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98 TMJ 2008, Vol. 58, No. 1

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REVIEW ARTICLES
abstract
Received for publication: Feb. 22, 2008. Revised: May 19, 2008.
rEZUMat
1
Department of Anatomy and Embryology,
2
Department of Endodontology,
Faculty of Dental Medicine, Carol Davila University of Medicine and Pharmacy,
Bucharest, Romania,
3
Department of Periodontology, Faculty of Dental
Medicine, Victor Babes University of Medicine and Pharmacy, Timisoara,
Romania,
4
Department of Oral Rehabilitation, Faculty of Dental Medicine, Carol
Davila University of Medicine and Pharmacy, Bucharest, Romania,
5
Department
of Orthodontics, Faculty of Dental Medicine, Victor Babes University of Medicine
and Pharmacy, Timisoara, Romania
Correspondence to:
Andreea Didilescu, 2 Iovita Str., Bl. P24, Apt. 32, Bucharest, Tel. + 40-722-536-798
Email: andreea.didilescu@gmail.com
INtrODUctION

The dental pulp is closely connected with the
periodontal ligament through the apical foramina,
accessory canals and dentinal tubules. Due to this
relationship, pulp diseases may infuence periodontal
health and vice versa, and the periodontal infection
may affect the pulp integrity. It is estimated that pulpal
and periodontal problems are responsible for more
than 50% of tooth mortality.
1
cUrrENt cONcEPts ON tHE rELatIONsHIP
bEtWEEN PULPaL aND PErIODONtaL DIsEasEs
Andreea Didilescu
1
, Radita Iliescu
2
, Darian Rusu
3
, Alexandru Andrei Iliescu
4
,
Alexandru Ogodescu
5
, Emilia Ogodescu
5
, Stefan Stratul
3
Combined endodontic-periodontal lesions represent a real challenge in the daily practice, both for the endodontist and periodontologist. The simultaneous
existence in the same tooth of pulpal problems and inflammatory periodontal disease can complicate the diagnosis and the treatment of the affected tooth. This
type of pathology represents a special situation in dentistry due to the complexity of anatomy and physiology of the pulp and periodontium. In this review, current
topics relating to etiology, pathways of dissemination and clinical concepts in combined endo-periodontal lesions are summarized. The poor prognosis of these
affections recommends an interdisciplinary approach with a good collaboration between specialists in endodontology, periodontology and microbiology.
Key Words: pulp infection, periodontal infection, bacterial migration
Leziunile combinate endo-parodontale reprezint\ o adevarat\ provocare n practica medicala curent\, att pentru specialistul n endodon]ie, ct [i pentru cel n
parodontologie. Existen]a simultan\ a problemelor pulpare [i parodontale la acela[i dinte poate complica diagnosticul [i tratamentul planificat pentru dintele
respectiv. Acest tip de patologie reprezint\ o situa]ie special\ datorit\ complexit\]ii anatomiei [i fiziologiei pulpare [i parodontale. Lucrarea prezent\ [i propune
s\ revizuiasc\ informa]iile din literatura de specialitate despre etiologie, c\i de diseminare [i aspecte clinice n leziunile endo-parodontale. Prognosticul rezervat
al acestor afec]iuni recomand\ o abordare interdisciplinar\, cu o bun\ colaborare ntre speciali[tii n endodon]ie, parodontologie [i microbiologie.
Cuvinte cheie: infec]ie pulpar\, infec]ie parodontal\, migrare bacterian\
Simon et al. (1972) have classifed the lesions based
on the primary source of infection, as follows:
2
1. Primary endodontic lesions;
2. Primary endodontic lesions with secondary
periodontal involvement;
3. Primary periodontal lesions;
4. Primary periodontal lesions with secondary
endodontic involvement;
5. True combined lesions.
In addition, Belk and Gutmann (1990) proposed
a sixth group of lesions - concomitant pulpal and
periodontal lesions.
3
EtIOLOGY
It has been demonstrated that the primary etiologic
agent in periodontitis is bacterial plaque adhering to
the teeth and other hard surfaces in the oral cavity. The
pulp may be affected by the invasion of bacteria or
their toxins, or by a direct trauma during the restorative
therapy.
4,5

Several factors make it diffcult to establish a correct
etiology of the combined endo-periodontal lesions.
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Andreea Didilescu et al 99
First, the pulpal pain may occur either in a primary
endodontic lesion or in a primary periodontal lesion
with secondary endodontic involvement. In the last
situation, the periodontal symptoms may be masked
by the pulpal symptoms. Second, the tests used for the
diagnosis of endo-periodontal lesions, such as vitality
tests and radiographic examinations, may lead to an
incorrect or incomplete diagnosis.
MIcrObIOLOGY
The literature contains few descriptions of the
periodontal-endodontic lesion microbiology. The
profles of the periodontal pathogens in simultaneous
pulpal and periodontal disease associated with the
same tooth, were investigated by Rupf et al.
6
The
periodontal pathogens displayed comparable profles
in pulpo-periapical lesions, except in progressive adult
periodontitis. Kobayashi et al. concluded that the
periodontal pocket in teeth with advanced periodontitis
may be a possible source of root canal infections.
7

