Pulpal diagnosisASGEIR 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 asympto-

matic, 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.

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, 6–9). 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

12

Endodontic Topics 2003, 5, 12–25Printed in Denmark. All rights reserved

Copyrightr Blackwell Munksgaard

ENDODONTIC TOPICS 2003

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 consulta-

tion 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 inmost 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 26–60% 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 inflam-

matory 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 (15–17) and there is a good indication for example

that somatostatin may inhibit pulpal pain activation

under certain conditions (17–19). The effects of the

central nervous system (CNS) should not be over-

looked either. It is clear that CNS plasticity can both

enhance and reduce pulpal pain (20–21); 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

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.

Pulpal diagnosis

13

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, throb-

bing, poorly localized), the more severe the inflamma-

tion 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

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 (27–29).

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 radio-

graphic 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 endo-

dontic 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

Fig. 2. Irreversible pulpitis due to a carious exposure. Themost predictable treatment to prevent apical periodontitis is apuplectomy.

Sigurdsson

14

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).

Acute apical periodontitis

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 radio-

graphic signs of apical periodontitis. Vitality tests

should confirm the diagnosis of a severely inflamed or

(more likely) a necrotic pulp.

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

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.

Fig. 3. Acute apical periodontitis: May result fromtraumatic occlusion, AP with acute pulpitis or an acuteexacerbation of CAP.

Pulpal diagnosis

15

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 veryminimal

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).

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,

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 system-

atically 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

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

11–13); 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

Fig. 5. Apical periodontitis with abscess.

Fig. 4. Chronic apical periodontitis.

Sigurdsson

16

neurofibers (only) that are normally active throughout

the dentin–pulp complex. Thus, complaints of sharp

provoked pain indicate mild and reversible inflamma-

tion 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 inflam-

matory 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 A-

fibers 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 inflam-

matory changes in deep class V preparations in canine

teeth, there was strong correlation between change in

the animal’s 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 comparedwith healthy pulps (38–40).

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 inflam-

mation 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

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

Pulpal diagnosis

17

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 frommyofacial 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).

Electric pulp tester (EPT)

The EPT uses electric current to stimulate the sensory

nerves of the dental pulp (47–49), specifically, the fast-

conducting 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).

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

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

Sigurdsson

18

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 distrib-

uted 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 themost 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

Table 1. Formulation of a pulpal diagnosis

Vital pulp

Symptom, test, supporting information Necrotic pulp Irreversible inflammation Reversible inflammation

Pulp test Negative Positive Positive

Key factors

Pulpal exposure Present Absent

Pain to percussion Present Absent

Related factors

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

Factors related to treatment plan

Age, periodontal disease, previous pulpal insults Questionable Questionable

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

Pulpal diagnosis

19

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 period-

ontium. A positive percussion test indicates inflamma-

tion 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

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

other diagnostic tests are used to differentiate period-

ontitis 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 radio-

graph will be most advantageous. If a vital tooth is

evaluated, a bitewing radiographwould 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 radio-

graphs 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-pathFig. 8. Percussion test.

Fig. 9. Palpation test.

Sigurdsson

20

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 dentino–enamel and denti-

no–pulpal interfaces using transmission and reflection

of sound from the dental hard tissues.

Crown surface temperature

Fanibunda (70–72) has performed extensive research

in the field of crown surface temperature. This pulp

vitality technique is based on the hypothesis that vital

teeth are warmer and will rewarm quicker after cooling

than non-vital teeth. Fanibunda’s experiments con-

cluded that time–temperature 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).

133Xenon radioisotope

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 700nm 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 full-

scale deflection at a given gain.

The technique appears objective, non-invasive and

accurate. A growing number of reports indicate that it

is a methodwhich can easily be adapted to the testing of

Fig. 10. Bite stent used for every radiography to ensurethat positioning is consistent.

