Invited Review

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Endoperio lesion: Adilemma from 19th until

21stcentury
Abhishek Parolia, Toh Choo Gait1, Isabel C. C.M. Porto2, Kundabala Mala3
Faculty of Dentistry, Divison of Oral Clinical Sciences, 1School of Dentistry, International Medical University, Kuala
Lumpur, Malaysia, 2Department of Restorative Dentistry, Cesmac University Center, Macei, Alagoas, Brazil,
3
Department of Conservative Dentistry and Endodontics, Manipal College of Dental Sciences, Manipal University,
Mangalore, Karnataka, India

Address for correspondence: Dr. Abhishek Parolia, Email:abhishek_parolia@imu.edu.my

ABSTRACT
The interrelationship between endodontic and periodontal diseases has been a subject of speculation, confusion and controversy
for many years. Pulpal and periodontal problems are responsible for more than 50% of tooth mortality today. An endoperio
lesion can have a varied pathogenesis which ranges from quite simple to relatively complex one. These lesions often present
challenges to the clinician as far as diagnosis and prognosis of the involved teeth are concerned. It is very essential to make a
correct diagnosis so that the appropriate treatment can be provided. To make a correct diagnosis the clinician should have a
thorough understanding and scientific knowledge of these lesions and may need to perform restorative, endoontic or periodontal
therapy, either singly or in combination to treat them. Therefore, this presentation will highlight the diagnostic, clinical guidelines
and decisionmaking in the treatment of these lesions from an Endodontists point of view to achieve the best outcome.

CLINICAL RELEVANCE TO INTERDISCIPLINARY DENTISTRY

Perioendo lesions are very complex in nature and can have a varied pathogenesis.
Treatment decisionmaking and prognosis depend primarily on the diagnosis of the specific endodontic and/or periodontal diseases.
To have the best prognosis, clinician should refer the case to various areas of specialization, to perform restorative,
endodontic or periodontal therapy, either singly or in combination. Therefore, to achieve the best outcome for these
lesions, a multidisciplinary approach should be involved.
Key words: Diagnosis, endoperio lesions, management

INTRODUCTION

he pulpperiodontal interrelationship is a
unique one and can consider them as a
single continuous system or as one biologic unit in
which there are so many paths of communication.
The interrelationship of these structures influences
each other during health, function and disease.
They can get affected individually or combined;
when both systems are involved they are called true
endoperio lesions. Endodonticperiodontal problems
are responsible for more than 50% of tooth mortality
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DOI:
10.4103/2229-5194.120514

today.[1] They present challenges to the clinician as

far as diagnosis and prognosis of the involved teeth
are concerned. It is very essential to make a correct
diagnosis so that the appropriate treatment can be
provided. The relationship between the periodontium
and the pulp was first discovered by Simring and
Goldberg in 1964.[1] Since then, the term perioendo
lesion has been used to describe lesions due to
inflammatory products found in varying degrees in
both periodontium and pulpal tissues.
The pulp and periodontium have embryonic, anatomic
and functional interrelationship. There are various
pathways for the exchange of infectious elements
and irritants from the pulp to periodontium or vice
versa, leading to the development of endodontic
periodontal lesions.[2,3]
Pathways of developmental origin (anatomical
pathways):
Apical foramen, accessory canals/lateral canals
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Parolia, etal.: Endoperio

Congenital absence of cementum exposing dentinal

tubules
Developmental grooves
Pathways of pathological origin:
Empty spaces on root created by Sharpeys fibers
Root fracture following trauma
Idiopathic root resorptioninternal and external
Loss of cementum due to external irritants.
Pathways of iatrogenic origin:
Exposure of dentinal tubules following root planning
Accidental lateral root perforation during endodontic
procedures
Root fractures during endodontic procedures.
The main etiological factors for endoperio lesions are
living(bacteria, fungi and viruses) and nonliving pathogens.
Along with these, many contributing factors such as trauma,
root resorptions, perforations, and dental malformations
also play an important role in the development and
progression of such lesions[4,5][Figure1]. The condition of
the pulp is an important factor in susceptibility to microbial
invasion. Avital pulp is very resistant to microbial invasion.
Penetration of the surface of a healthy pulp by oral bacteria
is relatively slow or may be blocked entirely. In contrast,
a necrotic pulp is rapidly invaded and colonized by
bacteria. When the pulp becomes necrotic, inflammatory
byproducts of pulpal origin may leach out through these
pathways and initiate/trigger an inflammatory vascular
response in the periodontium, cause destruction of
periodontal tissue fibers, resorption of adjacent alveolar
bone and cementum. Nature and extent of periodontal
destruction depends on various factors such as virulence

