Endodontic Topics 2003, 5, 1225

Printed in Denmark. All rights reserved

Copyright r Blackwell Munksgaard

ENDODONTIC TOPICS 2003

Pulpal diagnosis
ASGEIR SIGURDSSON
Correct pulpal diagnosis is the key to all predictable endodontic treatment. It is paramount that prior to proceeding
with a treatment that will affect the contents of the pulp chamber that a clinical diagnosis of the pulp and the
periapical tissues is established. This diagnosis should be based on presenting symptoms, history of symptoms,
diagnostic tests and clinical findings. If it is not possible to establish the diagnosis or one diagnosis is not dominant
within a differential diagnosis, therapy should not be initiated until further evaluation has been performed. In this
review, current knowledge on pulpal and periapical status as it pertains to diagnosis will be reviewed. Additionally,
most common diagnostic tests will be presented and critically reviewed.

In the past, there have been a variety of different pulpal

diagnostic terms introduced in the literature (1, 2).
Many have been very elaborate and most attempted to
describe the histological status of the pulp. However,
with the limitations of current technology the attempt
to predict the histological status of the pulp is
impossible without prior removal of the tissue to be
evaluated. In more recent times, the trend has been to
move away from these elaborate classifications and use
a somewhat modified version of the classification
suggested by Morse et al. in 1977 (3). Even though
this classification refers to some degree to histological
status of the pulp, it directs the clinician to a specific
treatment because there is no crossover between
classification categories in terms of treatment needs.

Healthy pulp
According to the classification a healthy pulp is vital,
without inflammation. A healthy pulp will be asymptomatic, react to vitality tests such as heat, carbon dioxide
(CO2) snow, ice and/or electric pulp tester (EPT).
Once the pulp gets older it forms increasing amount
of secondary dentin in the pulp chamber such that its
reaction to thermal test might be diminished, but even
in those cases a healthy pulp should predictably react to
EPT (4). With the limitations of the diagnostic tests
presently available, it would be unrealistic to assume
that our diagnosis of a healthy pulp is definitely correct.

12

However, this diagnostic term describes the treatment

of a tooth that needs pulp removal because of
prosthodontic or restorative needs. Another example
would be pulp therapy after a traumatic injury whether
it is pulp capping or pulpotomy in an immature tooth
or pulpectomy in a mature tooth when it is judged to
be the treatment with the best prognosis of preventing
apical periodontitis (5).

Reversible pulpitis
This diagnosis implies that the pulp is vital, but has
some local area/s of inflamed tissue that will heal after
conservative vital pulp therapy (Fig. 1). Symptoms can
be very misleading in this diagnostic category, from
none at all to very intense and sharp sensation
associated with thermal stimuli. It is well established
that there is a poor correlation between clinical
symptomalogy and the pulpal histopathological state
(1, 2, 69). The history of symptoms will most often
reveal pain or sensation on stimulation only, such that
the tooth will only bother the patient when the tooth is
exposed to a stimulus that is hot and/or cold.
According to the classification, reversible pulpitis
should heal once the irritant is removed or, in case of
an exposed dentin surface, the exposed dentin is
adequately sealed. The mild trauma with subsequent
inflammation can cause small regions of neurogenic
inflammation and sufficient mechanical damage to

Pulpal diagnosis

Fig. 1. Moderate carious lesion results in a localized pulpitis. Since nothing in the history points to irreversible pulpitis,
it is assumed that after vital pulp therapy this pulp inflammation will heal.

stimulate a nerve sprouting reaction (10) and thereby

possibly cause exaggerated response to vitality tests,
indicating more severe inflammation than actually is
present. However, there is a much higher risk of
diagnosing a pulp with mild symptoms as being
reversible inflamed, when in actuality the pulp is
irreversible inflamed (see below). Thus, mistakes in
diagnosis of this pulpal category are common and
understandable. Therefore, it is essential to recall and
test all patients who have had treatment based on this
diagnostic category in order to confirm that the
progression of pulpal reaction has gone according to
expectation, i.e. the pulp has healed. Phone consultation is not enough in these cases, because failure of
diagnosis and treatment is conceivably pulp necrosis
which will in most cases start asymptomatically. The
lack of symptoms may be misinterpreted by the patient
as resolution of the problem and a successful outcome.

Irreversible pulpitis
In case of irreversible pulpitis, the pulp is still vital but is
severely inflamed so that healing is an unlikely outcome
with conservative pulp therapy. Thus, ultimately, pulp
necrosis and infection is the predicted outcome if vital
pulp therapy is attempted. Apical periodontitis will be
the final outcome. In order to avoid pulp necrosis, the
pulp is aseptically removed and the entire space filled
with a root canal filling material (Fig. 2). As with
reversible pulpitis, symptoms can be very misleading. It
has been well documented that in most cases a pulp that
is irreversibly inflamed is asymptomatic. It has been
reported that dental pulps can progress from vitality to

necrosis without pain in 2660% of all cases (11, 12).

According to a recent study, neither gender nor tooth
type appears to matter in case of asymptomatic pulpitis;
however, the older the patient was (over 53 vs. under
33 years of age) the less likely there was any pain
associated with the pulpitis (13). This phenomenon has
been in the past termed as painless pulpitis (14).
Currently, it is not known how asymptomatic pulp
death can happen; one suggestion is that at least in
some cases, the progression of inflammation to pulp
death is so rapid that there is no pain or conversely that
the inflammation is so slow that the classical inflammatory mediators that participate in the pain process
never reach a critical level (13). A more likely
explanation may be that there is effective modification
by local as well as centrally mediated systems. It has
been shown that there are several local regulatory
factors and systems in the pulp. Several studies have
recently indicated that endogenous opioid, adrenergic
sympathetic and nitric oxide systems do exist in the
pulp (1517) and there is a good indication for example
that somatostatin may inhibit pulpal pain activation
under certain conditions (1719). The effects of the
central nervous system (CNS) should not be overlooked either. It is clear that CNS plasticity can both
enhance and reduce pulpal pain (2021); however, the
detailed function and ability of the CNS to modulate
pain is as of yet poorly understood.
If the pulp is symptomatic it is most often very
sensitive to thermal changes, and the pain sensation has
the tendency to linger as a dull ache after the stimulus
has been removed. This fact can be used with caution to
predict if the pulp is likely to be irreversibly inflamed or

