of the pulp. the low compliance environment, created by
dentin and enamel. Figure l represents a schematic illustra-
tion of events involving inflammation in general, in which
noxious stimuli have profound effects on the tissue cells.
Mechanical stimuli, such as drilling or cutting tooth structure
generate noxious vibration or frictional heat; chemical com-
ponents of various dental materials and cavity washing agents
and bacterial byproducts as a result of caries are considered
chemical and bacterial stimuli, respectively. When reaching
the noxious range, the stimuli degranulate mast cells, disrupt
important nutrient flow, damage cells, and in the process
lower the excitability threshold of sensory nerves. The attend-
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
cause pain indirectly by vasodilating arterioles and by pro-
moting vascular leakage in venules, resulting in edema and
subsequent elevation in tissue pressure, which is of critical
importance in pulpal inflammation. Finally, the mediators
cause chemotaxis via leukocytes. Pulpal inflammation, if
unattended, eventually leads to pulpal necrosis, which in turn
causes periapical pathosis. An example of such a case is shown
in Fig. 2. a radiograph of fully crowned mandibular anterior
teeth of a healthy female patient. There was no pulpal or
periapical pathosis prior to the prosthodontic procedures, but
as shown in the radiograph, periapical radiolucencies are
present on all of the treated anterior teeth. Since these teeth
had no history, of decay or trauma prior to the restoration,
the probable cause of the periapical pathosis was the restora-
tive procedure. The questions are "Why does tooth prepara-
tion result in periapical pathosisT' and "What are the mech-
anisms of this process?" This fundamental problem in clinical
dentistry can be partially explained by the dynamic relation-
ship between blood vessels and sensory nerves in the pulp.
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
intradental recording technique for measuring the sensory
nerve activities in feline teeth. More recently, a modified
intradental recording technique and laser Doppler flowmetry
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-
sponse to osmotic stimulation with 3 M NaCI applied to a
deep dentin cavity. NaCI applied in dentinal cavities caused
increases in both PBF and 1NA, with PBF increases preceding
the INA increases. This sequence suggests that PBF changes
have an effect on INA.
ROLE OF PULPAI. TISSUE P R E S S U R E IN
PULPAL INFLAMMATION
Pulpal tissue pressure measurements, like PBF and sensory
nerve recordings, have benefited from technological advance-
ments in research equipment and increased sophistication in
research methods and can now be measured very precisely.
Using a micropipettc with a 2- to 4-~,m tip diameter, con-
trolled by a servo-nulling counter-pressure system, precise
pulpal tissue and intravascular pressures were recorded (27).
The normal resting tissue pressure has been recorded at 6 to
10 mm Hg, but when the pulp is locally inflamed, the local
FIG 4. A polygraph tracing of simultaneous recordings of PBF and
INA in response to application of 3 M NaCI into a dentinal cavity in a
cat canine tooth. The top racing represents PBF measured with laser
Doppler flowmetry and the bottom tracing represents INA recorded
with the intradental recording technique.
tissue pressure rises to about 16 mm Hg (28). This tissue
pressure increase would be insignificant in other tissues, but
in the low compliance environment of the pulp, even a small
rise can a have significant impact on local circulation as well
as sensory nerve activities. Nfirhi (18), recording from the
single nerve fiber, has found that an increase in the tissue
pressure increases sensory nerve activity.
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
ACrlVITIES
A number of separate studies on microcirculation and
sensory nerve activity in the dental pulp have shown that an
interrelationship exists and several investigators state that
local microcirculatory changes may have profound effects on
sensory nerve functions in the pulp (1, 4, 30, 31). A severe
reduction in PBF in feline teeth, caused by the apical injection
of adrenaline or electrical stimulation of the sympathetic