Pulpal diagnosis

21

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 deox-

ygenated blood. This gives the percentage of oxygena-

tion 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 wave-

length 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

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 thick-

ness 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

verymuch of clinical significance in the decision of need

for endodontic care, only it needs to be remembered

Fig. 11. Laser Doppler flowmeter. Left set up andcomputer read out of pulp status. Right, probe showingthe small dimensions suitable for accurate placement onthe tooth.

Fig. 12. Dual wavelength spectrophotometer. Machineattached to recorder (left) and light source and detector(right).

Sigurdsson

22

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 SurgOral Med Oral Pathol 1970: 29: 102–116.

2. Seltzer S. Classification of pulpal pathosis.Oral SurgOralMed Oral Pathol 1972: 34: 269–280.

3. Morse DR, Seltzer S, Sinai I, Biron G. Endodonticclassification. J Am Dent Assoc 1977: 94: 685–689.

4. FullingHJ, Andreasen JO. Influence ofmaturation statusand tooth type of permanent teeth upon electrometricand thermal pulp testing procedures. Scand J Dent Res1976: 84: 291–296.

5. Heide S, Mjor IA. Pulp reaction to experimentalexposures in young permanent monkey teeth. Int EndodJ 1983: 16: 11–19.

6. Seltzer S, Bender IB, Zionitz M. The dynamics of pulpinflammation: correlation between diagnostic data andactual histologic finding in the pulp.Oral Surg Oral MedOral Pathol 1963: 16: 846–871.

7. Lundy T, Stanley HR. Correlation of pulpal histopathol-

ogy and clinical symptoms in human teeth subjected to

experimental irritation. Oral Surg Oral Med Oral Pathol1969: 27: 187–201.

8. Dummer PMH, Hicks R, Huws D. Clinical signs andsymptoms in pulp disease. Int Endod J 1980: 13: 27–35.

9. Garfunkel A, Sela J, Almansky M. Dental pulp pathosis:Clinicopathologic correlation based on 109 cases. OralSurg Oral Med Oral Pathol 1987: 35: 110–117.

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: 872–883.11. Barbakow F, Cleaton-Jones P, Friedman D. Endodontic

treatment of teeth with periapical radiolucent areas in ageneral practice. Oral Surg Oral Med Oral Pathol 1981:51: 552–559.

12. Bender IB. Reversible and irreversible painful pulpitides:

diagnosis and treatment.Aust Endod J 2000: 26: 10–14.13. Michaelson PL, Holland GR. Is pulpitis painful? Int

Endod J 2002: 35: 829–832.14. Hasler JE, Mitchell DF. Painless pulpitis. J Am Dent

Assoc 1970: 81: 671–677.15. Olgart LM.Neural control of pulpal blood flow.Crit Rev

Oral Biol Med 1996: 7: 159–171.16. Byers MR, Narhi MVO. Dental injury models: Experi-

mental tools for understanding neuroinflammatory

interactions and polymodal nocicpetor functions. CritRev Oral Biol Med 1999: 10: 4–39.

17. Hirvonen T, Hippi P, Narhi M. The effect of an opioidantagonist 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: 1366–1369.19. Casasco A et al. Peptidergic nerves in human dental pulp:

an immunocytochemical study.Histochemistry 1990: 95:115–121.

20. Dubner R, Ruda MA. Activity-dependent neuronalplasticity following tissue injury and inflammation.

Trends Neurosci 1992: 15: 96–103.21. Sigurdsson A, Maixner W. Effects of experimental and

clinical noxious counter irritants on pain perception.

Pain 1994: 57: 265–275.22. Narhi MVO, Hirvonen T, Hakumaki MOK. Activa-

tion of intradental nerves in the dog to some stimuliapplied 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 –

andC – fibers and human sensations. J Physiol 1987: 391:193–207.

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: Quin-tessence Publ., 1996, 136–140.

