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53
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contamination from periodontal fluids and blood, challenges in identifying and collecting pulp
tissue from appropriate control teeth, and the limited volume of vital tissue that can be collected
from inflamed dental pulps. A recent systematic review highlighted further issues with
biomarkers for pulpal diagnosis that further delay progress in the field(59). The review aimed to
calculate sensitivity, specificity and DOR of previously investigated pulpitis biomarkers and to
determine if biomarker levels discriminate between clinical diagnoses of pulpitis based on
presence or absence of spontaneous pain. As shown in Table3.2, IL-
8 and IL- 6 can discriminate
with high accuracy between healthy pulps and that with irreversible pulpitis. None, however, of
the biomolecule’s studies can differentiate between reversible and irreversible pulpitis, where
the distinction is needed most.
The decision to treat the dental pulp depends heavily on the results of sensibility testing, which, as
discussed before, may correlate poorly with the actual histopathology of the dental pulp under examination. In addition, these clinical testing methods are non-
Table3.2 Summary findings andevidence certainty forall outcomes using GRADE (59).
standardized and not objective. As a
Outcomes Impact
Diagnostic accuracy:
healthy versus
pulpitis with
spontaneous pain
Diagnostic accuracy:
pulpitis with
spontaneous versus
spontaneous
nonpain
Evaluate if the level
of biomarkers
correlates with and
can predict VPT
outcomes
The inflammatory
cytokines ILIL- 8have high sensitivity,
specificity and DOR to
discriminate between
healthy and pulpits with
spontaneous pain
suggestive of IRP, while the
diagnostic accuracy of
TNFα and IL-
None of the biomarkers
showed high sensitivity,
specificity or DOR to
discriminate between
pulpitis and spontaneous
versus nonpain. IL- 6 showed moderate
DOR with very wide
Confidence Interval (CI)
and no significant
difference in standardized
mean between spontaneous
versus non- spontaneous
pain
Limited data suggests high
levels of activemetalloproteinase 9
(MMP- 9) correlate with
poorer outcomes of full
coronal pulpotomy
6 and
1β is low
spontaneous
matrix
№ofparticipants
(studies)
IL-
6: 4 studies;
69healthy; 108 IRP
8: 4 studies;
IL77healthy; 91 IRP
5 studies; 100 healthy;
134 IRP
IL- 1β: 3 studies;
44healthy; 50 IRP
IL- 6: 2 studies; 77 RP
72 IRP
IL-
8: 2 studies; 77 RP
72 IRP
IL- 1β: 2 studies; 37 RP
33 IRP
TNFα: 2 studies; 77 RP
72 IRP
MMP- 9: 1 study;
40IRP, 10 healthy
Certaintyofthe
evidence(GRADE)
IL-
6 ⨁⨁◯◯ (b,c,d)
Low
IL- 8 ⨁⨁◯◯ (b,c,d)
Low
TNF α⨁◯◯◯ (c,d)
Very low
IL- 1β⨁⨁◯◯ (b,c,d)
Low
⨁◯◯◯(c,d)
Very low
⨁◯◯◯(c,d)
Very low
⨁◯◯◯(c,d)
Very low
⨁◯◯◯(c,d)
Very low
⨁◯◯◯(c,d)
Very low
(Continued)
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Pulpal Diagnosis54
Chairside (or adjacent lab) analysis for
biomarker of interest, for example MMP9
Level of biomarker compared with
established reference standar
Objective measure of pulpitis
obtained to inform clinician and
patient of treatment options
Sample taken using paperpoint,
microcapillary tube or other
collection vessel
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Table3.2 (Continued)
Outcomes Impact
№ofparticipants
(studies)
Certaintyofthe
evidence(GRADE)
GRADE Working Group grades of evidence:
High certainty: We are very confident that the true effect lies close to that of the estimate of the effect.
Moderate certainty: We are moderately confident in the effect estimate. The true effect is likely to be
close to the estimate of the effect, but there is a possibility that it is substantially different.
Low certainty: Our confidence in the effect estimate is limited. The true effect may be substantially
different from the estimate of the effect.
Very low certainty: We have very little confidence in the effect estimate. The true effect is likely to be
substantially different from the estimate of the effect
Downgraded due to high risk of bias on randomization and selection of reported results.
