An endodontic conundrum:
• Highlights the anatomical link between
the association between pulpal
infection and periodontal disease
P. A. Heasman*1
This paper reviews the classification of periodontal-endodontic lesions and considers the pathways through which
inflammatory lesions or bacteria may communicate between the pulp and the periodontium. Such communications have
previously underpinned the classification of periodontal-endodontic lesions but a more up-to-date approach is to focus
specifically on those lesions that originate concurrently as pulpal infection (and necrosis) and periodontal disease on the
affected teeth. In doing so, both conventional periodontal and endodontic treatments are indicated for the affected teeth,
although more complex management strategies may occasionally be indicated.
INTRODUCTION
The periodontal-endodontic interface has
provided significant challenges for clinicians
over several decades. The diagnosis and
management of the so-called ‘periodontal-
endodontic’ group of lesions is based upon
the known continuum between the otherwise
anatomically distinct environments of the
dental pulp and the periodontal ligament.
This continuum, which is dependent upon a
series of anatomical communications, has of
course, not changed over time although our
knowledge and understanding of the impacts
of pulpal disease on the periodontium and
chronic periodontitis on the pulp most
certainly have. It is important to have
a thorough understanding of the basic
anatomy, the aetiology and the development
of periodontal-endodontic lesions (PEL) if
they are to be managed successfully and
for both clinicians and patients to be able
to confidently base decisions regarding
appropriate treatment options and long-term
prognoses for affected teeth.
CLASSIFICATION
While there have been a number of
attempts to classify PEL1–4 the most quoted
classification remains that of Simon et al.5
which was first published in 1972. This
classification is based on the observation
1
Professor of Periodontology, School of Dental Sciences,
Framlington Place, Newcastle upon Tyne
*Correspondence to: Professor Peter Heasman
Email: p.a.heasman@ncl.ac.uk
Refereed Paper
Accepted 27 November 2013
DOI: 10.1038/sj.bdj.2014.199
© British Dental Journal 2014; 214: 275-279
BRITISH DENTAL JOURNAL VOLUME 216 NO. 6 MAR 21 2014
PRIMARY ENDODONTIC LESION
PERIAPICAL INFECTION
PRIMARY ENDODONTIC
SECONDARY PERIODONTAL
LESION
‘TRUE’
COMBINED PERIODONTAL -
ENDODONTIC LESION
that most PELs will have originated in
either the pulp or the periodontium and
classifies the initial lesions as being primary
periodontal or primary endodontic lesions
respectively. As the inflammation spreads
from the original site the lesions develop
to effect secondary involvement of the
adjoining anatomical site, for example,
into a primary endodontic and secondary
periodontal lesion. When a PEL develops
simultaneously as periapical pathology
and chronic (or aggressive) periodontitis
then it is classified as a ‘true’, combined
periodontal-endodontic lesion. While this
classification has certainly stood the test
of time it is often difficult to confidently
compartmentalise PELs into one  of the
five  categories (Fig.1). This classification
identifies pulpal/periapical infection and
© 2014 Macmillan Publishers Limited. All rights reserved
IN BRIEF
the dental pulp and the periodontal
PRACTICE
ligament.
• Presents an update on the classification
of periodontal-endodontic lesions.
• Discusses the treatment options for
periodontal-endodontic lesions.
Fig. 1 Classification of
periodontal-endodontic
PRIMARY PERIODONTAL LESION lesions (based on
Simon et al. 1972)5. The
CHRONIC PERIODONTITIS ‘True’, combined lesion
is the only lesion that is
considered in the more
recent classification
of Abbott and Castro
PRIMARY PERIODONTAL
Salgado9 who then
make the distinction
SECONDARY ENDODONTIC
between endodontic
LESION and periodontal lesions
that do, or do not
communicate
periodontal infections as primary, separate
entities that may spread to cause secondary
infections. Where does a primary endodontic
lesion end and a primary endodontic with
secondary periodontal involvement begin?
It might also be considered unnecessary
and confusing to include the singular,
primary lesions in such a classification.
