ENDODONTIC-PERIODONTAL INTERACTIONS

GUIDED BY: PRESENTED BY:

DR. AMIT GOEL DR. VIRSHALI GUPTA

PG 2ND YEAR

CONTENTS

Introduction

Pathways connecting endodontic and periodontal tissues

Etiology of endo-period 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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INTRODUCTION

Endodontic-periodontal 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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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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ETIOLOGICAL AND CONTRIBUTING FACTORS IN ENDO-PERIO LESIONS4/27

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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Most of the species that have

been found in infected root

canals can also be present in

the periodontal pocket.

(Moore 1987, Sundqvist 1994).

Rupf et al (2000) studied the profiles periodontal pathogens in pulpal and

periodontal diseases associated with the

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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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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II. Based on clinical presentation strategies for each (by Weine, 1982)

Class 1 -tooth that clinically and radiographically stimulateperiodontal involvement but is truly due to pulpal inflammation or

necrosis.

Class II – tooth with both pulpal and periodontal diseaseconcomitantly

Class III – tooth that has no pulpal problem but requires endodontictherapy with root amputation to receive periodontal healing

Class IV- tooth that clinically and radiographically stimulate pulpal orperiapical disease but in fact has periodontal disease.

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IV. 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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III. 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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V. Classification as recommended by the World Workshop for ClassificationPeriodontal Diseases (1999)

Endodontic-periodontal lesion

Periodontal-endodontic lesion

Combined lesion

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DIAGNOSTIC PROCEDURES USED TO IDENTIFY THE ENDO-PERIO LESION

Examination/ tests

1º endodontic lesion

1º periodontallesion

1º endodontic2º periodontal

1º periodontal2º endodontic

True combinedlesion

Visual Soft tissue -sinus opening

Tooth -decay/ largerestoration/ fractured restoration ortooth/erosions/abrasions/cracks/ discolorations/ poor RCT

Inflamedgingiva/ recession (multiple teeth)

Plaque & subgingival calculus (multiple teeth)

swellingindicatingperiodontal abscess

Plaque formsat the

gingival margin of the sinus tractleads to inflammationof marginal gingiva exudate Root

perforation/ fracture

plaque,subgingival calculus &swelling (multiple teeth)

pus, exudate localized/

generalisedrecession &exposure of

root

Plaque, calculus &

periodontitis will be present in varying degrees Swelling

around single or multiple teeth

pus, exudate

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Examination/ tests

1º endodontic lesion

1º periodontallesion

1º endodontic2º periodontal

1º periodontal2º endodontic

True combined lesion

Pain Sharp Usually dull ache

Sharp only in acutecondition

Usually sharp shooting

Dull ache in chronicconditions

Usually dull ache

Sharp only in acuteperiodontal

abscess

Dull ache usually

Only in acute conditions itis severe

Palpation does not indicate whetherthe inflammatory process isof endodontic or periodontalorigin

Pain on Pain on Pain on Pain on

Percussion Normally tender percussion

sensitivity of theproprioceptive fibers in an inflamed pdl will help identifythe location of the pain

Tender on percussion

Tender on percussion

Tender on percussion

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Examination/ tests

1º endodontic lesion

1º periodontallesion

1º endodontic2º periodontal

1º periodontal2º endodontic

True combined lesion

Mobility Fractured roots and recentlytraumatized teeth often present high mobility

Localized to generalizedmobility of teeth

Localized mobility

Generalized mobility

Generalized mobility withhigher grade of mobility related to the involvedtooth

Pulp vitality test,

A lingeringresponse-rreversible pulpitis No response -Necrotic pulp (non-vital)

pulp is vital andresponsive to testing

Pulp vitality testsnegative

Pulp vitality maybe positive inmultirooted teeth

Usually negative becauseof non-vital pulp.

Pocket probing A deep narrow solitary pocket*

Multiple wide deeppockets

Presence ofsolitary widepocket

Presence of multiplewide and deepperiodontal pockets

Probing reveals typical conical periodontal type of probing

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Examination/ tests

1º endodontic lesion

1º periodontallesion

1º endodontic2º periodontal

1º periodontal2º endodontic

True combined lesion

Sinus tracing A radiograph with GP points to apex or furcation area in molars

Sinus tract mainly at thelateral aspect of the root

Sinus tract mainly at the apex/furcationarea

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 onchewing

No symptoms Painful response on chewing

No symptoms Painful response on chewing

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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 rootusually 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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ENDODONTIC PERIODONTAL-CONTROVERSY

• Two basic questions have been raised and continue tobe a matter of dispute :

1) Is periodontal disease a cause of pulp necrosis?

2) Can a pulpless tooth be the cause of periodontaldisease?

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EFFECT OF PULPAL DISEASE ON THE PERIODONTIUM

Bacteria and toxic irritants in pulp increase intrapulpal pressure. Inc pressure may cause toxic

to be expressed through patent channels which results in retrograde periodontitis.

Unresolved endodontic lesion causes bone loss, pocket formation and impair wound healing.

Potential effect of tooth with a necrotic pulp has been described as a risk factor (Jansson,

Ehnevid and Blomlof 1998) in the initiation and progression of periodontal disease, and the initiation of periodontal pockets.

Diem et al (2002) reported that all tissues of the periodontium had a potential for regeneration regardless of the status of the pulp.

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INFLUENCE OF ENDODONTIC PROCEDURES ON PERIODONTIUM

Endodontic therapy adversely affects periodontal healing.

Mechanical preparation, sealers, surgical trauma hinder new bone, cementum andconnective tissue repair.

Precautions to be taken when periodontal therapy to follow endodontic treatment.

Induce less mechanical trauma

Use more biocompatible sealers

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CONTRADICTING STUDY

Sanders et al. (1983) reported that after the use of freeze dried bone allograft, 65% ofthe teeth that did not have root canal treatment showed complete or greater than 50%bone-fill in periodontal osseous defects; while only 33% of the teeth which had rootcanal treatment prior to the periodontal surgical procedure had complete or greaterthan 50% bone-fill.

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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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Seltzer et al (1978) found inflammatory alterations

and localized pulp

necrosis adjacent to

lateral canals in roots

exposed by periodontal

disease.

Mazur and Massler (1979) found that only

periodontitis involving

apical foramen can lead

to pulp necrosis.

Cohen, 2002 have suggested that periodontal disease causes pulpal

necrosis. Periodontal disease is a

direct cause of pulpal atrophy

necrosis.

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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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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 (1979) found no relationship and disclaimed

relationship of periodontal

disease as a causative factor in

pulpal disease.

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TREATMENT

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CONCLUSION

Endo perio lesions present challenges to the clinicians in their proper diagnosis, treatment and prognosis of the involved teeth.

They have a varied pathogenesis which ranges from quite simple to relatively complex.

Knowledge of these diseases is essential in coming to the correct diagnosis and proper treatment plan.

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REFERENCES

Carranza, Newman 1Oth 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 21stcentury. J Interdiscip Dentistry 2013;3: 2-11.

Syed Wali Peeran et al, endo- perio lesions, international journal of scientific & technologyresearch volume 2, issue 5, may 2013

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