International Journal of Applied Dental Sciences 2018; 4(4): 223-228

ISSN Print: 2394-7489

ISSN Online: 2394-7497 Endodontic-periodontal lesion: A two-way traffic
IJADS 2018; 4(4): 223-228
© 2018 IJADS
www.oraljournal.com
Received: 15-08-2018
Dr. Anindya Priya Saha, Dr. Anindya chakraborty and Dr. Sananda Saha
Accepted: 17-09-2018
Abstract
Dr. Anindya Priya Saha
Endodontic-Periodontal lesions are complicated disease entity, frequently encountered in day-to-day
MDS (Periodontology), Guru
Nanak Institute of Dental
dental practice, difficult to diagnose and treat. The success of management of a combined periodontal
Science & Research Kolkata, and endodontic lesion depends on the elimination of both of the disease processes. In the case of a
West Bengal, India. combined endo-perio lesion, the endodontic therapy results in healing of the endodontic component,
while the prognosis of tooth would finally depend on the healing of the periodontal lesion. This literature
Anindya chakraborty review aims to assess the causes and consequences of periodontal-endodontic lesions, as well as its
MDS (Oral & Maxillofacial clinical, radiographic and microbiological aspects, and presents a comprehensive outline of diagnosis of
Surgery), Rajarajeswari Dental perio-endo lesions and a sequential treatment protocol to the same.
College & Hospital, Bengaluru,
Karnataka, India. Keywords: Retrograde pulpitis, retrograde periodontitis, pulp, periodontium.
Dr. Sananda Saha
MDS (Periodontology),
Introduction
Dr. R Ahmed Dental College & The tooth, the pulp within it and its supporting periodontal tissues should be viewed as one
Hospital, Kolkata, west Bengal, biological unit. The interrelationship among these structures influences themselves during health
India. and disease [1]. The periodontal-endodontic lesions are characterized by the co-existence of the
pulpal and periodontal disease in a same tooth, which makes complex its diagnosis, as well as
management, because a single lesion often present signs of endodontic and periodontal
involvement. This suggests that one disease might be the cause or consequence of the other, or had
originated from two different and independent processes which were mingled by their advancement [2].
The relation between the pulp and the periodontium was a matter of concern since long back.
Effects of periodontal disease on pulp was first depicted by Turner and Drew (1919) [1] The reverse
was first narrated by Simring and Goldberg (1964) [2] Cahn (1927) and Sicher (1936) [3] first pointed
the communicating channels between pulp and periodontal tissues.

Pathways of Communication
The periodontium and pulp have embryonic, structural and functional interrelationship. From ecto
Mesenchymal cells develop the dental papilla and follicle, which differentiate into periodontium
and the pulp respectively. This developmental origin results anatomical connections, which remain
throughout life [4]. Three main pathways have been attributed to the development of periodontal-
endodontic lesions (Rotstein & Simon, 2004) [5].
 Apical foramen
 Lateral & Accessory canals
 Dentinal tubules

Correspondence
Dr. Anindya Priya Saha
MDS (Periodontology), Guru
Nanak Institute of Dental
Science & Research Kolkata,
West Bengal, India.