25. Hoshino et al. In-vitro antibacterial susceptibility ofbacteria taken from infected root dentine to a mixture of

Pulpal diagnosis

23

ciprofloxacin, metronidazole and minocycline. Int EndodJ 1996: 29: 125–130.

26. Iwaya S, Ikawa M, Kubota M. Revascularization of an

immature permanent tooth with apical periodontitis and

sinus tract. Dent Traumatol 2001: 17: 185–187.27. Strindberg LZ. The dependence of the results of pulp

therapy on certain factors. An analytic study based onradiographic and clinical follow-up examinations. ActaOdont Scand 1956: 14: 1177–1180.

28. Seltzer S, Bender IB, Zionitz M. The interrelationship of

pulp an periodontal disease. Oral Surg Oral Med OralPathol 1963: 16: 1474–1490.

29. Sjogren U, Hagglund B, Sundqvis G, Wing K. Factors

affecting the long-term results of endodontic treatment.

J Endod 1990: 16: 498–504.30. Bergenholtz G. Microorganisms from necrotic pulp of

traumatized teeth. Odont Revy 1974: 25: 347–358.31. Bender IB, Seltzer S. Roentgenographic and direct

observation of experimental lesions in bone. J Am DentAssoc 1961: 62: 152.

32. SjogrenU, FigdorD, Perssbon S, Sundqvist G. Influenceof infection at the time of root filling on the out come of

endodontic treatment of teeth with apical periodontitis.

Int Endod J 1997: 30: 297–306.33. Fouad AF, Rivera EM, Walton RE. Penicillin as a

supplement in resolving the localized acute apicalabscess. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 1996: 81: 590–595.

34. Okeson JP. Orofacial Pain. Chicago: Quintessence

Publishing Co, Inc, 1996.35. Olgart LM. The role of local factors in dentin and pulp

intradental pain mechanisms. J Dent Res 1985: 64: 572–578.

36. Lepinski M, Hargreaves KM, Goodis HE, Bowles WR.

Bradykinin levels in dental pulp by microdialysis. J Endod2000: 26: 744–747.

37. Chaisin-Chattipakorn S, Sigurdsson A, Light AR, Narhi

M, Maixner W. Trigeminal c-Fos expression andbehavioral responses to pulpal inflammation in ferrets.

Pain 2002: 99: 61–69.38. 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 pulptissue from painful and healthy human teeth. Int Endod J2002: 35: 30–36.

39. Bowles WR,Withrow JC, Lepinski AM,Hargreaves KM.

Tissue levels of immunoreactive substance P are in-

creased in patients with irreversible pulpitis. J Endod2003: 29: 265–267.

40. Narhi M, Jyvasjarvi E, Hirvonen T, Huopaniemi T.Activation of heat sensitive nerve fibers in the dental pulp

of the cat. Pain 1982: 14: 317–326.41. Grushka M, Sessle BJ. Application of the McGill pain

questionnaire to the differentiation of toothache pain.

Pain 1984: 19: 49–57.42. Sessle BJ. The neurobiology of facial and dental pain:

present knowledge, future direction. J Dent Res 1987:66: 962–981.

43. Glick DH. Locating referred pulpal pain.Oral Surg OralMed Oral Pathol 1962: 15: 613–623.

44. Travell J. Myofacial trigger points: A clinical view. In:

Bonica J, Albe-FessardD, eds.Advances in PainResearchand Therapy,Vol. 1. NewYork: Raven Press, 1976: 919–926.

45. Eli I. Dental anxiety: A cause for possible misdiagnosis oftooth vitality. Int Endod J 1993: 26: 251–253.

46. Klepac RK, Dowling J, Hauge G, McDonaldM. Reportsof pain after dental treatment, electrical tooth pulp

stimulation and cutaneous shock. J AmDent Assoc 1980:100: 692–695.

47. Bjorn H. Electrical stimulation of teeth and its applica-

tion to dentistry. Sven Tandlaek Tidskr 1946: 39(Suppl):39–45.

