J Clin Periodontol 2002: 29: 781–783 Copyright C Blackwell Munksgaard 2002

Printed in Denmark . All rights reserved

0303-6979

Case Report

Endoperiodontal lesion Stefano Sartori, Maurizio Silvestri

and Vitaliano Cattaneo
UDA Periodontology & Maxillofacial Surgery,
A case report S. Matteo Hospital, Pavia, Italy

Sartori S, Silvestri M, Cattaneo V. Endoperiodontal lesion. J Clin Periodontol

2002; 29: 781–783. CBlackwell Munksgaard, 2002.

Abstract
The purpose of this case report is to present an unusual endoperiodontal lesion
on tooth 46 in an 8-year-old child. The absence of any carious process and the
presence of the typical radiographic aspect of an infrabony defect, led us to con-
sider the periodontal aetiopathogenesis. In spite of all this, an accurate peri-
odontal probing of all the teeth and the use of the pulp tester for teeth 46 and Key words: endoperiodontal lesion;
36 led us to diagnose properly a truly endodontic lesion. The endodontic treat- periapical lesion; pulp necrosis
ment of the involved tooth achieved the complete healing of the lesion. Accepted for publication 23 May 2001

Introduction
Apical foramina and accessory root ca-
nals can lead to the transmission of an
infection from the endodontic spaces to
the periodontium and vice versa. Every
time dentine is exposed to the oral en-
vironment, pulp reacts with a defensive
inflammatory reaction. In fact, when a
tooth is involved by a carious process
or restorative procedures, oral bacteria
or their components can arrive at the
pulp via dental microtubules. Often in
these cases, some typical signs of a peri-
odontal involvement can be observed.
In addition to thermal hypersensitivity,
pain caused by percussion, a slight en-
largement of the periapical periodontal
space may be radiographically detected
(Langeland 1987). If dental pulp does
not degenerate into a necrotizing pro-
cess, it reacts by producing reparative
dentine and, after removal of the aeti-
opathogenetic factor (e.g. carious
tissue), symptoms and periapical radio-
graphic signs should disappear.
Pulp necrosis is always associated
with a periapical response and its na-
ture, as many studies have demon-
strated, is microbiological (Bergenholtz
1974, Sundqvist 1976). After an initial
phase in which the pathologic phenom-
enon expands itself from the apical part
of the pulp to the periapical tissue, the
second phase may evolve in two poss-
ible ways: the formation of an acute ab-
scess or the establishment of a balance
between the bacterial challenge and the
host response (Yu & Stashenko 1987,
Stashenko & Yu 1989). This balance
consists of an inflammatory process
that leads to the formation of a richly
vascularized granulation tissue, which
is infiltrated by different inflammatory
cells (Stashenko 1995, Nair 1987, Mar-
ton & Kiss 1993). The inflammatory
tissue may stay the same size for many
years or can increase, sometimes be-
coming a cystic lesion. An abscess may
arise every time the balance between
bacteria and the host breaks down. The
radiographic aspect of the periodontal
response to the pulp necrosis and bac-
terial contamination consists of an area
of radiolucency generally localised in
the proximity of the apical foramen or
sometimes the accessory lateral endo-
dontic canals. Lateral canals contain
vessels and connective tissue. The width
of lateral canals is reduced by continu-
ous deposition of dentine and root ce-
mentum, which could explain why lat-
eral endodontic lesions are more fre-
quent in young permanent molars with
infected pulp than in the molars of
adults. Many authors have studied the
location and the frequency of lateral ca-
nals in permanent teeth, finding the
highest concentration in the apical part
of the root and at the furcation level
(Lowman et al. 1973, Burch & Hulen
1974, Koenigs et al. 1974, Vertucci &
Williams 1974, De Deus 1975, Gut-
mann 1978). Periapical acute manifes-
tations due to canal infections can in-
crease in size, causing a progressive de-
struction of the periodontal apparatus.
If this lesion evolves into an abscess the
suppurative exudate tries to find a
drainage to the gingival sulcus (or peri-
odontal pocket), generally through the
periodontal ligament or perforating the
bone wall and running, in this last case,
along the soft tissues. When the endo-
dontic infection drains through the
periodontal ligament, a typical narrow
and deep probing site can be detected
or, rarely, as in the reported following
case, an unusual extensive destruction
of the periodontal tissue. Even in this
latter case, if the origin of the lesion is
truly endodontic, a proper endodontic
treatment will lead to a complete heal-
ing of the periodontal tissues.
Case report
An 8-year-old male was referred to our
attention for a deep pocket (16 mm)
(Fig. 1) all along the buccal and distal
aspect of the 46. The absence of any
carious process was verified, the pulp
782 Sartori et al.
Fig. 1. A 16 mm probing depth at time 0.
Fig. 2. Tooth 46 at time 0 after the cavity test.
Fig. 3. Four months after the treatment with
Ca(OH)2.
tester and the cavity test confirmed the
vitality of the tooth but with a slightly
inferior response with respect to the 36.
A wide periodontal defect involving the
furcation (Fig. 2) could be observed
radiographically at the distal aspect of
the mesial root (except 1 mm apically)
and the bone around the distal root, ex-
cept for its most apical portion. No
deep caries or fractures had been de-
tected and the history had not revealed
any traumatic injuries in the past few
years.
For these reasons one of the diagnos-
tic hypotheses was a periodontal lesion.
This diagnosis was reinforced by the
typical morphology of the defect, the
wide extension of the probing site all
along the buccal and distal aspect of the
Fig. 4. Eight months after Ca(OH)2 appli-
cation.
Fig. 5. Eight months after the final endodon-
tic treatment.
Fig. 6. Probing depth of 5 mm 8 months after
the final endodontic treatment.
tooth, the absence of deep caries and
the positivity of the pulp tester and cav-
ity test.
The probing of all the other primary
and permanent teeth revealed probing
depths ⱕ3 mm. The pulp tester applied
to tooth 46 revealed a slightly inferior
response compared to tooth 36. There-
fore another diagnostic hypothesis was
partial pulp necrosis of a not well
known nature, involving the most co-
ronal portion of the pulp, which could
have promoted the periodontal involve-
ment through the wide lateral canals
present in such young patients, espe-
cially at the furcation level (Lowman
et al. 1973, Burch & Hulen 1974, Ko-
enigs et al. 1974, Vertucci & Williams
1974, Gutmann 1978). In spite of the
unclear nature of this supposed endo-
dontic lesion, we decided to perform an
endodontic treatment.
The first step in our therapeutic plan
was initially to promote the apex for-
mation by means of Ca(OH)2. After
opening the pulp chamber, the non-vi-
tal pulp tissue was removed and the en-
dodontic spaces were shaped by Nickel
Titanium instruments (LightspeedA??)
and washed out with a sodium hypo-
chlorite 5% solution. After an accurate
drying of the canals they were filled
with a pure Ca(OH)2 powder. Four
months later (Fig. 3), we could detect a
partial apex closure and a reduction of
the lesion. It was decided to wait an-
other 4 months. Eight months later
(Fig. 4), apex formation was completed
and the original lesion disappeared. It
was decided to perform the final endo-
dontic treatment by filling the endodon-
tic spaces with vertically condensed gut-
tapercha. Eight months after the treat-
ment (Fig. 5), complete healing of the
periodontal tissues could be seen. At
this time, the probing attachment level
(PAL) was 5 mm (Fig. 6) with a PAL
gain of 11 mm. No periodontal treat-
ment was performed.
Conclusions
The morphology of the bone defect de-
tected in the X-ray and the probing
depth measured all along the buccal
and distal aspect of the involved tooth
seemed to indicate a diagnosis of the
periodontal origin of the lesion. How-
ever, the pulp vitality test, the history of
the patient and the healthy periodontal
state of all the other teeth strongly sup-
ported the endodontic nature of the de-
fect. Following endodontic treatment
with an appropriate healing period, the
PAL gain and the filling of the defect
detected by X-ray confirmed the purely
endodontic origin of the lesion.
This case report demonstrates that a
correct diagnosis is necessary for se-
lecting the best treatment plan and for
avoiding over-treatment.
Zusammenfassung
Der Zweck dieses Fallberichtes ist die Dar-
stellung einer ungewöhnlichen endoparodon-
talen Läsion an Zahn 46 bei einem 8 Jahre
alten Kind. Die Abwesenheit jeglicher kariö-
sen Läsion sowie das typische röntgenologi-
sche Bild eines infraalveolären Defekts führ-
ten ursprünglich zur Annahme einer paro-

