ENDODONTIC-

PERIODONTIC
LESIONS

LIBRARY DISSERTATION

DR NISHAT ZAIDI
(2017-2020)
 LIBRARY DISSERTATION

ENDO-PERIO LESIONS

GUIDED BY: BY:

1. Dr P.KARUNAKAR Dr NISHAT ZAIDI.S
2. Dr RAJI VIOLA SOLOMON
3. Dr SHANTHI PRIYA

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 ACKNOWLEDGEMENTS
A lot of people have contributed and supported me throughout this endeavour and I am extremely
grateful to each and every one of them.

To begin, it is with supreme sincerity and deep sense of appreciation that I acknowledge my
esteemed Professor & Head of Department Dr. P.Karunakar Sir for his valuable suggestions,
critical judgment and thought provoking advices, rendered for the betterment of this work as well as
for framing my personality.

My PG Guide, Dr.Raji Viola Solomon, Professor of Department of Conservative dentistry &

endodontics ,Panineeya Mahavidyalaya Institute of dental sciences and Research center, Hyderabad
for always giving me excellent guidance, exemplary encouragement, undying spirit in igniting the
flame of knowledge in me and friendly help during the course of my entire post-graduation. I am
indebted to her for having sculpted me and made me do things which I would never have dreamt of.
A mere word of thanks is not sufficient to express their unflinching support, keen surveillance,
inestimable aid and continued inspiration during the preparation of this dissertation.

It is my greatest fortune to express my heartful thanks to Dr. M.S Ranga Reddy Sir Professor in
Department of Conservative dentistry & endodontics ,for constant encouragement and motivation
and giving me an opportunity to utilize the facilities in the institution for this dessertation.

My heartfelt grateful to Dr.Umrana FaizuddinProfessor in the Department of Conservative

Dentistry and Endodontics for hes valuable guidance, sheer tenacity, selfless dedication, and
personal interest rendered at every level for the better outcome of this dissertation.

I would like to acknowledge the contribution of my Mentor Dr. Shanthi Priya, Senior lecturer who
with hes knowledge and experience guided me in this dissertation and for her constant support and
guidance during this endeavor.

A special thanks to Dr Karthik Basa, for answering all my doubts and also in training me in my
clinical activities.

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I would also like to acknowledge dr Ashish Jain And Dr Shravan kumar for their ever extending
support.

I would also like to thank, Dr.Syed Wali Ahmed, Dr.G.Shivani Reddy , Dr.Akula Sarika &
Dr Ramidi Deepika for their help and support rendered throughout my post- graduate course. My
heart fills with fond gratitude as I reminisce the cherishable moments of benevolence and selfless
co-operation I received from my batchmates and friends

I would like to thank the almighty and my Grandmother Smt Fatima Unissa Begum, My parents Dr
S.M.H Zaidi & Dr Najafi Begum, My Uncle, and friend Mr Aijaz Hussain and My Mother in law
Mrs Marzia Begum for all the sacrifices they made for me, for always believing in me and
supporting me in all ways possible. I would also like to thank my brothers Mr Anwar Zaidi & Mr
Aman Zaidi and my lovely kids Zainab Hyder & Zehra Hyder for giving me constant moral support
whenever needed.

I also thank my beloved Husband Mr Mustafa Hyder, for making my dull moments lively with his
cheerful words and providing enormous computer assistance with innovative ideas required for the
outcome of this dissertation

Last but not the least I would like to thank my house help Mrs Parveen(Choti Ma) without whose
support my PG Course would not have been possible.

Above all I thank the Almighty for giving me strength, blessings, will-power and wisdom to
perform this research work effectively and succeed in all my endeavours during this course.

DR. NISHAT ZAIDI.S

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 TABLE OF CONTENTS:

1. INTRODUCTION 6-9
2. PATHWAYS OF COMMUNICATIONS 10-20
BETWEEN PULP AND PERIODONTIUM

3. ETIOPATHOGENESIS 21-30

4. CONTRIBUTING FACTORS 31-51

5. CLASSIFICATION OF ENDODONTIC- 52-62

PERIODONTAL LESIONS

7. DIAGNOSIS 63-82
8.DIFFERENTIAL DIAGNOSIS 82-95
9. TREATMENT OF ENDODONTIC- 96-103
PERIODONTIC LESIONS
10.RECENT ADVANCES IN TREATMENT 104-119

11. SUMMARY 120-123

12.CONCLUSION 124-126

13. BIBLOGRAPHY 127-132

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INTRODUCTION

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 INTRODUCTION:

The relationship of the pulp and the periodontium is dynamic. The periodontium and the pulp are
closely related, they have embryonic, anatomic and functional interrelationships. In 1919 Turner
and Drew first described the effect of periodontal disease on the pulp. The relationship between
periodontal and pulpal disease was first described by Simring and Goldberg in 19641. The clinician
should be aware that endodontic and periodontal lesions arise from inflammation or degeneration of
both tissues. The function of a tooth depends on the health and vitality of the periodontium and not
on the state of the pulp. Thus, the tooth and its supporting structure form a biological unit.

Understanding the interrelationship between endodontic and periodontic diseases is crucial for
correct diagnosis, prognosis, and treatment decision making. The interrelationships between pulpal
and periodontal disease primarily occur by way of the intimate anatomic and vascular connections
between the pulp and the periodontium2.

The main pathways of for communications between the dental pulp and periodontium are dentinal
tubules, lateral and accessory canals and the apical foramen3. These interrelationships have been
traditionally demonstrated using radiographic, histologic, and clinical criteria.2

Pulpal and periodontal problems are responsible for more than 50% of tooth mortality. Diagnosis is
often challenging because these diseases have been primarily studied as separate entities, and each
primary disease may mimic clinical characteristics of the other disease. Some studies suggest that
these two diseases may have etiologic influences on the progression of the other disorder.2

Pulp tissue succumbs to degeneration by way of a multitude of insults such as caries, restorative
procedures, chemical and thermal insults, trauma, and periodontal disease. When products from
pulp degeneration reach the supporting periodontium, rapid inflammatory responses can ensure that
are characterized by bone loss, tooth mobility, and sometimes sinus tract formation.

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If this occurs in the apical region, a periradicular lesion forms. If this occurs with crestal extension
of the inflammation, a retrograde periodontitis or reverse pocket is formed. However, the lesion
formed has little anatomic similarity to a periodontally induced defect.2

Periodontal disease, by contrast, is a slowly progressing disease that may have a gradually atrophic
effect on the dental pulp. A periodontal lesion is used to denote an inflammatory process in the
periodontal tissues resulting from dental plaque accumulation on the external tooth surfaces.
Research has shown that periodontitis is characterized by the presence of localized inflammation or
tissue infarction, a decrease in cells, resorption, fibrosis, and coagulation necrosis. Dystrophic
calcification may cause some degeneration in the pulp and further influence periodontal disease. In
addition, periodontal treatments such as deep root planing and/or curettage, use of localized
medicaments, and gingival injury or wounding may accelerate further pulpal inflammation and
provoke the interrelated disease process.2

Periodontal and pulpal disease have some common clinical symptoms, most probably tenderness to
percussion and swelling. Either disease may mimic the other, clinically or radiographically.
Therefore an accurate evaluation of the etiologic factors involved is needed for the correct
diagnosis and treatment planning.4

The establishment of a correct diagnosis may complicate when both endodontic and periodontal
lesion affect the same tooth simultaneously and may present a single lesion. Proper diagnosis of
various disease affecting the pulp and periodontium is important to exclude unnecessary and even
detrimental treatment.4

The concern with which the dental profession regards the subject of teeth which are affected by
both endodontic and periodontal disease is evidenced by the abundance of literature dealing with
this subject much of it published within the past decade. Descriptions of endodontic and periodontal
lesions have been appearing for a considerable period but confusion still exists with regard to
etiology, diagnosis and therapy. Much of what has been written is based upon trial and error-some
are successful, some are quite questionable.5

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Attempts have been made to develop a rationale for combined “endo-perio therapy". It has been
suggested that the elimination of etiologic factors is essential to success.5 What we have developed
through the years are analyses of endodontic problems and periodontic problems as separate
entities, which may occasionally occur simultaneously and have some abstract relationship to one
another. The nature of the endodontic or periodontal problem seems to be the usual factor,
responsible for the incidence of lesions that apparently affect both tissues. Though there may be
considerable truth to this hypothesis in many instances.5

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.6

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PATHWAYS OF COMMUNICATIONS
BETWEEN PULP AND PERIODONTIUM

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 PATHWAYS OF COMMUNICATIONS
BETWEEN PULP AND PERIODONTIUM

The pulp and periodontium have embryonic, anatomic and functional interrelationship. There are
various pathways for the exchange of infectious elements and irritants from the pulp to
periodontium or vice versa, leading to the development of endodontic periodontal lesions.7

Pathways of developmental origin (anatomical pathways):8

 Apical foramen

 Dentinal tubules

 Lateral and accessory canals

 Palatogingival groove

Pathways of pathological origin:

 Perforations

 Vertical root fracture

 Loss of cementum

Pathways of iatrogenic origin:

 Perforation during endodontic therapy.

 Root fracture during root canal therapy

 Exposure of dentinal tubules during root planning

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 Anatomical pathways of communication between the pulp and the periodontium

I.Pathways of Developmental Origin (Anatomical Pathways):

1. Apical Foramen :

The apical foramen is the principal route of communication between the pulp and the periodontium.
Bacterial by-products and inflammatory mediators in a diseased pulp may exit readily through the
apical foramen to cause periapical pathosis. The apex is also a portal of entry of inflammatory
elements from deep periodontal pockets to the pulp.

Pulp inflammation or pulp necrosis extends into the periapical tissues, causing a local inflammatory
response often associated with bone and root resorption. It has been shown that when apical
granulomas from necrotic pulps are extensive, the granulomatous tissue can be present along the
lateral aspects of roots, which may also cause extensive resorption of the alveolar crest.9

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Although communication between pulp and periodontium can be focused on the vascular route,
many other possible avenues exist such as: lingual grooves, root/tooth fractures, cemental
agenesis/hypoplasia, root anomalies, intermediate bifurcation ridges, fibrinous communications,
and trauma-induced root resorption.10

Root apex Scanning electron micrograph of the apical third of a root

2. Lateral and Accessory Canals:

In addition to the apical foramen, which is the main avenue of communication, there are a multitude
of branches connecting the main root canal system with the periodontal ligament. These root canal
ramifications were first described nearly 100 years ago by Preiswerk (1901). These ramifications
are now currently termed as ‘accessory canals’. The term accessory canal is now used to describe
any ramification that connects the root canal system to the periodontal ligament.7

Considerable speculation exists about the role that lateral or accessory canals may play in the
spread of inflammation from a periodontal pocket into the dental pulp or vice versa. Lateral and
accessory canals may result from a lack of dentin elaboration around a blood vessel located in the
periradicular connective tissue.

When the roots begin to mature, lateral and accessory canals are generated. They contain blood
vessels and nerve bundles that penetrate the apices from different directions. Foramina are also
formed if a break develops in the continuity of root sheath.9

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Lateral canals normally harbor connective tissue and vessels which connect the circulating system
of the pulp with that of the periodontal ligament. In some instances, the lateral or accessory canal is
obliterated by calcification, but patent communications of varying sizes (10-250μm) may remain in
many cases.10

The majority of the accessory canals are found in the apical part of the root and lateral canals in the
molar furcation region. The frequencies of these ramifications on the root surface are as follows:
apical third 17%, coronal third 1.6% and body of the root 8.8%.11

Lateral and accessory canals may be present anywhere along the root

Studies of human teeth have shown that lateral and accessory canals and foramina are present in
great numbers, especially in the bifurcation and trifurcation regions of molars. It is estimated that
30–40% of all teeth have lateral or accessory canals and the majority of them are found in the apical
third of the root.9

DeDeus found that 17% of teeth presented lateral canals in the apical third of the root, about 9% in
the middle third, and less than 2% in the coronal third. Some investigators found accessory canals
in molar furcation in 20% to 60% of permanent teeth, and 23% of deciduous molars examined. In a
study of 1,140 extracted adult human teeth, lateral canals were found in 27% of teeth, and
distributed at various levels of the root.11

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In another report, 2% of 100 teeth studied had accessory canals located within a periodontal pocket
and 23% of the periodontal pockets had 1 or 2 accessory canals. A fairly high prevalence of lateral
canals in posterior teeth that communicate with the floor of the pulp chamber and the periodontal
ligament has been reported in animals. Thus, there is ample evidence to indicate that infection of
the pulp can potentially communicate with the periodontium at locations other than the apex of the
tooth.9

Bender et al., stated that periodontal endodontic problems were much more frequent in the molars
than in the anterior teeth because of the greater number of accessory canals present in the molars.
The percentage of lateral canals in the furcation is 46% in first molars and 50 to 60% in any
multirooted teeth.10

Radiographically, it is seldom possible to identify lateral canals unless they have been filled with a
contrasting root canal filling material following endodontic therapy. The radiographic indications of
the presence of lateral canals before obturation are:

1. Localized thickening of periodontal ligament on the lateral root surface

2. A frank lateral lesion

It is essential that the dentist recognizes and is familiar with canal ramifications and variations. The
ideal treatment of periodontal pocket formation associated with untreated accessory root canals is
total debridement and total obturation of the root canal system.12

3. Dentinal Tubules:

Dentinal tubules which contain the odontoblastic process that extends from the odontoblast at the
pulpal dentin border to the dentino-enamel junction or the cement-dentinal junction. Passage of
microorganisms between the pulp and periodontal tissues is possible through these tubules, when
the dentinal tubules are exposed in areas of denuded cementum. Exposed dentinal tubules in areas
devoid of cementum may serve as communication pathways between the pulp and the periodontal
ligament. Exposure of dentinal tubules may occur due to developmental defects, disease processes,
or periodontal or surgical procedures.13

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Radicular dentin tubules extend from the pulp to the cemento-dentinal junction. They run a
relatively straight course. The diameter ranges from 1 mm in the periphery to 3 mm near the pulp.
The tubular lumen decreases with age or as a response to chronic low-grade stimuli causing
apposition of highly mineralized peritubular dentin. The density of dentin tubules varies from
approximately 15,000 per square millimetre at the cemento-dentinal junction in the cervical portion
of the root to 8000 near the apex, whereas at the pulpal ends the number increases to 57,000 per
square millimetre.9

Thus it is apparent that when such a large number of dentinal tubules are exposed, a pulpal response
to such a trauma will occur. The nature of the response will depend upon the severity of the trauma
imposed and will vary from laying down of peritubular dentin in teeth with minimal trauma, to
irreversible pulpitis and pulpal necrosis in teeth with severe trauma. It is therefore preferable to
perform root canal therapy prior to periodontal procedures, particularly if periodontal surgery is
indicated. 9

Scanning electron micrograph of the Dentinal tubules at root surface

When the cementum and enamel do not meet at the cemento-enamel junction, these tubules remain
exposed, thus creating pathways of communication between the pulp and the periodontal ligament.
Cervical dentin hypersensitivity may be an effect of such a phenomenon.9

Scanning electron microscopic studies have demonstrated that dentin exposure at the cemento-
enamel junction occurred in about 18% of teeth in general and in 25% of anterior teeth in particular.
In addition, the same tooth may have different cemento-enamel junction characteristics presenting
dentin exposure on one side while the other sides are covered with cementum. \This area becomes
important in assessing the progressions of endodontic pathogens, as well as the effect of root
scaling and planing on cementum integrity, trauma, and bleaching-induced pathosis.14

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4. Palatogingival groove:

It is a development groove, a common anomaly in maxillary lateral incisors. It begins in the central
fossa or across the cingulum, extends varying distances apically. It is located in the midpalatal or
mesial or distal regions of the tooth palatally or even bucally. It provide funnel like areas for plaque
retention. Periodontal probing is advised for patients with palatogingival grooves. Palatogingival
grooves are associated with deep isolated “tubular-shaped” periodontal pockets with intrabony
defects.

They may bleed and suppurate. On radiographs they appear as a “tear drop shaped area” and dark
lines parallel or imposed on the root canal can be noticed. These lines are termed as parapulpal lines
(dark vertical line). They are related to the incidence of localized periodontitis with or without
pulpal pathosis, depending on the depth, extent, and complexity of the groove.1

Palatogingiva development groove in maxillary lateral incisors

5. Root perforations:

Perforations of root are undesirable clinical complications that open up a communication between
the root canal system and the periodontal ligament/oral cavity and may lead to treatment failure.
They occur due to extensive carious lesion, internal and external resorption, over instrumentation
(iatrogenic) and post preparation (iatrogenic).1

6. Vertical root fractures:

A vertical root fracture is defined as a fracture of the root that is longitudinally oriented at a more or
less oblique angle towards the long axis of the tooth. Root fractures occur accidently and may
involve cementum, dentine and pulp. Mobility of the involved teeth, Pain on biting, pain on
selective loading of the cusps, discomfort, periodontal defect, radiographic bone destruction,
abscess formation and a narrow sinus tract-type of probing defect may at instances be present on
one side in the line of fracture are all seen.1

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 Illustration & IOPA showing vertical root fracture

II. Pathological Pathways Of Communication

1. Empty Spaces Created By Destroyed Sharpey’s Fibres

Due to destruction of periodontium in cases of periodontal disease, the contents of the root canal
system get exposed to the toxic products. Thus there is direct communication established between
the pulp and the oral cavity through the exposed dentinal tubules.15

2. Root Fractures Following Trauma

A vertical root fracture is defined as a fracture of the root that is longitudinally oriented at the more
or less oblique angle towards the long axis of the tooth. It can traverse the root in different
directions, mesially/distally or facially/lingually.
It may or may not involve the pulp chamber. A vertical root fracture can extend the entire length of
the tooth and involve the gingival sulcus or pocket area but may also be incomplete and confined to
either the coronal or the apical portions.

As a result of bacterial growth in the fracture space, the adjacent periodontal ligament will become
the seat of an inflammatory lesion causing breakdown of the connective tissue fibers and alveolar
bone.15

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3. Loss of Cementum
Loss of cementum can occur because of gingival recession, due to presence of inadequate attached
gingiva, improper brushing technique, periodontal surgery, overzealous tooth cleansing habits, etc.

III.Iatrogenic Pathways Of Communication

1. Perforation during endodontic therapy

Perforation is basically a mechanical or pathological communication between the root canal system
and the external tooth surface.