13

Sigurdsson

Fig. 2. Irreversible pulpitis due to a carious exposure. The most predictable treatment to prevent apical periodontitis is a
puplectomy.

not. It has been established for some time that in a

healthy pulp only very intense stimuli will activate the
more centrally located C fibers (22, 23). When a long
and intense enough stimulus is placed on a healthy
pulp, there is first sharp pain, mediated by the A-delta
fibers, followed by second poorly localized dull pain
sensation (23). In case of severe inflammation, it is clear
that there are several inflammatory mediators that can
cause increased sensitivity in the pulpal nociceptors.
Initially, these effects will be primarily on the more
peripheral A-delta fibers, but when the inflammation
reaches deeper structures, the C fibers will be affected.
This will cause their firing threshold to be lower and
receptive field larger (24). Therefore, it is important
when the patient is questioned about lingering pain
after the stimulus has been removed to not only ask
about the time it took the pain to go away, but also
about a description of the lingering sensation. The
more C-fiber-mediated pain complaint (dull, throbbing, poorly localized), the more severe the inflammation might be and thus the more likely to be irreversible
in nature.
It has also been shown that the more severe the pain
and the longer it has been symptomatic, the more likely
it is irreversibly inflamed (12). Probably though the
clearest sign of irreversible inflamed pulp is the history
of spontaneous pain, which will hit the patient
without any thermal stimulation to the teeth, and even
wake the patient from sound sleep (6).

Necrotic pulp
This diagnostic category implies partial (below the
cemento-enamel junction) or total pulp space with no
vital structures. The distinction between partial and

14

total necrosis can be very important in cases of

immature teeth. The only way to confirm vitality in
those cases is to enter the pulp chamber and remove the
necrotic debris down to a vital pulp stump. If the pulp is
completely necrotic in a tooth with undeveloped root,
it is now possible in some cases to disinfect the canal
space and stimulate the root to continue formation (see
(25, 26)).
In case of a fully formed tooth, root canal therapy is
always indicated for both partially and fully necrotic
pulp. If the pulpal space is not already infected it will in
most cases become so in time if left untreated.
Prevention of formation of periapical lesion has been
shown to have much more reliable outcome than a
treatment on a tooth with a periapical lesion (2729).
The key question is when is a necrotic root canal space
infected? It has been shown that all teeth with periapical
lesions do have infected pulp space (30). Teeth that do
not have periapical lesion may or may not be infected,
but because it is well known that there has to be a
significant loss of bone structure before it becomes
radiographically apparent (31), using lack of radiographic signs may be unreliable. Therefore, it is
recommended to treat all necrotic teeth as being
infected. Disinfection of the canal space will lead to
predictable and high success (32).
In summary, we do vital pulp therapy in cases when
the pulp is healthy or reversibly inflamed but endodontic therapy when it is irreversibly inflamed or
necrotic.

Periapical diagnosis
The term apical periodontitis implies that there is
inflammation in the periapical tissues. Like pulpal

Pulpal diagnosis
inflammation, the periapical inflammation can be
symptom free and then may only be diagnosed on a
periapical radiograph; however, it is very important to
appreciate that a periapical lesion is most likely caused
by an infection in the root canal system, irrespective of
the patient having history or being symptomatic (30).
As always, if the patient is symptomatic then it is very
important to be able to diagnose the source, prior to
any treatment. Treatment of such is always to remove
the irritant that causes the symptoms or lesion. This
could be accomplished by simple occlusal adjustment in
case of occlusal trauma, but more likely the cause is
bacteria in the root canal system and the only
predictable treatment is to effectively disinfect the
canal space followed by filling of the canal and coronal
cavity. Antibiotics cannot penetrate into a root canal
space with necrotic tissue since the blood supply that
would transport the antibiotic is not viable. Therefore,
antibiotics will not accomplish disinfection and any
relief in symptoms will be temporary (33).

Chronic apical periodontitis

This diagnostic category implies that the patient is
asymptomatic with the only sign a periapical lesion
radiographically (Fig. 4). Frequently, the patient will
deny any previous history of pain in the tooth. Vitality
test and test cavity preparation will confirm a necrotic
pulp. Occasionally, an acute flare up occurs in a chronic
lesion that will cause swelling and/or pain in the area.
This is commonly termed Phoenix abscess or acute
exacerbation of a chronic apical periodontitis (Fig. 5).

Apical periodontitis with abscess

Acute apical periodontitis

When the pulp space infection and the periapical

inflammation cause purulent breakdown there is a
possibility of accumulation of pus in the periodontium
or subperiosteal. This, as with the Phoenix abscess,
commonly occurs in an area of chronic apical periodontitis
(Fig. 5). As stated before, treatment should be primarily
aimed at eliminating the source of the abscess, the pulpal
space, and antibiotics only used as supplemental treatment
if the patient is showing systemic effects of the infection.

This diagnostic category suggests that there is an acute

inflammation in the periodontal ligament space that
causes the involved tooth to be tender to touch/
percussion and/or palpation. By definition, there are
minimal or no radiographic changes associated with
this diagnostic term. There can be several causes for this
inflammation. Most benign would be occlusal trauma.
If that is the case, the pulp should be vital and
unaffected, but in case of bacteria the pulp is either
obviously irreversibly inflamed or more likely already
necrotic. In case of occlusal trauma, evaluation of the
dentition will point to a new filling in the opposite arch
or in the tooth involved or the patient will reveal that
he/she was chewing and happen to accidentally bite
into something unexpectedly hard. If the trauma is
recent then there will be no signs on a radiograph, but if
the traumatic occlusion has been there for a long time,
the periodontal ligament space could be slightly
widened all around the tooth.
When the acute apical periodontitis (Fig. 3) is caused
by a severely inflamed or necrotic pulp the signs of pain
to chewing, percussion (both in a vertical and a lateral
direction) and periapical palpation will precede radiographic signs of apical periodontitis. Vitality tests
should confirm the diagnosis of a severely inflamed or
(more likely) a necrotic pulp.

