This document discusses the relationship between endodontic and periodontal tissues. It begins by introducing endo-perio lesions and noting they are responsible for over 50% of tooth mortality. It then covers pathways connecting endodontic and periodontal tissues, the etiology and classification of endo-perio lesions, diagnostic procedures, differences between periodontal and periapical abscesses, the endo-perio controversy, and treatment approaches. The document provides an overview of the interactions between the endodontic and periodontal systems and debates around their relationships.

1. ENDO-PERIO INTERACTIONS
GUIDED BY: PRESENTED BY:
DR. AMIT GOEL DR. VIRSHALI GUPTA
PG 2ND YEAR
From Endo to perio From Perio to endo

2. CONTENTS
 Introduction
 Pathways connecting endodontic and periodontal tissues
 Etiology of endo-perio lesions
 Classification of endo-perio lesions
 Clinical diagnostic procedures
 Differences b/w periodontal and periapical abscess
 Endo-perio controversy
 Therapeutic management of pulpal and periodontal diseases
 Conclusion
 References
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3. INTRODUCTION
Endo-perio problems are responsible for more than 50% of tooth mortality today.
In 1919 Turner and Drew first described the effect of periodontal disease on the pulp. The
relationship between the periodontium and the pulp was first discovered by Simring and
Goldberg in 1964.
Since then, the term ‘endo- perio 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.
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4. PATHWAYS CONNECTING ENDODONTIC &
PERIODONTAL TISSUES
 Anatomical pathways:
 Apical foramen, accessory canals /lateral canals
 Congenital absence of cementum exposing
dentinal tubules
 Developmental grooves
 Non-physiological pathways:
 iatrogenic root canal perforations
 vertical root fractures caused by trauma,
pathway created due to resorption etc.
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5. ETIOLOGICAL AND CONTRIBUTING FACTORS
IN ENDO-PERIO LESIONS4/27