Observational studies upgraded due to effect size.
Downgraded due to lack of precision (small sample size)
Observational studies graded as low
With permission from Karrar etal.(59)/John Wiley & Sons.
consequence, endodontic diagnosis in many clinical situations can be challenging, and the resulting
treatment becomes a defensive reaction to simply extirpate the dental pulp. This dilemma is exacerbated when clinical diagnosis becomes difficult in real- case scenarios where the patient cannot identify the offending tooth in the arch, and the potential offending tooth has a full coverage restoration
(which makes pulp sensibility testing difficult) or a history of recent trauma, among others.
Measuring biomarker expression rather than relying on subjective responses to sensibility
testing may lead to a biologically based diagnostic tool that can stage pulpal inflammation,
which typically progresses from the coronal to the apical pulp (Figure 3.1). However, In the
Developing next-generation
pulp diagnostic tools using
blood and biological fluids
Figure3.1 Illustration of potential next- generation pulp diagnostic tests and customized therapeutics.
Reproduced with permission from Duncan(31).
Developing targeted pulp
capping materials aimed at
biological processes
d
e.g materials ‘doped’ with epigentic
modifiers, growth factors or inhibitors
Permanent
restoration
Dental
pulp
Odontoblast
Odontoblast-like cell
Progenitor cell
Blood vessel
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References 55
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absence of a clinical biomarker test to stage pulpitis into initial, mild, moderate and severe
inflammation (2, 33), direct observation of the dental pulp using magnification is recommended(3). The European Society of Endodontology’s position statement on the management
of deep caries and exposed pulp(33) recommends a detailed pain history and meticulous clinical
examination supplemented with a high- quality periapical radiograph and pulp sensibility testing using low-
temperature cold testing in combination with EPT are necessary to assess the
status of the pulp. The routine use of Cone Beam Computed Tomography (CBCT) is not justified
for assessing pulpitis. Vital pulps should be considered reversibly inflamed when the tooth is
symptomless or has sharp pain of short duration (<30 seconds), while irreversible pulpitis (partial or complete) is characterized by episodes of spontaneous, radiating pain that lingers after
removal of the stimulus.
Conclusion
Although fundamental for the provision of appropriate treatment, arriving at an accurate diagnosis of pulp disease is still challenging and problematic in everyday clinical practice. Relying on
subjective patients’ symptoms and diagnostic tools that are not fit for purpose are the major issues
that need to be addressed in future research in methods for pulpal diagnosis. Advances in pulp
biology and molecular diagnostics should be utilized for the development of novel chairside tests
that can accurately determine the degree of pulp inflammation and the healing potential of the
tissue that need to be maintained.
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52 Shin SJ, Lee W, Lee JI, Baek SH, Kum KY, Shon WJ, etal. Matrix metalloproteinase- 8 and
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59 Karrar RN, Cushley S, Duncan HF, Lundy FT, Abushouk SA, Clarke M, etal. Molecular
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8 changes in pulp tissue and gingival crevicular fluid samples of healthy
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Vital Pulp Treatment Modalities
The Management ofDeep Caries Using Selective andNon- Selective Removal
ofCarious Tissue, Stepwise Excavation andIndirect Pulp Capping
Helena Fransson1 and Lars Bjørndal
1
Department of Endodontics, Faculty of Odontology, Malmö University, Malmö, Sweden
2
Cariology and Endodontics, Section of Clinical Oral Microbiology, Department of Odontology, Faculty of Health and Medical Sciences,
University of Copenhagen, Copenhagen, Denmark
2
Introduction
When you first become a dentist and perhaps later pursue a career within a specialty, you are or
should be in your comfort zone. You are supposed to make qualified judgements and decisions and
carry out the treatments that are expected and evidence- based. You are an expert in the field. However,
acquired expertise is not permanent as the considered best choice of treatment for a given health
state may change over time, perhaps due to the impact of new research or a change in the demographics of the population. Within endodontics, the tradition has been to address two main domains:
the exposed vital pulp or the infected, necrotic root canal system associated with apical periodontitis.
In short, the prevention or treatment of apical periodontitis has been the focus of endodontics. The
question arises as to how far back in the disease development we would like to go to prevent apical
periodontitis. Does it include excavation of carious tissue in order to prevent pulp exposure?