This classification was challenged as being
primarily ‘academic’ and of little help to
the clinician who needs to know the precise
clinical need of a tooth (teeth or patient)
before making an informed decision as to
the appropriate treatment(s) to offer.6
Interestingly, the American Academy of
Periodontology’s (AAP) 1989 classification
of gingival and periodontal diseases did
not recognise the association between
periodontal and endodontic disease and it
275
 PRACTICE
was only in 1999 that the AAP workshop
included the simple term ‘periodontitis
associated with endodontic lesions – a
combined periodontal-endodontic lesion’.7,8
The consensus opinion was to propose a
classification that was not based on such
extensive ‘compartmentalisation’ of the
infections and a more recent classification
has also adopted this approach. 9 The
classification of Abbott and Salgado
focuses specifically on only those lesions
that are associated with both periodontal
and endodontic diseases that affect a tooth
or teeth simultaneously with the principal
distinction being whether or not the lesions
communicate with each other (Figs 2 and 3).
Thus there are only two possible categories
which, following clinical and radiographic
examinations facilitate the diagnosis and
therefore the management of the lesion:
• Concurrent endodontic and periodontal
disease without communication (Fig. 2)
• Concurrent endodontic and periodontal
disease with communication (Fig. 3).9
The former suggests a tooth that happens
to be affected by both pulpal and periodontal
disease at the same time and which requires
treatments targeting both causes; the latter can
be considered a lesion of singular aetiology (a
‘true’ periodontal-endodontic lesion) and for
which a considered judgement of prognosis
should be made before embarking on a more
intensive treatment regimen.
ANATOMICAL CONSIDERATIONS
Many of the classifications and the
management strategies for PELs have been
based upon the well-established anatomical
communications between the pulp and the
periodontium. It is pertinent to briefly review
these although the role of many of these
communicating pathways may not be as
crucial as once was believed.
Around 27% of teeth demonstrate lateral
or accessory canals. These can be found
along most parts of the root structure
with the majority (17%) being found in
the apical third, around 9% in the middle
third and 2% in the gingival third of the
root.10 The furcation region of molars has
the highest prevalence of accessory canals
with approximately 25% of molars showing
such features.11 It would appear, however,
that only around 10% of molars have
furcation canals that communicate directly
with the pulp chamber12 whereas up to 60%
have furcation canals that communicate
with the most coronal aspect of the root
canal.13 The potential relevance of these
canals is that they effect anastomoses
between the vast networks of capillary beds
in the pulp with the vascular supply to
276
the periodontal ligament, and in doing so
provide the opportunity for the spread of an
inflammatory lesion between the structures.
Another communication channel between
the pulp and the periodontium is through
patent dentinal tubules that may be exposed
at the cement-enamel junction due to
absence of cementum, or on a root surface of
a periodontally-involved tooth that has been
subjected to root surface instrumentation.
Unlike the accessory canals that transmit
blood vessels, however, the dentinal
tubules are occupied by the processes of
the odontoblasts and dentinal fluid, which
may underpin the symptoms of dentine
sensitivity.14 The role of dentinal tubules
in the aetiology of PELs is not necessarily
associated with spread of inflammation but
with the bacterial invasion and spread of the
microflora either from the root canal to the
periodontal ligament or from a periodontal
pocket in the opposite direction.15
The classification given in the previous
section 9 is based on an inflammatory
continuum that occurs only when a
progressing periodontal lesion and pulpal
infection extend to, and beyond the apex
of the tooth. This concurs with previous
histological evidence that suggests that
pulpal involvement from a PEL will only
develop once the periodontal lesion extends
to, and beyond the apex of the tooth.16
CONSEQUENCES OF
BACTERIAL INVASION
Both endodontic and periodontal infections
derive their microflora from the multitude of
organisms that reside in the oral cavity and
similar anaerobic conditions favour growth
of anaerobes both in the infected pulp and
periodontal pockets.17 This, together with
the numerous anatomical communications
between the pulp and the periodontium may
at least partly explain why these distinct
environments have similar microbiological
profiles.18–21 The dentinal tubules adjacent to
both the pulp and the diseased periodontium
may also be subject to bacterial invasion
from an adherent biofilm and even if the
contained organisms are unable to facilitate
free passage from one surface to the other,
they may still provide a potent reservoir of
persistent infection in a necrotic pulp or an
infected periodontal pocket.22–24 The invasion
of root dentine by bacteria, however, does
not necessarily imply that an inflammatory
periodontal lesion will initiate irreversible
pathological change in the pulp. Whether
or not the odontoblastic processes form
a protective barrier to bacterial exchange
is debatable 25 and although there is
histopathological evidence of pulpal change
in caries-free, periodontally-affected teeth,
BRITISH DENTAL JOURNAL VOLUME 216 NO. 6 MAR 21 2014
© 2014 Macmillan Publishers Limited. All rights reserved
Fig. 2 Radiograph of a 38-year-old patient
with generalised, moderately advanced
chronic periodontitis and affecting 47 which
demonstrates bone loss mesially and distally,
as well as a furcation involvement. 47 is also
non-vital and has extensive apical pathology
although the apical and periodontal lesions
remain separate and do not communicate9
Fig. 3 Radiograph of a 50-year-old
patient with generalised, advanced chronic
periodontitis affecting the entire dentition.