6. BACTERIA ASSOCIATED WITH PULPITIS
Eubacterium sp. 59 Gram-positive nonmotile
Peptostreptococcus sp. 54 Gram-positive nonmotile
Fusobacterium sp. 50 Gram-negative nonmotile
Porphyromonas sp. 32 Gram-negative nonmotile
Prevotella sp. 45 Gram-negative nonmotile
Streptococcus sp. 28 Gram-positive nonmotile
Lactobacillus sp. 24 Gram-positive nonmotile
Wolinella sp. 18 Gram-negative motile
Actinomyces sp. 14 Gram-positive nonmotile rods
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7. Moore 1987, Sundqvist 1994
Most of the species that have
been found in infected root
canals can also be present in
the periodontal pocket.
Rupf et al (2000) studied the profiles of
periodontal pathogens in pulpal and
periodontal diseases associated with
same tooth and concluded that
periodontal pathogens often
accompany endodontic infections
Didilescu AC et al (2012) - F.
nucleatum, P. micra and C.
sputigena may play a role in
the pathogenesis of endo-
periodontal lesions.
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8. CLASSIFICATION OF ENDO- PERIO LESIONS
I. Based on etiology, diagnosis, treatment and prognosis
(by Simon, 1972)
Primary endodontic lesions
Primary endodontic lesions with secondary
periodontal involvement
Primary periodontal lesions
Primary periodontal lesions with secondary
endodontic involvement
True combined lesions
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9. II. Based on clinical presentation strategies for each (by Weine, 1982)
Class 1-Tooth in which symptoms clinically and radiographically
simulate periodontal disease but are in fact due to pulpal
and/or necrosis.
Class II – Tooth that has both pulpal or periapical disease and
periodontal disease
Class III –Tooth that has no pulpal problem but requires endodontic
therapy plus root amputation to gain periodontal healing.
Class IV- Tooth that clinically and radiographically simulates pulpal or
periapical diseases but in fact has periodontal disease.
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10. III. Stock (1988) modified Simon’s classification
Omitted Class V of the classification.
He argued that both Class II and Class IV lesions in advanced
stages can become combined lesions and therefore a
class to describe these lesions was not necessary.
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11. IV. Based on treatment plan (Grossman classification,1991)
Type 1 – Requiring endodontic treatment only.
Type II – Requiring periodontal treatment only.
Type III – Requiring combined endo-perio treatment
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12. V. Classification as recommended by the World Workshop for Classification
Periodontal Diseases (1999)
Endodontic-periodontal lesion
Periodontal-endodontic lesion
Combined lesion
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13. DIAGNOSTIC PROCEDURES USED TO IDENTIFY
THE ENDO-PERIO LESION
Examination/
tests
1º endodontic
lesion
1º periodontal
lesion
1º endodontic
2º periodontal
1º periodontal
2º endodontic
True combined
lesion
Visual  Soft tissue -
sinus opening
 Tooth -
decay/ large
restoration/
fractured
restoration or
tooth/
erosions/abrasio
ns/cracks/
discolorations/
poor RCT
 Inflamed
gingiva/
recession
(multiple
teeth)
 Plaque &
subgingival
calculus
(multiple
teeth)
 swelling
indicating
periodontal
abscess
 Plaque forms
at the
gingival margin
of the sinus tract
leads to
inflammation
of marginal
gingiva
 exudate
 Root
perforation/
fracture
 plaque,
subgingival
calculus &
swelling
(multiple
teeth)
 pus, exudate
 localized/
generalised
recession &
exposure of
root
 Plaque,
calculus &
periodontitis will
be present in
varying degrees
 Swelling
around single
or multiple
teeth
 pus, exudate
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14. Examination/
tests
1º endodontic
lesion
1º periodontal
lesion
1º endodontic
2º periodontal
1º periodontal
2º endodontic
True combined
lesion
Pain Sharp  Usually dull
ache
 Sharp only in
acute
condition
 Usually sharp
shooting
 Dull ache in
chronic
conditions
 Usually dull
ache
 Sharp only in
acute
periodontal
abscess
 Dull ache
usually
 Only in acute
conditions it
is severe
Palpation does not indicate
whether
the inflammatory
process is
of endodontic or
periodontal
origin
Pain on Pain on Pain on Pain on
Percussion Normally tender
percussion
Tender on
percussion
Tender on
percussion
Tender on
percussion
Tender on
percussion
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15. Examination/
tests
1º endodontic
lesion
1º periodontal
lesion
1º endodontic
2º periodontal
1º periodontal
2º endodontic
True combined
lesion
Mobility Fractured roots and
recently
traumatized teeth
often present high
mobility
Localized to
generalized
mobility of teeth
Localized
mobility
Generalized
mobility
Generalized
mobility with
higher grade of
mobility related
to the involved
tooth
Pulp vitality
test,
 A lingering
response-
rreversible pulpitis
 No response -
Necrotic pulp
(non-vital)
pulp is vital and
responsive to
testing
Pulp vitality tests
negative
Pulp vitality may
be positive in
multirooted teeth
Usually negative
because
of non-vital pulp.
Pocket probing A deep narrow
solitary pocket*
Multiple wide
deep
pockets
Presence of
solitary wide
pocket
Presence of
multiple
wide and deep
periodontal
pockets
Probing reveals
typical conical
periodontal type
of probing
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16. Examination/
tests
1º endodontic
lesion
1º periodontal
lesion
1º endodontic
2º periodontal
1º periodontal
2º endodontic
True combined
lesion
Sinus tracing A radiograph with
GP points to apex
or furcation area in
molars
Sinus tract mainly
at the
lateral aspect of
the root
Sinus tract mainly
at the apex/
furcation
area
Sinus tract mainly
at the lateral
aspect of the root
Difficult to trace
out the origin of
the lesion *
Radiographs
Cracked tooth
testing
Painful response on
chewing
No symptoms Painful response
on chewing
No symptoms Painful response
on chewing
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17. DIFFERENCES BETWEEN PERIODONTAL AND
PERIAPICAL ABSCESS
PERIODONTAL ABSCESS PERIAPICAL ABSCESS
Periodontal pocket is present caries/ fracture is present
May occur after periodontal treatment May occur after endodontic or restorative
Tooth is vital Tooth is non - vital
Pain is usually dull and localized Pain is severe and difficult to localize
Swelling is present on the lateral surface of root
usually without fistulous track as abscess usually
drains from pocket opening.
Swelling is present at the apical portion of tooth
which drains by formation of a fistulous track.
Tender on lateral percussion Tender on vertical percussion
Usually not visible on radiographs Appears as a periapical radiolucency
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18. ENDO – PERIO – CONTROVERSY
• Two basic questions have been raised and continue to
be a matter of dispute :
1) Is periodontal disease a cause of pulp necrosis?
2) Can a pulpless tooth be the cause of periodontal
disease?
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19. EFFECT OF PULPAL DISEASE ON THE
PERIODONTIUM
Early inflammatory changes in the pulp very little effect on the
periodontium.
Necrotic pulp produces inflammatory response transverse into
periodontal tissues.
Nature and extent of periodontal destruction depends on:
1. Virulence of pathogens in the canal system
2. Duration of the disease
3. Defense mechanism of the host.
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CARRANZA 12TH EDITION, 2016