of microorganisms, duration of the disease and the host

defense mechanism. Similarly, the reverse of the effect
of a necrotic pulp on the periodontal ligament, has been
referred to as retrograde pulpitis.[5]
Over the past century, the dental literature has
consistently reflected a controversy related to the effect
of periodontal disease on the dental pulp. It has been
found that the pulp has a quite sophisticated vasculature
system with a network of capillary beds, precapillary
sphincters and arteriovenous shunts, which provides a
significant capacity for the pulp to survive. From clinical
observations, it is rare to find a virgin tooth(no decay,
restorations, fracture, perforation) with evidence of
periapical pathosis for which cause for the pulp becoming
necrotic cannot be determined. Many studies have
demonstrated that periodontal disease or sequelae of
periodontal treatment does not affect the pulp.[68] On
the other hand, studies have suggested that the effect
of periodontal disease on the pulp is atrophic and
degenerative in nature including a decrease in number of
pulp cells, an increase in dystrophic calcifications, fibrosis,
as well as a direct inflammatory affect.[911] Therefore,
periodontal disease and periodontal treatments should
be regarded as potential causes of pulpitis and pulpal
necrosis. [12] However, It has been advocated that
periodontal disease has no effect on the pulp, unless it
extends all the way to the tooth apex, the dental pulp is
capable of surviving significant insults and that the effect
of periodontal disease as well as periodontal treatment
on the dental pulp is negligible.[13]
Though there are many conflicting studies abound,
Harrington etal.[14] mentioned another parameter which

Figure1: Etiological and contributing factors in endoperio lesions

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Parolia, etal.: Endoperio

may influence our clinical impressions related to the

dental pulp, and indeed many of our misinterpretations,
from early histological observations. They explained the
importance of adequate fixation of pulp tissue as it has
always been, and continues to be, a challenge, and artifacts
resulting from inadequate fixation continue to be described
as evidence of pathosis. They recommended careful
reviewing of the papers published prior to 1975, as well as
some written since if their descriptions of perceived pulp
pathosis are in fact simply histological artifacts.
Historically the effect of periodontal disease on the dental
pulp has been a source of discussion but recently the
effect of pulpal necrosis on the initiation and progression
of marginal bone loss has been discussed.[13] The potential
effect of a tooth with a necrotic pulp or a tooth with
previous root canal treatment has been taken into account
as a risk factor in the initiation, progression of periodontal
disease, and the resolution of periodontal pockets.
Many studies have stated that a pulpless tooth with a
periapical lesion promotes the initiation of periodontal
pocket formation, progression of periodontal disease,
and interferes with healing of a periodontal lesion after
periodontal treatment.[1517] It has also been found that
the periapical trauma may occur by over instrumentation
during shaping and cleaning of the root canal, extrusion
of irrigants, sealer and gutta percha points that may
hinder new bone, cementum and connective tissue repair.
Therefore, precautions should be taken when periodontal
therapy has to be followed by endodontic treatment.

CLASSIFICATION OF
PERIODONTALENDODONTIC LESIONS
The first classification of endodonticperiodontal lesions
based on pathology of origin was proposed by Simon
etal.[18] as follows:
Primary endodontic lesions
Primary periodontal lesions
Primary endodontic lesions with secondary periodontal
involvement
Primary periodontal lesions with secondary endodontic
involvement
True combined lesions.
Though Simon etal. have classified these lesions into
five types but actually three, four and five can be
considered as combined lesions. There have been many
classifications suggested by several other authors such
as independent periodontal and endodontic lesions[19]
or concomitant pulpal and periodontal lesions[20,21] to
describe endoperio lesions. In contrast to combined
perioendo lesions, concomitant pulpal and periodontal
lesions reflect the presence of two separate and distinct
disease states with different causative factors and with
no clinical evidence that one disease state has influenced
4

the other. Recently, von Arx and Cochran[22] proposed a

clinical treatment classification of perioendofurcation
lesions based on the role of membrane application in
endodontic surgery. Singh[23] classified endoperio lesions
based on the pathogenesis and added the term iatrogenic
lesions, usually endodontic lesions produced as a result
of treatment modalities. There are many classifications for
endoperio lesions, but for differential diagnostic purposes,
the socalled endoperio lesions are best classified as
endodontic, periodontal, or a combined disease.[24] These
lesions can also be classified by treatment depending
on whether endodontic, periodontal, or combined
treatment modalities are needed. All these classifications
are mainly based on the theoretic pathways explaining
how these radiographic lesions are formed. Therefore, by
comprehensive understanding of the pathogenesis and
investigations, the clinician can make a sound diagnosis,
formulate an appropriate treatment plan and assess the
prognosis of these lesions.