It can occur at any stage while performing endodontic therapy that is during access cavity
preparation or during instrumentation procedures leading to canal perforations at cervical, midroot
or apical levels.15

Diagram illustrating Perforation during endodontic therapy

2. Root fracture during root canal therapy

Root fracture can occur at any stage of root canal treatment, that is during biochemical preparation,
obturation or during post placement. The common reasons for root fracture are excessive dentin
removal during biomechanical preparation and weakening of tooth during postspace preparation.
Whatever is the reason, the fracture site provides entry for bacteria and their toxic products from
root canal system to the surrounding periodontium. 15

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3. Exposure of dentinal tubules during root planning

Exposure of dentinal tubules during periodontal surgery or root planning procedures can result in a
pathway of communication between pulpal and periodontal space.15

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ETIOPATHOGENESIS

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 ETIOPATHOGENESIS
The etiologic factors involved in the evolution of perio-endo lesions can be of a varied natureThe
main etiological factors for endo-perio lesions are living (bacteria, fungi and viruses) and nonliving
pathogens. Along with these, many contributing factors such as trauma, root resorptions,
perforations, and dental malformations also play an important role in the development and
progression of such lesions . Paul and Hutter reported that despite our substantial understanding of
the etiology of periodontal and endodontic disease, we are frequently at a loss to explain how one
process occurring primarily in the pulpal or periodontal tissues might affect the other process.

The transfer of bacterial flora between periodontal and pulpal tissues is summarized in a schematic
diagram. Ross et al studied the relationship between periodontal and pulpal disorders & concluded
that concurrent periodontal and pulpal disorders may related to, or independent of, each other.16

Schematic diagram illustrating possible pathways as well as the direction within these pathways for
spread of infection between pulpal and periodontal tissues.7

A. INFLUENCE OF PULPAL PATHOLOGIC CONDITION ON PERIODONTIUM

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1. Impact of disease conditions in the vital pulp
Disease processes, caries, restorative procedure and traumatic injuries of the dental pulp frequently
involve inflammatory changes.

The resulting inflammation will then be directed towards the source of irritation and be confined for
as long as the inflammatory defence does not collapse and convert into a destructive breakdown of
the pulpal tissue. Consequently inflammatory alterations in the vital pulp will not sustain distinct
lesion in the adjoining periodontium. Yet occasionally, disruption of the apical lamina dura or
widening of the periodontal ligament space may seen in the periodontium. Even minor periapical
radiolucency may be present in spite of that vital pulp functions prevail. In such instances, typical
clinical signs of pulpitis, including spontaneous pain, thermal sensitivity or tenderness to
percussion, may or may not be present.17

If the pulp survives the acute phase of the inflammatory response, repair and scarring of the tissue
frequently develop. Reparative dentin with in areas of the previous lesion, fibrosis and dystrophic
mineralization represent typical sequelae to pulpal repair. Such tissue changes may interfere with
the nervous and vascular supply of the tissue, which in turn may jeopardize its continued vital
function.18

Inference:
From a diagnostic point of view it is important to realize that as long as the pulp maintains vital
functions, although inflamed or scarred. It is unlikely to produce irritants that are sufficient to cause
pronounced marginal breakdown of the periodontium. Consequently no benefit will be gained from
pulp.

2. Impact of pulpal necrosis

Contrary to disease conditions in the vital pulp, pulp necrosis is frequently associated with
inflammatory involvement of periodontal tissue. The location of this lesion is most often at the
expense of the tooth. They may also occur at any site where lateral canals exit into the
periodontium.

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While sterile necrotic pulps are unable to sustain overt inflammation in the periodontal tissue. In
this respect pulpal disease shares an identical etiology with periodontal disease. In fact, the two
disease entities show many characteristics in common in terms of their microbiologic and
immunologic histopathology features.17

Similar to periodontal disease, potential pathogen most often associated with endodontic infection
are found in the anaerobic segment; Fusobacterium, Provotella, Porphyromonas,
Peptostreptococcus, Eubacterium, Capnocytophaga and Lactobacillus belonging to the genera most
frequently isolated by culture5. Also Spirochete and Fungi may reside in infected root canals.19
It should be noted that the composition of the micro biota in necrotic pulps is not as complex as one
in deep periodontal pockets associated with periodontal disease and usually comprises a limited
number of bacterial species of with or two many predominate.

The host tissue response to the infection will take the form of either an acute abscess or a chronic
inflammatory response. Which of the forms occurs is largely depends on the quality and quantity of
bacteria present in the root canal and capacity of the host defense to confine and neutralize the
bacterial elements that are released from the root canal into the periodontium.Following the initial
expansion, which involves destruction of the periodontal ligament and the adjunct alveolar bone, a balanced
host parasite relationship is usually established. The inflammatory processes may then remain unchanged in
size for years.9

Histologically, the established lesion is characterized by a richly vascularized granulation tissue,

infiltrated by inflammatory cells, neutrophils, remainder lesion comprises of mixed cellularity and
varying immunocompetent cells are prevalent in long standing infection . With increasing distance
from root canal apertures and lesion harbors a decreasing number of inflammatory cells and
increasing amount of fibrovascular element representing attempts to repair. More peripherally there
is much stronger expression of fibroblastic activity and formation of new vessels and in the most
peripheral portion of the lesion, a collagen rich connective tissue normally separates it from the
surrounding bone tissue.

Some but far from all lesions containing proliferating epithelial cells, they originate from epithelial
rests of malassez. In its established form, a lesion is clearly localized and constitutes an
immunologically active protection zone of importance, to preventing the dissemination of
intracanal pathogens into surrounding periodontal tissue.Bacteria occasionally overcome the host
defense and be present in the periapical tissue. This is particularly true for purulent lesion.

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Inference :
The essential difference between the two disease (pulpal and periodontal) entities is their respective
source of infection. Periodontal ligament disease is maintained by bacterial accumulation in the
dentogingival region, while endodontic lesions are directed towards infectious elements released
from pulpal space.

Rarely well established lesions of pulpal origin involves marginal periodontium; unless they are
developing close to the bone margin. A potential pathway for infectious element in root canal in
such instances may be lateral canal.

3. Manifestations of endodontic lesions in the marginal periodontium from lateral canals

Endodontic lesions, where bacterial elements reach the periodontium by way of lateral canals, may,
except for lateral aspects of roots, appear in furcation areas of 2 and 3 rooted teeth.
If there is an existing periodontal lesion, the two soft tissue lesions may merge and in the
radiographically appear as one lesion.

Although clinically, one may be able to bring a probe through both lesions, it is important from a
therapeutic point of view to understand that the coronal part is directed towards an infection in the
marginal periodontium and the apical part to an infection emanating from the sources of infection is
required.

Lateral canals normally harbour connective tissue and blood vessels, which connect the circulatory
system of the pulp with periodontium. Such anastomosis is formed during the early phases of tooth
development. During the completion of the root formation, severe anastomosis are blocked and
reduced in width by continuous deposition of dentin and cementum.

This may explain why endodontic lesions are rarely seen in furcal areas of adult dentition, while in
primary and young permanent molars, such lesions are often the first signs of infected pulpal
necrosis. Patent communications may bring about endodontic lesions in the adult dentition.
Although clinical observations demonstrate that occurrence, the rate at which endodontic lesion
appears in the marginal periodontium seems to be low20.An intact layer of cementum evidently acts
as an effective barrier against passage of both, bacteria and its components.

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Inference:

Inflammatory lesions may develop from a root canal infection at the lateral aspects of the root and
in furcation regions of two and multirooted teeth. These types of lesions appear to be rare and do
not seem to emerge at a rate that corresponds to the frequency associated with lateral canals occur
in teeth.

B. INFLUENCE OF PERIDONTAL DISEASES ON THE PULP

Bacterial products and substances released by the inflammatory process in the periodontium may
gain access to the pulp along the very same pathways as an endodontic infection can affect the
periodontium in the opposite direction. A clear-cut relationship between progressive periodontal
disease and pulpal involvement, however does not invariably exist.

While inflammation as well as necrosis of pulp tissue have been observed adjacent to lateral canal
in teeth exposed by periodontal disease, a number of clinical studies have failed to confirm a direct
correlation between periodontal disease and pulp tissue changes.
Observation suggests that the presence of an intact cementum layer is important for the protection
of the pulp from injurious elements produced by the plaque microbiota. Once the dentin pulp
complex has been exposed to the bacterial challenge, repair and healing will be instituted, leaving
the remaining tissue relatively unaffected.21

In the study by Bergenholtz & Lindhe, destructive periodontal disease was produced experimentally
during a comparatively short period [5-7 months], while in humans a similar degree of destruction
of periodontal tissue normally requires several years.
It has been reported that the pulp of teeth with long standing periodontal\pulp disease develops
fibrosis and various forms of mineralization. The number of blood vessels and nerve fibres can also
be reduced.22

Zarneck and Shilder evaluated 40 teeth and also concluded that periodontal disease had no effect on
the pulp. The pulpal changes reported by previous researchers as pathology was distributed instead
to, inadequate histologic fixation and varying degrees of normal between young and old pulps.
They further noted that each of the teeth with a necrotic pulp had either extensive caries or massive
restorations. Finally in their study of 34 asymptomatic teeth with periodontitis only 6 showed
evidence of pulpal pathosis.

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Inference:
Thus it can be said that periodontal disease rarely jeopardizes the vital functions of the pulp. In
teeth with moderate breakdown of the attachment apparatus, the pulp usually remains in the proper
function. Breakdown of the pulp presumably does not occur until the periodontal disease process
has reached a terminal state, i.e. when bacterial plaque involves the main foramina.

Apparently, as long as the blood supply through the apical foramen remains intact, the pulp is
capable of withstanding injurious elements released by the lesion in the periodontium.

Periodontal disease is an inflammatory and effective process; however, it does not appear to have a
direct inflammatory effect on pulp. The initial effect of periodontal inflammation may be
degenerative. This is evident histological as an increase in secondary dentin formation, dystrophic
calcification, fibrosis and collagen resorption.23

ATROPHIC CHANGES

Teeth with caries or restorations that also have periodontal ligament disease have more atrophic
pulps than teeth with caries or restorations but no periodontal disease18. A larger collagen content in
the pulp, with more dentin and dystrophic calcification, is found in teeth with periodontal ligament
disease, and the canal space may be markedly narrowed.24

Changes occur in the relationship between surface and inflammatory root resorption and in the
pulp after reimplantation. Thus due to these atrophic changes, there is a disruption of blood flow
through lateral canals which leads to localized areas of coagulation necrosis in the pulp.21
Root planning have the same affect on the pulp and has been shown to increase the rate of
reparative dentinogenesis .One possible explanation for his is that blood vessel leading into lateral
canals are severed, causing localized areas of pulpal necrosis.21

In cases of slowly developing periodontal disease, cementum deposition may act to obliterate a
lateral canal before pulpal irritation occurs. Hence this cementum deposition along with the absence
of lateral canal explain swhy not all periodontally involved teeth demonstrate pulpal atrophy and
cause narrowing.

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INFLAMMATORY CHANGES:

The causative agents of periodontal disease are found in the sulcus and are continually challenged
by host defenses. An immunologic or inflammatory response is elicited in response to this
microbiologic challenge.

This results in the formation of granulomatous tissue in the periodontium. When periodontal
disease extends from the gingival sulcus towards the apex, the inflammatory products attack the
elements of the periodontal ligament and the surrounding alveolar bone.

A clear cut relationship between progressive periodontal disease and pulpal involvement, however,
does not invariably exist. The most common periodontal lesion produced by the pulp disease is the
localized apical granuloma. It is produced by the diffusion of bacterial products through the root
apex, with the formation of vascular granulation tissue. Subsequently, resorption of the alveolar
bone and occasionally of the root itself may occur.21

INFLUENCE OF PERIDONTAL TREATMENT MEASURES ON THE PULP

SCALING AND ROOT PLANNING:
They are indispensable procedures in the treatment of periodontal disease. However, not only will
bacterial deposits be removed from the root surface but also may cementum & superficial dentin.
Therefore by this instrumentation dentinal tubule will be exposed and normally left unprotected to
the oral environment.

Subsequently microbial colonization of the exposed root dentin may result in bacterial invasion of
the dentinal tubule. As a consequence, inflammatory lesion may develop in the pulp.21Yet the
vitality of the pulp is not normally put at risk even though hypersensitivity frequently develops
following such measures presenting an uncomfortable and difficult problem to manage.

During the maintenance phase of periodontal ligament therapy scalling and planning of root are
frequently repeated procedures. At each recall session the root surfaces are debribed and some
dentin is removed. This therapy can result not only in weakening of tooth structure but also in
extensive reparative dentin formation in pulp. However on rare occasions deep periodontal
ligament scalling may expose lateral canals that in turn can induce severe painful symptoms of
pulpitis.24

28
Inference:
Results of clinical observations and animal experiments support the view that scalling and root
planning procedures normally do not threaten the vitality of the pulp. Adjacent to instrumented root
surfaces localized inflammatory alterations may on occasion emerge, but in most instances these
will be followed by repair processes.

ROOT DENTIN HYPERSENSITIVITY

Patient subject to root planning & scaling in periodontal ligament therapy may after the
instrumentation procedure experience increased sensitivity of the treated teeth to evaporation,
tactile, thermal and osmotic stimuli. Usually the symptom, most often a temporary and sustainable.
However, occasionally the condition may become a chronic pain problem and may persists for
months or years. In a clinical trial comprising 35 patients, Tommaro et al observed that, while a
majority of patients subjected to non- surgical periodontal instrumentation developed sensitive
teeth, only a few teeth in a small number of patient developed highly sensitive root surfaces.25

Initial symptom is sharp pain of rapid onset that disappears once the stimulus is removed. In more
severe, long standing cases, shorter or longer periods of lingering, dull or aching pain symptoms
may be provoked. Even a minimal contact of a tooth brush with root dentin surface may result in
intense pain that hinder proper oral hygiene measures.25
This pain condition is termed dentin hypersensitivity by Holland et al. But the Ailment has also
been given many other names such as sensitive dentin, cervical dentin sensitivity and root
sensitivity. After periodontal instrumentation dentinal tubules becomes uncovered to oral
environment and subject to hydrodynamic forces. Hence a variety of pain evoking stimuli elicits
sudden fluid shifts in the exposed tubules thereby inducing a painful sensation according to
hydrodynamic theory of dentin sensitivity.

The increase in pain intensity may have one or both of the following two explanations. Firstly the
smear layer formed on the root surface by the scaling procedure will be dissolved within a few
days. This in turn will increase the hydraulic conductance of the involved dentinal tubule and thus
decrease the peripheral resistance to fluid flow across dentin. Thereby pain sensation is more
readily provoked. Secondly open dentinal tubule serve as pathways for diffusive transport of
bacterial elements in the oral cavity to the pulp, which is likely to cause a localized inflammatory
pulpal response.

29
In addition, shallow exposures of root dentin are accompanied by sprouting of new terminal braches
from pulpal axons in areas subjacent to root surface injury. Sprouting of nerves is a temporary
event and will subside if inflammation disappears- a feature consistent with their involvement in
root dentin hypersensitivity.26

The fact that root dentin hypersensitivity often disappears a few weeks after the scaling procedure is
best explained by the development of natural occlusion of the exposed dentinal tubules by mineral
deposits. Hypersensitive root areas show large numbers of tubular apertures on their surfaces than
non-sensitive radicular dentin support this view. The fact that only certain individuals become
seriously affected may be related to local factors in oral cavity, as well as the level of pain
perception.

Inference:
Root dentin hypersensitivity develops as an uncomfortable and sometimes difficult ailment to treat,
subsequently scalling and root planning procedure in periodontal therapy. Although the exact
mechanism is not well established, the condition is clearly related to open dentinal tubule that
allows hydrodynamic mechanism to elicit painful sensation upon external stimuli. Root dentin
hypersensitivity should be checked against other conditions that can cause similar symptoms, for
example cracked teeth.

ACID ETCHING

Root conditioning using citric acid during periodontal regenerative therapy helps to remove
bacterial endotoxin and anaerobic bacteria and to expose collagen bundles to serve as a matrix for
new connective tissue attachment to cementum.

Though beneficial in the treatment of periodontal disease, citric acid removes the smear layer, an
important pulp protector. Cotton and Siegel reported that citric acid, when applied to freshly cut
dentine, has a toxic effect on the human dental pulp. However, several other studies have concluded
that pulpal changes after the application of citric acid does not show any significant changes in the
pulp.21

30
CONTRIBUTING FACTORS

31
 CONTRIBUTING FACTORS:

Chart of Factors Associated With Endo-Perio Lesion 6

1. Poor endodontic treatment

Correct endodontic procedures and techniques are key factors for treatment success. It is imperative
to completely clean, shape and obturate the canal system in order to enhance successful outcomes.
Unfortunately, poor endodontic treatments are often found associated with periradicular
inflammation. Poor endodontic treatment allows canal reinfection, which may often lead to
treatment failure. Clinical signs and symptoms as well as radiographic evidence of periradicular
lesions are usually associated with endodontic failure.9

32
(A) Maxillary lateral incisor with necrotic pulp and periapical lesion. (B)over obturation and poor
endodontic treatment Nine months after endodontic treatment the tooth is symptomatic and the
lesion is larger. (Courtesy: Rotstein & Simon)

A)Non-healing due to insufficient root canal preparation and obturation in a maxillary second
premolar. (B) Two-year follow-up radiograph showing evidence of bony healing.
(Courtesy: Rotstein & Simon)

Endodontic failures can be treated by either orthograde or retrograde retreatment with good success
rates. It seems that the success rate is similar to that of initial conventional endodontic treatment if
the cause of failure is properly diagnosed and corrected. In recent years, retreatment techniques
have improved dramatically due to use of the operating microscope and development of new
armamentarium.9

33
2. Poor restorations

I. Overhanging dental restorations

Overhanging dental restorations are major dental health problem. An Overhanging dental restoration
is defined as an extension of restorative material beyond the confines of a cavity, preparation. They
have been strongly implicated as an etiologic factor in the progression of periodontal disease and are
alarmingly prevalent.27

Radiograph showing inadequate overhanging dental restorations and bone loss

In addition to promoting plaque accumulation, they change a nondestructive subgingival flora to a

destructive one. There is good documentation that bleeding, gingivitis, and bone loss increase in
tissues adjacent to overhanging dental restorations as compared to homologous teeth. Removal of
overhanging dental restorations enhances the effectiveness of the hygienic phase of periodontal
therapy. Many overhanging dental restorations, however, are not detected on radiographs and are
evident only by use of an explorer directed subgingivally. For this reason and others, many are not
removed.27

II. Coronal leakage

Coronal leakage is the term used to designate leakage of bacterial elements from the oral
environment along restoration margins to the endodontic filling. Studies have indicated that this factor
may be an important cause of endodontic treatment failure. Root canals may become re-
contaminated by microorganisms due to delay in placement of a coronal restoration and fracture of
the coronal restoration and/or the tooth. Defective restorations and adequate root canal fillings will
have a higher incidence of failures than teeth with inadequate root canal fillings and adequate
restorations.9

34
 Poor coronal seal in a maxillary second premolar. (A) Radiograph showing inadequate coronal
restoration and root canal treatment. Note the lateral apical lesion associated with the tooth. (B)
Radiograph taken upon completion of endodontic retreatment. The old restoration was removed and
the canal system properly prepared and obturated. (Courtesy: Rotstein & Simon)

In an in-vitro study, they found that packing excess gutta-percha and sealer over the floor of the
pulp chamber, after completion of root canal filling, did not provide a better seal of the root canals.
It was therefore recommended that excess of gutta-percha filling should be removed to the level of
the canal orifice sand that the floor of the pulp chamber be protected with a well sealed restorative
material.9

Coronal restoration is the primary barrier against coronal leakage and bacterial contamination of the
root canal treatment. It has been shown that lack of coronal coverage following endodontic
treatment can significantly compromise tooth prognosis. Therefore, it is essential that the root canal
system be protected by good endodontic obturation and a well-sealed coronal restoration.10

3. Trauma

Traumatic injuries to the teeth result in damage to many dental and periradicular structures. Trauma
to teeth and alveolar bone may involve the pulp and the periodontal ligament. Both tissues can be
affected either directly or indirectly.