Fig. 3. Acute apical periodontitis: May result from

traumatic occlusion, AP with acute pulpitis or an acute
exacerbation of CAP.

15

Sigurdsson

Fig. 4. Chronic apical periodontitis.

Apical periodontitis with sinus tract

Similar to the apical periodontitis with abscess, the
infection in the pulpal space and subsequent reaction in
periapical area is causing purulent breakdown but in this
case rather then collect subperiosteally and thereby
cause pain and swelling, the exudate has found its way to
a surface, most commonly on the gingiva or mucosa,
but sometimes on to the surface of the skin. Because of
the lack of pressure buildup there is usually very minimal
pain associated with this diagnostic category and after
the tract has found its way to the surface swelling will
not occur. Once the source of the infection has been
eliminated, by disinfection the pulpal space of the
involved tooth, the sinus tract should heal within a few
days without any specific need for treatment (Fig. 6).

Fig. 5. Apical periodontitis with abscess.

most of the diagnosis should be done by what we hear

and not what we see. In fact, visual clues might throw us
off track resulting in incorrect diagnosis. Therefore, it is
essential to carefully listen to the patient and systematically review his/her present symptoms as well as the
pain history prior to coming to any conclusions about
the cause.
It is often stated that once a comprehensive history
has been taken the practitioner should in most cases
know the diagnosis of the problem. The clinical
examination and diagnostic tests should then be done
to ascertain which tooth fits this diagnostic category.

Pain complaint

Diagnostic procedures
It has been stated by Dr Okeson (34) that dentists are
disadvantaged by their dental training because it
focuses primarily on diagnosing a problem by visual
means. However, when diagnosing the origins of pain,

16

As stated previously, pulpitis is as a rule painless (4, 8,

1113); therefore, lack of pain is not a good indicator
of severity of pulpal/periapical inflammation. However
pain, when present, is obviously an indicator of disease.
If the pain is short and directly associated with a
stimulus, it is likely to be mediated by the A-delta

Pulpal diagnosis

Fig. 6. Histological, clinical and radiographic appearance of a apical periodontitis with sinus tract.

neurofibers (only) that are normally active throughout

the dentinpulp complex. Thus, complaints of sharp
provoked pain indicate mild and reversible inflammation and that vital pulp therapy would be sufficient to
reverse the pulpal inflammation. Examples would be
the removal of a shallow carious lesion, replacing a leaky
restoration or covering exposed root surfaces.
There is building evidence that the classical inflammatory mediators, capable of causing pain, are released
in the pulp in direct proportion to the insult. Serotonin
(5-TH) is for example able to sensitize intra-dental Afibers resulting in increased responsiveness (35) and
bradykinin have shown to be in significant higher
concentration in irreversibly inflamed human pulps
(36). In addition, recently in a ferret model where
lipopolysaccharide (LPS) was used to induce inflammatory changes in deep class V preparations in canine
teeth, there was strong correlation between change in
the animals behavior and C-fos expression in the area
of subnucleous caudalis and interpolaris. The findings
were consistent with mild-to-moderate pain felt by the
animals for some time after the exposure to the LSP
(37).
It is not only the inflammatory mediators that are
associated with pulpal pain. Recent studies have also
demonstrated that neuropeptides from the nociceptive
nerve fibers present in the pulp (calcitonin gene-related
peptide (CGRP), Neurokinin A (NKA) and substance P)
are found in significantly higher concentrations in
symptomatic pulp compared with healthy pulps (3840).
The history of the pain has been found to be as
important as the presenting symptoms. As stated before
there is a difference between the pain sensations

conveyed by the two main pain fibers in the pulp. The

rapid pain sensation associated with the A-delta fibers is
part of the normal function of the pulp, the deeper
seated slower and unmyelinated C-fiber are for most
part unresponsive to all but very intense stimulus in
normal, uninflamed pulp (16, 40). When asking about
the history of the pain it can be very revealing to note
that the pain initially started as primarily temperature
sensitivity, with sharp defined pain episodes, but then
changed to more dull throbbing ache that has become
more severe in nature. This is important for many
reasons, first it indicates a shift to pain consistent with
activation of the C-fibers indicating increased inflammation and second it has been shown that self-reports
of intensity and quality of dental pain is a valid predictor
of whether or not the pulpal inflammation is reversible
or not (41, 42).
It is extremely important to remember that the
primary source of the pain does not have to be in the
location of chief complaint of the patient. Therefore, all
possible sources need to be investigated and ruled out
because in order for a treatment to be effective it must
be directed towards the source of the pain and not the
site of the pain.
Dr Glick (43) in 1962 investigated the referral
pattern from teeth with toothache. He noticed certain
trends that still for most part hold true. He concluded
that toothache never crossed the midline, the pain was
frequently referred from one tooth to another and the
referred pain was not only felt in the deep but also to
the superficial or cutaneous tissues. There were also
certain patterns observed, the upper teeth tended to
refer the pain up to the upper face and temporalis

17

Sigurdsson
muscle area, where the lower teeth tended to be
referred to the body of the mandible and back to the
ear. However, not only the pulp can refer pain to a
remote area. It has been shown that certain muscle
groups can refer pain from myalgia to the dentition
(44) confusing the patient into thinking that he/she is
suffering from toothache when they actually are
suffering from myofacial pain (muscle ache). Therefore,
clearly it is very important to palpate facial structures
where pain is felt by the patient. If pain is felt in a tooth
that is made worse by palpation of the temporalis
muscle it is much more likely that the patient is
suffering from myalgia than toothache (see Table 1).

Diagnostic tests
Unfortunately, many clinicians rely solely on diagnostic
tests to make a definitive diagnosis. It is very important
to remember that most commonly used test systems do
not actually assess the vitality (blood circulation) of the
pulp and most do not give much if any indication about
presence or severity of inflammation in the pulp. So
why are these tests used? The main reasons for doing
pulpal test are to reproduce the symptoms, to localize
the symptoms and to access the severity of the
symptoms. With every test it has to be remembered
that the responses are going to be subjective and some
patients will have the tendency to exaggerate while
others will understate the pain felt (45, 46).