DIAGNOSIS
Nomenclature distinguishes between lesions caused by
periodontal pathogens, as seen in chronic periodontitis,
and lesions of the apical periodontal tissues associated with
endodontic pathology. When the location is distinct and the
lesion is discrete, the two are easy to differentiate. When
they simultaneously affect the marginal and apical areas of
the periodontium, thus making it essential to ascertain their
true cause through differential diagnosis.[25] If a patient has
been monitored over a period of time diagnosis of primary
endodontic disease and primary periodontal disease
usually can be easily done; once the lesions progress
to their final stage, they usually give similar clinical and
radiographic appearance and the differential diagnosis
becomes more challenging. For example, a similar in
clinical and radiographic features will be seen with both, a
growing periapical lesion with secondary involvement of
periodontal tissues and a longstanding periodontal lesion
that has progressed to the apex.
It is easier to determine the origin of the lesion when a
pulp vitality test is positive because this will rule out an
endodontic etiology. However, pulp tests may not be
always reliable. This consideration is particularly relevant
when challenges to pulpal status arise from periodontal
diseases such as partial necrosis of a pulp in a multirooted
tooth due to long standing periodontal lesions. If pulpal
necrosis is associated with inflammatory involvement of
the periodontal tissue, it presents a greater diagnostic
problem. In this situation, the location of these pulpal
lesions is most often at the apex of the tooth, but they may
also occur at any site where lateral and furcal canals exit
into the periodontium.[26] Therefore, accurate diagnosis can
be made by careful history taking, thorough oral hard and
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Parolia, etal.: Endoperio

soft tissue examination, the use of pulp testing procedures

and periodontal probing.[19]

The following steps help in diagnosing the exact lesion

[Table1].

Table1: Diagnostic procedures used to identify the endo-perio lesion

Examination/tests

Primary endodontic lesion

Primary periodontal
lesion

Primary endodontic
secondary periodontal

Primary periodontal
secondary
endodontic
Presence of plaque,
subgingival calculus
and swelling around
multiple teeth
Presence of pus,
exudate
Presence of
localized/
generalized gingival
recession and
exposure of root
Usually dull ache
Sharp only in acute
periodontal abscess
Pain on palpation

True combined
lesionorconcomitant pulpal
and periodontal lesions
Plaque, calculus and
periodontitis will be
present in varying degrees
Swelling around single or
multiple teeth
Presence of pus, exudate

Visual(magnifying loupes
and operative microscope
can be effective)

Soft tissuepresence of sinus

opening
Toothpresence of decay/
large restoration/fractured
restoration or tooth/
erosions/abrasions/cracks/
discolorations/poor RCT

Inflamed gingiva/gingival
recession around multiple
teeth
Accumulation of plaque
and subgibgival calculus
around multiple teeth
Intact teeth
Presence of swelling
indicating periodontal
abscess

Plaque forms at the

gingival margin of
the sinus tract and
leads to inflammation
of marginal gingiva
exudate
Root perforation/
fracture/misplaced
post

Pain

Sharp

Palpation(a positive
response to palpation may
indicate active periradicular
inflammatory process)
Percussion(it indicates the
presence of a periradicular
inflammation that may be
either from pulpal or PDL
origin)
Mobility(tooth mobility is
directly proportional to the
integrity of the attachment
apparatus or to the extent
of inflammation in the PDL
ligament)
Pulp vitality using cold test,
electric test, blood flow
tests, and cavity test(an
abnormal response may
indicate degenerative
changes in the pulp)
Pocket probing

It does not indicate whether

the inflammatory process is
of endodontic or periodontal
origin
Normally tender on
percussion

Usually dull ache

Sharp only in acute
condition
Pain on palpation

Usually sharp shooting

Dull ache in chronic
conditions
Pain on palpation

The sensitivity of the

proprioceptive fibers in
an inflamed periodontal
ligament will help identify
the location of the pain
Localized to generalized
mobility of teeth

Tender on percussion

Tender on
percussion

Tender on percussion

Localized mobility

Generalized mobility Generalized mobility with

higher grade of mobility
related to the involved
tooth

The pulp is vital and

responsive to testing

Pulp vitality tests

negative

Pulp vitality may

be positive in
multirooted teeth

A deep narrow solitary

Multiple wide and deep
pocket in the absence of
pockets
periodontal disease may
indicate the presence of a
lesion of endodontic origin or
a vertical root fracture

Presence of
solitary wide
pocket[Figure2ad]
but if periodontal
lesion is due to
fracture of root then
solitary deep narrow
pocket(mainly
localized)

Presence of multiple
wide and deep
periodontal pockets

Sinus tracing(by inserting

a semi rigid radiopaque
material into the sinus tract
until resistance is met)

A radiograph with gutta

percha points to apex or
furcation area in molars

Sinus tract mainly at the

lateral aspect of the root

Sinus tract mainly at

the apex or furcation
area

Radiographs

Presence of deep carious

lesions/extensive or defective
restorations/previous poor
root canal treatment/possible
mishaps/root fractures/root
resorption with peripical
radiolucency
Often, the initial phases of
periradicular bone resorption
from endodontic origin is
confined only to cancellous
bone. Therefore it cannot be
detected unless the cortical
bone is also affected
Painful response to the
patient at the time of
chewing, especially on
releasing the biting pressure