Dental injuries may take many shapes but generally can be classified as enamel fractures, crown
fractures without pulp involvement, crown fractures with pulp involvement, crown–root fracture,
root fracture, luxation, and avulsion. Treatment of traumatic dental injuries varies depending on the
type of injury and it will determine pulpal and periodontal ligament healing prognosis.3

35
4. Vertical Root Fracture

In general, vertical root fractures occur most often on endodontically treated teeth. The clinical
features of vertical root fractures in non endodontically treated teeth can sometimes appear as
combined endodontic and periodontal lesions. Cemental tears or detachment of cementum from a
root surface by means of trauma or aging has been reported; the lesion often results in periodontal
destruction and endodontic involvement.20

Vertical root fractures have been associated with root-filled teeth where excessive lateral forces
were applied during compaction or possibly with stress induced by a post placement in root-filled
teeth. Clinical survey of fractured teeth also reveals that fractures are more common in teeth with
extensive restorations, in older patients, and in mandibular posterior teeth.20

Pain during occlusion or mastication is the principal symptom. Thermal sensitivity, gingival
swelling, and periodontal abscess or sinus tracts are also common. Narrow or localized deep
pockets are usually detected by periodontal probing. Widening of the root canal space and
periapical and/or periodontal radiolucency are radiographic characteristics which may aid in
diagnosis.20

Root fractures frequently occur on endodontically treated teeth and are associated with a deep
pocket on a surface of the tooth which may or may not be abscessed.
Symptoms and signs associated with vertical root fractures show a variety of characteristics and are
difficult to distinguish from those associated with periodontal and endodontic lesions. Pain on
selective loading of cusps may be an indication of a root fracture. Sometimes the definitive
diagnosis of vertical root fractures has to be confirmed by exploratory surgical exposure of the root
for direct visual examination.20

The development of periodontal disease may be a contributory factor in the deterioration of the
tissues surrounding a pre-existent root fracture. Widening of the fracture space may result from
communication between the fracture site and the oral fluids.

Vertical root fractures that involve the gingival sulcus and periodontal pocket area usually have a
hopeless prognosis because of continuous bacterial invasion of the fracture space from the oral
environment. Single-rooted teeth are generally extracted. In multirooted teeth, a treatment
alternative is hemisection or resection of the fractured root.

36
Vertical root fracture. A, Radiograph revealed widened periodontal ligament with J-shaped
radiolucency around the apex. B, Periodontal probe indicated more than 12 mm of probing depth. C,
Exploratory surgery confirmed vertical root fracture. (Courtesy: Ingle’s Endodontics)

5. Root Perforations

Root perforations are undesirable clinical complications that may lead to periodontal lesions. When
root perforation occurs, communications between the root canal system and either peri-radicular
tissues or the oral cavity may often reduce the prognosis of treatment. Root perforations may result
from extensive carious lesions, resorption, or from operator error occurring during root canal
instrumentation or post preparation.10

Iatrogenic root canal perforations: They are serious complications during dental treatment and have
a rather poor prognosis. Perforations may be produced by powered rotary instruments during the
attempt to gain access to the pulp or during preparation for a post. Improper manipulation of
endodontic instruments can also lead to a perforation of the root. When root perforation occurs,
communications between the root canal system and either periradicular tissues or the oral cavity
may often reduce the prognosis of treatment.

37
At the site of perforation, an inflammatory reaction in periodontal ligament occurs and leads to the
formation of a lesion which can progress as a conventional primary endodontic lesion.10

Perforation in the middle or apical third of root

Inflammatory lesions in the marginal periodontium as manifested by increased probing depth,

suppuration, increased tooth mobility, and loss of fibrous attachment may result from an undetected
or unsuccessfully treated root perforation. A periodontal abscess may also occur in the absence of
any previous periodontal disease, following perforation of the lateral wall of the root during
endodontic therapy.3

Treatment prognosis of root perforation depends on the size, location, time of diagnosis and
treatment, degree of periodontal damage as well as the sealing ability and biocompatibility of the
repair material.10
6. Resorptions

Root resorption is a condition associated with either a physiologic or a pathologic process resulting
in a loss of dentin, cementum and/or bone5. It may be initiated in the periodontium and affect
initially the external surfaces of the tooth (external resorption) or it may start within the pulp space
affecting primarily the internal dentin surfaces (internal resorption)

. If not diagnosed and treated, external root resorption may invade cementum, dentin and ultimately
the pulp space. In cases of untreated internal resorptions the process may advance and perforate to
the external root surface.27

38
(A) Radiograph showing an internal inflammatory resorptive defect in the coronal third of the root
canal of a maxillary central incisor. The tooth tested positive to pulp sensitivity tests.
(B) Postoperative radiograph showing obturation of root canal and resorptive defect.
(Courtesy: Rotstein & Simon)

Practically all teeth with apical periodontitis will exhibit a certain degree of inflammatory root
resorption. This can be located on either the apical or lateral aspects of the root but is more frequent
at the apex. During the initial stages the resorption cannot be detected radiographically; however, it
is evident in histologic sections.27

7. Developmental Malformations
Teeth with developmental malformations tend to fail to respond to treatment when they are directly
associated with an invagination or a vertical developmental radicular groove.

Such conditions can lead to an untreatable periodontal condition. These grooves usually begin in
the central fossa of maxillary central and lateral incisors crossing over the cingulum, and continuing
apically down the root for varying distances. Such a groove is probably the result of an attempt of
the tooth germ to form another root.3

Probing deep lingual pocket associated with radicular invagination. Raised flap reveals the depth

39
 and length of deep lingual groove. (Courtesy: Ingle’s Endodontics)

As long as the epithelial attachment remains intact, the periodontium remains healthy. However,
once this attachment is breached and the groove becomes contaminated, a self-sustaining infrabony
pocket can be formed along its entire length. This fissure-like channel provides a nidus for
accumulation of bacterial biofilm and an avenue for the progression of periodontal disease that may
also affect the pulp. Radiographically, the area of bone destruction follows the course of the
groove.3

From the diagnosis standpoint, the patient may present symptoms of a periodontal abscess or a
variety of asymptomatic endodontic conditions. If the condition is purely periodontal, it can be
diagnosed by visually following the groove to the gingival margin and by probing the depth of the
pocket, which is usually tubular in form and localized to this one area, as opposed to a more
generalized periodontal problem. The tooth will respond to pulp-testing procedures. Bone
destruction that vertically follows the groove may be apparent radiographically.10

If this condition is also associated with an endodontic disease, the patient may present clinically
with any of the spectrum of endodontic symptoms. The prognosis of root canal treatment in such
cases is guarded, depending upon the apical extent of the groove.
The clinician must look for the groove as it may have been altered by a previous access opening or
restoration placed in the access cavity. The appearance of a teardrop-shaped area on the radiograph
should immediately arouse suspicion.

The developmental groove may actually be visible on the radiograph. If so, it will appear as a dark
vertical line. This condition must be differentiated from a vertical fracture, which may give a
similar radiographic appearance. Treatment consists of burring out the groove, placing bone
substitutes, and surgical management of the soft tissues and underlying bone. Radicular grooves are
self-sustaining infrabony pockets and therefore scaling and root planing will not suffice. Although
the acute nature of the problem may be alleviated initially, the source of the chronic or acute
inflammation must be eradicated by a surgical approach. Occasionally, the tooth needs to be
extracted due to poor prognosis.10

40
ETIOLOGICAL FACTORS:
LIVE PATHOGENS
Among the live pathogens encountered in a diseased pulp and periapical tissues are: 28
 Bacteria

 Fungi

 Viruses

These pathogens and their by-products may affect the periodontium in a variety of ways and need
to be eliminated during root canal treatment.

1. BACTERIA

Endodontic disease is caused by bacteria. The periapical tissues become involved when bacteria
invade the pulp, causing either partial or total necrosis.10

The relationship between the presence of bacteria and pulpal and periapical diseases was
demonstrated by Kakehashi et al..In that study, pulps of normal (conventional) rats were exposed
and left open to the oral environment. Consequently, pulp necrosis ensued, followed by periapical
inflammation and lesion formation. The study demonstrated that without bacteria and their
products, periapical lesions of endodontic origin do not occur.

Moller et al 28 confirmed these findings in monkeys. They reported that non-infected necrotic pulp
tissue did not induce periapical lesions or inflammatory reactions. However, once the pulp became
infected, periapical lesions and inflammation in the apical tissues occurred.9

Jansson et al., in a retrospective radiographic 3-year study, evaluated 175 endodontically treated
single-rooted teeth of 133 patients. Patients who were more prone to periodontitis and exhibited
evidence of endodontic treatment failures showed about a 3-fold increase in marginal bone loss as
compared to patients without endodontic infection. Jansson & Ehnevid also investigated suggested
that endodontic infection in molars associated with periodontal disease may enhance periodontitis
progression by spreading pathogens through accessory canals and dentinal tubules. These

41
Proteolytic bacteria predominate in the root canal flora, which changes over time to a more
anaerobic microbiota.10

Rupf et al. studied the profiles of periodontal pathogens in pulpal and periodontal diseases
associated with the same tooth.10

Specific PCR methods were used to detect Actinobacillus actinomycetemcomitans, Tannerella

forsythensis, Eikenella corrodens, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella
intermedia, and Treponema denticola. These pathogens were found in all endodontic samples and
the same pathogens were found in teeth with chronic apical periodontitis and chronic periodontitis.
They concluded that periodontal pathogens often accompany endodontic infections and supported
the idea that endodontic–periodontal interrelationships are a critical pathway for both diseases.10

Spirochetes are another type of microorganism associated with both endodontic and periodontal
diseases. Spirochetes are usually found more frequently in subgingival plaque than in root canals.
Several studies revealed a large diversity of oral treponemes present in subgingival biofilms of
periodontal pockets. It has been suggested that the presence or absence of oral spirochetes can be
used to differentiate between endodontic and periodontal abscesses.10

Today, the presence of spirochetes in the root canal system is well documented and has been
demonstrated by different identification techniques such as dark field and electron microscopy,
checkerboard DNA–DNA hybridization analysis, and 16S rRNA gene profiles. Recent studies
demonstrated that the spirochete species most frequently found in root canals are T. denticolaand
Treponema maltophilum. This organism possesses an array of virulence factors associated with
periodontal disease and may also participate in the pathogenesis of periradicular disease. T.
maltophilum is a small, motile treponeme with two periplasmic flagella. T. maltophilum has also
been frequently isolated from patients with rapidly progressing forms of periodontitis. It has also
been suggested that L-form bacteria may have a possible role in periapical disease. 29

Some bacterial strains can undergo morphological transition to their L-form after exposure to
certain agents particularly penicillin. Under certain conditions, depending on host resistance factors
and bacterial virulence, the L-forms revert to their original pathogenic bacterial form and may be
responsible for acute exacerbation of chronic apical lesions.29

42
 A B C

D E F

G H I.

Periapical Actinomyces infection. This case graphically shows the growth of bacteria past the
apical foramen and its invasion of apical cementum and periapical tissues. (A) Radiograph of a
maxillary central incisor with a necrotic pulp showing a large periapical lesion. (B) Nonsurgical
endodontic therapy was done but the tooth continued to be symptomatic. (C) Apical surgery was
then performed. Photomicrograph shows part of the root with the attached lesion. (D) Colonies of
Actinomyces in the lumen of the lesion are evident.(E)Higher magnification shows large colony of
Actinomyces. (F) Foamy macrophages attacking the bacteria. (G) Edge of the bacterial megacolony
showing the absence of inflammatory cells that are unable to penetrate the colony. (H) Higher
magnification of the bacterial colony. (I) Center of the colony untouched by the inflammatory cells.
(Courtesy: Rotstein & Simon)29

43
2. FUNGI (YEASTS)

The presence and prevalence of fungi associated with endodontic disease is well documented. Yeast
colonization associated with radicular pathosis has been demonstrated in untreated root caries,
dentinal tubules, failing root canal treatments, apices of teeth with asymptomatic apical
periodontitis, and in periapical tissues.

Many studies reported that the prevalence of fungi in cultured root canal systems varied from 0.5%
to 26% in untreated root canals and from 3.7% to 33% in cases of previously treated canals.

The majority of the recovered fungi were Candida albicans. C. albicans also showed the ability to
colonize canal walls and penetrate into dentinal tubules. Other species such as Candida glabrata,
Candida guillermondii, and Candida incospicia and Rodotorula mucilaginosa were also detected.10

Factors affecting the colonization of the root canal by fungi are not fully understood. It appears,
however, that among the predisposing factors of this process are immunocompromising diseases
such as cancer, certain intracanal medicaments, local and systemic antibiotics, and previous
unsuccessful endodontic therapy. It has been hypothesized that the reduction of specific strains of
bacteria in the root canal during endodontic treatment may allow fungal overgrowth in the low
nutrient environment.10

Another possibility is that fungi may gain access from the oral cavity during treatment as a result of
poor asepsis. As in endodontic infections, C. albicans was also the most common species of fungi
isolated. Recently, it has been demonstrated that the presence of fungi in root canals is directly
associated with their presence in saliva. These findings further stress the importance of using
aseptic endodontic and periodontal techniques, maintaining the integrity of dental hard tissues and
periodontium.10

44
 A B C

D E F

Fungi in persistent periapical lesion: Fungi in a persistent periapical lesion. (A) Radiograph of
maxillary lateral incisor with necrotic pulp and periapical radiolucency. (B) Immediate
postoperative radiograph showing good nonsurgical treatment. (C)At the 3-month recall the patient
is still symptomatic and the periapical radiolucency is larger. (D) Transmission electron micrograph
shows growing hyphae of a fungus. (E) Higher magnification of the hyphae showing the cell wall.
(F) Reproductive fungi spores. (Courtesy: Ingle’s Endodontics)3

3. VIRUSES

There is increasing evidence to suggest that viruses play an important role in both endodontic and
periodontal diseases.9 In patients with periodontal disease, herpes simplex virus is frequently
detected in gingival crevicular fluid and in gingival biopsies of periodontal lesions.
Human cytomegalo virus was found in about 65% of periodontal pocket samples and in about 85%
of gingival tissue samples. Epstein–Barr virus type I was detected in more than 40% of pocket
samples and in about 80% of the gingival tissue sample.9

45
Gingival herpes viruses were associated with increased occurrence of subgingival P. gingivalis, T.
forsythensis, P. intermedia, Prevotella nigrescens, T. denticola, and A. actinomycetemcomitans,
suggesting that they may play a role in promoting overgrowth of pathogenic periodontal bacteria.9

In endodontics, the presence of viruses in the dental pulp was first reported in a patient with AIDS.
DNA of HIV virus has also been detected in periradicular lesions. However, it has not been
established that HIV virus can directly cause pulpal disease. Herpes simplex virus was also studied
in relation to endodontic disease. However, unlike its role in periodontal disease, it appears that
herpes simplex virus is not associated with endodontic disease.30

On the other hand, recent data suggest that other common types of human viruses may be involved
in pulpal disease and in the development of periapical lesions. Sabeti et al. suggested that human
cytomegalovirus and Epstein– Barr virus play a role in the pathogenesis of symptomatic periapical
lesions.

Herpesvirus activation in periapical inflammatory cells may impair the host defence mechanisms
and give rise to overgrowth of bacteria, as seen in periodontal lesions. Herpesvirus-mediated
immune suppression may be detrimental in periapical infections due to alreadycompromised host
responses in the granulomatous tissue. Alterations between prolonged periods of herpesvirus
latency interrupted by periods of activation may explain some burst-like symptomatic episodes of
periapical disease.

Frequent reactivation of periapical herpesvirus may support rapid periapical breakdown. Absence
of herpesvirus infection or viral reactivation may be the reason that some periapical lesions remain
clinically stable for extended periods of time.30

NON-LIVING ETIOLOGIC AGENTS

Depending on their origin and nature, non-living etiologic agents can be either extrinsic or intrinsic.

I. EXTRINSIC AGENTS

FOREIGN BODIES

Foreign bodies are frequently found to be associated with inflammation of the periradicular tissues.

46
Although endodontic and periodontal diseases are primarily associated with the presence of

microorganisms, some treatment failures may be explained by the presence of certain foreign
substances in situ. These include substances such as dentin and cementum chips, amalgam, root
canal filling materials, cellulose fibers from absorbent paper points, gingival retraction cords,
leguminous foods, and calculus-like deposits.

A foreign-body response may occur to any of these substances and the clinical reaction may be
either acute or chronic. Therefore, such conditions may be either symptomatic or asymptomatic.
Microscopically, these lesions demonstrate the presence of multinucleated giant cells surrounding
the foreign material in a chronic inflammatory infiltrate. Mechanical or surgical removal of the
foreign bodies is usually the treatment of choice.10

A B

C D

Foreign-body particles in a periapical lesion. (A) Radiograph of a symptomatic maxillary central

incisor with a large periapical lesion. Endodontic treatment was done 27 years ago. (B) Apical
surgery was done and apical tissue submitted for histologic analysis. Photomicrograph shows
foreign-body particles in the presence of giant cells. (C) Higher magnification of the foreign-body
particles and giant cells. (D) Part of the foreign body. When put under polarized light, the presence
of vegetable matter was apparent. The diagnosis was confirmed when parts of a paper point
penetrated past the apical foramen. (Courtesy: Rotstein & Simon)3

47
II.INTRINSIC AGENTS

1. CHOLESTEROL

The presence of cholesterol crystals in apical periodontitis is a common histopathologic finding.