A positive response to the electric pulp test is an

indication of vital pulp tissue in the coronal aspect
of the root canal space. However, it is not an indication
of the reversibility of the inflammation within the
pulp. No correlation has been found between the
pain thresholds and the condition of the pulp (6,
55, 56).
A negative response was found by Seltzer et al. (6) to
indicate a total necrosis in 72% of cases and localized
necrosis in 25.7 % of cases. Thus, if it is accepted that
even localized necrosis is an indication for the need of
pulpectomy in a mature tooth, in 97.7% of cases a
negative response to the electric pulp test would
indicate that clinically a pulpectomy or debridement
of a necrotic pulp should be performed.
The response of the young pulps (teeth with open
apices) to the EPT is unreliable (4, 57) since the
complete development of the plexus of Raschkow does
not occur until the final stages of root development
(58). Thus, pulpal nerves do not end amongst the
odontoblasts, predentin or dentin, as in fully developed
teeth in occlusion (59). In young teeth, sensitivity
testing with cold is a more effective method (57).
Where the electric pulp tested is placed on the tooth
crown is critical. It has been shown that the incisal edge
on anterior teeth and the mesio-buccal incisal edge on
lower teeth is the optimal placement site for the EPT to
determine the lowest response threshold (60). This is
true of the cold tests as well (Fig. 7).

Thermal tests
Electric pulp tester (EPT)
The EPT uses electric current to stimulate the sensory
nerves of the dental pulp (4749), specifically, the fastconducting myelinated fibers (A-Delta) at the pulp
dentin junction. The unmyelinated (C) fibers of the
pulp may (50) or may not respond (51). Measurement
of electric voltage in teeth may be inconsistent due to
thickness of enamel and dentin, dryness and electrical
resistance of enamel (52), infractions, restorations, pits,
fissures and caries. In addition, the movement of the
electric current to the pulp may be impossible if the
tooth is covered with a crown or large restoration.
Bipolar and monopolar are the two stimulating
modes available. The bipolar mode is presumably more
accurate because the current is confined the coronal
pulp (53, 54). However, most EPTs are still monopolar
(51).

18

These tests are thought to work by hydrodynamic

forces in the dentin-initiating generator potentials in
the nerve endings by displacing surface membranes. By
this theory, fluid movement in the tubules (due to the
thermal stimulation) is responsible for activation of
sensory receptor units in the pulp (61).

Cold test
The most effective cold tests are those with frozen
sticks of carbon dioxide ( ! 781C; CO2 snow) or a
cotton pellet sprayed with difluordichlormethane
(DDM) ( ! 501C) (57). Older techniques of using
refrigerator ice or ethyl chloride ( ! 41C) are less
reliable (57) and should be replaced by the newer
techniques. A major advantage of these newer thermal
tests may be their ability to effectively move cold

Pulpal diagnosis
Table 1. Formulation of a pulpal diagnosis
Vital pulp
Symptom, test, supporting information

Necrotic pulp

Irreversible inflammation

Reversible inflammation

Pulp test

Negative

Positive

Positive

Pulpal exposure

Present

Absent

Pain to percussion

Present

Absent

Severe pain

Present

Absent

Spontaneous pain

Present

Absent

Past history of pain

Present

Absent

Deep throbbing lingering pain

Present

Absent

Pain to hot relieved by cold

Present

Absent

Questionable

Questionable

Key factors

Related factors

Factors related to treatment plan

Age, periodontal disease, previous pulpal insults

Fig. 7. Correct placement of pulp-testing devices. Left: CO2 ice stick placed on the incisal edge. Right: the electric pulp
tester placed on the mesio-buccal cusp of the lower molar.

through crowns and large restorations. Concern about

the potential for extreme cold to cause cracks in the
dentin or irreversibly damage the pulp have been shown
to be unfounded (62, 63).
Abnormal but positive responses are equally distributed among the pulps of teeth in all diagnostic
categories (6, 8). Therefore, a positive response is an
indication that the pulp is vital but does not indicate if
inflammation is reversible. The same authors showed
that a negative response is highly indicative of necrosis
and this test result can be used to predict the need for
root canal therapy.
The advantages of frozen CO2 over other sensitivity
tests is that it can be used with metallic restorations,

orthodontic bands, metallic splints, temporary and

permanent crowns, and is also the most effective vitality
test for immature teeth (4, 57, 64).

Heat test
The heat test is a difficult test to perform since too
much heat can in itself cause irreversible harm to the
pulp. The reaction to heat has been described as
biphasic. Initially, there is a sharp localized pain reaction
due to stimulation of A-delta fibers (65), and with
continued stimulation, a dull radiating pain follows
(66) due to activation of the C fibers (22, 40). No
correlation has been found between an abnormal

19

Sigurdsson
response to heat and a histologic diagnosis including
liquefaction necrosis. A negative response is indicative
of necrosis in the pulp (6, 8). Thus, as with the other
sensitivity tests, this test only differentiates a vital from a
non-vital pulp. Degrees of inflammation or the
reversibility of an inflamed pulp cannot be ascertained
from this test.

Mechanical tests
Percussion and palpation
These are not true vitality tests but rather are indicative
of periodontal ligament inflammation (67). Pain is
elicited on percussion more frequently in all pulp
conditions where partial or total necrosis is present (49)
and as such is an indirect method of assessing the status
of the pulp. Also, the presence of percussion and/or
palpation sensitivity in conjunction with a vital pulp is
indicative of a pulp that is severely and thus (probably)
irreversibly inflamed.
Percussion (Fig. 8). This test is performed with digital
pressure or more commonly with the handle of a
mouth mirror. The aim of this test is to determine the
presence/absence of inflammation in the apical periodontium. A positive percussion test indicates inflammation of the periradicular tissues. However, a negative
percussion test does not rule out the presence of such
inflammation (6). As already mentioned, a positive
response to percussion in a tooth which tests vital to
sensitivity testing is an indication of severe and
probably an irreversible inflammation in that pulp
(49). Care must be taken, when interpreting the results
of the percussion tests, to rule out a positive response
due to marginal periodontitis, i.e. due to periodontal
disease. This is particularly difficult in those cases where

Fig. 8. Percussion test.