Vertical bone loss and

more generalized than
to lesions of endodontic
origin
Bone loss wider coronally

Presence of deep
carious lesions/
extensive or defective
restorations/previous
poor root canal
treatment/diminution
of the pulp canal space/
possible mishaps/root
fractures[Figure3a and
b]/root resorption with a
wide base radiolucency
around the apex of the
root[Figure4ae]

No symptoms

Painful response to the

patient at the time of
chewing, especially
on releasing the biting
pressure

Cracked tooth testing using

transillumination wedging
staining

Fractured roots and recently

traumatized teeth often
present high mobility

A lingering
responseirreversible pulpitis
No responsenecrotic
pulp(nonvital)

Dull ache usually

Only in acute conditions it
is severe
Pain on palpation

Usually negative because

of nonvital pulp. Vitality
tests may give a positive
response in multirooted
teeth

Probing reveals the typical

conical periodontal type of
probing with the exception
that at the base of the
periodontal lesion, the
probe will abruptly drop
further down the lateral
root surface and may even
extend to the apex of the
tooth
Sinus tract mainly at Difficult to trace out the
the lateral aspect of origin of the lesion, if a
the root
sinus tract is present, it
may be necessary to raise
a flap to determine the
etiology of the lesion
Angular bone loss in The radiographic
multiple teeth with a appearance of combined
wide base coronally endodonticperiodontal
and narrow at the
disease may be similar to
apex of the root
that of a vertically fractured
tooth

No symptoms

Painful response to the

patient at the time of
chewing, especially
on releasing the biting
pressure

RCT= Root canal therapy, PDL= Periodontal ligament

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Parolia, etal.: Endoperio

TREATMENT AND PROGNOSIS OF

ENDOPERIO LESIONS

Primary endodontic lesions

Primary endodontic diseases usually heal following root
canal therapy. The outcome of endodontic treatment is
influenced by the presence of microorganisms within the
root canal system. Good prognosis is to be expected if
treatment is carried out properly with a focus on infection
control. The sinus tract extending into the gingival sulcus

Treatment decisionmaking and prognosis depend primarily

on the diagnosis of the specific endodontic and/or periodontal
disease [Table 2]. The main factors to consider are pulp vitality
and the type and extent of the periodontal defect.

Table 2: Treatment map of endodontic-periodontal lesions

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Parolia, etal.: Endoperio

or furcation area disappears at an early stage once the

affected pulp has been removed and the root canals
well cleaned, shaped, and obturated. In case of tooth
with large periapical lesion, orthograde endodontic
therapy has been advised instead of surgical endodontic
therapy.[27,28] Placement of intracanal medicaments such
as calcium hydroxide has found to be very effective in
the healing of large periapical lesion. Calcium hydroxide
works in many ways, [29] chemically it damages the
microbial cytoplasmic membrane by the direct action
of hydroxyl ions, suppresses enzyme activity, disrupts
the cellular metabolism and inhibits deoxyribonucleic
acid(DNA) replication by splitting DNA. Physically it acts
as a physical barrier that fills the space within the canal
and prevents the ingress of bacteria into the root canal
system. It also kills the remaining microorganisms by
withholding substrates for growth and limiting space for
multiplication. Biologically it encourages the periapical
hard tissue healing around teeth with infected canals,
inhibits root resorption and stimulates periapical healing
after trauma.[3034]
Primary periodontal lesions
Primary periodontal disease should only be treated by
periodontal therapy. In this case, the prognosis depends
on the severity of the periodontal disease, efficacy of
periodontal therapy and patient response; however,
prognosis of primary periodontal lesions is not as favorable

as primary endodontic lesions. Primary periodontal

lesions should be treated by hygiene phase therapy
in the first instance. Subsequently, poor restorations
and developmental grooves that are involved in the
lesion must be removed. Periodontal surgery should be
performed after the completion of hygiene phase therapy
if deemed necessary. Since, the presence of an intact
cementum layer is important for the protection of the
pulp and vigorous surgical periodontal procedures may
remove cementum and expose dentinal tubules, which in
turn transport irritants, thereby cause pulpal inflammation
and necrosis of the dental pulp. Therefore, clinicians should
take precautions during periodontal therapy and avoid the
use of irritating chemicals, minimize the use of ultrasonics
and rotary scaling instruments when<2 mm of dentin
thickness remaining. Judicious use of periodontal surgical
intervention is advantageous to treat this lesions.[35]
Primary endodontic with secondary
periodontal lesions [Figure 2]
The treatment and prognosis of the tooth with these
lesions are different from those of teeth involved with
only primary endodontic disease. The prognosis for
treatment of primary endodontic disease with secondary
periodontal involvement depends primarily on the
severity of periodontal involvement. Tooth with these
lesions should first be treated with endodontic and
simple hygiene phase therapy. In this case, multivisit
endodontics should be practiced and the placement of
intracanal medicament was found to be very useful in
reducing inflammation and favoring repair.[36] Treatment
results should be evaluated in 23 months and only then
further periodontal treatment should be considered. This
sequence of treatment allows sufficient time for initial