With time, the cholesterol crystals would be dissolved and washed away, leaving behind the spaces
they occupied as clefts. The reported prevalence of cholesterol clefts in periapical disease varies
from 18% to 44%.10

It has been suggested that the crystals could be formed from cholesterol released by disintegrating
erythrocytes of stagnant blood vessels within the periapical lesion, lymphocytes, plasma cells and
macrophages, which die in great numbers and disintegrate in chronic periapical lesions, or by the
circulating plasma lipids..30

However, it is possible that all of these factors may contribute to the accumulation, concentration
and crystallization of cholesterol in a periapical lesion. Accumulation of cholesterol crystals in
inflamed periapical tissues in some cases has been suggested to be one of the causes of failure of
endodontic therapy.10

A B

Cholesterol clefts in a periapical lesion. (A)Photomicrograph stained with Masson‟s Trichrome of a

cyst with a thick fibrous wall. Embedded in the wall is a large collection of cholesterol clefts. (B)
Higher magnification showing empty clefts where cholesterol was dissolved during the histologic
preparation.3

It seems that the macrophages and the multinucleated giant cells that congregate around cholesterol
crystals are not efficient enough to destroy the crystals completely. In addition, the accumulation of
macrophages and giant cells around the cholesterol clefts in the absence of other inflammatory
cells, such as neutrophils, lymphocytes and plasma cells, suggests that the cholesterol crystals

48
induce a typical foreign-body reaction.10

2. RUSSELL BODIES

Russell bodies can be found in most inflamed tissues throughout the body including the
periradicular tissues. These are small, spherical accumulations of an eosinophilic substance found
within or near plasma cells and other lymphoid cells. The presence and occurrence of Russell
bodies in oral tissues and periapical lesions is well documented35. Several studies have indicated
the presence of Russell bodies in about 80% of periradicular lesions. Recently, large intracellular
and extracellular Russell bodies were found also in inflammatory pulpal tissue of carious primary
teeth.10

It is hypothesized that Russell bodies are caused by the synthesis of excessive amounts of normal
secretory protein in certain plasma cells engaged in active synthesis of immunoglobulins. The
endoplasmic reticulum becomes greatly distended, producing large homogeneous eosinophilic
inclusions. However, the mechanisms of Russell bodies production, and their exact role in pulpal
inflammation have not yet fully elucidated.10

(A) Photomicrograph of a periapical

lesion showing presence of Russell
bodies.
A (B) Transmission electron micrograph
demonstrates the round amorphous
shape of these bodies.

(Courtesy: Rotstein & Simon)10

3. RUSHTON HYALINE BODIES

The presence of Rushton hyaline bodies (RHB) is a feature unique to some odontogenic cysts.
Their frequency varies from 2.6% to 9.5%. Rushton hyaline bodies usually appear within either the

49
epithelial lining or the cyst lumen. They have a variety of morphologic forms, including linear
(straight or curved), irregular, rounded and polycyclic structures, or they may appear granular.

The exact nature of Rushton hyaline bodies is not fully understood. It has been variously suggested
that they are keratinous in nature , of hematogenous origin, a specialized secretory product of
odontogenic epithelium, or degenerated red blood cells.

Photomicrograph showing Rushton hyalinebodies in the

epithelial lining of a periapical cyst. (Courtesy: Rotstein &
Simon)10

4. CHARCOT-LEYDEN CRYSTALS

Charcot-Leyden crystals (CLC) are naturally occurring hexagonal bipyramidal crystals derived
from the intracellular granules of eosinophils and basophils. Their presence is most often associated
with increased numbers of peripheral blood or tissue eosinophils in parasitic, allergic, neoplastic,
and inflammatory diseases.31

Activated macrophages were reported to have an important role in the formation of CLC in several
disease processes. CLC and damaged eosinophils, along with their granules, have been observed
within macrophages. It has been proposed that after the degranulation of eosinophils, CLC protein
could be phagocytized into acidified membrane-bound lysosomes. Although the biological and
pathologic role of CLC in endodontic and periodontal disease is still unknown, they may be
associated with some cases of treatment failures.

5. EPITHELIAL RESTS OF MALASSEZ

Epithelial rests of Malassez are normal constituents of both the lateral and apical periodontal
ligament. The term ‘‘rests,’’ is misleading in that it evokes a vision of discrete islands of epithelial
cells. It has been shown that these rests are actually a fishnet-like, three-dimensional,
interconnected network of epithelial cells. In many periapical lesions, epithelium is not present and

50
therefore is presumed to have been destroyed. If the rests remain, they may respond to a stimulus by
proliferating to wall off the irritants coming through the apical foramen. The epithelium is
surrounded by chronic inflammation and is termed an epitheliated granuloma. If this lesion is not
treated, the epithelium continues to proliferate in response to the bacteria and inflammatory
products from the apical foramen.10

The term ‘‘bay’’ cyst has been introduced for the microscopic representation of this situation. This
is a chronic inflammatory lesion that has epithelium lining surrounding the lumen, but the lumen
has a direct communication with the root canal system through the foramen. On the other hand, a
‘‘true’’ cyst is the completion of the epithelial proliferative lesion. It is a three-dimensional,
epithelium-lined cavity with no communication between the lumen and the canal system.
When periapical lesions are studied in relation to the root canal a clear distinction between these
two entities should be made.
There has been some confusion in the diagnosis when lesions are studied only on curetted biopsy
material. Since the tooth is not attached to the lesion, orientation to the apex is lost. Therefore the
criterion used for diagnosis of a cyst is a strip of epithelium that appears to be lining a cavity. It is
apparent that curetting both a bay cyst and a true cyst could lead to the same microscopic diagnosis.

A bay cyst could be sectioned in such a way that it could resemble or give the appearance of a true
cyst. This distinction between a bay and a true cyst is important from the standpoint of healing. It
may be that true cysts must be surgically removed, but bay cysts that communicated with the root
canal may heal with nonsurgical root canal therapy.

Since root canal therapy can directly affect the lumen of the bay cyst, the environmental change
may bring about resolution of the lesion. The true cyst is independent of the root canal system;
therefore conventional therapy may have no effect on the lesion. The formation of a cyst and its
progression from a bay cyst to a true cyst occurs over time. Thus the longer a lesion is present, the
greater the chance of becoming a true cyst. However, the incidence of true cysts is probably less
than 10%.10

51
CLASSIFICATION OF ENDO-
PERIO LESIONS

52
 CLASSIFICATION OF ENDODONTIC
PERIODONTAL LESIONS
Because of the close relationship between endodontics and periodontics, various classifications
have been suggested for lesions affecting the pulpal and periodontal tissues. A good classification
system will help clinician to differentiate whether the lesion is of periodontal or endodontic in
origin and to dictate the correct plan of treatment.

1. CLASSIFICATION BY GULDENER, HIATT AND SIMON 32

The classification of teeth with pulpo-periodontal changes suggested by these authors is based
mainly on the aetiology of the disease.

Class I: primary endodontic lesions

Class I (A): Accidental perforations (intralveolar) or resorptive perforations (internal resorption).
Class I (B): Chronic periradicular lesion (granuloma or cyst) or acute periradicular lesion (alveolar
abscess).

Class II: primary periodontal lesions

Class II (A): Advanced periodontal disease with or without extension to the apical area (pulp vital)
Class II (B): Secondary endodontic involvement. Infection through lateral canals or dentinal
tubules. Pulpal necrosis with or without secondary periapical involvement (pulp non-vital)

Class III: combined lesion

True combined lesion (coalescence between periodontal and endodontic lesion) or vertical crown-
root fracture with pulpal involvement.

(A) primary endodontic lesions (B) primary periodontal lesions (C) True combined lesion

53
2. CLASSIFICATION BY FRANKLIN S.WEIN 4

This classification is based on the fact that four types of endodontic-periodontal cases are commonly
encountered. Divisions of the cases are based on the etiology of the disease.

Class I - Tooth in which symptoms clinically and radiographically simulate periodontal disease but are
in fact due to pulpal inflammation and/or necrosis.

Class II - Tooth that has both pulpal or periapical disease and periodontal disease concomitantly

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 disease but in fact
has periodontal disease.

3. CLASSIFICATION BY GULDENER AND LANGELAND 33

(BASED ON POSSIBLE PATHOLOGIC RELATIONSHIPS)

A. Endodontic – Periodontal Lesions: In endodontic-periodontal lesions, pulpal necrosis precedes

periodontal changes. A periapical lesion originating in pulpal infection and necrosis may drain to
the oral cavity through the periodontal ligament and adjacent alveolar bone.
This may present clinically as a localised, deep, periodontal pocket extending to the apex of the
tooth. Pulpal infection also may drain through accessory canals, especially in the area of the
furcation & may lead to furcal involvement through loss of clinical attachment and alveolar bone.

B. Periodontal – Endodontic Lesions: In periodontal-endodontic lesions, bacterial infection from

a periodontal pocket associated with loss of attachment & root exposure may spread through
accessory canals to the pulp, resulting in pulpal necrosis. In the case of advanced periodontal
disease, the infection may reach the pulp through the apical foramen. Scaling & root planing
removes cementum & underlying dentin and may lead to chronic pulpitis through bacterial
penetration of dentinal tubules.

C. Combined Lesions: Combined lesions occur when pulpal necrosis and a periapical lesion occur
on a tooth that also is periodontally involved combined lesions could display interesting
correlations between specific microbiota of endodontic lesion and periodontal pockets.4
54
4. CLASSIFICATION BY SIMON .J.H.S, GLICK.D.H AND FRANK.A.L 34
(BASED ON ETIOLOGY, DIAGNOSIS, PROGNOSIS AND TREATMENT)
To clarify the interrelationship of pulpal and periodontal disease state, a classification system was
developed in 1972, classified on the basis of theoretic pathways of lesion formation.

1. Primary endodontic lesion: Necrotic pulp draining coronally through the periodontal ligament
into the gingival sulcus with acute exacerbation of chronic apical lesion. The necrotic pulp may
drain through the apical foramen, lateral canal or through the accessory canals at the furcal area.
The pocket that forms is narrow and has little or no local factors. Radiographs with gutta-percha
cone tracing the sinus tract point towards the origin of the lesion. Root canal treatment is the
treatment of choice. Prognosis is excellent with complete and rapid resolution of the lesion occurs.

2. Primary periodontal lesion: It is chronic periodontitis progressing apically along the root
surface. It is characterized with wide periodontal pocket along with presence of local factors, a vital
pulp, minimal or no pain, periodontal pockets in multiple teeth. Periodontal therapy is the available
treatment option. Root canal therapy must not be carried as the pulp is vital.
Only Periodontal therapy should be carried out. Prognosis is related to the amount of attachment
loss, the effectiveness of the periodontal treatment accomplished and the patient response.

3. Primary endodontic with secondary periodontal involvement: Primary endodontic lesion with a
draining abscess through the periodontium if left untreated over a period of time may lead to local
factors accumulating in the sinus tract and a creation of secondary periodontal problem. It may also be
caused due to root fractures, iatrogenic perforations by improper placement of pins and post. 9 Evidence
of both pulpal and periodontal disease can be seen in radiographs. Root canal therapy is carried out and
certain time is allowed for periodontal tissues to heal. After this evaluation period of 2-3 months
periodontal therapy is carried out if required. Prognosis depends on the amount of attachment loss and
severity of periodontal disease.

4. Primary periodontal with secondary endodontic involvement: Retrograde pulpitis can occur
when the periodontal disease exposes lateral canal to oral environment or involves the apical canal.
In such a case primary periodontal lesion with secondary endodontic involvement can be observed.
Patients reports with severe pain, signs of pulpal disease concomitant with deep pocketing and
history of extensive periodontal disease. Microbiota of the root canal shows strong correlation with
that of periodontal pockets.
55
Radiographically these lesions are similar to primary endodontic lesions with secondary
periodontal involvement. Both periodontal and endodontic therapies are required. prognosis
depends on the severity of the periodontal disease and periodontal response to treatment.

5. True combined lesions: Pulpal pathosis progressing coronally and periodontal pathoses
progressing apically may develop independently around the same tooth and concomitantly unite.
They are relatively infrequent and when occur may have significant periodontal involvement with
considerable attachment loss. Clinically necrotic pulp or failing endodontic treatment with presence
of local factors (plaque and calculus), deep pockets and periodontitis are present in varying degrees.
Radiographically these lesions appear similar to that of the tooth with vertical fractures. Immediate
sealing of root perforations, root canal therapy, advanced endodontic surgery, periodontal therapy
with procedures such as hemisection, root resection may be required treatment options. Prognosis is
guarded and depends on the amount of destruction caused by periodontal disease.9

6. Concomitant pulpal and periodontal lesions: This additional group of lesions was proposed by
Belk and Guntmann Pulpal and periodontal diseases can co-exist with different aetiologies. Thus
the lesions will consist of an endodontic lesion and a non communicating periodontal lesion. In this
situation both the diseases should be treated individually.1

(a) Endodontic Lesions. (b) Periodontal Lesion (c) Primary Endodontic Lesion with Secondary
Periodontic Involvement. (d) Periodontic Lesions. (e) Primary Periodontic Lesion with Secondary
Endodontic Involvement.(f) "True" Combined Lesions.

56
 True combined lesions Concomitant pulpal and periodontal lesions

35
5. CLASSIFICATION BY RATEITSCHAK ET AL (Based On Endodontic Therapy)
A. Type I: It is primarily of endodontic origin and the pulp is usually dead.

B. Type II: It is basically periodontal disease, which sometimes affects the pulp, and the pulp is
usually normal or sometimes damaged by ascending pulpitis.

C. Type III: It is a combined case of a root canal problem and periodontal disease, and the pulp is
usually dead .

Primary endodontic lesion Primary periodontal lesion

57
 True combined endo-perio lesion

6. CLASSIFICATION BY GROSSMAN(BASED ON THERAPY PROTOCOL) 1

a. Teeth that require endodontic therapy alone.

b. Teeth that require periodontal therapy alone.

c. Teeth that require endodontic as well as periodontal therapy.

7. CLASSIFICATION BY TORABINEJAD (BASED ON THE ORIGIN OF THE

PERIODONTAL POCKET) 36
(1) Periodontal pocket of endodontic origin.
(2) Periodontal pocket of periodontal origin.
(3) Combined endodontic-periodontal lesion.
• Separate endodontic and periodontal lesions without communication
• endodontic and periodontal lesions with communication.

8. GLICKMAN’S CLASSIFICATION (BASED ON THE PATHWAYS OF THE SPREAD OF

INFLAMMATION) 37
1) A periapical lesion originating in pulpal infection may have a pathway of fistulization from the
apex and along the root to the gingiva.

2) Marginal periodontitis can progress to the apex of a root or to the emergence of an accessory
canal and induce a secondary pulpal involvement.

3) A true combined lesion is present when two separate lesion of endodontic and periodontal origin
coalesce.

58
9. Classification of Von Arx and Cochran (Based on the clinical treatment with the employment
of a membrane) 38
Class I: lesion with bone defect in the apex which may invade the buccal/labial and lingual cortex.
However, the periapical lesion cannot be measured through the gingival sulcus of the affected
tooth, that is, the periodontal pocket does not reach the apex.
Class II: apical lesion with the concomitant marginal involvement, also referred as a combined
periodontal-endodontic lesion, with great periodontal pocket deepness around the affected tooth.
The treatment uses the membrane for the guided tissue regeneration
Class III: furcation lesion, coming from the accessory canals or from iatrogenic perforation and the
marginal lesion may or may not occur.Also, the use of the membrane for guided tissue regeneration
can be used as treatment.

10. Classification of Oliet and Pollock 15

This classification system is based on treatment procedures. It is less complicated and directs the
clinical to the appropriate treatment with an improved prognosis.
According to this classification the endodontic- periodontic lesion can be classified into 3 different
treatment categories.

[I] Lesions that require endodontic treatment procedures only:

1. Any tooth with necrotic pulp and apical granulomatous tissue replacing periodontium and bone,
with or without a sinus tract (chronic periapical abscess).

2. Chronic periapical abscess with a sinus tract draining through the gingival crevice, thus passing
through a section of attachment apparatus in its entire length alongside the root.

3. Root fractures, longitudinal and horizontal.

4. Root perforations: Pathologic, iatrogenic.

5. Teeth with incomplete apical root development and inflamed or necrotic pulps with and without
periapical pathosis.

6. Endodontic implants.

7. Re-implantation, intentional or traumatic.

8. Transplants, autotransplants or allo transplants.

59
9. Teeth requiring hemisection or radisectomy.

10. Root submergence.

[II] Lesions that require periodontal treatment procedures only:

1. Occlusal trauma causing reversible pulpitis.

2. Occlusal trauma plus gingival inflammations resulting in pocket formation.

a. Reversible but increased pulpal sensitivity caused by trauma or possibly by exposed dentinal
tubules.

b. Reversible but increased pulpal sensitivity caused by uncovering lateral or accessory canals
existing into the periodontium.

3. Suprabony or infrabony pocket formation treated with overzealous root planning and curettage,
leading to pulpal sensitivity.

4. Extensive infrabony pockets formation extending beyond the root apex and sometimes coupled
with lateral or apical resorption yet with pulp that responds within normal limits to clinical testing.

[III] Lesion that require combined endodontic–periodontic treatment procedures:

1. Any lesion in group I that results in irreversible reactions in the attachment apparatus and
requires periodontal treatment.

2. Any lesion in group II that results in irreversible reactions in pulp tissue and also requires
endodontic treatment.

A clinically useful classification should be clear and easy to understand. It should also be based on
information that can be obtained from the history provided by the patient along with the findings of
the clinical examination and other diagnostic procedures such as percussion, palpation, mobility
testing, pulp sensibility tests, periodontal probing and periapical radiographs which are all
particularly useful, and essential, for diagnosing endodontic and periodontal conditions.

60
It is therefore proposed that the classification of endodontic and periodontal diseases be limited to
those teeth that have both endodontic and periodontal diseases occurring at the same time – hence,
it is proposed that they should be called “concurrent diseases” rather than combined endo-perio-
lesions since the suggested term is more appropriate as well as being more accurate, clinically
useful and easy to use.39

Hence, only two categories are required, as follows:

1. CONCURRENT ENDODONTIC AND PERIODONTAL DISEASES WITHOUT

COMMUNICATION

This applies to a tooth that has an infected root canal system with some form of apical periodontitis
PLUS marginal periodontal disease with pocketing but the periapical and periodontal diseases do
not communicate with each other .

That is, clinically when probing the periodontal pocket it does not extend as far as the periapical
lesion; radiographically the periodontal pocket does not extend as far as the apical foramen of the
root canal, and bone can be seen between, and separating, the periapical radiolucency and the base
of the periodontal pocket.39

Concurrent endodontic & periodontal lesions without communication

2. CONCURRENT ENDODONTIC AND PERIODONTAL DISEASES WITH

COMMUNICATION
This applies to a tooth that has an infected root canal system with some form of apical periodontitis
PLUS marginal periodontal disease with pocketing that extends to the periapical lesion such that

61
the periapical and periodontal diseases communicate with each other; radiographically the
periodontal pocket and the periapical radiolucency appear as one radiolucency, and there is no bone
between the periapical radiolucency and the base of the periodontal pocket.39

Concurrent endodontic & periodontal lesions with communication

Latest classification by Khalid et al published in the International journal of Dentistry in 2014

A new endodontic-periodontal interrelationship classication, based on the primary disease with its
secondary effect,is suggested as follows:

(1) retrograde periodontal disease:

(a) primary endodontic lesion with drainage

through the periodontal ligament,

(b) primary endodontic lesion with secondary peri-

odontal involvement;

(2) primary periodontal lesion;

(3) primary periodontal lesion with secondary endodon-

tic involvement;

(4) combined endodontic-periodontal lesion;

(5) iatrogenic periodontal lesions.