20

Fig. 9. Palpation test.

the pulp vitality tests indicate a vital pulp. The results of

other diagnostic tests are used to differentiate periodontitis of periodontal or endodontic origin.
Palpation (Fig. 9). This test is used to detect
inflammation in the mucoperiosteum around the root
of the tooth. It may be possible to detect tenderness,
fluctuation, hardness or crepitus before extensive
swelling is present.

Diagnostic information
As has been discussed for the percussion test, a positive
response when palpating over the root tip is a reliable
indicator of periapical inflammation. However, if a
positive response is not elicited, inflammation is not
necessarily absent (6).

Radiographic examination
The radiographic examination is one of many tests and
the findings should always be evaluated together with
those of the other tests and the clinical examination.
Initial sensitivity tests can suggest which type of radiograph will be most advantageous. If a vital tooth is
evaluated, a bitewing radiograph would be advantageous
to detect caries or other causes of pulpal inflammation. If
periapical disease is suspected by the previous tests, a
periapical radiograph is indicated. All radiographs should
be taken using holders which allow parallelism and
standardization. If comparative radiographs will be
required on follow-up, it is useful to fabricate a rubber
biteblock so that the angulation of follow-up radiographs will be as similar as possible (Fig. 10).
The radiograph cannot detect pulpal inflammation
directly. However, caries or defective restorations seen
on the radiograph will suggest pulp inflammation
(68). Condensing apical periodontitis is a near-path

Pulpal diagnosis
teeth are warmer and will rewarm quicker after cooling
than non-vital teeth. Fanibundas experiments concluded that timetemperature curves comparing the
warming of vital vs. non-vital teeth were diagnostically
informative.
Additionally, it has been attempted to use color
change of cholisteric liquid crystals as a diagnostic tool
to measure crown temperature change (73) with some
success. And a more recent study using an infrared
thermographic camera showed crown temperature
patterns of non-vital teeth to be slower to re-warm
than those of vital teeth (74).
Fig. 10. Bite stent used for every radiography to ensure
that positioning is consistent.

133Xenon radioisotope
gnomonic sign of pulpitis. Also, the presence of an
apical radiolucency of endodontic origin may be a good
indication that necrosis or a necrotic zone is present in
the pulp space.

Additional tests
Test drilling
This test has been used when full coverage restorations
are present making other forms of testing impossible.
The use of CO2 frozen sticks has diminished the need
for test drilling. Some practitioners use the test drill
method as the final diagnosis of pulp necrosis. As with
the other sensitivity tests, a positive response to this test
indicates a vital pulp but gives no information about the
pathologic involvement of the pulp.

Experimental testing methods

Attempts have been made to demonstrate pulpal
circulation rather than the neural integrity of the pulp.
Tests include:

Ultrasonic pulse echo

Barber et al. (69) used an ultrasonic pulse echo
instrument to detect the dentinoenamel and dentinopulpal interfaces using transmission and reflection
of sound from the dental hard tissues.

Crown surface temperature

Fanibunda (7072) has performed extensive research
in the field of crown surface temperature. This pulp
vitality technique is based on the hypothesis that vital

Radioactive materials for measurement of pulpal blood

circulation were previously used in the radiolabelled
microsphere injection method (75, 76). A method
utilizing a radiation probe with 133 xenon radioisotope
to differentiate between vital and pulpless teeth on the
basis of blood supply has been found effective (77).
However, the use of radioactive materials is expensive,
restricted on humans, and requires special licencing
requirements. To this point the most promising of
these experimental methods are those using the
measurement of light passing through or deflected
from the blood in the pulp.

Laser Doppler flowmetry

This technique was developed to assess blood flow in
microvasculature systems, e.g. retina, mesentery, renal
cortex and skin (78) (Fig. 11). It has recently been used
in intact teeth in animals (79, 80) and in man (79, 81).
It utilizes a light beam (Helium Neon 632.8 nm),
which is scattered by moving red blood cells (82).
Newer machines have varied the wavelength between
600 and 700 nm depending on the light absorption
properties of tissue which is tested. This light beam
undergoes a frequency shift, according to the principle
of Doppler. The back-scattered light is picked up by
photodetectors, and produces a signal which is
proportional to the red cell flux (number of
cells " average velocity). This can be used as a measure
of pulpal blood flow, expressed as a percentage of fullscale deflection at a given gain.
The technique appears objective, non-invasive and
accurate. A growing number of reports indicate that it
is a method which can easily be adapted to the testing of

21

Sigurdsson

Fig. 11. Laser Doppler flowmeter. Left set up and

computer read out of pulp status. Right, probe showing
the small dimensions suitable for accurate placement on
the tooth.

a tooth and which is promising as a pulp vitality tester.

It is especially effective in young traumatized teeth with
large pulps that do not respond well to other forms of
sensitivity testing (79, 81, 83).

Pulse oximetry
This technique has been used to detect vascular
integrity in the tooth (84). A modified probe was used
and two wavelengths used to provide a ratio of the
absorption of wavelengths for oxygenated and deoxygenated blood. This gives the percentage of oxygenation of blood (84). This method has the potential of
not only assessing the presence of a vital pulp but also of
assessing pathological processes (84).

Dual wavelength spectrophotometry

Oximetry by spectrophotometry uses a dual wavelength light source (760 and 850 nm) to determine the
oxygen saturation level of the pulpal blood supply (85
87). Preliminary tests on teeth were promising since the
blood oxygenation and volume could be detected (88)
(Fig. 12). Thus, the instrument might be useful not
only in determining pulp necrosis, but also the
inflammatory status of the pulp. The instrument shows
promise as a pulp tester as it is non-invasive, objective,
small and portable.

Clinical findings
The findings of the clinical examination in addition to
an extensive knowledge of the pulpal reaction to
external irritants is important for arriving at a correct
diagnosis. A thorough clinical examination is critical

22

Fig. 12. Dual wavelength spectrophotometer. Machine

attached to recorder (left) and light source and detector
(right).

since pulpitis is usually painless and also because of the

lack of correlation between symptomatology and
diagnostic tests and the histopathologic state of the
pulp.

Clinical findings of significance

Carious pulpal exposure
Scientific evidence indicates that when the pulp is
exposed to caries, bacteria have penetrated the pulp
directly with abscess formation (68). Long-term vital
treatment of a cariously exposed pulp has reported
success rate from just over 20% to below 50% (89, 90)
so that the pulp should be considered irreversibly
inflamed. Only in cases where root development is
incomplete should an attempt be made to estimate the
level at which the pulp is uninflamed and apexogenesis
attempted.