The microbiology of endodontic infections
Root canal infections are mixed and semispecifc
infections with a great predominance of obligate and
facultative anaerobic bacteria. However, only a small
group is commonly isolated from infected dental pulp
cavities. The relative proportion of strict anaerobic
bacteria to facultative aerobic bacteria increases with
the time, and so does the total number of bacteria.
8-12

According to recent reports, it is presumed that over
700 bacterial species inhabit the oral cavity and more
than half of these cannot be cultivated.
13,14
Specifc
combinations of bacteria can be found in the root
canal and they can contribute to ecological shifts of
the fora by different mechanisms of interaction.
15
Bacteria may not only reside in the main canal,
but they also invade the dentinal tubules, making
them act as a reservoir for future dental and
systemic infections.
16,17
Porphyromonas gingivalis,
Tannerella forsythensis and Fusobacterium nucleatum
are associated with extraradicular bioflm formation
and refractory periapical chronic periodontitis.
18
The
presence of T. forsythensis, P. gingivalis and Treponema
denticola was demonstrated in root canal samples
collected from patients with carious lesions, necrotic
pulp and radiographic evidence of periradicular
bone loss.
19
T. denticola was highly associated with
symptomatic endodontic infections and periapical
bone resorption, whereas Enterococcus faecalis
was associated with asymptomatic chronic apical
periodontitis and secondary endodontic infections in
endodontic failures.
20
Black-pigmented bacteria have
been isolated from acute abscesses of dental origin,
suggesting an active role in the pathogenesis of acute
symptoms.
21-23

The microbiology of periodontal infections
The periodontal infection is caused by
microorganisms colonizing the tooth surface at supra
or subgingival level. Living, dying and dead bacteria
and their metabolic byproducts form a resistant
bioflm by attaching to the tooth, to the epithelial cells
and to the underlying exposed tissues.
24
The onset
of the infectious periodontal disease depends on the
simultaneous occurrence of a number of factors for
initiation and progression, such as the virulence of
periodontal pathogens, the local environment and the
host defense mechanisms. It is already documented
that approximately 15 host genes are involved in the
onset and progression of the periodontal disease in
humans.
25
Different studies used various criteria such as the
association between the pathogens and the disease,
the elimination or decrease of species and the parallel
remission of disease due to specifc treatment, the
host response, the virulence factors, associated different
bacteria with different periodontal pathoses.
26-30
Actinobacillus
actinomycetemcomitans, P. gingivalis, T. forsythensis,
Prevotella intermedia, F. nucleatum, Campylobacter
rectus, Eikenella corrodens, Peptostreptococcus micros and
Eubacterium are the best studied periodontal pathogens.
31

However, their proportion in the dental bioflm and their
virulence may differ among individuals with periodontal
disease.
32

PatHWaYs OF DIssEMINatION
Both endodontic and periodontal diseases are
caused by mixed anaerobic infections. Bacteria and
their infammatory by-products can penetrate through
the pathways connecting the periodontium and the
pulp. Kerns and Glickman described six groups of
normal and pathological pathways:
33
(Fig. 1)
1. The apical foramen may be the most signifcant
direct route of communication between the pulp
and the periodontium. The apical foramina represent
also a portal of entry towards the pulp from deep
periodontal pockets. Pulp infection extends into
the periapical tissues causing a local infammatory
response, followed by alveolar bone and sometimes by
focal root resorptions.
34
2. Lateral and accessory canals appear mainly in
the apical area and in the furcation area of molars.
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Figure 1. The normal pathways of communication between the endodontium
and the periodontium (1 -the apical foramen, 2, 3 - lateral and accessory
canals, 4 - dentinal tubules).
They have been suggested to be direct pathways
between the pulp and the periodontium and contain
connective tissue and blood vessels that connect the
circulatory systems of the two tissues.
33
The presence
of patent accessory canals is a potential pathway for
the spread of bacteria and toxic substances from the
pulp, resulting in an infammatory process within the
periodontal ligament.
34
3. Dentinal tubules contain odontoblastic processes
that extend from the odontoblasts to the dentin-enamel
junction or the dentin-cementum junction. Fluid may
fow through patent dentinal tubules. In absence of
an intact enamel or cementum covering, the pulp may
be considered exposed to the oral environment. The
number of dentinal tubules per square millimetre
varies from 8,000 to 57,000 and the diameter ranges
from 0.5 m in the peripheral dentin to 3-4 m near
the pulp. The permeability of root dentin depends
upon dentin thickness, the number of tubules/mm
2
,
and the diameter and patency of the tubules.
35
4. Palatogingival grooves are developmental
anomalies of the maxillary incisor teeth, with lateral
incisors more often affected than centrals. Grooves
usually begin in the central fossa, cross the cingulum
and extent apically to vary distances.
36
(Fig. 2)
Sometimes, a radicular groove is located on the buccal
aspect of maxillary central incisors.
37
5.