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The apical foramen represent the principal route of incidence of pulpal inflammation and degeneration was
communication between pulp and periodontal ligament. reported in periodontally involved teeth than teeth with no
Bacteria themselves, or their products, and inflammatory periodontal involvement, in a study on 85 human teeth by
factors can exit through apical foramen, resulting peri-apical Bender & Seltzer (1972) [11]. Periodontal disease has seen to
pathosis; or reverse happens in deep periodontal pockets. exert no effect on pulp until the pocket has extended to the
Lateral and accessory canals present a possible route for apex (Czarnecki & Schilder, 1979); or periodontal damage
spread of pathogens from pulp to periodontal tissues, and vice has opened an accessory canal to oral environment (Rubach &
versa. De Deus (1975), studying 1140 human teeth, observed Mitchel, 1965) [26]. If the microvasculature of apical foramen
that, about 17% of all teeth presented lateral canals in apical remains intact, pulp maintains its vitality (Langeland et al,
third, about 9% in middle third and 2% in coronal third of 1974) [12].
root [3]. Gutmann (1978), studying 102 human teeth, noticed The effects of periodontal inflammation on pulp is atrophic in
25.50% sample presented lateral canals in furcation area alone nature; including calcification, increase in collagen content,
[4]
. Kirkham (1975), studying 1000 human teeth with formation of reparative dentine and narrowing of canal
advanced periodontal involvement, observed only 2% of spaces; or resoroptive; in addition to direct inflammatory
lateral canals associated with periodontal pocket. sequel. (Mandi et al, 1974) [5] Root planing may exert same
Exposed dentinal tubules, in area where dentine is devoid of effects on pulp and has been shown to increase the rate of
cementum, can act as pathway for communication between formation of reparative dentine. (Hattler & Listgarten, 1984).
pulp and periodontium. Exposures take place from
development defects, wear defects, restorative procedures and Microbiota
periodontal therapies. The density of dentinal tubules varies The oral cavity contains more than 600 species of
from 15000 per Sq. mm. at C.D. Junction cervically, while microorganisms, and the gram negative anaerobic onesare
8000 near apex; to 57000 at pulpal end. Again, the diameter directly related to both the peri-apical and periodontal lesion,
ranges from 1µm in periphery to 3µm toward pulp. Dentine among which the endodontic is less complex than periodontal
exposure occurs at C.E. Junction in 18% of teeth in general pathogen [13].
and 25% of anterior Teeth.
Palato-gingival grooves are found in maxillary lateral incisor, Bacteria: Aggregatibacter actinomycetemcomitans,
extending varying distance apically from cingulam. Bacteroides frosythus, Ekinella corrodens, Fusobacterium
Radiographically they appear as ‘tear drop shaped area’ and nucleatum, Porphyromonas gingivalis, Prevotella
para-pulpal line’ (dark vertical line parallel to canal). They intermediate and Treponema denticola are seen to exist in
provide funnel like area aiding into plaque retention. These both endodontic and periodontal infection [12].
are related to deep ‘tubular’ periodontal pocket, with localized
periodontal disease, with/without pulpal pathosis, depending Fungi: Candida albicans is prevalent in both in endodontic
on their depth and extent. lesion as well as sub-gingival plaque [6, 7]

Literature Review Viruses: Recent study indicates Cytomegalo virus, Epstein-

Pulpal Disease & Periodontal Health Barr virus, herpes virus could be involved in pathogenesis of
Pulpal lesion involves in inflammatory changes, causing periodontal and endodontic disease [8, 9].
inflammatory response of the periodontal ligament at the Kobayashi et al. [15] detected microorganisms common to
apical foramen and at the opening of the accessory canals [7], canal and p pockets were detected from endodontic samples
resulting rapid and wide spread destruction of PDL, with the in 15 devitalized teeth, without caries and with periodontal
production of radiolucency peri-apically, or in the furcation or advancement including: Eubacterium and Fusobacterium spp,
at various points along the root. This is referred to as Porphyromonas gingivalis, Prevotella intermedia,
‘Retrograde periodontitis’ with signs and symptoms including Peptostreptococcus spp, Capnocytophaga spp, Actinomyces
deep localized periodontal pocket, purulent inflammatory spp and Streptococcus spp.
exudates, angular bone loss, swelling and bleeding of the The similarity between the endodontic and periodontal
gingival tissues and increased tooth mobility. Osseous microbiota indicates the possibility of the occurrence of cross
destruction involves furcal area much earlier, because of [1] infection between the root canal and periodontal pocket.
greater incidence of furcal canal and [2] furcal bone, being
thinner, resorbes faster (Moss, 1965). Classification of endodontic-periodontal lession
In animal model, change in periodontal ligament were found Simon, Glick & Frank (1972) [10] classified endodontic-
after pulpotomy and placement of caustic agent in pulp periodontal lesion, based upon origin of the disease and its
chamber (Seltzer et al, 1967) [7]. Periodontal therapy of a spread, as following:
tooth with pulpal disease and peri-apical radiolucency results 1. Primary endodontic lesion (when the lesion is entirely
in poor periodontal healing (Ehnevid et al, 1993) [8]. In animal endodontic in origin)
model, free autogenous soft tissue graft failure rate was 2. Primary endodontic lesion with secondary periodontal
greater, when graft was placed over untreated teeth with involvement (when periodontal defect develops in
diseased pulp (Perlmutter et al, 1987). Hence, precious pre- endodontic ally affected teeth)
assessment of pulpal status is critical for a successful 3. Primary periodontal lesion (when the lesion is entirely
periodontal therapy. periodontal in origin)
4. Primary periodontal lesion with secondary endodontic
Periodontal Disease & Pulpal Health involvement (when endodontic problem arises in
Controversies and conflicts exist regarding the effects of periodontally diseased teeth)
periodontal inflammation on the pulp. Theoretically 5. True combined lesion (when both endodontic and
periodontal pathosis can adversely affect pulp, producing periodontal disease develop independently and unite)
retrograde pulpitis (Simring & Goldberg, 1964) [2]. A greater
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Stock (1988) [11] modified Simon et al classification and