43, 31, 32, 37 and 38 are all non-vital
and demonstrate apical pathology as well
as periodontal involvement. The lesions are
communicating9 and as such, will compromise
the prognosis for the involved teeth
these are likely to be limited to fibrosis,
dystrophic calcifications and reduced
vascularity.14 Indeed, it has been suggested
that irreversible inflammatory change of the
pulp only occurs once the apical vessels have
become involved16 and this latter observation
would further corroborate the adoption of
a classification that distinguishes simply
between PELs that do or don’t communicate
in the vicinity of the apex of a tooth.9 These
observations have further been corroborated
by the findings of a classic animal study
that exposed root surfaces to experimental
periodontitis and found that while there
were concurrent pathological changes
in the pulp, these were mainly limited to
mild inflammation and secondary dentine
formation, again suggesting the pulp has an
inherent capacity to protect itself. Failure
to detect any accessory root canals implied
that the bacterial challenge would, most
likely, have occurred through patent dentinal
tubules.26 Furthermore, when extensive root
instrumentation that removed most of the
cementum was undertaken and followed by
further plaque accumulation there appeared to
be little, if any, additional pulpal pathology.26
Although the communication and passage
of inflammation between the pulp and the

Fig. 4a Periapical radiographs of a rotated
and grade 2 mobile 14, which clinically had
an associated sinus opening on the adjacent
attached gingiva. The radiograph taken along
the buccal-palatal axis suggests that the root
fillings in both roots appear to be adequate
Fig. 4b When the tube and film are
positioned so that the primary beam is in the
mesial-distal axis it becomes clear that the
root fillings are inadequately condensed and
not achieving apical seal
periodontal ligament is possible, it is when
the pulp has necrosed and an apical infection
has developed that the periodontium may
be further compromised. This relationship
between established periapical pathology
and periodontal disease has been evaluated
in several studies that have suggested
that teeth with necrotic pulps and apical
pathology can both exacerbate periodontal
disease and compromise healing following
non-surgical periodontal treatment. 27–29
For example, a cohort study of patients
with endodontically-involved, single
rooted teeth demonstrated an association
between periapical pathology and vertical
periodontal bone lesions. It was concluded
that intrapulpal infection, evident as
periapical radiolucency, may promote bone
loss and be considered a risk factor for
periodontal progression.29
BRITISH DENTAL JOURNAL VOLUME 216 NO. 6 MAR 21 2014
THE DIAGNOSIS OF PERIODONTAL-
ENDODONTIC LESIONS
The diagnosis of pulpal/periapical or
periodontal disease as distinct entities is
based on a thorough clinical examination
utilising pulp sensibility tests, percussion,
transillumination, test cavities, probing
pocket depths, an assessment of mobility,
and identification of bleeding and, or
suppurating pockets. 9,30 Occasionally, a
localised problem such as an extensive
periapical lesion that tracks coronally
through an otherwise healthy periodontal
ligament may present as a narrow sinus tract
and mimic periodontal disease. This might
be classified as a primary endodontic lesion
with secondary periodontal involvement5
although this would not be included in the
definition of a concurrent PEL suggested
earlier in this paper.9 Consequently, the
management would simply involve root
canal therapy of the affected tooth.