48. Reynolds RL. The determination of pulp vitality by

means of thermal and electrical stimuli. Oral Surg OralMed Oral Pathol 1966: 22: 231–236.

49. Seltzer S, Bender IB. The Dental Pulp, 3rd edn.Philadelphia: J.B. Lippincott, 1985.

50. Mumford JM. Evaluation of gutta percha and ethylchloride in pulp testing. Br Dent J 1964: 116: 338–342.

51. Narhi M, Virtanen A, Kuhta J, Huopaniemi T. Electricalstimulation of teeth with pulp tester in the cat. ScandJ Dent Res 1979: 87: 32–38.

52. McGrath PA, Gracely RH, Dubner R, Heft MW. Non-

pain and pain sensations evoked by tooth pulp stimula-

tion. Pain 1983: 15: 377–388.53. 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: 245–251.

55. Mumford JM. Thermal and electrical stimulation ofteeth in the diagnosis of pulpal and periapical disease.

Proc R Soc Med 1967: 60: 197–202.56. Lundy T, Stanley HR. Correlation of pulpal histopathol-

ogy and clinical symptoms in human teeth subjected to

experimental irritation. Oral Surg Oral Med Oral Pathol1969: 27: 187–201.

57. Fuss Z, Trowbridge H, Bender IB, Rickoff B, Sorin S.

Assessment of reliability of electrical and thermal pulptesting agents. J Endod 1986: 12: 301–305.

58. Fearnhead RW. The histologic demonstration of nervefibers in dentin. In: Andersen DJ, ed. Sensory Mechanismsin 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: 406–416.

60. Bender IB, Landau MA, Fonsecca S, Trowbridge HO.

The optimal placement-site of the electrode in electricpulp testing of the 12 anterior teeth. J Am Dent Assoc1989: 118: 305–310.

61. Brannstrom M, Astrom A. The hydrodynamics of the

dentine: its possible relationship to dentinal pain. IntDent J 1972: 22: 219–303.

62. Ingram TA, Peters DD. Evaluation of the effects of

carbon dioxide uses as a pulpal test. Part 2. In vivo effect

Sigurdsson

24

on canine enamel and pulpal tissues. J Endod 1983: 9:296–303.

63. Rickoff B, Trowbridge H, Baker J, Fuss Z, Bender IB.Effects of thermal vitality tests on human dental pulp.J Endod 1988: 14: 482–485.

64. Ehrmann EH. Pulp testers and pulp testing withparticular reference to the use of dry ice. Aust Dent J1977: 22: 272–279.

65. Narhi M. The characteristics of intradental sensory unitsand their responses to stimulation. J Dent Res 1985:64(Special Issue): 564.

66. BrannstromM, Johnson G.Movement of the dentin andpulp liquids on application of thermal stimuli. An in vitrostudy. Acta Odont Scand 1970: 28: 59–70.

67. Klausen B, Helbo M, Dabelsteen E. A differentialdiagnostic approach to the symptomatology of acutedental pain. Oral Sur Oral Med Oral Pathol 1985: 59:297–301.

68. Massler M. Pulpal reaction to dental caries. Int Dent J1967: 17: 441–460.

69. Barber FE, Lees S, Lobene RR. Ultrasonic pulse–echomeasurements in teeth. Arch Oral Biol 1969: 14: 745–751.

70. Fanibunda KB. A laboratory study to investigate thedifferentiation of pulp vitality in human teeth bytemperature measurement. J Dent 1985: 13: 295–303.

71. Fanibunda KB. The feasibility of temperature measure-ment as a diagnostic procedure in human teeth. J Dent1986: 14: 126–129.

72. Fanibunda KB. Diagnosis of tooth vitality by crownsurface temperature measurement: a clinical evaluation.J Dent 1986: 14: 160–164.

73. Howell RM, Duell RC,Mullaney TP. The determinationof pulp vitality by thermographic means using cholestericliquid crystals. Oral Surg Oral Med Oral Pathol 1970:29: 763–768.