62
DIAGNOSIS

63
 DIAGNOSIS
It is incumbent to gather all relevant information via history and examination. So, appropriate
diagnostic aids are needed to correlate this information to determine the condition which might be
consistent with the findings. It also helps to differentiate between various conditions and to arrive at
the correct diagnosis.

Diseases of pulpal or periodontal origin involving the other tissue secondarily or occurring in
combination are found when the patient has pain or an abscess or some other kind of discomfort in
the area of the involved tooth. On occasion however the situation may be uncovered during a
routine examination. The clinician should be able to determine whether the existing tissue changes
came from either of one or both processes (pulpal + periodontal) so that appropriate treatment can
be given. It may happen that the existing lesion may be result of one process only, although at the
first look it may appear that both processes are involved. One process may have started the
destruction and the second may have contributed at a later time.

History
Considerable information may be gained from the patient’s medical and dental history. A through
history of the onset, duration and progress of the problem should be noted. This should include sign
and symptoms relating to present or past pulpal or periodontal disease and also a history of trauma
to the tooth. The chief complaint itself may establish the diagnosis. Usually pulpal problems are of
acute onset whereas periodontal problems are chronic in nature. 2

Clinical diagnostic procedures

Clinical tests are imperative for obtaining correct diagnosis and differentiating between endodontic
and periodontal disease. The extraoral and intraoral tissues are examined for the presence of any
abnormality or disease. One test is usually not sufficient to obtain a conclusive diagnosis.2

Visual examination
A thorough visual examination of the lips, cheeks, oral mucosa, tongue, palate and muscles should
be done routinely. Digital examination of the same tissues is performed simultaneously. The
alveolar mucosa and attached gingiva are examined for the presence of inflammation, ulcerations,
or sinus tracts. Frequently, the presence of a sinus tract is associated with a necrotic pulp.

64
The teeth are examined for abnormalities such as caries, defective restorations, erosions, abrasions,
cracks, fractures, and discolorations. A discolored permanent tooth may often be associated with a
necrotic pulp. A ‘‘pink spot’’ detected in the tooth crown may indicate an active internal resorption
process. A conclusive diagnosis for pulpal disease cannot be achieved by visual examination alone.
It therefore must always be accompanied by additional tests.

Visual examination is dramatically improved by the use of enhanced magnification and

illumination. Magnifying loops and the operating microscope are currently widely used among
dental professionals. These accessories facilitate the location of calculus, caries, coronal and
radicular fractures, developmental defects, and areas of denuded dentin mainly at the cementum–
enamel junction.9

Pain
Several aspects of pain should be considered when differentiating between pulpal and periodontal
pathosis. They include the type, intensity, frequency, duration and activators of pain. Questions
such as the following should be answered by the patient:
- Is the pain sharp or dull, throbbing or steady? (type)
- Is the pain mild, moderate, or severe? (intensity)
- Is the pain constant or intermittent? (frequency)
- Does heat, cold or both stimuli cause pain?
- Is the pain related to biting? (activators of pain)
- Is the pain felt only in one tooth? (location)

Early pulpitis gives pain on cold, which is mild and is of short duration. Pain occurs spontaneously
during these early stages of pulpal inflammation, where there is poor localization and the pain may
be referred to other sites. Pain due to the pulpal involvement is usually acute in onset and severe.
Heat produces pain that is sharper, more severe and of longer duration. It does not usually respond
to potent analgesics. As the inflammation increases in intensity, the pain becomes more severe, of
longer duration and is felt with hot or cold. Finally continuous severe pain may be felt even at room
temperature, suggesting pulpal degeneration and necrosis.

Pain of periodontal origin is chronic and usually mild or moderate which can sometimes cause
acute exacerbation resulting in periodontal abscess formation. In case of combined pulpal-
periodontal lesions, there is minimal pain as drainage occurs through the periodontal pocket formed
due to excess bone loss, thereby reducing the pressure and pain.2
65
Palpation
Palpation is performed by applying firm digital pressure to the mucosa covering the roots and
apices. With the index finger the mucosa is pressed against the underlying cortical bone. This will
detect the presence of periradicular abnormalities or ‘‘hot’’ zones that produce painful response to
digital pressure. A positive response to palpation may indicate active periradicular inflammatory
process. However, this test does not indicate whether the inflammatory process is of endodontic or
periodontal origin. Also, as with any other clinical test, the response should be compared to control
teeth. 9

Palpation

Percussion
Percussion is performed by tapping on the incisal or occlusal surfaces of the teeth either with the
finger or with a blunt instrument such as the back end of a mirror handle. The tooth crown is tapped
vertically and horizontally. Although this test does not disclose the condition of the pulp, it
indicates the presence of a periradicular inflammation. An abnormal positive response indicates
inflammation of the periodontal ligament that may be either from pulpal or periodontal origin.

The sensitivity of the proprioceptive fibers in an inflamed periodontal ligament will help identify
the location of the pain. This test should be done gently, especially in highly sensitive teeth. It
should be repeated several times and compared to control teeth. 9

The sensitivity of the proprioceptive fibers in an inflamed periodontal ligament will help identify the
location of the pain. This test should be done gently, especially in highly sensitive teeth. It should be
repeated several times and compared to control teeth. 2

66
 Vertical and Horizontal Percussion

Mobility
Mobility testing can be performed using two mirror handles on each side of the crown. Pressure is
applied in a facial–lingual direction as well as in a vertical direction and the tooth mobility is
scored.
Tooth mobility is directly proportional to the integrity of the attachment apparatus or to the extent
of inflammation in the periodontal ligament. Teeth with extreme mobility generally have little
periodontal support, indicating that the primary cause may be periodontal disease. Fractured roots
and recently traumatized teeth often present high mobility. 2

Frequently, however, a periradicular abscess of pulpal origin may cause similar mobility. This can
only be verified if other tests indicate pulp necrosis or if mobility improves a short time after
completion of endodontic therapy. Pressure exerted by an acute apical abscess may cause transient
tooth mobility. This may also occur as a result of orthodontic movement and pulp necrosis of
previously traumatized teeth.9

Pocket probing
Periodontal probing is an important test that should always be performed when attempting to
differentiate between endodontic and periodontal disease. A blunt calibrated periodontal probe is
used to determine the probing depth and clinical attachment level.

67
It may also be used to track a sinus resulting from an inflammatory periapical lesion that extends
cervically through the periodontal ligament space.

probing reveals a deep defect 15

A deep solitary pocket in the absence of periodontal disease may indicate the presence of a lesion of
endodontic origin or a vertical root fracture. Periodontal probing can be used as a diagnostic and
prognostic aid. For example, the prognosis for a tooth with a necrotic pulp that has developed a
sinus track is excellent following adequate root canal therapy. However, the prognosis of root canal
treatment in a tooth with severe periodontal disease is dependent on the success of the periodontal
therapy. Therefore, correct identification of the etiology of the disease, whether endodontic,
periodontal or combined, will determine the course of treatment and long-term prognosis.9

Fistula tracking
Endodontic or periodontal disease may sometimes develop a fistulous sinus track. Inflammatory
exudates may often travel through tissues and structures of minor resistance and open anywhere on
the oral mucosa or facial skin. Intraorally, the opening is usually visible on the attached buccal
gingiva or in the vestibule. Extraorally, the fistula may open anywhere on the face and neck.
However, it is most commonly found on the cheek, chin, and angle of the mandibule, and
occasionally also on the floor of the nose. If the etiology is pulpal, it usually responds well to
endodontic therapy.

The identification of the sinus tract by simple visual examination does not necessarily indicate the
origin of the inflammatory exudate or the tooth involved. Occasionally, the exudate exists through
the periodontal ligament, thus mimicking a pocket of periodontal origin.

Identifying the source of inflammation by tracking the fistula will help the clinician to differentiate
between diseases of endodontic and periodontal origin.40Fistula tracking is done by inserting a
semi-rigid radiopaque material into the sinus track until resistance is met. Commonly used
materials include gutta-percha cones or pre softened silver cones. A radiograph is then taken that
will reveal the course of the sinus tract and the origin of the inflammatory process.9

68
 Fistula tracking with GP point

Pulp vitality testing

These tests are designed to assess the response of the pulp to different stimuli. An abnormal
response may indicate degenerative changes in the pulp. In general, no response indicates pulp
necrosis, and moderate transient response indicates normal vital pulp. A quick painful response may
often indicate reversible pulpitis and lingering painful response indicate irreversible pulpitis. Since
some of these tests may provoke a painful reaction they should be carefully performed and their
nature and importance explained to the patient. When correctly performed and adequately
interpreted these tests are reliable in differentiating between pulpal disease and periodontal disease.
The most commonly used pulp vitality tests are: cold test, electric test, blood flow tests, and cavity
test.40

1. Thermal
Various methods and materials have been used to test the pulp’s response to thermal stimuli. The
baseline or normal response to either hot or cold is a patient’s report that a sensation is felt but
disappears immediately on removal of the thermal stimulus.
Abnormal responses include a lack of response to the stimulus, the lingering or intensification of a
painful sensation after the stimulus is removed, or an immediate, excruciatingly painful sensation as
soon as the stimulus is placed on the tooth.2

(A) Heat Test

Heat testing is most useful when a patient’s chief complaint is intense dental pain on contact with
any hot liquid or food. When a patient is unable to identify which tooth is sensitive, a heat test is
appropriate. Starting with the most posterior tooth in that area of the mouth, each tooth is
individually isolated with a rubber dam. An irrigating syringe is filled with a liquid (most
commonly plain water) that has a temperature similar to that which would cause the painful
sensation. ‘’

69
The liquid is then expressed from the syringe onto the isolated tooth to determine whether the
response is normal or abnormal. The clinician moves forward in the quadrant, isolating each
individual tooth until the offending tooth is located. That tooth will exhibit an immediate, intense
painful response to the heat. With heat testing a delayed response may occur, so waiting 10 seconds
between each heat test will allow sufficient time for any onset of symptoms.

Another method for heat testing is to apply heated gutta-percha or compound stick to the surface of
the tooth. If this method is used, a light layer of lubricant should be placed onto the tooth surface
before applying the heated material to prevent the hot gutta-percha or compound from adhering to
the dry tooth surface. Heat can also be generated by the friction created when a dry rubber-
polishing wheel is run at a high speed against the dry surface of a tooth. However, this latter
method is seldom used today.

Often a tooth that is sensitive to heat may also be responsible for some spontaneous pain. In these
cases the patient may present with cold liquids in hand just to minimize the pain. Typically, a tooth
that responds to heat and then is relieved by cold is found to be necrotic.2

“ Touch’n Heat” device manufactured by SybronEndo, using the specific tip.42

(B) Cold test

This test is performed by applying a cold substance, or agent, to a well-isolated tooth surface. Tooth
isolation can be achieved by drying the crown surfaces with cotton rolls, gauze and a very gentle air
blast. Several cold methods are used: ice sticks, ethyl chloride, carbon dioxide (dry ice), and
refrigerants such as dichlorodifluoromethane. Carbon dioxide (–78 oC) and DDM (–50 oC) are
extremely cold and are only used when the pulp does not respond to less cold agents. Extremely
cold agents may cause crazing and infraction lines on the enamel.9

70
 Cold Vitality Test with cold spray and ice stick42

Teeth with vital pulps will react to cold with sharp brief pain response that usually does not last
more than a few seconds. An intense and prolonged pain response often indicates abnormal pulpal
changes and irreversible pulpitis. Lack of response may indicate pulp necrosis. When adequately
performed, this test is reliable in determining whether the pulp has undergone irreversible damage.
However, false-positive and false-negative responses may occur, especially in multiradicular teeth
where not all roots are affected or in teeth with calcified root canals.

2. Electric test
This test is performed by applying an electric stimulus to the tooth using a special pulp tester
device. The tooth is first cleaned, dried and isolated. A small amount of toothpaste is placed on the
electrode of the pulp tester, which is then put into contact with the clean tooth surface. Only sound
tooth structure should be contacted.

Electric current is gradually applied until the patient reports sensation. Many devices are currently
available; all are effective and used in a similar manner. The purpose of the test is to stimulate the
sensory nerve fibers of the pulp to produce a response. No response frequently indicates pulp
necrosis. A positive response may be interpreted as either intact vital pulp or partially necrotic
pulp.9

Electric Tooth Vitality Test6

71
However, the electric test does not provide any information about the condition of the vascular
supply of the pulp. While interpreting the results the clinician must take into consideration the
various false-positives and false-negatives of this test. The most common causes for false-positive
responses are: partial pulp necrosis, patient anxiety, ineffective isolation, and inadvertent contact
with metallic restorations.

The most common causes for false-negative responses are: obliterated root canals, recently
traumatized teeth, teeth with immature apices, patient taking drugs that elevate the pain threshold,
and poor electrode–tooth contact. In general, however, the electric pulp test is easy to perform and
provides accurate determination of pulp necrosis in adult teeth.9

3. Cavity test
This test is highly reliable in determining the vitality of the pulp. It basically consists of creating a
cavity in the tooth without anesthesia.

A high-speed handpiece with a new sharp bur is generally used. A positive response indicates
presence of vital pulp tissue, while a negative response accurately indicates pulp necrosis. If no
response is obtained, the cavity is extended into the pulp chamber and endodontic treatment is
initiated. This test is not routinely performed since it may produce pain in cases where the pulp is
vital. It should only be limited to cases where all other tests proved inconclusive and a definitive
diagnosis of the pulp condition could not be established.40

4. Restored teeth testing

Testing teeth with extensive coronal restorations is somewhat more challenging. Whenever
possible, the restoration should be removed to facilitate pulp testing. In cases where restoration
removal is not feasible, a small access opening is made through the restoration until sound tooth
structure is reached. Cold test and cavity test will give the most reliable results. In most instances
electric pulp testing will not prove beneficial.

Access through full gold crowns can usually be done without affecting the strength and stability of
the restoration. Access repair is done with amalgam, or another permanent filling material. Access
for pulp testing can be done through porcelain restorations as well. In such cases, access is done
slowly and with copious water irrigation.9

72
5. Selective anesthesia test
This test is useful in cases where the source of pain cannot be attributed to a specific arch.
Disappearance of pain following a mandibular block will confirm the source of pain originating
from a mandibular tooth.

The periodontal ligament injection is often used to narrow down the zone in question, however, it
cannot anesthetize a single tooth without affecting adjacent teeth. In the maxillary arch the test may
be more focused to a specific tooth by injecting a small amount of anesthetic solution in an
anterior–posterior direction at the root apex level. No conclusive diagnosis differentiating between
endodontic and periodontal disease can be made using this type of test.9

6. Blood flow test

This test is designed to determine the vitality of the pulp by measuring its blood flow rather than the
response of its sensory nerve fibers. Different systems such as dual wavelength spectrophotometry,
pulse oximetry, and laser Doppler have been developed to measure either oxyhemoglobin, low
concentration of blood, or pulsation of the pulp.44,45

Sensors are applied to the external surfaces of the crown and the pulp blood flow is recorded and
compared to controls. The procedure is non-invasive and painless. These tests are relatively new
and are not used routinely.2

(A) Laser Doppler Flowmetry

Laser Doppler flowmetry (LDF) is a method used to assess blood flow in microvascular systems.
Attempts are being made to adapt this technology to assess pulpal blood flow. A diode is used to
project an infrared light beam through the crown and pulp chamber of a tooth. The infrared light
beam is scattered as it passes through the pulp tissue. The Doppler principle states that the light
beam will be frequency-shifted by moving red blood cells but will remain unshifted as it passes
through static tissue. The average Doppler frequency shift will measure the velocity at which the
red blood cells are moving.2

Several studies have found LDF to be an accurate, reliable, and reproducible method of assessing
pulpal blood flow. Even with these positive findings, the technology is not advanced enough for
this method to be used on a routine basis in a dental practice. In one clinical trial fabricating the
individualized stabilization jig, making the LDF recordings took approximately 1 hour, a finding
not unique to this study.41

73
If technology can be developed whereby testing by LDF can be accomplished in minutes, it will
likely replace the thermal and electric pulp testing methods. A certain luxation injuries will cause
inaccuracies in the results of electric and thermal pulp testing. LDF has been shown to be a great
indicator for pulpal vitality in these cases.2

(B) Pulse Oximetry

One of the great advantages of pulp testing with devices such as the laser Doppler flowmeter is that
the collected data are based on objective findings rather than subjective patient responses.2

The pulse oximeter is another such noninvasive device. Widely used in medicine, it is designed to
measure the oxygen concentration in the blood and the pulse rate. A pulse oximeter works by
transmitting two wavelengths of light, red and infrared, through a translucent portion of a patient’s
body (e.g., a finger, earlobe, or tooth). Some of the light is absorbed as it passes through the tissue;
how much is absorbed depends on the ratio of oxygenated to deoxygenated hemoglobin in the
blood.

On the opposite side of the targeted tissue, a sensor detects the absorbed light, and on the basis of
the difference between the light emitted and the light received, a microprocessor calculates the
pulse rate and oxygen concentration in the blood. The transmission of light to the sensor requires
that there be no obstruction from restorations, which can sometimes limit the usefulness of pulse
oximetry to test pulp vitality.

Attempts to use the pulse oximeter to diagnosis pulp vitality have met with mixed results. Some
studies have reported that pulse oximetry is a reliable method for assessing pulp vitality. Most of
the problems appear to be related to the currently available technology. Some investigators have
concluded that these devices used for pulp testing are too cumbersome and complicated to be used
on a routine basis in a dental practice. 41

Cracked Tooth Testing

(A) Transillumination
This test is designed to aid in the identification of cracks and fractures in the crown. A fiber optic
connected to a high-power light source is used to illuminate the crown and gingival sulcus.

74
The contrast between the dark shadow of the fracture and the light shadow of the surrounding tissue
will clearly reveal the size and orientation of the fracture line. An existing restoration may need to
be removed to enhance visibility.9

(B) Wedging
This technique aids in the identification of vertical crown fractures or crown–root fractures. Such
fractures cause a painful response to the patient at the time of chewing. During the test, wedging
forces are created as the patient is instructed to chew on a cottonwood stick or other firm material.

This test is fairly reliable in identifying a single tooth causing pain during mastication. Many of
these fractures involve only the tooth crown and terminate in the pulp chamber. Such cases are
treated successfully with endodontic therapy.

(C) Staining
Staining identifies lines of fracture in the crown and root and is often used in conjunction with the
wedging test. The tooth crown is dried and a cotton pellet soaked with methylene blue dye is
swabbed on the occlusal surface of the tooth. The patient is asked to bite on a stick and perform
lateral jaw movements.

This way the dye penetrates well into the zone of the fracture. The dye is then rinsed from the tooth
surfaces and visual examination with magnifying loops or the microscope will reveal a distinctive
fracture line darkened with dye.9

Radiographs
Radiographs are essential for detection of anatomic landmarks and a variety of pathological
conditions. In addition, radiographs are of utmost importance for documentation and legal
purposes.

Radiographic examination will aid in detection of carious lesions, extensive or defective

restorations, pulp caps, pulpotomies, previous root canal treatment and possible mishaps, stages of

75
root formation, canal obliteration, root resorption, root fractures, periradicular radiolucencies,
thickened periodontal ligament, and alveolar bone loss.