Figure2: Primary endodontic lesion with secondary periodontal

involvement. (a) Clinical picture showing maxillary right first molar
with the presence of palatal swelling with 7mm deep periodontal
pocket mimicking primary periodontal lesion.(b) Radiograph showing
presence of deep coronal restoration and mesial caries approaching
the pulp with periapical radiolucency, confirming primary endodontic
lesion.(c) Radiograph showing completion of root canal therapy in
maxillary molar with periapical healing.(d) Clinical picture showing
complete resolution of periodontal pocket
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b
Figure3: Primary endodontic secondary periodontal lesion. (a) Intraoral
periapical radiograph showing root canal treated maxillary left first
premolar with radiolucency along the root. Clinically, a deep narrow
pocket was found on the mesial aspect of the root suggesting the
presence of vertical root fracture.(b) Clinical view of the extracted tooth
showing two fractured fragments of the tooth
7

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Parolia, etal.: Endoperio

Figure4: Patient complained of pus discharge from gums in between central incisors. Patient gave a history mild impact trauma on mandibular
anterior 10years ago.(a) Clinical picture showing the presence of sinus opening in between central incisors.(b) Radiograph of mandibular
anterior teeth showing the presence of large radiolucency in between central incisors with a wide base at the apex suggesting primary endodontic
lesion(both centrals did not respond to vitality tests).(c) Radiograph showing initiation of root canal therapy and placement of calcium hydroxide
as an intracanal medicament.(d) Radiograph showing completion of root canal treatment.(e) Radiograph showing healing after 1year

tissue healing and better assessment of the periodontal

condition. [37,38] It also reduces the potential risk of
introducing bacteria and their byproducts during the initial
phase of periodontal healing. In this regard, it has been
suggested that aggressive removal of the periodontal
ligament and underlying cementum during interim
endodontic therapy may adversely affect periodontal
healing, therefore, should be avoided.[39] But in cases
where healing with only endodontic therapy does not
occur then both endodontic and periodontal treatments
should be carried out since with endodontic treatment
alone, only part of the lesion may heal up to the level
of the secondary periodontal lesion. If the endodontic
treatment is adequate, the prognosis depends on the
severity of the marginal periodontal damage and the
efficacy of periodontal treatment. Primary endodontic
lesions with secondary periodontal involvement may
also occur as a result of iatrogenic damage such as root
perforation or fracture during root canal treatment or
placement of pins or posts. Root perforations are treated
according to their aetiology. The outcome of the treatment
of root perforations depends on the size, location, time of
diagnosis and treatment, degree of periodontal damage as
well as the sealing ability and biocompatibility of the sealer.
8

It has been recognized that the success of the treatment

depends mainly on immediate sealing of the perforation
and appropriate infection control. Several materials such as
mineral trioxide aggregate, reinforced zinc oxideeugenol
cementglass ionomer cements and Vitremer have been
recommended to seal root perforations. [4042] Root
fractures may also present as primary endodontic lesions
with secondary periodontal involvement. These typically
occur on roottreated teeth, often with post and crowns.
Treatment depends on the tooth type, extent, duration
and location of fracture, for example, single rooted tooth
with lesions caused by vertical root fracture has a hopeless
prognosis and should be extracted[43] while molars can
be treated by root resection or hemisection.[44] However,
many case reports are described in literature where many
innovative techniques to treat and retain anterior teeth
have been attempted with varying success. Clinician
have either removed the fractured segment or attempted
to bond the root using a biocompatible material.[4548]
Therefore, before considering any complex or extensive
restructure treatment, the desirability for retention of
the tooth root should be carefully weighed up against
extraction and replacement with a denture, bridge or
implant.
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Parolia, etal.: Endoperio