Vol. 16, No. 2, February 1990
nerve, resulted in concomitant decreases in INA (1, 32); the
excitability of intradental sensory, units seems thus modulated
by sympathetic vasoconstrictor fibers. This linear relationship
between the reduction of pulpal blood flow and ofintradental
nerve activity has not been duplicated in our laboratory.
Careful examinations reveal that pulpal blood flow must be
reduced significantly (approximately 90%) for a substantial
duration of more than 10 min, in order to have an effect on
intradental nerve activities. It has been hypothesized that the
fast-conducting A fibers lose their function rapidly as a result
of ischemia, to which the slow-conducting C fibers are less
sensitive (28). [his suggests that C fibers may maintain their
functional capacity longer than A-delta fibers during inflam-
mation, in which PBF and therefore O2 content are reduced
as a result of the low compliance system of the pulp (30, 33).
A systematic study of the possible modulating effect of ische-
mia on nerve fiber activity should provide important insights
into dentinal pain mechanisms, especially during inflamma-
tion. Changes in pulpal blood flow may not have a direct
effect on pulpal C fiber activities; however, increases in pulpal
tissue pressure by flow elevation cause excitation of the sen-
sory nerves. Increased tissue pressure is a function of an
increase in blood flow accompanied by an increase in vascular
permeability. Thus, we could conclude that changes in blood
flow have a direct effect on pulpal A fiber activities but
minimum effect on C fibers. However, tissue pressure eleva-
tion excites all sensory nerves (Fig. 5).
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
AS|
l |
C| = tPBF
FIG 5. Relationship of pulpal tissue pressure and A-delta and C fiber
nerve activities. + represents excitation or an increase in nerve
activity. An increase in pulpal tissue pressure as a consequence of
an increase in PBF has an excitatory effect on both A-delta (A-d) and
C fibers. An excitation of C fibers in turn causes pulpal flow increase
via neurokinins released from the C fiber nerve endings.
Neurovescular Reactions in Pulp 51
changes depend on the degree of neural stimulation. For
instance, weak orthodromic stimulation of the tooth surface,
which excites only A-delta fibers, causes no changes in PBF,
suggesting that excitation of the A-delta fibers has no signifi-
cant effect on PBF (Fig. 6). However, strong orthodromic
stimulation of the tooth surface causes erratic changes in PBF,
most likely by C fiber excitation (Fig. 6). Antidromic stimu-
lation of the inferior alveolar nerve in cats, pretreated with an
a-adrenergic blocker, caused an increase in PBF and biphasic
neural activity; an increase followed by a prolonged depres-
sion (31). This neurogenic vasodilation is mediated by the
neurokinin SP, which is released from unmyelinated C fiber
endings when antidromic stimulation is applied (35, 36).
Recent evidence suggests that this neurogenic vasodilation is
mediated not only by SP, but also by neurokinin A, B, and
especially by calcitonin gene-related peptides. The biphasic
neural response following the antidromic stimulation may be
related to the biphasic PBF response after i.a. infusion of SP
(16), since SP effects are both vascular and neural. Another
explanation for the biphasic neural response is that SP triggers
the release of histamine, which causes an elevation of pulpal
tissue pressure via an increase in vascular permeability (31).
Thus, an increase in PBF by vasoactive substances, released
either from the sensory nerve endings or from other cellular
components, may have profound effects on both circulatory
and neural behavior.
'9
PBF
(low flow)
NEUROPEPTIDES
SP, CGRP etc. )
C PBF
TISSUE PRESSURE
FiG 6. Relationship of pulpal blood flow and A-delta (A-d) and C fiber
nerve activities. Excitation of A-~, has little effect on PBF. while a
decrease in flow has an inhibitory effect on A-~ fiber excitability.
Excitation of C fibers increases PBF via neuropeptides, namely, SP
and calcitonin gene-related peptide (CGRP). An increase in PBF per
se has little effect on C fiber activity, but an increase in tissue pressure
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
References