Perforations of the roots create a communication
between the root canal system and the periodontal
ligament. This usually occurs as a result of iatrogenic
factors (overinstrumentation), internal or external
resorption (Figs. 3, 4) or caries penetrating through the
foor of the pulp chamber.
33

Figure 2. Intraoperative photo of a palatogingival groove of a lateral upper
incisor, sealed with glass-ionomer cement.
Figure 3. X-ray image of an endodontic-periodontal lesion caused by an
internal root resorbtion.
The closer the perforation is to the gingival
sulcus / periodontal pocket, particularly into the
coronal third of the root or the furcation region,
the greater is the probability of a periodontal
lesion by migration towards apical of the gingival
epithelium.
38,39

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Andreea Didilescu et al 101
Figure 5. Endodontic-periodontal lesion with primary endodontic lesions
and secondary periodontal involvement of 16. Initial (A) and after re-entry (B)
X-ray of the upper first molar. Intra-operatory image of the initial periodontal
defect (C) and the re-entry image after the 6 months (D).
endodontic origin of this condition, due most probably
to the second mesio-buccal canal, very often ignored
during the endodontic therapy. (Fig. 5)
Figure 4. Pre-operatory image of the same lesion while measuring the
initial pocket depth.
6. Vertical root fractures occur accidentally. A
periapical lesion often forms, which may have the
radiographical appearance of a pulpal related lesion.
A way of communication between root canal and
periodontium is created, giving possibility to bacteria
and their by-products to invade the surrounding
periodontal ligament.
34,39
cLINIcaL cONcEPts
Primary endodontic lesions with secondary
periodontal involvement
A causal relationship between root canal infection
and periodontal disease requires a patent route to
the periodontium, an infected root canal system and
suffcient virulence of the pulpal bacteria to promote
marginal periodontitis.
40
In the absence of treatment,
the pulpal infection will continue, leading to destruction
of the periapical alveolar bone and progressing into
the area of furcation. Due to drainage through the
gingival sulcus and accumulation of plaque in the
purulent pocket, periodontal disease progresses and
the further apical migration of the attachment may
occur.
33
Extensive pulpal infection spreading through
patent lateral canals or dentinal tubules in the absence
of an intact cementum may alter the periodontium,
too.
40
Radiographs show evidence of both pulpal and
periodontal disease.
A typical situation: the upper frst molar displays
signs of periodontal disease with loss of attachment of
mesio-buccal root. Radiographic examination reveals
the presence of periapical and periodontal radiolucency,
and a complete obturation of three canals. Usually, in
this case, the symptoms are misinterpreted and the
diagnosis is of localized periodontitis; consequently, the
applied treatment consists of scaling and root-planning,
associated with local antiseptics and irrigations with
clorhexidine. Healing does not occur because of the




A
B
C
D
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102 TMJ 2008, Vol. 58, No. 1

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Therefore, the correct diagnosis is of primary
endodontic lesion with secondary periodontal
involvement.
Primary endodontic lesions with secondary
periodontal involvement may also be the results of
iatrogenic factors, such as root perforations, root
fracture or misplacement of posts during coronal
restorations.
34

Figure 6. Primary periodontal lesions with secondary endodontic
involvement lesion. Initial x-ray of the defect (A) and initial probing of the PD
(B). Intra-operatory aspect of the bone (C). Six months after x-ray (D) with
the root canal treatment completed and the bone defect filled.
Primary periodontal lesions with secondary
endodontic involvement
The effect of periodontitis on the healthy pulp
has been reported in several studies.
41,42
Periodontal
disease can affect the pulp through dentinal tubules,
lateral canals or apical foramina. Lateral canals and
dentinal tubules may be also infected through a
temporary opening to the oral environment during
surgical fap procedures. When the pulp is affected, the
patient reports acute pain and clinical signs of pulpal
infammation. Radiographically, these lesions may be
indistinguishable from the primary endodontic lesions
with secondary periodontal involvement.
33
(Fig. 6)
True combined lesions
Pulpal and periodontal diseases may occur
independently and concomitantly in and around the
same tooth. A necrotic pulp or a failing endodontic
treatment, plaque, calculus and periodontitis are present
in varying degrees.
33
True combined endo-periodontal
lesions present radiographic evidence of bone loss
surrounding a substantial area of the root. Periodontal
probing reveals a pocket extending to the apical region
of the tooth. However, a fully documented diagnosis
of a true combined lesion is hard to establish.
Concomitant pulpal and periodontal lesions
In this case, periodontal and pulpal diseases
coexist, but with different etiology. Radiographically,
the endodontic lesion and a noncommunicating
periodontal pocket are observed.
33

cONcLUsIONs
The tooth anatomy and the etiology of endodontic-
periodontal lesions offers a strong base for establishing
a correct diagnosis. Due to the complexity of these
affections, an interdisciplinary approach with a good
collaboration between endodontists, periodontologists
and microbiologists, is recommended.

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