Primary periodontal secondary endodontic

lesion and true combined lesions
Primary periodontal disease with secondary endodontic
involvement and true combined endodonticperiodontal
diseases require both endodontic and periodontal
regenerative procedures. The success rate of the
endodonticperiodontal combined lesion without a
concomitant regenerative procedure has been reported
to a range from 27% to 37%. [49] Combined lesions
can be classified into three types, first, tooth with two
separate lesions, one endodontic usually periapical and
one periodontal with no communication, second, teeth
with a single lesion that involves both endodontic and
periodontal pathoses and third, teeth with endodontic
and periodontal lesions that were once separate but
now communicate. Truecombined lesions should be
treated initially as primary endodontic lesions with
secondary periodontal involvement. Prior to surgery,
palliative periodontal therapy should be completed and
root canal treatment carried out. The prognosis of true
combined lesion is often poor or even hopeless, especially
when periodontal lesions are chronic and extensive.
The prognosis of combined diseases mainly rests with
the ef ficacy of periodontal therapy. [5] Though, root
amputation, hemisection or bicuspidization may allow the
root configurations to be changed sufficiently for a part
of the root structure to be saved, however, the operator
need to consider various factors before root resection
such as tooth function, root filling, anatomy, restorability,
bone support around the healthy root and patients
compliance. Atooth that requires a root to be resected
always needs root canal treatment; therefore, the surgery
must be planned with care, particularly with respect
to the timing of the root treatment. Ideally, the tooth
should be root filled prior to surgery.[36] The prognosis
of an affected tooth can also be improved by increasing
bony support, which can be achieved by bone grafting
and guided tissue regeneration(GTR). These advanced
treatment options are based on responses to conventional
periodontal and endodontic treatment over an extended
time period. These regenerative procedures with the aid
of the microscope, in the treatment of combined lesions
have been found to have a success rate of 77.5%.[50]
GTR therapy was first introduced in 1980s since then
both human and animal studies have demonstrated
various degrees of regeneration of bone and attachment
apparatus.[51,52] GTR therapy has also been implemented
in the endodontic surgeries as a concomitant treatment
during the management of the endodonticperiodontal
lesions.[5356] The decisions and treatment strategy for
the application of the regenerative procedures are
made at various levels such as presurgical, postroot
canal treatment, intrasurgical, and postsurgical. Factors
influencing treatment outcome should also be considered
at each level under patientspecific, defectspecific,
Journal of Interdisciplinary Dentistry / Jan-Apr 2013 / Vol-3 / Issue-1

and healing categories.[57] The presurgical assessment

includes establishing and verifying the nonvital status
of the pulp, the extent and severity of the periodontal
destruction, and therapeutic prognosis of the planned
regenerative procedure. Once the therapeutic prognosis
of the periodontal regenerative procedure is determined
to be favorable, then endodontic therapy should be
provided. Root canal therapy helps to reduce the mobility
of the involved tooth therefore, after a successful root
canal therapy; tooth mobility should be further assessed to
determine the necessity for splinting. Cortellini etal.[58,59]
have recommended splinting of the mobile tooth before
GTR procedure. The intrasurgical assessment should
include morphology of the periodontal defect, defect
type, material of choice to fill the defect and augment
healing, control of patients oral hygiene, and wound
stabilization.[60,61] Furthermore, long term follow up
is mandatory for these lesions. However, advanced
diagnostic tests like cone beam computer tomography to
check the conditions of the hard tissues, pulse oximetry
for evaluate the true vitality, polymerase chain reaction
to identify the specific microbes may add value in proper
diagnosis. Cases should be well discussed to achieve
good prognosis.

CONCLUSION
A perioendo lesion can have a varied pathogenesis which
ranges from quite simple to relatively complex one. To
make a correct diagnosis the clinician should have a
thorough understanding and scientific knowledge of these
lesions. Despite the segmentation of dentistry into the
various areas of specialization, a clinician needs to perform
restorative, endodontic or periodontal therapy, either
singly or in combination. Therefore, to achieve the best
outcome for these lesions, a multidisciplinary approach
should be involved.

REFERENCES
1. Simring M, Goldberg M. The pulpal pocket approach: Retrograde
periodontitis. JPeriodontol 1964;35:2248.
2. Mjr IA, Nordahl I. The density and branching of dentinal tubules
in human teeth. Arch Oral Biol 1996;41:40112.
3. Zehnder M, Gold SI, Hasselgren G. Pathologic interactions in pulpal
and periodontal tissues. JClin Periodontol 2002;29:66371.
4. Sunitha VR, Emmadi P, Namasivayam A, Thyegarajan R, Rajaraman
V. The periodontalendodontic continuum: Areview. JConserv Dent
2008;11:5462.
5. Rotstein I, Simon JH. Diagnosis, prognosis and decisionmaking
in the treatment of combined periodontalendodontic lesions.
Periodontol 20002004;34:165203.
6. Jaoui L, Machtou P, Ouhayoun JP. Longterm evaluation of
endodontic and periodontal treatment. Int Endod J 1995;28:24954.
7. Torabinejad M, Kiger RD. Ahistologic evaluation of dental pulp
tissue of a patient with periodontal disease. Oral Surg Oral Med
Oral Pathol 1985;59:198200.
9

[Downloaded free from http://www.jidonline.com on Monday, January 18, 2016, IP: 5.14.30.141]