omitted Class V lesions as he argued that both Class II and 3. Teeth requiring both endodontic-periodontal
Class IV lesions become combined lesion in advanced stage. procedures – it includes:
Similarly, one can argue on including ‘primary periodontal a) Any type 1 lesion causing irreversible reaction to a/a, and
lesion’ in the classification hence require periodontal therapy
Khalid Al-Faujan (2014) modified the primary endodontic b) Any type 2 lesion causing irreversible reaction to pulp,
lesions, ‘since it has no periodontal relationship; and and hence require endodontic therapy
proposed a new endo-periodontal interrelationship
classification as follows [12]: World workshop for classification of periodontal diseases
1. Retrograde periodontal disease (1999) (14) has presented a new classification depending on
a) Primary endodontic lesion with drainage through origin of disease as follows:
periodontal ligament a) Endodontic-periodontal lesion
b) Primary endodontic lesion with secondary periodontal b) Periodontal-endodontic lesion
involvement c) Combined lesion
2. Primary periodontal lesion
3. Primary periodontal lesion with secondary endodontic Primary Endodontic Lession
involvement  Pathogenesis
4. Combined endodontic-periodontal lesion o It arises as sequel of pulpitis from dental caries, wear
5. Iatrogenic periodontal lesion defects, trauma and fracture.
o A primary endodontic lesion presents a necrotic pulp and
Here, the primary endodontic lesion with/without periodontal a chronic peri-apical abscess with a sinus tract draining
involvement secondarily is referred as retrograde through periodontal ligament space or gingival sulcus.
periodontitis, (as such periodontal disease begins from apex
and then extends coronally- just reverse to common  Clinical Features
periodontal disease). o The lesion presents ‘isolated’ periodontal problem in
relation to the affected tooth only, without a generalized
Weine (1982) [13] presented a different classification periodontal disease.
depending on clinical presentation as follows: o H/O pulpitis.
1. Symptoms clinically and radiographically simulate o A sinus tract, originating from apex, is often present in
periodontal disease, but are in fact owing to pulpal sulcus.
lesions. o Negative pulp vitality test.
2. That has both pulpal and peri-apical disease and
periodontal disease concomitantly  Treatment
3. That has no pulpal disease but requires endodontic o Endodontic therapy – must be performed in multiple
therapy plus root amputation in order to gain periodontal appointment, to revaluate healing process between the
healing beginning and completion of treatment.
4. Symptoms clinically and radiographically simulate pulpal o Periodontal therapy isn’t required usually.
and peri-apical disease but in fact has periodontal origin.
 Prognosis
Grossman (1988) followed the oldest classification by Oliet o They exhibit good prognosis. Radiographic and clinical
and Pollock (1968) and classified the endo-perio lesions healing occurs rapidly.
according to treatment need, as follows: o A sinus tract heals soon after canal debridement. Healing
completes within 3-6 months.
1. Teeth requiring endodontic therapy only – it includes
a) Necrotic pulp and peri-apical lesion with/without sinus Primary Endodontic Lesion with Secondary Periodontal
tract Involvement
b) Chronic peri-apical abscess with sinus tract passing  Pathogenesis
through a/a. o It arises when periodontal problem develops on teeth
c) Root fracture with PEL.
d) Root resorption o If the primary endodontic lesion with a sinus tract isn’t
e) Replnatation detected and hence, treated early; plaque and calculus is
f) Intentional endodontic therapy often deposited in draining sinus tract; creating a
g) Radisectomy secondary periodontal problem
h) Incomplete closure of apex
 Clinical Features
2. Teeth requiring periodontal therapy only – it includes o Negative pulp vitality test.
a) Occlusal trauma causing reversible pulpitis o Presence of plaque and calculus, in the way of sinus tract.
b) Occlusal trauma plus inflammation of gingiva resulting in
pocket
 Treatment
c) Overzealous periodontal therapy causing pulpal
o Endodontic therapy
sensitivity
o Periodontal therapy – should not be employed until
d) Deep and extensive infra-bony pocket, extending beyond
complete debridement of canal is achieved.
apex, sometimes coupled with root desorption, yet with a
vital pulp.

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 Prognosis  Treatment
o Prognosis of endodontic therapy is usually predictable. o Endodontic therapy and periodontal therapy.
o Regeneration of periodontal tissue depends upon the o Root resection can be in need with regenerative therapy.
extent of tissue destruction.
 Prognosis
Primary Periodontal Lesion o Prognosis of lesion is related to extent of periodontal
 Pathogenesis damage.
o The lesion develops as sequelae of progressing o Though response of endodontic therapy is predictable,
periodontal problem extending to the apex. the tooth shows hopeless prognosis, if majority of
o Plaque represents the prime etiologic factor. osseous support is lost from periodontal lesion.