Often, pulp inflammation has been described without the associated cause(1). In this chapter,
we will focus on caries being the cause of inflammation, as it is one of the main indications for
endodontic treatment(2, 3). An insight into the dynamics of the pulp inflammation due to progressing stages of caries is presented. Instead of simply presenting a case with a deep carious lesion
being the cause of further treatment, it seems relevant to describe the carious lesion in more detail.
Is it possible to introduce a threshold for deciding on the need for an invasive pulp treatment, or
would the prognosis of the tooth be improved if pulp exposure was avoided?
It is perhaps the norm that dentists limiting their practice to endodontics only receive referrals on
root canal treatments that often have already been initiated; perhaps an emergency treatment has
been performed or attempts to negotiate the root canals have been made. It is tempting to suggest that
these dentists rarely perform primary carious- tissue removal close to the pulp, even though such a
dentist should have extensive theoretical knowledge about the pulp and its healing capacity. However,
there is a trend within the endodontic field that dentists and endodontists should also have knowledge
on the treatment when pulp exposure should be avoided. This is important not only for pre- and
postgraduate students but also for the trained endodontist in educating and training general dentists.
The development and updating of clinical guidelines are examples of ways to help dentists to
keep up with any changes regarding established treatments and to inform about potential new
59
Vital Pulp Treatment, First Edition. Editedby Henry F.Duncan andIkhlas A. El-Karim.
© 2024John Wiley & Sons Ltd. Published 2024 by John Wiley & Sons Ltd.
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treatment concepts. In this chapter, recently updated publications on evidence and guidelines on
the treatment of deep carious lesions will be included. From the perspective of a general dental
practitioner, this should form part of being an engaged and motivated dentist. It is, however, a
difficult task to implement new knowledge and change the behaviours or traditions related to
treatment. At the beginning of this chapter, we will present the treatment modalities as well as the
indications based on a pragmatic subdivision of an extensive carious lesion into three classes.
VitalPulpTreatmentModalitiesAimingNottoExposethePulp
Based on understanding the biological concepts behind treatment recommendations, the goal is to
provide the reader with tools to adopt a minimally invasive approach, such as the vital pulp treatments in teeth with well- defined deep carious lesions, as outlined in Table4.1.
Indications–APragmaticSubdivisionofExtensiveCariousLesions
For the management of extensive carious lesions, the clinical dilemma is obvious, as the presence
of infected dentine is not an objective clinical measure. Concomitantly, it is not possible to monitor
the degree of pulpal inflammation at the chairside based on the patient’s symptoms or other clinical findings(5). So what is meant by a ‘deep carious lesion’. The traditional wording of ‘complete’
and ‘partial’ removal of carious tissue is not precise and has unclear elements, and you may speculate on what is actually meant when the words are used. Is it the partial removal of microorganisms
or demineralized dentine?
Table4.1 Definitions of the vital pulp treatment modalities presented in this chapter were modified after
a position paper from the European Society of Endodontology(4).
Treatment Definition
Non- selective
caries removal
Selective caries
removal
Selective caries
removal in
one-
stage
Stepwise
excavation
Indirect pulp
capping
Source: Adapted from the European Society of Endodontology.
Complete removal of soft and firm carious dentine from the periphery and central
aspects of the cavity until hard dentine is reached
A collective name for several treatments: selective caries removal in onestepwise excavation
Application of a biomaterial onto a dentine barrier in an indirect onecarious- tissue removal technique. Removal of soft or firm dentine. Immediate
placement of a permanent restoration
Application of a biomaterial in an indirect twotechnique. Temporary restoration placement between visits and re- entry after
6–12mo. The first stage involves selective carious removal to soft dentine to the extent
that it facilitates proper placement of a temporary restoration, and the second stage
involves removal to firm dentine– the final placement of a permanent restoration
Application of a biomaterial onto a thin dentine barrier in a oneremoval technique generally to hard dentine. Leaves neither soft nor firm carious
dentine behind. Considered more aggressive than selective carious- tissue removal in
one- stage and stepwise excavation. However, if the excavation is successful, pulp
exposure is avoided. The problem is that the frequency of unintended exposures will
be more frequent than for selective caries removal in one- stage or stepwise excavation
stage selective carious- tissue removal
stage and
stage selective
stage carious- tissue
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(a) (b)
(c)
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The International Caries Consensus Collaboration have carried out a comprehensive
qualitative analysis of the nomenclature for excavation and treatment options, attempting to
simplify the topic and making it more suitable for dental practice(6, 7). This practiceterminology on carious-
tissue removal is based on the features of the carious tissue and presented
based
in Figure4.1(8).