Concurrent PELs will usually affect a
single tooth although multiple affected teeth
may present in a patient where there has
been widespread dental neglect (Fig. 3). The
teeth involved may have extensive carious
lesions and large restorations and will
consequently fail to respond to sensibility
tests. There will be increased, wide-based
probing depths with bleeding or suppuration
from the pockets and the tooth may be
tender to percussion in the presence of an
acute apical or periodontal abscess (or both).9
Panoramic oral radiographs will reveal the
extent, morphology and the severity of the
periodontal bone loss and supplementary,
conventional or digital periapical films may
be exposed for those teeth which, on the
basis of clinical findings and the panoramic
film, appear to have apical pathology.31 A
periapical film will provide the required
definition to ascertain the apical extent of
the periodontal lesion (the point at which
the periodontal membrane space assumes
normal width) and the coronal margin of a
periapical lesion and thus help in identifying
whether or not the separate periodontal and
pulpal inflammatory lesions communicate.
Periodontal-endodontic lesions may be
associated with teeth having previously
been root filled and the limitations of
conventional (two-dimensional) periapical
radiographs must be recognised as they may
not correlate with the three‑dimensional
quality of a root filling.32 An apparently
well-condensed and well-adapted root
filling associated with a PEL may need to
be retreated if the long-term outcome for the
tooth is to be assured (Fig. 4). Furthermore,
when conventional, plain films fail to
provide sufficient diagnostic information
limited-volume, high-resolution cone beam
© 2014 Macmillan Publishers Limited. All rights reserved
PRACTICE
computed tomography may be justifiable
for assessing and treatment planning
periodontal-endodontic lesions.33
THE TREATMENT OF CONCURRENT
PERIODONTAL-ENDODONTIC
LESIONS
While this section will consider the
management of the concurrent PEL, it is
important to recall that infected or necrotic
pulps (or indeed lesions associated with
root perforations or failing root canal
therapy) may lead to a narrow sinus tract
that mimics a periodontal pocket. Because
the aetiology of such lesions is pulpal in
origin, the indicated treatment is root canal
therapy (or replacement of a root filling(s)
where a previous treatment appears to have
failed and the infection has persisted) or,
where indicated, an attempted repair of a
perforated root. Long-term follow-up and
monitoring is required to assess healing and
to assess whether apical surgery or perhaps
extraction may be indicated should the
infection persist.
Similarly, if a vital tooth affected
by periodontal disease develops pulpal
symptoms then periodontal treatment is the
priority intervention, again with long-term
follow-up to ensure that what is likely to
be only a mild inflammatory reaction of
the pulp (which may exacerbate after root
instrumentation) resolves as the vital pulp
resists the spread of inflammation from the
periodontal lesion.
Thus concurrent periodontal-endodontic
infections that don’t communicate should
be managed by root canal therapy to
eliminate the source of pulpal infection and
instrumentation of root surfaces that are
then less likely to communicate residual
infection through dentinal tubules or
accessory canals.9
Before embarking on treatment of lesions
that communicate, however, it would be
pragmatic to ascertain the patient’s perspective
and views on treatment of the tooth, which
may carry no guarantee of long-term success;
and particularly so where multiple teeth may
be affected and considered to be unrestorable,
and where extraction would be the preferred
option. While there is evidence that root canal
treatment alone is a cost-effective approach
compared to extraction and restoration of
the space,34 there are no data available that
establish the cost-effectiveness of an approach
that may be expensive in terms of both time
and money and particularly so when advanced
management strategies may be indicated.
The initial objective for those PELs that
communicate should be to disinfect the
entirety of the affected site as quickly and
effectively as possible and by engaging a
277
 PRACTICE
strategy of shared care between dentist and
hygienist. The best approach would be to
manage the endodontic and periodontal
infections ‘aggressively’ and simultaneously:
initially thorough root instrumentation of
the periodontal site and application of
local delivery antimicrobials; together with
removal of the necrotic pulp, initial cleaning
and shaping of the root canal with liberal
irrigation and application of endodontic
medicaments such as non-setting calcium
hydroxide, Ledermix or TreVitaMix.