Parolia, etal.: Endoperio

8. Bergenholtz G, Nyman S. Endodontic complications following
periodontal and prosthetic treatment of patients with advanced
periodontal disease. JPeriodontol 1984;55:638.
9. Langeland K, Rodrigues H, Dowden W. Periodontal disease,
bacteria, and pulpal histopathology. Oral Surg Oral Med Oral Pathol
1974;37:25770.
10. Mandi FA. Histological study of the pulp changes caused by
periodontal disease. JBr Endod Soc 1972;6:802.
11. Petka K. The 14 warning signs. Endod Prac 2001;4:826.
12. Wang HL, Glickman GN. Endodontic and periodontic
interrelationships. In: Cohen S, Burns RC, editors. Pathways of the
Pulp.8th ed. St Louis: C. V. Mosby; 2002. p.65164.
13. Czarnecki RT, Schilder H. Ahistological evaluation of the human
pulp in teeth with varying degrees of periodontal disease. JEndod
1979;5:24253.
14. Harrington GW, Steiner DR, Ammons WF. The periodontalendodontic controversy. Periodontol 20002002;30:12330.
15. Jansson L, Ehnevid H, Lindskog S, Blomlf L. Relationship between
periapical and periodontal status. Aclinical retrospective study.
JClin Periodontol 1993;20:11723.
16. Jansson LE, Ehnevid H, Lindskog SF, Blomlf LB. Radiographic
attachment in periodontitisprone teeth with endodontic infection.
JPeriodontol 1993;64:94753.
17. Jansson L, Ehnevid H, Lindskog S, Blomlf L. The influence of
endodontic infection on progression of marginal bone loss in
periodontitis. JClin Periodontol 1995;22:72934.
18. S i m o n J H , G l i c k D H , F r a n k A L . T h e r e l a t i o n s h i p o f
endodonticperiodontic lesions. JPeriodontol 1972;43:2028.
19. H a r r i n g t o n G W, S t e i n e r D R . P e r i o d o n t a l e n d o d o n t i c
considerations. In: Walton RE, Torabinejad M, editors. Principles
and Practice of Endodontics. 3rd ed. Philadelphia: Saunders Co.;
2002.
20. Wang HL, Glickman GN. Endodotic and periodontic interelationships.
In: Cohen S, Burns RC, editors., Pathways of the Pulp.8th ed. St. Louis:
Mosby; 2002. p.65164.
21. Ammons WF, Harrington GW. The periodonticendodontic
continuum. In: Newman MG, Takei HH, Carranza FA, editors.
Carranzas Clinical Periodontology. 9 th ed. Philadelphia: W. B.
Saunders; 2002. p.84050.
22. von Arx T, Cochran DL. Rationale for the application of the GTR
principle using a barrier membrane in endodontic surgery:
Aproposal of classification and literature review. Int J Periodontics
Restorative Dent 2001;21:12739.
23. Singh P. Endoperio dilemma: Abrief review. Dent Res J (Isfahan)
2011;8:3947.
24. Rotstein I, Simon JH. The endoperio lesion: Acritical appraisal of
the disease condition. Endod Top 2006;13:3456.
25. Edoardo F. EndoPeriodontal Lesions. London: Quintessence
Publishing; 2011. p.12.
26. Meng HX. Periodonticendodontic lesions. Ann Periodontol
1999;4:8490.
27. Stock CJ. Endodontics in practice. Diagnosis and treatment planning.
Br Dent J 1985;158:16370.
28. Whyman RA. Endodonticperiodontic lesions. Part II: Management.
NZ Dent J 1988;84:10911.
29. Siqueira JF Jr, Lopes HP. Mechanisms of antimicrobial activity of
calcium hydroxide: Acritical review. Int Endod J 1999;32:3619.
30. Fava LR, Saunders WP. Calcium hydroxide pastes: Classification and
clinical indications. Int Endod J 1999;32:25782.
31. Rehman K, Saunders WP, Foye RH, Sharkey SW. Calcium ion
dif fusion from calcium hydroxidecontaining materials in
endodonticallytreated teeth: An invitro study. Int Endod J
1996;29:2719.
32. Lin YH, Mickel AK, Chogle S. Effectiveness of selected materials
against Enterococcus faecalis: Part3. The antibacterial effect of
calcium hydroxide and chlorhexidine on Enterococcus faecalis.
10