The integrity of the dental pulp cannot be determined by radiographic images alone. Radiographic
changes will only be detected once the inflammation or bacterial by products originating from the
dental pulp cause sufficient demineralization of the cortical bone.9

The initial phases of periradicular bone resorption from endodontic origin is usually confined only
to the cancellous bone. Therefore it cannot be detected unless the cortical bone is also affected.
Also, certain radiographic features are susceptible to multiple interpretations. On the other hand,
periodontal disease causing alveolar bone loss can be effectively detected by radiographs.

For purposes of differential diagnosis, periapical and bitewing radiographs should be taken from
several angles. Sometimes, other types of radiographs are also required. A number of radioloucent
and radiopaque lesions of non-endodontic and non-periodontal origin may simulate the
radiographic appearance of endodontic or periodontal lesions.
Therefore, clinical signs and symptoms as well as findings from the other clinical tests should
always be considered at the time of radiographic evaluation.

Primary endodontic lesion 46 True combined pulpal and periodontal Lesion

Cone-beam computed tomographic (CBCT)

Radiographic examination represents an essential part of the contemporary management of
endodontic periodontal problems, from diagnosis and treatment planning to outcome evaluation.
Intraoral and panoramic radiographic assessments have inherent limitations in the fact that 3-
dimensional (3D) anatomy is compressed in a 2-dimensional (2D) image; superimposition of
anatomic structures may result in geometric distortion of the area and anatomic noise that can hide
the region of interest. Cone-beam computed tomographic (CBCT) imaging may overcome these
problems by producing 3D images of teeth and surrounding tissues.43

CBCT is potential for an increase in diagnostic efficacy and characterization of the periodontal
76
bone status. Studies have shown that CT assessment of alveolar bone height and bony pockets is
reasonable, accurate, and precise.

Visualization of lamina dura, crater defects, furcation involvements, contrast, and bone quality were
also evaluated. In measurements of buccal and lingual defects, CBCT proved superior to
conventional radiography. Low dosage and superior image quality in comparison with conventional
CT are promising for periodontal applications, especially in the areas of intrabony defects,
dehiscence and fenestration defects, and periodontal cysts, and in the diagnosis of furcation-
involved molars. 4
CBCT imaging has the potential to replace intraoral imaging for the assessment of periodontal
architecture. However, clinical studies would be helpful in supporting this conclusion. CBCT may
be a useful and more practical clinical tool than digital subtraction radiography for the assessment
of changes in periodontal bone over time.45

Radiologic examination is an essential part of the diagnosis and management of endodontic

treatments. At this time, intraoral radiography is the imaging technique of choice for the
management of endodontic disease, but CBCT imaging appears to provide a superior validity and
reliability in the detection of periapical lesions. CBCT imaging has been used in endodontics to
study root canal anatomy and the prevalence of apical periodontitis to evaluate root canal
preparation and filling and for retreatment, surgical endodontics. The superior accuracy of CBCT
imaging may result in the early detection of periapical lesions and may help to determine their exact
locations and extents.44
CBCT imaging has the potential to become the first choice for endodontic treatment planning and
outcome assessment, especially when new scanners with lower radiation doses and better
resolutions become available.43

Three images depicting a complete periodontal furcation involvement of a second molar. The figure
on the left visualizes a furcation involvement delineated by the circle. The center and right images
demonstrate the extent of the lesion (arrows) from facial-lingual and axial views. These 300-mm
images were obtained with the Sirona Galileos CBCT system (Sirona Dental Systems, Bensheim,

77
Germany).

In this case, the standard 2D periapical radiograph did not reveal the true extent of the apical lesion
(circle). The pattern of the lesion suggests a root fracture (arrow). In this case, the treatment of the
tooth was changed from re-treating the root canal to extracting the tooth. These 300-mm images
were obtained with the Sirona Galileos CBCT system (Sirona Dental Systems, Bensheim,
Germany).

78
 Table 1 DIFFERENTIAL DIAGNOSIS OF PULPAL AND

PERIODONTAL FINDINGS 2

ETIOLOGY Pulp-infection Pulp-infection

PULP TEST Non-vital Vital
MICROBIAL Fewer organisms Complex microbial plaque
TRAUMA May be primary or May be primary cause of
(OCCLUSION) secondary wide periodontal space or
secondary cause in pocket
formation
INFLAMMATION Mostly Acute Mostly Chronic
pH Usually acidic Usually alkaline
ROOT SURFACE No calculus Calculus
POCKET Narrow, one surface, often Wide coronally, narrow
facial. apically. Usually
interproximal & part of a
generalized disease.
BONE-LOSS One surface, often facial, Multiple surfaces , usually
wider apically, narrow interproximal, wider
coronally coronally, often intrabony
RADIOGRAPHIC Funnel shaped, wider at apex Generalized bone destruction
FINDINGS but often superimposed over coronally not involving
root in facial pocket periapical regions.
RESTORATIVE Deep restorations Carious or deep restorations
not related

79
 HISTOPATHOLOGY

PULPAL PERIAPICAL
EPITHELIUM No down growth Proliferation & down
growth
CONNECTIVE TISSUE Fibers residue on root No fibers except apical
surface, minimum portion, large quantity of
granulation tissue granulation in pocket
GINGIVAL Little or no recession Gingival recession in
chronic cases
THERAPY Pocket closure with Regeneration possible only
enododontic treatment or with advanced periodontal
with simple additional treatment, except in pocket
periodontal procedures of recent origin from acute
inflammation.

Table 2 DIFFERENTIAL DIAGNOSIS OF PULPAL, PERIAPICAL,

PERIODONTAL ABSCESSES FINDINGS

80
 PULPAL PERIAPICAL PERIODONTAL
TYPE OF PAIN Sharp lancinating Dull or continuous Dull or absent
SWELLING Absent Generalized Localized
COLOR OF Normal Darkened Normal
TOOTH
PERCUSSION Normal Sensitive Usually normal
EXTRUSION Absent Extruded Absent
VITALOMETER Low,normal or No response Normal
high range
PERIODONTAL No probable defects Normally single Probable defects in
of the mouth probable defect many areas
RADIOGRAPHIC Caries, recent shallow Deep caries, deep Pocket with calculus
EXAMINATION fillings fillings
LYMPHATIC Absent Enlarged Absent

TABLE 3 SUMMARIZES THE COMMON CLINICAL AND

RADIOGRAPHIC FINDINGS WHEN EXAMINING A PATIENT
FOR ENDODONTIC AND PERIODONTAL DISEASES. 3

Typical findings Pulp and Periapical Periodontal diseases Concurrent

diseases endodontic and

81
 periodontal diseases
Disease process Yes No Yes – but may have
localized more than one tooth
to just one tooth involved if the patient
has generalized
marginal periodontal
disease
Extensive caries or Yes No Yes – likely there is
restorations pulp ⁄ periapical
disease present
Responds to pulp No Yes No – due to the pulp ⁄
sensibility periapical
Tests disease process
Periodontal probing No – but may have a Yes – usually a deep, Yes – usually a deep,
defect deep, wide-based pocket wide-based
narrow probing defect if pocket due to the
there is a draining sinus periodontal
that exits in the gingival disease process
sulcus

Crestal bone loss No Yes Yes – usually a deep,

evident on wide-based pocket due
Radiographs to the periodontal
disease process

Periapically – loss of Yes No Yes – due to the pulp ⁄

lamina periapical
dura or the presence Diseas
of a e process
radiolucency
Tenderness to No – unless acute apical No – unless No – unless acute
percussion periodontitis or acute acutePeriodontal apical periodontitis,
and ⁄ or palpation apical abscess is abscess is acute apical abscess or
present; present; may „„feel acute periodontal
may „„feel different‟‟ if different‟‟ if chronic abscess is
chronic apical marginal periodontitis present; may „„feel
periodontitis is present is present different‟‟ if chronic
apical periodontitis or
chronic marginal
periodontitis is
present

82
DIFFERENTIAL DIAGNOSIS

DIFFERENTIAL DIAGNOSIS
For differential diagnostic purposes the "endo-perio lesions" are best classified as endodontic,
periodontal or combined diseases.39 They can also be classified by treatment depending on whether
endodontic, periodontal or combined treatment modalities are necessary.

83
They include: primary endodontic disease, primary periodontal disease, and combined diseases.
The combined diseases include: primary endodontic disease with secondary periodontal
involvement, primary periodontal disease with secondary endodontic involvement, and true
combined diseases. Once the lesions progress to their final involvement, they give a similar
radiographic picture and the differential diagnosis becomes more challenging. 9

PRIMARY ENDODONTIC DISEASE:

An acute exacerbation of a chronic apical lesion on a tooth with a necrotic pulp may drain coronally
through the periodontal ligament into the gingival sulcus. This condition may mimic clinically the
presence of a periodontal abscess. In reality, it is a sinus tract from pulpal origin that opens through
the periodontal ligament area. For diagnosis purposes, it is imperative for the clinician to insert a
gutta-percha cone into the sinus tract and to take one or more radiographs to determine the origin of
the lesion.

When the pocket is probed, it is narrow and lacks width. A similar situation occurs where drainage
from the apex of a molar tooth extends coronally into the furcation area.

This may also occur in the presence of lateral canals extending from a necrotic pulp into the
furcation area. Primary endodontic diseases usually heal following root canal treatment. 9 The sinus
tract extending into the gingival sulcus or furcation area disappears at an early stage once the
necrotic pulp has been removed and the root canals are well sealed. It is important to recognize that
failure of any periodontal treatment will occur when the presence of a necrotic pulp has not been
diagnosed, and endodontic treatment has not followed.39

84
 A B

C D

Primary endodontic disease in a mandibular first molar with a necrotic pulp. (A) Preoperative
radiograph showing periradicular radiolucency associated with the distal root. (B) Clinically, a deep
narrow buccal periodontal defect can be probed. (C) One-year after root canal therapy, resolution of
the periradicular bone lesion is evident. (D) Clinically, the buccal defect healed and pocket probing
depth is normal. (Courtesy: Ingle’s Endodontics) 3

PRIMARY PERIODONTAL DISEASE:

These lesions are caused primarily by periodontal pathogens. In this process, chronic periodontitis
progresses apically along the root surface. In most cases, pulp tests indicate a clinically normal
pulpal reaction.There is frequently an accumulation of plaque and calculus and the pockets are
wider.

The prognosis depends upon the stage of periodontal disease and the efficacy of periodontal
treatment. The clinician must also be aware of the radiographic appearance of periodontal disease
associated with developmental radicular anomalies.9

A B

Primary periodontal lesion simulating an endodontic lesion. (A) Radiograph of mandibular first
85
 molar showing periradicular radiolucency and periapical resorption. (B) Lingual view of the
affected tooth. Note,gingival swelling and evidence of periodontal disease. In addition, an occulsal
filling is present close to the pulp chamber. Inspite of the clinical and radiographic picture, the pulp
responded normal to vitality testing procedures indicating the radiolucency, resorption and gingival
swelling are of periodontal origin. (Courtesy: Ingle’s Endodontics)

A B

D E

Primary periodontal disease in a maxillary second premolar (A)Radiograph showing alveolar bone
loss and a periapical radiolucency. Clinically, a deep narrow pocket was found at the mesial aspect
of the root. There was no evidence of caries and the tooth responded normally to pulp sensitivity
tests. (B) Radiograph showing pocket tracking with gutta-percha cone to the apical area. It was
decide to extract the tooth. (C) Clinical view of the extracted tooth with the attached lesion. Note a
deep mesial radicular development groove. (D) Photomicrograph of the apex of the tooth with the
attached lesion. (E) Histologic section of the pulp chamber shows uninflammed pulp tissue.
(Courtesy: Rotstein & Simon) 3

COMBINED LESIONS:

86
a. Primary Endodontic Disease with Secondary Periodontal Involvement:
If after a period of time a suppurating primary endodontic disease remains untreated, it may become
secondarily involved with periodontal breakdown. Plaque forms at the gingival margin of the sinus
tract and leads to plaque-induced periodontitis in the area. When plaque or calculus is detected, the
treatment and prognosis of the tooth are different that those of teeth involved with only primary
endodontic disease. The tooth now requires both endodontic and periodontal treatments. If the
endodontic treatment is adequate, the prognosis depends on the severity of the plaque-induced
periodontitis and the efficacy of periodontal treatment.

Using endodontic treatment alone, only part of the lesion will heal to the level of the secondary
periodontal lesion. In general, healing of the tissues damaged by suppuration from the pulp space
can be anticipated. Primary endodontic lesions with secondary periodontal involvement may also
occur as a result of root perforation during root canal treatment, or where pins or posts have been
misplaced during coronal restoration.

Symptoms may be acute, with periodontal abscess formation associated with pain, swelling, pus or
exudate, pocket formation, and tooth mobility. A more chronic response may sometimes occur
without pain, and involves the sudden appearance of a pocket with bleeding on probing or
exudation of pus. When the root perforation is situated close to the alveolar crest, it may be possible
to raise a flap and repair the defect with an appropriate filling material. In deeper perforations, or in
the roof of the furcation, immediate repair of the perforation has a better prognosis than
management of an infected one.

Use of mineral trioxide aggregate has resulted in cemental healing following immediate repair.
Root fractures may also present as primary endodontic lesions with secondary periodontal
involvement. These typically occur on root-treated teeth, often with post and crowns. The signs
may range from a localdeepening of a periodontal pocket to more acute periodontal abscess
formation. Root fractures have also become an increasing problem with molar teeth that have been
treated by root resection.9

b. Primary Periodontal Disease with Secondary Endodontic Involvement

The apical progression of a periodontal pocket may continue until the apical tissues are involved. In
this case the pulp may become necrotic as a result of infection entering via lateral canals or the
apical foramen. In single-rooted teeth the prognosis is usually poor.

87
In molar teeth the prognosis may be better. Since not all the roots may suffer the same loss of
supporting tissues, root resection can be considered as a treatment alternative. The effect of the
progression of chronic periodontitis on the vitality of the pulp is controversial. 3 If the blood supply
circulating through the apex is intact, the pulp has good prospects for survival. It has been reported
that pulpal changes resulting from periodontal disease are more likely to occur when the apical
foramen is involved. In these cases, bacteria originating from the periodontal pocket are the most
likely source of root canal infection.

A strong correlation between the presence of microorganisms in root canals and their presence in
periodontal pockets of advanced periodontitis has been demonstrated. Support for this concept has
come from research in which cultured samples obtained from the pulp tissue and radicular dentin of
periodontally involved human teeth showed bacterial growth in 87% of the teeth.

The treatment of periodontal disease can also lead to secondary endodontic involvement. Lateral
canals and dentinal tubules may be opened to the oral environment by scaling and root planning or
surgical flap procedures. It is possible for a blood vessel within a lateral canal to be severed by a
curette and for microorganisms to be pushed into the area during treatment, resulting in pulp
inflammation and necrosis.9

A B

Primary periodontal disease with secondary endodontic involvement in a maxillary premolar. (A)
Radiograph showing bone loss in one third of the root and separate periapical radiolucency. The
crown was intact but pulp sensitivity tests were negative and the pulp was necrotic on entry. (B)
Radiograph taken immediately after root canal therapy showing sealer in lateral canal that was
exposed due to the bone loss. (Courtesy: Rotstein & Simon)3

c. True Combined Disease:

True combined endodontic–periodontal disease occurs less frequently than other endodontic–
periodontal problems. It is formed when an endodontic disease progressing coronally joins with an
infected periodontal pocket progressing apically.34

The degree of attachment loss in this type of lesion is invariably large and the prognosis guarded.

88
This is particularly true in single-rooted teeth. In molar teeth, root resection can be considered as a
treatment alternative if not all roots are severely involved. Sometimes, supplementary surgical
procedures are required. In most cases periapical healing may be anticipated following successful
endodontic treatment. The periodontal tissues, however, may not respond well to treatment and will
depend on the severity of the combined disease.

The radiographic appearance of combined endodontic- periodontal disease may be similar to that of
a vertically fractured tooth. A fracture that has invaded the pulp space, with resultant necrosis, may
also be labeled a true combined lesion and yet not be amenable to successful treatment. If a sinus
tract is present, it may be necessary to raise a flap to determine the etiology of the lesion.9

True combined endodontic-periodontal disease in a mandibular first molar. Radiograph showing

separate progression of endodontic disease and periodontal disease. The tooth remained untreated
and consequently the two lesions joined together. 3

A B

True combined endodontic-periodontal disease. (A) Radiograph showing bone loss in two thirds of
the root with calculus present and separate periapical radiolucency. (B) Clinical examination
revealed coronal color change of the tooth involved and pus exuding from the gingival crevis. Pulp
sensitivity tests were negative. (Courtesy: Rotstein & Simon) 3

89
 A B

C D

True combined endodontic-periodontal diseases in a mandibular first molar. (A) Preoperative

radiograph showing periradicular radiolucencies. Pulp sensitivity tests were negative. (B)
Immediate postoperative radiograph of nonsurgical endodontic treatment. (C) Six-month follow-up
radiograph showing no healing. Gutta-percha cone is inserted in the buccal gingival sulcus. (D)
Clinical photograph showing treatment of the root surfaces and removal of the periradicular lesion.
(E) One-year follow-up radiograph demonstrating healing. (Courtesy: Rotstein & Simon) 9

The clinical diagnosis of the pulp status can be difficult at times. Unfortunately, there is no single
test available that will accurately and reliably determine the true status of the pulp or root canal in
all cases. The commonly-used thermal and electric pulp sensibility tests can only indicate the ability
of the pulp's nerve supply to respond to that particular stimulus. These tests do not provide any
information about the presence or absence of the pulp's blood supply, which is more relevant when
determining whether the pulp is healthy or diseased. However, reliable pulp and root canal
diagnoses can be made with a thorough understanding of the disease processes, the nature of the
test and the meaning of the test results.39

Pulp sensibility tests cannot be interpreted accurately without the use of periapical radiographs
since conditions such as pulp canal calcification, previous root fillings, pulpotomies, porcelain
90
crowns, etc., can lead to false test results. Teeth with previous endodontic treatment must be
assessed with extreme caution since radiographs do not provide information regarding the quality of
the endodontic treatment or the root canal fillings. Radiographs essentially only show how
radiopaque the root filling material is and where the material has been placed.

It is important to recognize that a tooth with a radiographically-determined good root canal filling
can still contain bacteria and this must be considered carefully when formulating a management
plan for diseased teeth.