Placement of the definitive root filling
should be delayed until the healing response
to periodontal management can be assessed
after three to six months (Fig. 5).
At this point it is worth noting that the
channels of communication between the pulp
and the periodontium, the accessory canals,
dentinal tubules and the apical foramen,
which have thus far been a hindrance,
may now work in favour of the clinician.
Although there is as yet no evidence to
suggest that antimicrobials delivered locally
to periodontal pockets can influence bacteria
that may have invaded root dentine there
is some evidence to suggest that bacterial
inhibition can occur after penetration
through dentine of antimicrobials that
have been placed in the pulp. This effect
also seems to occur irrespective of whether
or not the cementum layer has been
removed through root instrumentation. It
is conceivable, therefore, that medicaments
placed in the pulp and then renewed on a
regular basis will contribute to disruption of
root surface microorganisms and healing of
the periodontal site.35
From the periodontal viewpoint, teeth
with extensive PELs may require more
complex management strategies to improve
the likelihood of long-term success. For
example, in cases where only one  root of
a molar appears to be affected then there
is an option of root resection of an upper
molar or hemi-section of a lower molar
following placement of the definitive root
filling. In such cases, the remaining root(s)
should have sufficient periodontal support
to maintain the tooth in function and the
procedures are usually limited to cases
where the objective is to maintain an intact
dental arch, function or a key tooth that
may ultimately be helpful as an abutment
for a fixed or removable prosthesis.
Similarly, when a definitive root filling
has been placed, symptoms and signs of
infection have resolved, but a furcation
lesion or a deep vertical defect persists,
then an exploratory surgical procedure
may reveal a periodontal morphology that
is conducive to a periodontal regenerative
procedure.
278
Fig. 5 A non-mobile, functional 26 with a
communicating periodontal-endodontic lesion.
The initial phase of periodontal treatment
and root canal therapy has stabilised the
tooth, which is symptom free. Further
treatment options include periodontal surgery
with guided tissue regeneration or root
resection. Note the sealant extruded from
the mesiobuccal canal has migrated along the
communication between the periodontal and
endodontic lesions.
PROGNOSIS
The long-term, successful prognosis for teeth
with periodontal-endodontic lesions depends
on a number of crucial and key factors
including the severity and extent of the
initial periodontal and periapical infections,
correct treatment planning and decision-
making, the skill and experience of the
clinician(s) and the motivation of the patient,
particularly with long-term periodontal care.
It would seem logical to suggest that
the prognosis for any tooth affected by
lesions that communicate as a single,
extensive infection must be guarded at
best as the outcome ultimately depends on
both successful periodontal and endodontic
management. There are, as yet, few data
available on the long-term outcomes for
teeth affected by PELs. One study, however,
identified teeth as having hopeless prognoses
as a consequence of PELs with attachment
loss to their apices.36 The teeth were treated
endodontically and periodontally with the
latter including a surgical approach with
periodontal regenerative procedures. After
five years, 23 out of 25 teeth were maintained
in situ in good health and function and 83%
were free from any complications during the
review period. While one has to be careful
not to conclude that all teeth with hopeless
prognoses should be managed this way, these
data do demonstrate the remarkable healing
potential of the perio-pulpal complex.36
The considerable data on the ten-year
outcomes of teeth having been root resected
are also favourable and show tooth retention
rates in the region of 60‑100%.37–41 But again,
it must be emphasised that such outcomes are
usually achieved with extremely motivated
patients who have been treated by experienced
clinicians and under ideal conditions.
BRITISH DENTAL JOURNAL VOLUME 216 NO. 6 MAR 21 2014
© 2014 Macmillan Publishers Limited. All rights reserved
CONCLUSION
Periodontal-endodontic lesions present
on teeth that are affected concurrently by
periodontal and pulpal infections, which
lead to pulpal necrosis and attachment loss
respectively. These lesions may or may not
communicate in the vicinity of the apex of
the tooth. Both endodontic and periodontal
treatments are indicated in the first instance,
although where lesions are more advanced,
the long-term prognosis may be improved by
careful treatment planning and scheduling
more complex management strategies
such as root resection and periodontal
regeneration.
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PRACTICE
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39. Carnavale G, Pontoriero R, Di Febo G. Long-term
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