Age
Through the years, the pulpal space will be reduced and
thereby the pulp tissue becomes less. At the same time,
the cellular components decrease with increased thickness of the collagen fibers and number of nerves and
blood vessels are lost (6, 91). It is not clear how much
effect all these changes do have on the defense
capability of the pulp. It could be speculated that the
pulp has less ability to reverse an inflammatory response
to an insult; however, there is neither any research that
has confirmed that nor is there any indication that older
patients are more likely to need root canal therapy.
Therefore, increased age on its own does not seem to be
very much of clinical significance in the decision of need
for endodontic care, only it needs to be remembered

Pulpal diagnosis
that responses to tests might be greatly diminished with
increased age.

Periodontal disease
Severe periodontal disease can prematurely age the pulp
(6, 60, 92). However, again the aging of the pulp will
not necessary cause the pulp to be less able to defend it
self and it has been demonstrated that there is no
difference in the pulp status of teeth with or without
periodontal disease (93).

Previous pulpal insults

It is clear that any pulpal insult will affect the pulp in
someway and the more severe it was, the more reaction
will be seen (6). If a tooth has history of deep
restorations, possible incomplete caries removal or
carious pulp capping the more likely is that the pulp has
been damaged beyond repair and therefore a root canal
therapy would be needed.
Again if tests are inconclusive especially when there is
no reaction to thermal tests but some reaction to EPT
then a test cavity preparation is advisable. Then the
access is cut into the tooth without anesthesia. It is
important to explain to the patient that there is a good
likelihood that the pulp is necrotic and therefore no
pain is expected, but he/she is instructed to give a
signal if and when any sensation is felt. If the patient
feels sensation as soon as the dentin is exposed, then it is
likely that the periodontitis is of different origin that
needs then to be further investigated.

References
1. Baume LJ. Diagnosis of diseases of the pulp. Oral Surg
Oral Med Oral Pathol 1970: 29: 102116.
2. Seltzer S. Classification of pulpal pathosis. Oral Surg Oral
Med Oral Pathol 1972: 34: 269280.
3. Morse DR, Seltzer S, Sinai I, Biron G. Endodontic
classification. J Am Dent Assoc 1977: 94: 685689.
4. Fulling HJ, Andreasen JO. Influence of maturation status
and tooth type of permanent teeth upon electrometric
and thermal pulp testing procedures. Scand J Dent Res
1976: 84: 291296.
5. Heide S, Mjor IA. Pulp reaction to experimental
exposures in young permanent monkey teeth. Int Endod
J 1983: 16: 1119.
6. Seltzer S, Bender IB, Zionitz M. The dynamics of pulp
inflammation: correlation between diagnostic data and
actual histologic finding in the pulp. Oral Surg Oral Med
Oral Pathol 1963: 16: 846871.

7. Lundy T, Stanley HR. Correlation of pulpal histopathology and clinical symptoms in human teeth subjected to
experimental irritation. Oral Surg Oral Med Oral Pathol
1969: 27: 187201.
8. Dummer PMH, Hicks R, Huws D. Clinical signs and
symptoms in pulp disease. Int Endod J 1980: 13: 2735.
9. Garfunkel A, Sela J, Almansky M. Dental pulp pathosis:
Clinicopathologic correlation based on 109 cases. Oral
Surg Oral Med Oral Pathol 1987: 35: 110117.
10. Byers MR, Narhi MV, Mecifi KB. Acute and chronic
reactions of dental sensory nerve fibers to hydrodynamic
stimulation or injury. Anat Rec 1988: 221: 872883.
11. Barbakow F, Cleaton-Jones P, Friedman D. Endodontic
treatment of teeth with periapical radiolucent areas in a
general practice. Oral Surg Oral Med Oral Pathol 1981:
51: 552559.
12. Bender IB. Reversible and irreversible painful pulpitides:
diagnosis and treatment. Aust Endod J 2000: 26: 1014.
13. Michaelson PL, Holland GR. Is pulpitis painful? Int
Endod J 2002: 35: 829832.
14. Hasler JE, Mitchell DF. Painless pulpitis. J Am Dent
Assoc 1970: 81: 671677.
15. Olgart LM. Neural control of pulpal blood flow. Crit Rev
Oral Biol Med 1996: 7: 159171.
16. Byers MR, Narhi MVO. Dental injury models: Experimental tools for understanding neuroinflammatory
interactions and polymodal nocicpetor functions. Crit
Rev Oral Biol Med 1999: 10: 439.
17. Hirvonen T, Hippi P, Narhi M. The effect of an opioid
antagonist and a somatostatin antagonist on the nerve
function in normal and inflamed pulp. J Dent Res 1998:
77(abstract): 1329.
18. Taddese A, Nah S-Y, McClesky EW. Selective opioid
inhibition of small nociceptive neurons. Science 1995:
270: 13661369.
19. Casasco A et al. Peptidergic nerves in human dental pulp:
an immunocytochemical study. Histochemistry 1990: 95:
115121.
20. Dubner R, Ruda MA. Activity-dependent neuronal
plasticity following tissue injury and inflammation.
Trends Neurosci 1992: 15: 96103.
21. Sigurdsson A, Maixner W. Effects of experimental and
clinical noxious counter irritants on pain perception.
Pain 1994: 57: 265275.
22. Narhi MVO, Hirvonen T, Hakumaki MOK. Activation of intradental nerves in the dog to some stimuli
applied to the dentin. Arch Oral Biol 1982: 27: 1053
1058.
23. Jyvasjarvi E, Kniffki DK. Cold stimulation of teeth: a
comparison between the responses of cat intradental A
and C fibers and human sensations. J Physiol 1987: 391:
193207.
24. Narhi MVO, Yamamoto H, Ngassapa D, Hirvonen T.
Function of interadental nociceptors in normal an
inflamed teeth. In: Shjimono M, Maeda T, Suda H,
Takahashi K, eds. Dentin/pulp Complex. Tokyo: Quintessence Publ., 1996, 136140.
25. Hoshino et al. In-vitro antibacterial susceptibility of
bacteria taken from infected root dentine to a mixture of

23

Sigurdsson

26.