 Clinical Features Diagnosis

o Patient presents with generalized chronic periodontitis, The correct diagnosis of the periodontal-endodontic lesions is
sometimes having a sinus tract, with periodontal probing fundamental to set the treatment plant and asses the prognosis.
even extending to apex of the affected tooth, showing no Diagnosis of primary endodontic disease and primary
pulpal exposure through caries/trauma/fracture. Patient periodontal disease usually present no clinical difficulty. In
can experience minimal or no pain. primary periodontal lesion, the pulp is vital and responds to
o Positive pulp vitality test. pulp vitality test. In primary endodontic lesion, the pulp is
infected and non-vital and doesn’t respond.
 Treatment However, primary endodontic disease with secondary
o Surgical/ non-surgical periodontal therapy. periodontal involvement, primary periodontal disease with
o Re-evaluation must be done periodically to check for secondary endodontic involvement, or true combined diseases
retro-infection of pulp. are clinically and radio graphically very similar [1]. Accurate
diagnosis can be achieved by detailed history taking
Prognosis According to the studies of Goldman and Schildert [22], cases
The prognosis is entirely dependent on periodontal therapy of caries, traumas, defective restorations and wear defects,
and hence, extent of periodontal damage. which can develop a pulp necrosis, indicate the endodontic
origin of the lesion. Absence of these and presence of
Primary Periodontal Lesion with Secondary Endodontic calculus, plaque, inflammation of marginal tissue and
Involvement generalized perioddontitis, indicate periodontal lesion [23].
 Pathogenesis
o It arises as retro-infection of pulp, when periodontal Treatment Sequence
lesion extends to apex. Before the doing an advanced restorative treatment for an
o It may also follow the path through a lateral canal. endodontic-periodontal lesion, the prognosis of the involved
Cervical abrasion and SRP also can add to such problem. tooth should be evaluated thoroughly. Whether there is a
functional need for the tooth, whether the tooth is restorable
 Clinical Features after the lesion will heal and whether the patient is suitable for
o Negative/ altered pulp vitality test (as pulp can be a lengthy, costly and invasive treatment are crucial factors
necrotic/ partially vital, especially in multi-rooted teeth) that should be taken into account. If any of those appears
negative, extraction is the treatment of choice [15].
 Treatment When the pulp is non-vital and infected, conventional
o Surgical/ non-surgical periodontal therapy endodontic therapy alone will resolve the lesion. Endodontic
o Endodontic therapy surgery is not necessary, even with the presence of large peri-
radicular radiolucency’s and abscesses, but can be of need
 Prognosis when large peri-apical radiolucency remains even after the
o The prognosis depends upon periodontal therapy and non-surgical endodontic therapy. Johnson and Orban showed
hence, extent of periodontal damage. that periodontal disease that remained after unsuccessful
o Healing of peri-apical lesion isn’t predictable owing to endodontic therapy cleared up after successful endodontic
periodontal communication therapy [31].
If primary endodontic lesions persist, despite extensive
True Combined Lesion endodontic therapy, thenit may also have secondary
periodontal involvement or it can be a true combined lesion.
 Pathogenesis
Hiatt and Amen suggested that persistent periodontal disease
o Here pulpal and periodontal lesions develop and unite
resolves only after definitive periodontal therapy is
independently.
accompanied by successful endodontic therapy [33].
o It develops when an endodontic lesion progressing
In case of secondary periodontal involvement, rootcanal
coronally joins with a pre-existing periodontal defect
treatment is employed immediately and the cleaned and
progressing apically.
shaped canal is filled with calcium hydroxide paste, which has
anti-microbial, anti-inflammatory and proteolytic property,
 Clinical Features
inhibiting resorption and favouring repair. It also prevents
o Features are similar to that of primary periodontal lesion.
periodontal contamination of instrumented canals via patent
In addition, there must be some caries, trauma, fracture,
channels connecting the pulp and periodontium, before
wear defects, deep restoration or history of endodontic
periodontal treatment removes the contaminants. Treatment
therapy. So patient often has severe pain.
results should be evaluated after two to three months and only
o Negative pulp vitality test.
then should periodontal treatment be considered.
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Primary periodontal lesions should be treated first by non- would obtain the correct diagnosis and treatment plan,
surgical periodontal therapy. Periodontal surgery, in the form achieving greater chances of success in the management of
of pocket surgery and ressective and regenerative procedure, the periodontal-endodontic lesions.
is required for deeper pockets and angular bone defects.
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