(c)
(d)
Figure4.1 Macroscopic view of an extracted tooth with a proximal extensive carious lesion (a) and a
longitudinal mesial/distal axial crosscut (b). Higher magnification shows the pre- cavitated enamel- dentine
lesion (c) originating from the occlusal surface with the following zones: i = demineralized enamel, ii = black/
dark brown discolouration of demineralized dentine, iii = light brown discolouration of demineralized
dentine (the darker zones reflects areas of arrested caries), iv = hypermineralized dentine equivalent to zone
of sclerosis, v = tertiary dentine. The proximal carious lesion (d) with the following zones: i = retrograde
enamel demineralization, which typically is seen in the proximity to the open dentine lesion, ii = soft, dark
brown dentine, iii = destructed dentine, iv = pulp close demineralized dentine, v = tertiary dentine. Selective
removal to soft or firm dentine would be in the area iv. Selective removal to soft dentine should not be
interpreted as a stop excavating within the destructed dentine, as seen in iii, as this area is too soft. The
definition of soft is that it can be excavated with minimum resistance to a hand excavator, and firm would be
resistant to hand instrumentation. Source: John Wiley & Sons, Inc.
(d)
i
ii
iii
iv
v
iii
ii
v
iv
i
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The common subdivision of caries diagnoses in thirds, denoting caries superficialis, media and
profunda is a widely accepted terminology(9). However, for extensive carious lesions, the
diagnosis
caries profunda can further be subdivided into three classes, which could be related to evidencebased treatments(10).
CariesProfunda1
Radiographic features: This stage is defined as a lesion penetrating 2/3–3/4 of the dentine, with a
radiopaque zone separating the advancing front of the lesion and the pulp.
Histologic features: Microorganisms are located in the carious dentine. Evidence of chronic
pulp inflammation, but not associated with invasion of microorganisms into the pulp cavity
(Figure4.2).
Recommended treatment: Selective carious removal in one step to either soft or firm dentine
(Figure4.3e–h). This particular lesion class is most often treated with a selective caries removal
strategy(11–13).
CariesProfunda2
Radiographic features: This stage, described as deep caries, is defined as a lesion penetrating 3/4 or
more of the dentine, but still with a radiopaque zone separating the advancing front of the lesion
and the pulp.
Histologic features: Microorganisms are located in the carious dentine. Evidence of chronic pulp
inflammation with a low probability of the presence of invading microorganisms in the pulp cavity
(Figure4.2).
Recommended treatment: Stepwise excavation (Figure 4.3a–d). Evidence for selective carious
removal in one step to either soft or firm dentine is available but mainly based on children and
adolescent patients. See also Table4.1(13).
CP1
Figure4.2 Schematic drawing of a cavitated coronal carious lesion. In Caries Profunda (CP) 1, the
microorganisms are located in the carious dentine. There is evidence of pulp inflammation, but
microorganisms are not invaded into the pulp cavity. Without any intervention, the process will develop, and
in CP2, the bulk of microorganisms are still located in the carious dentine, and there is pulp inflammation,
as indicated by the pink zone. At this stage, there is a low probability of invading microorganisms in the
pulp cavity. However, from this point, a spread along the enamelcarious lesion has progressed further, and microorganisms are in the carious lesion extending into the
tertiary dentine and are also present within the pulp cavity (purple zone). The pulpal status includes severe
inflammation, and the pulp in the proximity of the carious lesion is partially or fully necrotic. At CP3, a pulp
invasive treatment is needed. Green indicates cariogenic microbiota and yellow dentine demineralization.
Light grey reflects demineralized enamel, and dark grey is the hypermineralized zone in the dentine. A basic
sketch is available from smart.servier.com. Source: With permission from Karger.
CP2 CP3
dentine junction is noted. In CP3, the
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