27.

28.

29.

30.
31.

32.

33.

34.
35.

36.

37.

38.

39.

40.

41.

42.

24

ciprofloxacin, metronidazole and minocycline. Int Endod

J 1996: 29: 125130.
Iwaya S, Ikawa M, Kubota M. Revascularization of an
immature permanent tooth with apical periodontitis and
sinus tract. Dent Traumatol 2001: 17: 185187.
Strindberg LZ. The dependence of the results of pulp
therapy on certain factors. An analytic study based on
radiographic and clinical follow-up examinations. Acta
Odont Scand 1956: 14: 11771180.
Seltzer S, Bender IB, Zionitz M. The interrelationship of
pulp an periodontal disease. Oral Surg Oral Med Oral
Pathol 1963: 16: 14741490.
Sjogren U, Hagglund B, Sundqvis G, Wing K. Factors
affecting the long-term results of endodontic treatment.
J Endod 1990: 16: 498504.
Bergenholtz G. Microorganisms from necrotic pulp of
traumatized teeth. Odont Revy 1974: 25: 347358.
Bender IB, Seltzer S. Roentgenographic and direct
observation of experimental lesions in bone. J Am Dent
Assoc 1961: 62: 152.
Sjogren U, Figdor D, Perssbon S, Sundqvist G. Influence
of infection at the time of root filling on the out come of
endodontic treatment of teeth with apical periodontitis.
Int Endod J 1997: 30: 297306.
Fouad AF, Rivera EM, Walton RE. Penicillin as a
supplement in resolving the localized acute apical
abscess. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 1996: 81: 590595.
Okeson JP. Orofacial Pain. Chicago: Quintessence
Publishing Co, Inc, 1996.
Olgart LM. The role of local factors in dentin and pulp
intradental pain mechanisms. J Dent Res 1985: 64: 572
578.
Lepinski M, Hargreaves KM, Goodis HE, Bowles WR.
Bradykinin levels in dental pulp by microdialysis. J Endod
2000: 26: 744747.
Chaisin-Chattipakorn S, Sigurdsson A, Light AR, Narhi
M, Maixner W. Trigeminal c-Fos expression and
behavioral responses to pulpal inflammation in ferrets.
Pain 2002: 99: 6169.
Awawdeh L, Lundy FT, Shaw C, Lamey PJ, Linden GJ,
Kennedy JG. Quantitative analysis of substance P,
neurokinin A and calcitonin gene-related peptide in pulp
tissue from painful and healthy human teeth. Int Endod J
2002: 35: 3036.
Bowles WR, Withrow JC, Lepinski AM, Hargreaves KM.
Tissue levels of immunoreactive substance P are increased in patients with irreversible pulpitis. J Endod
2003: 29: 265267.
Narhi M, Jyvasjarvi E, Hirvonen T, Huopaniemi T.
Activation of heat sensitive nerve fibers in the dental pulp
of the cat. Pain 1982: 14: 317326.
Grushka M, Sessle BJ. Application of the McGill pain
questionnaire to the differentiation of toothache pain.
Pain 1984: 19: 4957.
Sessle BJ. The neurobiology of facial and dental pain:
present knowledge, future direction. J Dent Res 1987:
66: 962981.

43. Glick DH. Locating referred pulpal pain. Oral Surg Oral
Med Oral Pathol 1962: 15: 613623.
44. Travell J. Myofacial trigger points: A clinical view. In:
Bonica J, Albe-Fessard D, eds. Advances in Pain Research
and Therapy, Vol. 1. New York: Raven Press, 1976: 919
926.
45. Eli I. Dental anxiety: A cause for possible misdiagnosis of
tooth vitality. Int Endod J 1993: 26: 251253.
46. Klepac RK, Dowling J, Hauge G, McDonald M. Reports
of pain after dental treatment, electrical tooth pulp
stimulation and cutaneous shock. J Am Dent Assoc 1980:
100: 692695.
47. Bjorn H. Electrical stimulation of teeth and its application to dentistry. Sven Tandlaek Tidskr 1946: 39(Suppl):
3945.
48. Reynolds RL. The determination of pulp vitality by
means of thermal and electrical stimuli. Oral Surg Oral
Med Oral Pathol 1966: 22: 231236.
49. Seltzer S, Bender IB. The Dental Pulp, 3rd edn.
Philadelphia: J.B. Lippincott, 1985.
50. Mumford JM. Evaluation of gutta percha and ethyl
chloride in pulp testing. Br Dent J 1964: 116: 338342.
51. Narhi M, Virtanen A, Kuhta J, Huopaniemi T. Electrical
stimulation of teeth with pulp tester in the cat. Scand
J Dent Res 1979: 87: 3238.
52. McGrath PA, Gracely RH, Dubner R, Heft MW. Nonpain and pain sensations evoked by tooth pulp stimulation. Pain 1983: 15: 377388.
53. Mumford JM. Orofacial Pain. Aetiology, Diagnosis and
Treatment, 3rd edn. Edinburgh: Churchill Livingstone,
1982.
54. Matthews B, Searle BN. Electrical stimulation of teeth.
Pain 1976: 2: 245251.
55. Mumford JM. Thermal and electrical stimulation of
teeth in the diagnosis of pulpal and periapical disease.
Proc R Soc Med 1967: 60: 197202.
56. Lundy T, Stanley HR. Correlation of pulpal histopathology and clinical symptoms in human teeth subjected to
experimental irritation. Oral Surg Oral Med Oral Pathol
1969: 27: 187201.
57. Fuss Z, Trowbridge H, Bender IB, Rickoff B, Sorin S.
Assessment of reliability of electrical and thermal pulp
testing agents. J Endod 1986: 12: 301305.
58. Fearnhead RW. The histologic demonstration of nerve
fibers in dentin. In: Andersen DJ, ed. Sensory Mechanisms
in Dentine. New York: Pergamon Press, 1963: 15.
59. Bernick S. Differences in nerve distribution between
erupted and non-erupted human teeth. J Dent Res 1964:
43: 406416.
60. Bender IB, Landau MA, Fonsecca S, Trowbridge HO.
The optimal placement-site of the electrode in electric
pulp testing of the 12 anterior teeth. J Am Dent Assoc
1989: 118: 305310.
61. Brannstrom M, Astrom A. The hydrodynamics of the
dentine: its possible relationship to dentinal pain. Int
Dent J 1972: 22: 219303.
62. Ingram TA, Peters DD. Evaluation of the effects of
carbon dioxide uses as a pulpal test. Part 2. In vivo effect

Pulpal diagnosis

63.