20. CONTRADICTING STUDY
 Sanders et al. (1983) reported that after the use of freeze dried bone allograft, 65% of the
teeth that did not have root canal treatment showed complete or greater than 50% bone-fill
periodontal osseous defects; while only 33% of the teeth which had root canal treatment
to the periodontal surgical procedure had complete or greater than 50% bone-fill.
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Diem et al (2002) reported that all
tissues of the periodontium had a
potential for regeneration regardless
of the status of the pulp. With proper
endodontic treatment, periodontal
disease of pulpal origin should heal.
Jansson et al (1998) Potential effect
of tooth with a necrotic pulp has
been described as a risk factor in
the initiation and progression of
periodontal disease, and the
resolution of periodontal pockets.

21. INFLUENCE OF ENDODONTIC PROCEDURES
ON PERIODONTIUM
 Aggressive removal of PDL and underlying cementum during interim endodontic therapy
adversely affects periodontal healing.
 Precautions to be taken when periodontal therapy to follow endodontic treatment.
 Induce less mechanical trauma
 Use more biocompatible sealers
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22. EFFECT OF PERIODONTITIS ON THE PULP
Result in atrophic and other degenerative changes like
 reduction in the number of pulp cells,
 dystrophic mineralization,
 fibrosis,
 reparative dentin formation,
 inflammation and
 resorption.
CAUSE:
Disruption of blood flow through the lateral canals localized areas of coagulation
necrosis in the pulp.
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CARRANZA 12TH EDITION, 2016

23. Seltzer et al (1978) found
inflammatory alterations
localized pulp necrosis
adjacent to lateral canals in
roots exposed by
periodontal disease.
Cohen, 2002 have
suggested that periodontal
disease causes pulpal
necrosis. Periodontal
is a direct cause of pulpal
atrophy and necrosis.
Rathod et al 2014 severe
chronic periodontitis can
affect dental pulp
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24. CONTRADICTING STUDIES
Kirkham (1975) studied 100
periodontally involved
& found 2% had lateral
canals in the periodontal
pocket.
Tagger & Smukler (1979)
removed roots from
extensively involved with
periodontal disease in
which root amputation was
necessary. Pulps of these
showed no inflammatory
changes.
Mazur and Massler (2009)
found no relationship of
periodontal disease as a
causative factor in pulpal
disease.
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25. EFFECT OF PERIODONTAL PROCEDURES ON
PULP
Scaling and root planing: removes the
bacterial plaque and calculus. However,
improper root planing procedures can also
remove cementum and the superficial parts
of dentin, thereby exposing the dentinal
tubules to the oral environment.
Acid etching: citric acid removes the smear
layer, an important pulp protector.
Application of citric acid may have a
detrimental effect on the dental pulp.
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26. TREATMENT
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27. CONCLUSION
 A perio-endo 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 multi-disciplinary approach
should be involved.
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28. REFERENCES
 Carranza, Newman 1Oth edition. Endodontic and Periodontics consortium.
 Carranza, Newman 12th edition. Endodontic and Periodontics consortium.
 Jan Lindhe. Endodontics and Periodontics. Clinical Periodontology and Implant Dentistry. 318-
351.
 Shalu Bathla, PERIODONTICS REVISITED – 1st edition.
 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.
 Syed Wali Peeran et al, endo- perio lesions, international journal of scientific & technology
research volume 2, issue 5, may 2013
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