dontalen Ätiopathogenese der Läsion.
Nachdem die Erhebung von Sondierungs-
parametern an allen Zähnen nur an Zahn 46
erhöhte Werte und Sensibilitätstests an Zahn
46 eine im Vergleich zu Zahn 36 verzögerte
Reaktion ergeben hatten, wurde die Diagno-
se einer primär endodontalen Läsion gestellt.
Allein die Wurzelkanalbehandlung von Zahn
46 führte zu einer vollständigen Ausheilung
des Defektes.
Résumé
Le but de ce rapport de cas était de présenter
une lésion endo-parodontale inhabituelle sur
une 46 chez un enfant de 8 ans. L’absence
de tout processus carieux et la présence d’un
aspect radiographique typique d’un défaut
intra-osseux nous a conduit à considérer une
étio-pathogènie parodontale. En dépit de
tout cela, un sondage parodontal précis de
chaque dent et l’utilisation d’un pulp-tester
sur les dents 46 et 36 ont permis de diagnosti-
quer vraiment une réelle lésion endodonti-
que. Le traitement endodontique des dents
impliquées entraı̂na la guérison complète de
la lésion.
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Address:
Dr Stefano Sartori
Via Scalabrini næ 9 31
29100 Piacenza
Italy
Tel: π39 328 9773427
Fax: π39 0523 314248
e-mail: stefano.sartori/unipv.it