74. Pogrel MA, Yen CK, Taylor R. Studies in tooth crowntemperature gradientswith theuseof infrared thermography.Oral Surg Oral Med Oral Pathol 1989: 67: 583–587.

75. Kim S, Schuessler G, Chien S. Measurement of bloodflow in the dental pulp of dogs with Xe-133 washoutmethod. Arch Oral Biol 1983: 28: 501–505.

76. Kim S, Dorscher-Kim J, Liu MT, Trowbridge H.Biphasic pulp blood flow response to substance P in thedog as measured with radiolabeled, microsphere injec-tion method. Arch Oral Biol 1988: 33: 305–309.

77. Trope M, Jaggi J, Barnett F, Tronstad L. Vitalitytesting of teeth with a radiation probe using 133xenon radioisotope. Endod Dent Trauma 1986: 2:215–218.

78. Holloway GA Laser Doppler measurement of cutaneousblood flow. In: Rolfe P, ed. Non-Invasive PhysiologicalMeasurements. London: Academic Press Inc., 1983: 11.

79. Gazelius B, Olgart L, Edwall B, Edwall L. Non-invasiverecording of blood flow in human dental pulp. EndodDent Trauma 1986: 2: 219–221.

80. Gazelius B, Edwall B, Olgart L, Lundberg JM, HokfeltT, Fisher JA. Vasodilatory effects and coexistence ofcalcitonin gene-related peptide (CGRP) and substance Pin sensory nerves of cat dental pulp. Acta Physiol Scand1987: 130: 33–40.

81. Mesaros SV, Trope M. Revascularization of traumatizedteeth assessed by laser Doppler flowmetry: Case report.Endod Dent Trauma 1997: 13: 24–30.

82. Wilder-Smith PE. A new method for the non invasiverecording of blood flow in human dental pulp. Int EndodJ 1988: 21: 307–312.

83. Yanpiset K, Vongsavan N, Sigurdsson A, Trope M.Efficacy of laser Doppler flowmetry for the diagnosis ofrevascularization of reimplanted immature dog teeth.Dent Trauma 2001: 17: 63–70.

84. Schnettler JM,Wallace JA. Pulse oximetry as a diagnostictool of pulpal vitality. J Endod 1991: 17: 488–490.

85. MillikanGA. The oxymeter, an instrument for measuringcontinuously the oxygen saturation of arterial blood inman. Rev Sci Inst 1942: 13: 434–437.

86. Wood EH, Geraci JE. Photoelectric determination ofarterial oxygen saturation in man. J Lab Clin Med 1949:34: 387–311.

87. Chance B. Rapid and sensitive spectrophotometry: III. Adouble beam apparatus. Rev Sci Inst 1951: 22: 634.

88. Nissan R, Trope M, Zheng C-D, Chance B. Dualwavelength spectrophotometry as a diagnostic test ofthe pulp chamber contents. Oral Surg Oral Med OralPathol 1992: 74: 508–514.

89. Barthel CR, Rosenkranz B, Leuenberg Roulet JF. Pulpcapping of carious exposures: treatment outcome after 5and 10 years: a retrospective study. J Endod 2000: 26:525–528.

90. Tronstad L, Mjor IA. Capping the inflamed pulp. OralSurg Oral Med Oral Pathol 1972: 34: 477–485.

91. Ikawa M, Komatsu H, Ikawa K, Mayanagi H, ShimauchiH. Age-related changes in the human pulpal blood flowmeasured by laser Doppler flowmetry. Dent Traumatol2003: 19: 36–40.

92. RubachWC,Mitchell DF. Periodontal disease, accessorycanals and pulp pathosis. J Periodontol 1965: 36: 34.

93. Mazur B, Massler M. Influence of periodontal disease onthe dental pulp. Oral Surg Oral Med Oral Pathol 1964:17: 592–599.

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