BK -- 1. Edwall L, Scott D Jr. Influence of changes in microoirculation on the

excitability of the sensory unit in the tooth of the cat. Acta Physiol Scand
1971 ;82:55-6.

roll
~'~I>"
t ---

J ~
'
PGs-

- ~
/ Hyp . . . . c i t a t i o n
I r
L LOW Comphance Environment
F,G 7. Relationship between loulpal inflammation and inflammatory
mediators, See text for explanation.
~
t Vasodi|ation
2. Haegefstam G The origin of impulses recorded from dentinal cavdies m
the tooth of the cat. Acta Physiol Scand 1976;97:121-8.
3. Matthews B Responses of intradental nerves to electrical and thermal
SP G ~-- ~) Leakage - 7 stimulation of teeth in dogs. J Physio11977;264:641-64.
i / % | 4. Olgart L. Excitation of intradental sensory units by pharmacological
agents. Acta Physiol Scand 1974;92:48-55.
! ', I 5. Narhi MVO, Hirvonen TJ, Hakumaki MOK. Responses of intradental
nerve fibers to stimulation of dentine and pulp. Acta Physiol Scand
1982:115:173-8.
6. Tender KH, Naess G. Nervous control of blood flow in the dental pulp in
dogs. Acta Phys~ol St.,and 1978;104:13-23.
7. Kim S. Edwall U Trowbndge H, C h i n S. Effects of local anesthetics on
pulpal blood flow in dogs. J Dent Res 1984;63:650-2.
8. Kim S Microcirculation of the dental pulp in health and disease. J
Endodont 1985;11:465-71.
9. Kim S, Trowbridge H, Dorscher-Kim J. The effects of 5-hydroxytrypta-
mine on pulpal hemodynames in dogs. J Dent Res 1986;65:682-5.
10. Kim S, Schuessler G, Chlen S. Measurement of blood flow in the dental
pulp of dogs with the Xe-133 washout method. Arch Oral Bio11983;28:501-5.
11. Shoher I, Mahler Y, Samueloff S. Dental pulp photoplethysmography in
Vol. 16, No. 2, February 1990
human beings. Oral Surg, Oral Meal, Oral Pathol 36:914. 1973.
12. Gazelius B, Olgart L, Edwall B, Edwall L Non-invaswe recording of
blood flow in human dental pulp. Endod Dent Traum 2"219-21. 1986.
13. Kim S. Regulation of pulpal blood flow. J Dent Res 64(spaciai is-
sue):590-6. 1985.
14. Kim S. Fan FC, Chen RYZ, Simchon S, Schuessler GB, Chien S. Effects
of changes in the systemic hemodynamic parameters ~n pulpal hemodynam~cs.
J Endodon 1980;63:394-9.
15. K,m S. Fleguiation of blood flow of the dental pulp: macrocirculat~on
and mlcrocirculation studies IPhD Dissertation}. New York, NY: Columbia
University, 1981.
16. Kim S, D0rscher-Kim J, Liu M-T, Trowbridge H. Biphasic pulp blood-
flow response to substance P in the dog as measured with a rad=olabeled.
microsphere injection method. Arch Oral B=o11988;33:305-9.
17. Bilotto G, Markowitz K. Kim S. Experimental procedure to test the
efficacy of chemical agents ~n altenng intradental nerve actwity J Endodon
1987;13:459-65.
18. Narhi M Activation of dental pulp nerves of the cat and the dog with
hydrostatic pressure. Proc Finn Dent Soc 1978;1-64.74(suppl V):
19. Narhi M, Virtanen A, Huopaniemi T, Hirvonen T. Conduction velocities
of single pulp nerve units in the cat. Acta Physiol Scand 1982;116:209-13.
20. N~irhi M. Jyvasjarvi E, Huopaniemi T. Functional differences in intraden-
tal A- and C-nerves units in cats. Abstracts of the IVth World Congress on
Pain. IASP, Seattle, Washington, 1984.
21. Narhi M. The characteristic of intradentai sensory units and their
responses to stimulation. J Dent Res 1985;64(special issue):564-71.
22. Brannstrom M, Astrom A. The hydrodynamics of the dentine; its pos-
sil04e relationship to dentinal pain. Int Dent J 1972:22:219-27.
23. Orchardson R The generation of nerve ~mpulses in mammalian axons
by changing the concentration of the normal constituents of extracelfular fluid.
J Physlo11978;275:177-89.
24. Bilotto G, Markowitz K, Kim S. Effects of ~omc and non-ionic solutions
Neurovascular Reactions in Pulp 53
on intradentaJ nerve activity in the cat. Pain f 988:32:231-8.
25. Mumford JM, Orofacial pain. Aetiokx:jy, diagnosis and treatment. 3rd
ed, Edinburgh: Churchill Livingston, 1982.
26. Markowrtz K. Bilotto G, Liu M, et al. Intradental nerves and pulpal blood
flow measured by a laser Doppler flowmeter. J Dent Res 1988;67:215.
27. Markowtiz K, Bilotto G, Liu M, Jo~ YT, Kim S. Physiokxjicai studies of
neurogenic inflammation in the dental pulp. J Endodon 1989; 15:170.
28. Tender K, Kvinnsland I. Micropuncture measurements of interstitial fluid
pressure in normal ancl inflamed dental pulp in cats. J Endodon 1983;9;105-9
29. Tonder K. Blood flow and vascular pressure in the dental pulp [Doctoral
dissertation]. Bergen, Norway: University of Bergen, 1980
30. Olgart L. The role of tocat factors in dentin and putp in intradentat pain
mechanisms. J Dent Res. 1985;64(special issue):572-8.
31. Gazelius B Studies on the release and effects of putative mediators of
pain in the dental pulp [Thesis[. Stockholm, Sweden: Karolinska Institute, 1981.
32. Olgart L, Gazelius B. Effects of adrenaline and felypressm (Octapressin)
on Izdood flow and sensory nerve activity =n the tooth Acta Odontol Scand
1977;35:69-75.
33. Jyvasjarvi E, Nat'hi M, Virtanen A, Huopaniem= T. Differential blockade
of intradental A-delta fibers by ischemia. J Dent Res 1983;62(spec=al issue):35
34. Dorscher-Kim J, Liu M-T, Trowb{idge H, Kim S InferK)r alveolar nerve
stimulation and pulpal blood flow in dogs. J Dent Res. 1986;64(special is-
sue): 146.
35. Gazelius B, Brodin E, Olgart L, Panopoulos P Evidence that substance
P is a me~ator of antidromic vasodilation using sornatostatin as a re~ease
inhibitor. Acta Physiol Scand 1981 ;113: f 55-9.
36. Brodin E, Bazelius B, Olgart L, Nilsson G Tissue concentration and
release of substance P-like immunoreactivity in the dental pulp. Acta Physiol
Scand 1981;111:141-9.
37. Kroeger D. Possible role of neurohumoral substances in the pulp. In:
Ir~nn SB, ed. Biology of the dental pulp organ: a symposium. Birmingham:
University of Alabama Press, 1968;333-46.