DIAGNOSTIC PROCEDURES USED TO IDENTIFY THE ENDO-PERIO LESION 8

91
 RCT= Root canal therapy, PDL= Periodontal ligament

True
Primary Primary Primary combined
Examination/test Primary endodontic periodontal Lesion or
periodontal
s endodontic lesion secondary secondary concomitant
Lesion periodontal endodontic endo-perio
lesions
Inflamed
gingiva /
Presence of
gingival
plaque,
Soft Recession Plaque forms subgingival
at the calculus
tissue-presence of around multiple Plaque,
gingival and
calculus and
sinus opening teeth margin of swelling
Visual periodontitis
the sinus tract around
Tooth-presence of Accumulation of will be
(magnifying and multiple
present in
decay/large plaque and leads to teeth
loupes and varying
inflammation Presence of
restoration/fracture subgibgival degrees
operative of marginal pus,
Swelling
d calculus around gingiva Exudate
microscope around single
exudate Presence of
restoration or tooth/ multiple teeth or
can be effective) Root localized/
multiple teeth
erosions/abrasions/ Intact teeth perforation/ generalized
Presence of
fracture/misp gingival
cracks/discoloratio Presence of pus, exudate
laced recession
ns/poor RCT swelling post and
exposure of
indicating
root
periodontal
abscess
Usually dull
Usually dull
Usually sharp Dull ache
ache ache
shooting usually
Sharp only
Pain Sharp Sharp only in Dull ache in Only in acute
in acute
chronic conditions it
acute periodontal
Conditions is severe
abscess
Condition
Palpation (a It does not indicate
positive response whether the
to palpation may inflammatory
indicate active process is of
Pain on Pain on Pain on Pain on
periradicular endodontic or
palpation palpation palpation palpation
inflammatory periodontal

process) Origin
Percussion (it Normally tender on The sensitivity Tender on Tender on Tender on
percussion percussion percussion
92
 of the
proprioceptive
indicates the
fibers in
presence of a
an inflamed
peri radicular
periodontal
inflammation
Percussion ligament will
that may be
help
either from
identify the
pulpal or PDL
location of the
origin)
pain

Mobility (tooth
mobility is directly Generalized
Fractured roots and
proportional to the mobility with
recently
integrity of the Localized to Localized Generalized higher grade
traumatized teeth
attachment generalized mobility mobility of mobility
often present high
apparatus or to the mobility of teeth related to the
mobility
extent of involved
inflammation in the tooth
PDL ligament)

Pulp vitality Usually

using cold test, negative
electric test, because of
A lingering Pulp vitality
blood flow tests, non-vital
response-irreversibl The pulp is vital may
and cavity test Pulp vitality pulp. Vitality
e pulpitis and be positive
(an abnormal tests tests may
No response responsive to in
response may Negative give a
necrotic testing multirooted
indicate positive
pulp (non-vital) teeth
degenerative response in
changes in the multirooted
pulp) Teeth.

Pocket Probing A deep narrow Multiple wide Presence of Presence of

solitary pocket in and deep solitary wide multiple Probing
the absence of pockets pocket but if wide and reveals the
periodontal disease periodontal deep typical
may indicate the lesion is due periodontal conical

93
 periodontal
type of
probing with
the exception
that at the
to fracture of
base of the
root then
presence of a lesion periodontal
solitary deep
of endodontic lesion, the
narrow pockets
origin or a vertical probe will
pocket
root fracture abruptly drop
(mainly
further down
localized)
the lateral
root surface
and may even
extend to the
apex of the
tooth
Difficult to
trace out the
origin of the
lesion, if a
sinus tract is
Sinus tracing (by Sinus tract present, it
A radiograph with Sinus tract
inserting a semi Sinus tract mainly at may be
gutta percha points mainly at the
rigid radiopaque mainly at the the lateral necessary to
to apex or furcation apex or
material into the lateral aspect of aspect of raise a flap to
area in molars furcation area
sinus tract until the root the root determine the
resistance is met) etiology of
the lesion

Radiographs Presence of deep Vertical bone Presence of Angular The

carious lesions / loss and deep bone loss in radiographic
extensive more carious multiple appearance of
/defective generalized than lesions/ teeth with a combined
Restoration/previou to lesions of extensive/def wide base endodontic–
s poor root canal endodontic ective coronally periodontal
treatment/possible origin restorations / and narrow disease may
94
 mishaps/root
fractures/root
previous poor
resorption with
root canal
peripical
treatment
radiolucency
/diminution
Often, the initial
of the pulp
phases of
canal
periradicular bone
space/possibl
resorption from be similar to
e
endodontic origin Bone loss wider at the apex that of a
mishaps/root
is of the root vertically
coronally fractures
confined only to fractured
/root
tooth
cancellous bone. resorption
with a
Therefore it cannot
wide base
be detected unless radiolucency
around the
the cortical bone is
apex of the
also affected . root

Painful Painful
response to response to
Painful response to
Cracked tooth the patient at the patient at
the patient at the
testing using the time of No the time of
time of chewing, No symptoms
transilluminatio chewing, symptoms chewing,
especially on
n wedging especially on especially on
releasing the biting
staining releasing the releasing the
pressure
biting biting
pressure pressure .

95
TREATMENT OF ENDODONTIC-PERIODONTIC
LESIONS

TREATMENT OF ENDODONTIC-
PERIODONTIC LESIONS

96
97
Before the commencement of any kind of advanced restorative work to treat a perio-endo lesion,
the prognosis of the tooth should be considered carefully.

98
Whether there is a functional need for the tooth, whether the tooth is restorable after the lesion has
been treated and whether the patient is suitable for a lengthy, costly and invasive treatment are
factors that should be taken into consideration. Treatment of a tooth with pulpo-periodontal lesions
should not be started before a definitive diagnosis has been established. Then, it must be determined
whether or not the tooth involved can be saved. The success may be influenced by the technique
used and the sequence of therapy.

TREATMENT MODALITIES

I. TREATING PRIMARY ENDODONTIC LESIONS

Primary endodontic diseases usually heal following root canal treatment. The sinus tract extending
into the gingival sulcus or furcation area disappears at an early stage once the affected pulp has
been removed and the root canals well cleaned, shaped, and obturated. Surgical endodontic therapy
has been shown to be unnecessary even in the presence of large periradicular radiolucencies and
periodontal abscesses. Invasive periodontal procedures should be avoided as this may cause further
injury to the attachment, possibly delaying healing.46

II. TREATING PRIMARY ENDODONTIC LESIONS WITH SECONDARY

PERIODONTAL INVOLVEMENT
It will not completely resolve with endodontic treatment alone. Root/re-root canal treatment is
instituted immediately and the cleaned and shaped root canal filled with calcium hydroxide paste.
As it is bactericidal, anti-inflammatory and proteolytic, it inhibits resorption and favors repair. It
also inhibits periodontal contamination from instrumented canals via patent channels connecting the
pulp and periodontium before periodontal treatment removes the contaminants. The canals are
eventually filled with a conventional obturation when there is clinical evidence of improvement.
The prognosis for primary endodontic lesions is good but worsens in the advanced stages of
secondary periodontal involvement.46

III. TREATING PRIMARY PERIODONTAL LESIONS

Determining the prognosis depends upon the stage of periodontal disease and the efficacy of
periodontal treatment. Primary periodontal lesions are treated by hygiene phase therapy in the first
instance. Subsequently, poor restorations and developmental grooves that are involved in the lesion
are removed as these are difficult areas to treat successfully. Periodontal surgery is performed after
the completion of hygiene phase therapy if deemed necessary.46

99
IV. TREATING PRIMARY PERIODONTAL LESIONS WITH SECONDARY
ENDODONTIC INVOLVEMENT
It depends largely on the extent of the pulpal involvement. If diagnosed at an early stage, the
involvement may be limited to reversible pulpal hypersensitivity. Treatment of the periodontal
lesion removes the source of pulpal irritation and secondary mineralization of the dentinal tubules
allows resolution of the pulpal hypersensitivity. When the periodontal lesion has progressed to
involve accessory canals and caused irreversible pulpal inflammation or pulpal necrosis combined
endodontic and periodontal therapy is again required. Endodontic therapy should be completed
first.46

V. TREATING TRUE-COMBINED LESIONS

They are treated initially as primary endodontic lesions with secondary periodontal involvement.
The prognosis of a true-combined perio-endo lesion is often poor or even hopeless, especially when
periodontal lesions are chronic with extensive loss of attachment. The root configuration can be
changed sufficiently by root amputation, hemisection or separation allowing for part of the root
structure to be saved2. The prognosis of an affected tooth can also be improved by increasing bony
support which can be achieved by bone grafting and guided tissue regeneration. This is due to the
most critical determinant of prognosis being a loss of periodontal support.46

Root Amputation
Root amputation is the resection of one or two roots at the furcation. Root amputation is most often
performed on maxillary molar teeth. Root amputation in the lower jaw is rarely indicated and is
confined to a molar which already acts as a bridge abutment. Amputation of one root should not
jeopardize the stability of the bridge. Root amputated teeth should be crowned.

Indications:
1. Severe carious destruction:
When severe caries renders one segment of a tooth non-restorable, removal of the involved root
allows for retention of the remainder of the tooth with an optimal periodontal environmental.
2. Control of compromised embrasure due to tight root proximity:
Root in tight proximal position that do not permit access for cleaning also do not allow for normal
gingival form. Both conditions have obvious periodontal repercussions. The above problem is
obviated by removal of selected roots in order to re-establish proper embrasure space.
3. Severe bone loss of an isolated root: The instances of severe bone loss about an isolated root
which threatens adjacent healthier root support either by direct extension of the periodontal lesion
or by the extent of its osseous surgical correction.

100
The root removal reduces the risk to the surviving teeth, with the added value that healing at the
extraction site often improves the radiographic and clinical appearance of the surviving
approximating periodontal structures.
4. Untreatable furcation involvement:
Frequently, as a sequel to periodontal disease, furcations of molar teeth become exposed to the oral
environment. By virtue of the anatomic conformation, they have the potential for plaque
accumulation and retention and render plaque removal nearly impossible. Removal of the root will
facilitate oral hygiene in that area.

5. Endodontically Untreatable Roots:

They are

1. Mechanically inoperable roots

2. Broken instruments
3. Pathologic and artificial perforations

4. Root Fractures
5. Periapical areas which do not respond to conventional therapy

A B C

D E F G

101
(A) Clinical view of intraoral swelling in relation to 17 and 18. (B) Radiographic view showing
resorption in distobuccal root of 17 (white arrow) due to impingement of 18. (C) Surgical view,
following extraction of 18, revealing bone loss around distobuccal root of 17. (D) Clinical view of
17 following vertical cuts and separation of its distobuccal root. (E) Surgical view following
extraction of 18 and resection of distobuccal root of 17. (F) Radiographic view following resection
and extraction of distobuccal root of 17. (G) Extracted distobuccal root of 17 showing resorption
(black arrow) (Courtesy: Pai et al.)47

Hemisection:
It refers to separation of a two rooted tooth (lower molar or upper first premolar) and extraction of
one half. The remaining half is intended as a bridge abutment. While tooth separation or
bicuspidation is the division of a two-rooted tooth without extraction. Both halves are individually
crowned and appear as two premolars.48
Indications:
1) Severe vertical bone loss involving only one root of multi-rooted teeth
2) Through and through furcation destruction
3) Unfavorable proximity of roots of adjacent teeth, preventing adequate hygiene maintenance in
proximal areas.
4) Severe root exposure due to dehiscence.
5) Endodontic failure: Hemisection is useful in cases in which there is perforation through the floor
of the pulp chamber, or pulp canal of one of the roots of an endodontically involved tooth which
cannot be instrumented.
6) When the root has been destroyed by extensive decay.

Contraindications for Root Resection and Hemisection

1. Fused roots (along their length or at apex).
2. Roots in acutely close proximity.
3. Inability to utilize treated root in an approximate restoration.
4. Inability to treat tooth endodontically.

102
 A B C

(A) Clinical image of cariously involved lower right molar and root stumps on left molar, (B)
preoperative radiographic view of periodontally involved lower right molar with (C) Radiographic
view of lower right molar after endodontic treatment and hemisection of mesial port of root
(Courtesy: Prashant et al.

(A) Clinical image of molar tooth

after ceramic bridge placement, (B)
radiographic view of hemisectioned
molar with bridge at 1 month recall
A B
visit, (C) radiographic view of
hemisectioned molar at 3 months
recall visit, showing absence of the
periodontal ligament widening and
C bone formation at an extraction site
(Courtesy: Prashant et al.)48

103
RECENT ADVANCES
IN TREATMENT

104
PERIODONTAL-ENDODONTIC REGENERATION THERAPY:
Regardless of the treatment method used, healing occurred by repair (ie, long junctional epithelium)
rather than regeneration of the lost tissues of the periodontal attachment apparatus. The introduction
of bone grafts in the 1970s and 1980s and the concept of guided tissue regeneration (GTR) offered
new treatment options to regenerate lost periodontal tissues. In the 1990s and 2000s, enamel matrix
derivatives (EMDs), platelet-derived growth factor (PDGF),insulin like growth factor (IGF-I),and
bone morphogenetic proteins (BMPs)have given a new dimension to periodontal regeneration with
promising clinical results.

The aim of periodontal treatment is complete regeneration of the lost or damaged tissues. Despite
the success of the above-mentioned materials and methods, this aim has been partially but not
completely established. At present, stem cells (SCs) represent a new era in regenerative therapy
with the aim of complete regeneration.49

BONE REPLACEMENT GRAFTS

Perhaps the most commonly used technique for regeneration is the use of bone replacement grafts.
Bone replacement grafts can promote tissue/bone regeneration through a variety of mechanisms.
Some grafts actually contain cells that lay down bone matrix, ultimately resulting in new bone
formation. These grafts are referred to as having osteogenic properties. Other grafts release growth
factors and other mediators that signal the host to produce native bone.

These grafts are considered osteoinductive . Furthermore, other graft materials might simply act as
a scaffold on which host bone might grow. This property is referred to as osteoconductive. There
are many different sources of bone replacement grafts, each with different advantages,
disadvantages, and success rates. In general, grafts can be categorized into autogenous, allograft,
alloplast, and xenograft sources. 50

Autogenous Grafts
Autogenous grafts are those obtained from a remote location within the same host and are
considered the gold standard bone replacement graft. Typically, these grafts are obtained intraorally
from the extraction sockets, edentulous ridges, ramus, symphysis, tuberosity, or the surrounding
buccal plate. Alternatively, larger grafts can be obtained extraorally from areas such as the iliac
crest or tibia. Advantages to using autogenous grafts are that these grafts are osteogenic, prevent

105
disease transmission, and are low cost.

However, they do require a second surgical site at the donor site. Schallhornused iliac crest grafts in
the treatment of infrabony defects and reported up to a 4-mm gain in bone height. However, reports
of root resorption made this treatment option less favorable. Vertical bone gains in infrabony
defects average 3.5 mm for autogenous grafting materials, and several groups have shown that this
approach results in true periodontal regeneration with new cementum formation. 50

Allografts
A bone allograft refers to a graft between genetically dissimilar members of the same species. The
grafts are often obtained from tissue banks that process the donor tissues. Depending on the manner
in which these tissues are processed, allografts might be osteoconductive or osteoinductive. These
grafting materials have relatively high success rates and have an additional advantage in that no
additional surgical procedure is required to procure bone from a donor site.

Disadvantages of allograft potentially include a foreign body immune response, cost, and
contamination of the graft during processing. The most commonly used forms of allografts are
freeze-dried bone allografts (FDBA) and decalcified freeze-dried bone allografts (DFDBA). In
addition, these bone replacement grafts might be further separated into cortical or cancellous
components. Decalcifying the bone allograft exposes BMPs, which have osteoinductive properties.
However, decalcifying the bone graft also causes this type of graft to resorb much faster and act as
a less effective scaffold than its counterpart, FDBA.

Studies evaluating the clinical success of FDBA report bone fill between 1.3–2.6 mm in periodontal
defects. Mellonig found at least 50% bone fill in 67% of periodontal defects if FDBA was used, and
this percentage increased to 78% if FDBA was combined with autogenous bone. Studies evaluating
DFDBA report similar bone fill compared with FDBA, with an average range of 1.7–2.9 mm.
Conversely, in a systematic review, fresh-frozen and DFDBA allografts were associated with
significant improvements in bone level compared with open flap debridement, although this did not
hold true for FDBA.

When used in periapical defects after root end surgery, one endodontic study demonstrated that
FDBA results in histologic periodontal regeneration with no adverse tissue response. Similarly,
several case reports have demonstrated healing with mature bone and hemopoietic marrow in
periapical areas by using DFBA with or without a membrane.50
106
 A B

C D

Bone allograft material for treatment of intrabony periodontal defect. (A) Preoperative radiograph
of intrabony periodontal defect #19. (B) Clinical picture showing surgical exposure of the defect
extending mesiolingually. (C) Bone allograft material filling the defect. (D) Follow-up radiograph
(18 months) showing the presence of adequate bone fill. (Courtesy of Bassam M. Kinaia, DDS,
MS, Boston University Institute for Dental Research and Education, Dubai Healthcare City, Dubai,
UAE.)

Periodontal/endodontic regeneration has been demonstrated with both FDBA and DFDBA,
although one report from Dragoo and Kaldahl showed FBDA healing by repair. In an animal study,
FDBA or DFDBA was placed into surgically created infrabony defects and evaluated
histologically. Three months postoperatively, the FDBA group showed earlier, more rapid, and
more substantial new bone formation than DFDBA.50

Xenografts
A xenograft refers to tissue taken from one species and placed into another species. For intraoral
bone replacement grafts, the most common animal sources are bovine and porcine. Because
antigenicity is a concern with this type of graft, the tissues are processed to remove all organic
constituents, leaving only an inorganic matrix. Thus, xenografts are osteoconductive by nature.
Typically, these grafting materials resorb very slowly and might sequester or undergo fibrous
encapsulation.

107
Positive clinical results have been reported for xenografts in the treatment of infrabony, furcation,
and endodontic-related surgical defects. However, tissue/bone regeneration with xenografts might
be unpredictable. In a study of 8 infrabony defects treated with anorganic bovine bone, 7 defects
showed some evidence of regeneration, whereas 1 defect healed completely by repair. 50

One group evaluated the use of GTR by using anorganic bovine bone and a resorbable collagen
membrane in periapical defects after surgical endodontics. At 1 year, 78% of defects healed
successfully, although there were no differences in outcomes between GTR and no treatment of the
residual periapical lesion. In contrast, one group used anorganic bovine bone in combination with a
bioabsorbable collagen membrane to treat through-and-through endodontic lesions during root end
surgery.

This group reported a success rate of 88% in the treatment group compared with 57% in the control
group (no bone graft or membrane). Consequently, it might be concluded that GTR might be
beneficial in more difficult or compromised situations, but it is unnecessary for simple endodontic
surgery where sufficient bone remains around the defect to regenerate on its own.50

Alloplasts
An alloplast is a synthetic or inert foreign body that is implanted into host tissue. They are
osteoconductive only and can be further categorized as hydroxyapatite, beta-tricalcium phosphate,
non-ceramic,polymer, or bioactive glass. Alloplasts serve primarily to maintain space, and
consequently they are not ideal for promoting periodontal regeneration.