JEndod 2003;29:5656.
33. Evanov C, Liewehr F, Buxton TB, Joyce AP. Antibacterial efficacy of
calcium hydroxide and chlorhexidine gluconate irrigants at 37C
and 46C. JEndod 2004;30:6537.
34. Khan AA, Sun X, Hargreaves KM. Effect of calcium hydroxide
on proinflammatory cytokines and neuropeptides. JEndod
2008;34:13603.
35. Mhairi RW. The pathogenesis and treatment of endoperio lesions.
CPD Dent 2001;2:77104.
36. Carrotte P. Endodontics: Part9. Calcium hydroxide, root resorption,
endoperio lesions. Br Dent J 2004;197:73543.
37. Paul BF, Hutter JW. The endodonticperiodontal continuum revisited:
New insights into etiology, diagnosis and treatment. JAm Dent
Assoc 1997;128:15418.
38. Chapple IL, Lumley PJ. The periodontalendodontic interface. Dent
Update 1999;26:3316, 338, 340.
39. Blomlf L, Lindskog S, Hammarstrm L. Influence of pulpal
treatments on cell and tissue reactions in the marginal periodontium.
JPeriodontol 1988;59:57783.
40. Parir okh M, Torabinejad M. Mineral trioxide aggr egate:
Acomprehensive literature reviewPart III: Clinical applications,
drawbacks, and mechanism of action. JEndod 2010;36:40013.
41. Tsatsas DV, Meliou HA, Kerezoudis NP. Sealing effectiveness
of materials used in furcation perforation invitro. Int Dent J
2005;55:13341.
42. Weldon JK Jr, Pashley DH, Loushine RJ, Weller RN, Kimbrough WF.
Sealing ability of mineral trioxide aggregate and superEBA when
used as furcation repair materials: Alongitudinal study. JEndod
2002;28:46770.
43. Solomon C, Chalfin H, Kellert M, Weseley P. The endodonticperiodontal
lesion: Arational approach to treatment. JAm Dent Assoc
1995;126:4739.
44. Moule AJ, Kahler B. Diagnosis and management of teeth with vertical
root fractures. Aust Dent J 1999;44:7587.
45. Tamse A, Fuss Z, Lustig J, Kaplavi J. An evaluation of endodontically
treated vertically fractured teeth. JEndod 1999;25:5068.
46. Unver S, Onay EO, Ungor M. Intentional replantation of a vertically
fractured tooth repaired with an adhesive resin. Int Endod J
2011;44:106978.
47. zer SY, nl G, Deer Y. Diagnosis and treatment of endodontically
treated teeth with vertical root fracture: Three case reports with
twoyear followup. JEndod 2011;37:97102.
48. Hanada T, Quevedo CG, Okitsu M, Yoshioka T, Iwasaki N,
Takahashi H, etal. Effects of new adhesive resin root canal filling
materials on vertical root fractures. Aust Endod J 2010;36:1923.
49. Oh SL, Fouad AF, Park SH. Treatment strategy for guided tissue
regeneration in combined endodonticperiodontal lesions: Case
report and review. JEndod 2009;35:13316.
50. Kim E, Song JS, Jung IY, Lee SJ, Kim S. Prospective clinical
study evaluating endodontic microsurgery outcomes for cases
with lesions of endodontic origin compared with cases with
lesions of combined periodontalendodontic origin. JEndod
2008;34:54651.
51. Nyman S, Gottlow J, Karring T, Lindhe J. The regenerative potential
of the periodontal ligament: An experimental study in the monkey.
JClin Periodontol 1982;9:25765.
52. Nyman S, Lindhe J, Karring T, Rylander H. New attachment following
surgical treatment of human periodontal disease. JClin Periodontol
1982;9:2906.
53. Taschieri S, Del Fabbro M, Testori T, Saita M, Weinstein R.
Efficacy of guided tissue regeneration in the management of
throughandthrough lesions following surgical endodontics:
Apr eliminary study. Int J Periodontics Restorative Dent
2008;28:26571.
54. Britain SK, Arx TV, Schenk RK, Buser D, Nummikoski P, Cochran
DL. The use of guided tissue regeneration principles in endodontic
Journal of Interdisciplinary Dentistry / Jan-Apr 2013 / Vol-3 / Issue-1

[Downloaded free from http://www.jidonline.com on Monday, January 18, 2016, IP: 5.14.30.141]

Parolia, etal.: Endoperio

surgery for induced chronic periodonticendodontic lesions:
Aclinical, radiographic, and histologic evaluation. JPeriodontol
2005;76:45060.
55. Kerezoudis NP, Siskos GJ, Tsatsas V. Bilateral buccal radicular groove
in maxillary incisors: Case report. Int Endod J 2003;36:898906.
56. John V, Warner NA, Blanchard SB. Periodontalendodontic
interdisciplinary treatment:A case report. Compend Contin Educ
Dent 2004;25:6012,604.
57. Bashutski JD, Wang HL. Periodontal and endodontic regeneration.
JEndod 2009;35:3218.
58. Cortellini P, Tonetti MS, Lang NP, Suvan JE, Zucchelli G,
Vangsted T, etal . The simplified papilla preservation flap
in the regenerative treatment of deep intrabony defects:
Clinical outcomes and postoperative morbidity. JPeriodontol
2001;72:170212.

59. Schulz A, Hilgers RD, Niedermeier W. The effect of splinting of teeth

in combination with reconstructive periodontal surgery in humans.
Clin Oral Investig 2000;4:98105.
60. Tonetti MS, Prato GP, Cortellini P. Factors affecting the healing
response of intrabony defects following guided tissue regeneration
and access flap surgery. JClin Periodontol 1996;23:54856.
61. Trombelli L, Kim CK, Zimmerman GJ, Wikesj UM. Retrospective
analysis of factors related to clinical outcome of guided tissue
regeneration procedures in intrabony defects. JClin Periodontol
1997;24:36671.
How to cite this article: Parolia A, Gait TC, Porto IC, Mala K. Endo-perio
lesion: A dilemma from 19th until 21st century. J Interdiscip Dentistry 2013;3:
2-11.
Source of Support: Nil, Conflict of Interest: None declared.

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