64.

65.

66.

67.

68.
69.

70.

71.

72.

73.

74.

75.

76.

77.

on canine enamel and pulpal tissues. J Endod 1983: 9:

296303.
Rickoff B, Trowbridge H, Baker J, Fuss Z, Bender IB.
Effects of thermal vitality tests on human dental pulp.
J Endod 1988: 14: 482485.
Ehrmann EH. Pulp testers and pulp testing with
particular reference to the use of dry ice. Aust Dent J
1977: 22: 272279.
Narhi M. The characteristics of intradental sensory units
and their responses to stimulation. J Dent Res 1985:
64(Special Issue): 564.
Brannstrom M, Johnson G. Movement of the dentin and
pulp liquids on application of thermal stimuli. An in vitro
study. Acta Odont Scand 1970: 28: 5970.
Klausen B, Helbo M, Dabelsteen E. A differential
diagnostic approach to the symptomatology of acute
dental pain. Oral Sur Oral Med Oral Pathol 1985: 59:
297301.
Massler M. Pulpal reaction to dental caries. Int Dent J
1967: 17: 441460.
Barber FE, Lees S, Lobene RR. Ultrasonic pulseecho
measurements in teeth. Arch Oral Biol 1969: 14: 745
751.
Fanibunda KB. A laboratory study to investigate the
differentiation of pulp vitality in human teeth by
temperature measurement. J Dent 1985: 13: 295303.
Fanibunda KB. The feasibility of temperature measurement as a diagnostic procedure in human teeth. J Dent
1986: 14: 126129.
Fanibunda KB. Diagnosis of tooth vitality by crown
surface temperature measurement: a clinical evaluation.
J Dent 1986: 14: 160164.
Howell RM, Duell RC, Mullaney TP. The determination
of pulp vitality by thermographic means using cholesteric
liquid crystals. Oral Surg Oral Med Oral Pathol 1970:
29: 763768.
Pogrel MA, Yen CK, Taylor R. Studies in tooth crown
temperature gradients with the use of infrared thermography.
Oral Surg Oral Med Oral Pathol 1989: 67: 583587.
Kim S, Schuessler G, Chien S. Measurement of blood
flow in the dental pulp of dogs with Xe-133 washout
method. Arch Oral Biol 1983: 28: 501505.
Kim S, Dorscher-Kim J, Liu MT, Trowbridge H.
Biphasic pulp blood flow response to substance P in the
dog as measured with radiolabeled, microsphere injection method. Arch Oral Biol 1988: 33: 305309.
Trope M, Jaggi J, Barnett F, Tronstad L. Vitality
testing of teeth with a radiation probe using 133
xenon radioisotope. Endod Dent Trauma 1986: 2:
215218.

78. Holloway GA Laser Doppler measurement of cutaneous

blood flow. In: Rolfe P, ed. Non-Invasive Physiological
Measurements. London: Academic Press Inc., 1983: 11.
79. Gazelius B, Olgart L, Edwall B, Edwall L. Non-invasive
recording of blood flow in human dental pulp. Endod
Dent Trauma 1986: 2: 219221.
80. Gazelius B, Edwall B, Olgart L, Lundberg JM, Hokfelt
T, Fisher JA. Vasodilatory effects and coexistence of
calcitonin gene-related peptide (CGRP) and substance P
in sensory nerves of cat dental pulp. Acta Physiol Scand
1987: 130: 3340.
81. Mesaros SV, Trope M. Revascularization of traumatized
teeth assessed by laser Doppler flowmetry: Case report.
Endod Dent Trauma 1997: 13: 2430.
82. Wilder-Smith PE. A new method for the non invasive
recording of blood flow in human dental pulp. Int Endod
J 1988: 21: 307312.
83. Yanpiset K, Vongsavan N, Sigurdsson A, Trope M.
Efficacy of laser Doppler flowmetry for the diagnosis of
revascularization of reimplanted immature dog teeth.
Dent Trauma 2001: 17: 6370.
84. Schnettler JM, Wallace JA. Pulse oximetry as a diagnostic
tool of pulpal vitality. J Endod 1991: 17: 488490.
85. Millikan GA. The oxymeter, an instrument for measuring
continuously the oxygen saturation of arterial blood in
man. Rev Sci Inst 1942: 13: 434437.
86. Wood EH, Geraci JE. Photoelectric determination of
arterial oxygen saturation in man. J Lab Clin Med 1949:
34: 387311.
87. Chance B. Rapid and sensitive spectrophotometry: III. A
double beam apparatus. Rev Sci Inst 1951: 22: 634.
88. Nissan R, Trope M, Zheng C-D, Chance B. Dual
wavelength spectrophotometry as a diagnostic test of
the pulp chamber contents. Oral Surg Oral Med Oral
Pathol 1992: 74: 508514.
89. Barthel CR, Rosenkranz B, Leuenberg Roulet JF. Pulp
capping of carious exposures: treatment outcome after 5
and 10 years: a retrospective study. J Endod 2000: 26:
525528.
90. Tronstad L, Mjor IA. Capping the inflamed pulp. Oral
Surg Oral Med Oral Pathol 1972: 34: 477485.
91. Ikawa M, Komatsu H, Ikawa K, Mayanagi H, Shimauchi
H. Age-related changes in the human pulpal blood flow
measured by laser Doppler flowmetry. Dent Traumatol
2003: 19: 3640.
92. Rubach WC, Mitchell DF. Periodontal disease, accessory
canals and pulp pathosis. J Periodontol 1965: 36: 34.
93. Mazur B, Massler M. Influence of periodontal disease on
the dental pulp. Oral Surg Oral Med Oral Pathol 1964:
17: 592599.

25