Hydroxyapatite grafts can achieve attachment gains of around 1–1.5 mm, and polymer grafts can
average 2 mm of bone fill. However, tissue/bone regeneration is highly unpredictable in these
cases.Alloplast materials are perhaps the most commonly investigated grafting materials for
periapical defects. Positive results with respect to periodontal regeneration in periapical defects
have been reported by using calcium sulfate, ceramic hydroxyapatite, and polylactide/polyglycolide
copolymers. 50

108
GUIDED TISSUE REGENERATION
Melcher suggested that there are 4 different cell types dictating the type of periodontal healing that
occurs.

These cells originate from the gingival epithelial tissue, lamina propria of connective tissue,
alveolar bone, and Periodontal ligament. Cells derived from periodontal ligament and bone contains
the potential to heal by true regeneration when compared with cells from lamina propria of gingiva
or gingival epithelial tissue that heal by repair Understanding barrier 109 mediated selective cell
repopulation gave rise to the concept of epithelial exclusion to restore lost periodontal tissue and
obtain new attachment. Bowers and colleagues published a histologic report on the formation of
new periodontal attachment apparatus in humans.

The study included teeth with intrabony defects that needed to be extracted because of advanced
periodontal disease. The investigators performed flap, curettage, crown removal, and submersion of
the vital root beneath themucosa with biopsies obtained at 6 months after treatment. The
submersion of the teeth allowed epithelial exclusion similar to GTR. New attachment occurred in
the submerged group indicating regeneration. Healing by long junctional epithelium was observed
on the nonsubmerged teeth, indicating repair. Further, regeneration of new attachment apparatus,
cementum, and bone was more likely in submerged, intrabony grafted defects with demineralized
FDBA. New attachment in grafted sites measured 1.76 mm compared with 0.76 mm in nongrafted
sites.

The investigators concluded that healing with a new attachment was more predictable for
submerged teeth and more likely when a bone graft was added. The literature demonstrated that
GTR was biologically possible with promising clinical results in intrabony and furcation defects.
Although the concept of GTR was primarily established in periodontal regeneration, it also has
been applied in surgical endodontic treatment. A recent systematic review by Tsesis and colleagues
evaluated the efficacy of GTR in endodontic surgery. They found that large communicating lesions
healed better with GTR compared with those without GTR. However, GTR in small confined
lesions was of no added benefit. The use of a resorbable membrane was more favorable than
nonresorbable membranes, a finding that was similar to that obtained in the regeneration of
periodontal furcation defects.

109
Therefore, when a periapical lesion is confined, GTR may not be necessary. If there is a large
communication of the periapical lesion, GTR would be of potential benefit. Despite the success of
GTR in periodontal and endodontic treatments, complete regeneration of the periodontal attachment
apparatus is not always predictable. Thus, advances in molecular biology, such as EMDs and
growth factors, offer a new area of research with the hope of complete regeneration.49

A B

Illustration of GTR for periodontal intrabony defect. (A) Epithelium and connective tissue
migration into periodontal intrabony defect with PDL tissue and alveolar bone loss. (B) Membrane
to exclude the soft tissue coronally to allow selective PDL and alveolar bone regeneration. (C) Ideal
outcome of GTR showing complete reconstruction of the periodontal attachment apparatus.
(Courtesy of Bassam M. Kinaia, DDS, MS, Boston University Institute for Dental Research and
Education, Dubai Healthcare City, Dubai, UAE.)

110
 A B C

D E

Combination of bone allograft material and resorbable membrane (GTR) for the treatment of apical
periodontitis. (A) Periapical radiolucency on #10 after treatment (RCT completed 15 years ago).
(B) Immediate postsurgical radiograph showing retrograde fill.(C) Bone allograft material added.
(D) Resorbable membrane placed. (E) Follow-up radiograph (6 months) showing adequate bone
fill. (Courtesy of Bassam M. Kinaia, DDS, MS, and Sami Chogle, BDS, DMD, MSD, Boston
University Institute for Dental Research and Education, Dubai Healthcare City, Dubai, UAE.

ENAMEL MATRIX DERIVATIVES

Advances in molecular biology set the stage for a new era in periodontal regeneration for complete
regeneration. Studies reported that treatment of intrabony defects with EMDs led to decreased
probing depth, increased clinical attachment level (CAL), increased bone-fill, and periodontal
regeneration. EMD contains amelogenins among other enamel matrix proteins that mimic the
cementogenesis process during root formation.

These proteins, in primate studies, have demonstrated stimulation of the surrounding

undifferentiated mesenchymal cells into cementoblasts to form acellular cementum, a process
similar to the formation of the inner layer of Hertwig epithelial root sheath during tooth
development. Once the cementum is formed, collagen fibers attach from the adjacent PDL leading
to the restoration of the periodontal attachment apparatus. Although not consistent, EMD creates a
favorable environment at the cellular level for periodontal regeneration by improving the
attachment as well as differentiation of PDL fibroblasts compared with gingival fibroblasts.

111
Similarly, the amelogenins are involved in the differentiation of odontoblasts during development
indicating that they may play a role in odontogenesis. Nakamura and colleagues examined the
effect of EMD on pulpal wound healing in an animal study using premolars. They found that EMD
formed dentin like hard tissue with the presence of formative cells outlining the pulpal wound.
EMD had a 2-fold better reparative potential of the pulpal wound compared with the control
(calcium-hydroxide) group. At the microbiological level, EMD selectively inhibited the growth of
gram-negative pathogens although exhibiting no effect on gram-positive pathogens. EMD mainly
creates a positive environment, but it does not contain a specific growth factor that can be useful to
enhance regeneration. More recent advances in regenerative therapies include the use of growth and
differentiation factors for periodontal and endodontic regeneration.49

A B

C D

Illustration of EMD for treatment of periodontal intrabony defect. (A) Apical migration of
epithelium and connective tissue into periodontal intrabony defect with PDL tissue and alveolar
bone loss. (B) Diseased root surface and periodontal defect are surgically exposed. (C) Enamel
matrix derivatives added to repair the defect. (D) Ideal outcome showing complete reconstruction
of the periodontal attachment apparatus. (Courtesy of Bassam M. Kinaia, DDS, MS, Boston
University Institute for Dental Research and Education, Dubai Healthcare City, Dubai, UAE.)

112
GROWTH AND DIFFERENTIATION FACTORS
Growth and differentiation factors play an important role in regulating wound-healing events, such
as chemotaxis, cell adhesion, proliferation, and differentiation. These factors include platelet-
derived growth factor (PDGF), vascular endothelial growth factor (VEGF), transforming growth
factors (TGF) a and b, acidic and basic fibroblast growth factors, epidermal growth factor, IGF-I,
IGF-II, cementum-derived growth factor, parathyroid hormone-related protein, and BMPs. At
present, the most used factors are PDGF, IGF, and BMPs. PDGFs are dimeric glycoproteins
comprising 2 A (-AA), 2 B (BB) chains, or a combination of the 2 (-AB) chains. PDGF-BB has
been used in intrabony periodontal defects with significant improvement in clinical outcomes
demonstrated as CAL gain, bone growth, and percentage bone fill. IGF is a protein with 2 ligands
(IGF-1 and IGF-2).

Howell and colleagues reported CAL gain, periodontal probing depth (PPD) reduction, and bone
gain with use of a combination of IGF-1 and PDGF-BB. Further, a pulp-capping study in rat molars
by Lovschall and colleagues reported a positive effect of IGF-1 in dentin repair. IGF-1 improved
the reparative dentinogenesis in injured dental pulps. 49

Contrary to the Lovschall study, Regan and colleagues evaluated the use of the PDGF and IGF
combination in periapical surgery and reported no regeneration of the periapical tissues. PDGF and
IGF have shown promising results in periodontal regeneration but their results are controversial in
endodontic regeneration. BMPs are differentiating factors belonging to the TGF-b superfamily.
They play a major role in differentiation, cell migration, proliferation, and apoptosis. At present,
there are more than 20 BMPs with BMP-2 (osteogenic protein-2 [OP-2]), BMP-3 (osteogenin), and
BMP-7 (osteogenic protein-1 [OP-1]) being the most useful in regenerative therapy. In 2007, the
Food and Drug Administration approved the use of INFUSE Bone Graft containing BMP in dental
regeneration.

BMP-2 and -3 have shown potential in correcting intrabony and furcation bone loss. However,
BMP-2 has been associated with ankylosis histologically. Therefore, these molecules are generally
reserved for use around implants or for guided bone regeneration. However, BMP-7 has been used
successfully in periodontal regeneration with no ankylosis. Similarly, animal studies reported the
differentiation of pulp cells into odontoblasts leading to the formation of osteodentin when using
BMP-2 and BMP-7.

113
The current regenerative methods have shown adequate clinical results, but complete regeneration
as of yet is not predictably achievable. New research emphasizes the use of SCs with the aim and
hope of complete regeneration of the original periodontal and endodontic tissues. 49

STEM CELLS
Although growth and differentiating factors have shown positive clinical results, they possess a
short biologic half-life that may limit their use in complete regeneration of lost or damaged tissues.
Therefore, constant release of these factors may be essential for complete periodontal regeneration.
SCs are readily present in human tissues offering new horizons for complete regeneration. Dental
SCs are primarily found in the dental pulp and PDL.

Three dental SC populations have been identified based on their origin: dental pulp SCs (DPSCs),
SCs from human exfoliated deciduous teeth (SHED), and PDLSCs. Several preclinical studies have
been reported on PDLSCs. In 1 study, PDLSCs were isolated from extracted human third molar
PDLs and transplanted into immunocompromised mice and rats. PDLSCs differentiated into
cementoblastlike cells, adipocytes, and collagen-forming cells and generated cementum/PDLlike
tissues. PDLSCs are similar to DPSCs and SHED in their expression of surface markers of STRO-1
and CD146/MUC18. Further, they are superior to bone mesenchymal stromal SCs (BMSSCs) in
their high proliferation rate and differentiation capacity. Lin and colleagues examined human
periodontium of molar teeth. The investigators used SC markers STRO-1, CD146, and CD44, and
were able to identify PDLSCs in the regenerated tissue, indicating their involvement in periodontal
regeneration.

Another marker that has been seen in BMSSCs recruitment is stromal cell–derived factor-1 (SDF-
1). A recent study by Du and colleagues37, reported significant proliferation and stimulated the
migration of PDLSCs at concentrations of 100 and 400 ng/mL of SDF-1. This process suggests that
SDF-1 may play a role in periodontal tissue regeneration in addition to the previous cell markers
mentioned. PDLSCs require a scaffold such as hydroxyapatite/tricalcium phosphate to generate
periodontal tissues. PDL progenitor cells (PDLPs) are alternative cell sources to PDLSCs. PDLPs
have been shown to play a role in periodontal regeneration because both are driven from the PDL.
SCs differentiate into progenitor cells, which are more developmentally committed, yet are
undifferentiated in comparison to those cells that have differentiated into specialized tissue cells.
Fen and colleagues examined the use of PDLPs in the treatment of human intrabony periodontal
defects and compared it to PDLSCs. PDLPs were transplanted in defects measuring more than 6
mm depth in 3 patients. PDLPs were similar to PDLSCs in their high proliferation rate and
multipotent differentiation, resulting in therapeutic periodontal regeneration.

This study represents one of the early clinical studies examining the use of stem/progenitor cells in
114
periodontal regeneration in humans. 4examined human periodontium of molar teeth. The
investigators used SC markers STRO-1, CD146, and CD44, and were able to identify PDLSCs in
the regenerated tissue, indicating their involvement in periodontal regeneration. Another marker
that has been seen in BMSSCs recruitment is stromal cell–derived factor-1 (SDF-1). A recent study
by Du and colleagues37, reported significant proliferation and stimulated the migration of PDLSCs
at concentrations of 100 and 400 ng/mL of SDF-1.

This process suggests that SDF-1 may play a role in periodontal tissue regeneration in addition to
the previous cell markers mentioned. PDLSCs require a scaffold such as hydroxyapatite/tricalcium
phosphate to generate periodontal tissues. PDL progenitor cells (PDLPs) are alternative cell sources
to PDLSCs. PDLPs have been shown to play a role in periodontal regeneration because both are
driven from the PDL. SCs differentiate into progenitor cells, which are more developmentally
committed, yet are undifferentiated in comparison to those cells that have differentiated into
specialized tissue cells. Fen and colleagues examined the use of PDLPs in the treatment of human
intrabony periodontal defects and compared it to PDLSCs.

PDLPs were transplanted in defects measuring more than 6 mm depth in 3 patients. PDLPs were
similar to PDLSCs in their high proliferation rate and multipotent differentiation, resulting in
therapeutic periodontal regeneration. This study represents one of the early clinical studies
examining the use of stem/progenitor cells in periodontal regeneration in humans. 49

TREATING IATROGENIC LESIONS

Although the first priority is to close the iatrogenic communication, the aim is to produce a seal.
Root perforations are treated according to their aetiology. The outcome of the treatment of root
perforations depends on the size, location, time of diagnosis and treatment, degree of periodontal
damage as well as the sealing ability and biocompatibility of the sealer.

It has been recognized that the success of the treatment depends mainly on immediate sealing of the
perforation and appropriate infection control. Several materials such as MTA, Super EBA, Cavit,
IRM, glass ionomer cements, composites, and amalgam have been recommended to seal root
perforations. Palatal perforations are difficult to manage, even surgically, and frequently lead to
extraction. The successful treatment of root perforations depends principally on early detection and
sealing. Although the prognosis is deemed poor, it appears that a successful outcome can frequently
be achieved. 46

Therapy of accidental perforations

115
Accidental perforations are treated surgically or non-surgically, depending on their size and
location .They can be classified into four groups:

Class I: Crown or root perforations coronal to the epithelial attachment. If the perforation occurs
coronal to the gingival tissue, it is visible and can easily be sealed from the outside using composite
resin. This is the only perforation which does not damage the periodontal tissue.

If the perforation is located within a periodontal pocket, a small flap is raised to allow the
perforation to be treated in a similar manner.

Class II: Perforations in the middle third of the root. The treatment is either surgical or nonsurgical,
depending on the size and location of the perforation. If the perforation was created with a root
canal instrument, it is usually small. The perforation canal is then treated like an additional root
canal. Care has to be taken not to overfill this artificial canal into the periodontal ligament space. If,
on the other hand, the perforation is made with a bur during preparation for a post hole, the
perforation should be sealed from the outside with zinc free silver amalgam.

Class III: Perforation in the apical third of the root. Class III perforations are the most frequent
type, often due to the "zipping effect" .In many instances, the perforation can be sealed
conservatively. If the perforated canal is slightly overfilled and the symptom-free periapical lesion
heals uneventfully, no further treatment is indicated. But, if clinical symptoms occur or an area can
be detected radiographically, endodontic surgery is indicated.

Class IV: Perforations in the interradicular space of multirooted teeth. The type of treatment
indicated depends on the size of the perforation and also on the health of the periodontal tissue.
Perforations of small diameter are treated non-surgically. The perforation may be sealed with silver
amalgam, gold foil or gutta-percha and root canal sealer. If, however, the perforation is large (>
2mm) root separation or hemi section is the treatment of choice.

Endodontic apical surgery

Lesions attributable to over-filling of root canals and intra-canal medicaments can usually be
resolved by periradicular surgery or endodontic apical surgery.

Endodontic apical surgery mainly includes periapical curettage or Root end resection with
periapical curettage or apical fistulation.

(i) Periapical curettage: Periapical curettage is indicated mainly when root canal is over filled,
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persistent pain exists and root canal retreatment is usually not feasible, it also depends upon the
degree of lesion present.
A small flap is raised and surgical fenestration of the alveolar bone at the apex is performed. With a
small periodontal curette, the excess root filling material and granulation tissue, if present, is
removed. In most instances, resection of the root tip is not required.

(ii) Root end resection: When root resection is done, periapical curettage is always performed as
well.
The indication for this common surgical treatment is mainly limited to the following situations.
1. Obstruction of the root canal (posts, broken instruments, calcifications).
2. Tortuous root canal that cannot be prepared to the apex.
3. Canal that cannot be dried because of continuous exudates.
4. Periapical lesion that does not heal despite apparently correct root canal treatment having been
performed.
5. Apical perforation with symptoms.
6. Apical external resorption.

In all cases in which the root canal treatment cannot be negotiated to the apex the sequence of
treatment is as follows:
1. Reflection of the flap.
2. Location of the apex and surgical perforation of the alveolar bone.
3. Root end resection.
4. Periapical curettage.
5. Retrograde cavity preparation and retrograde filling, preferably with zinc-free silver amalgam or
a high-copper silver amalgam and varnish.
6. Suturing of the flap.

Endodontic apical surgery may be combined with periodontal surgery. In most instances, a full
thickness flap is made at the gingival margin, both on the lingual and buccal aspect.

(iii) Apical fistulation. This is the surgical creation of a hole through the alveolar mucosa and
cortical plate at the apex of a tooth with acute symptoms to relieve pain. The technique is dangerous
if it is performed without raising a flap and thus first locate the apex.

117
Anatomical landmarks such as the maxillary sinus, the mandibular canal or mental nerve in the
neighborhood of root apices of posterior teeth should be identified. In addition, apical fistulation is
never a definitive treatment, but only for emergency use in very rare cases.

THERAPY OF RESORPTIVE PERFORATIONS

Internal resorption that has perforated into the periodontal ligament space must be distinguished
from external resorption that perforate into the pulp.

Perforated internal resorption can be treated non-surgically, but more frequently require surgical
therapy. The conservative approach, suggested by Frank (1967)38, consists of filling the entire root
canal with calcium hydroxide, after the root canal system has been thoroughly cleaned and shaped,
to induce cementogenesis.

After 2-3 months, calcium hydroxide is replaced by the definitive root canal filling, gutta-percha
and sealer. The surgical treatment consists of reflecting a flap and sealing the perforation from the
outside with silver amalgam.

DIODONTIC IMPLANTS
This rather rare procedure is occasionally performed on a mobile lower anterior tooth with
advanced periodontal disease (Frank 1967)39. After normal preparation of the root canal, a drill is
used through the root canal to create a space 6-8 mm into the alveolar bone.

Diodontic implants function primarily by improving the crown-root ratio, thereby stabilizing the
compromised tooth. Pocket elimination is performed when necessary, and healing should be
complete prior to the implant procedure. Where the pulp of the tooth is non-vital, the implant
should not be inserted at the first visit of endodontic treatment.

INTENTIONAL REPLANTATION
Intentional replantation of a tooth is the last resort when no other treatment is possible involves
extraction of the affected tooth, apicectomy and retro filling out of the mouth and finally
replantation of the tooth in its socket. The replanted tooth should be stabilized to the adjacent teeth
for several weeks. The prognosis of replanted teeth is not favorable because more than one-third
show root resorption or ankylosis after 5-10 years. Therefore, this procedure can only be
recommended with great reservation.

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PLATELET-RICH FIBRIN, “A FASTER HEALING AID”
Anatomically the pulp and periodontium are connected through apical foramen, and the lateral,
accessory, and furcal canals. Diseases of one tissue may affect the other. In the present case report
with two cases, a primary periodontal lesion with secondary endodontic involvement is described.
In both cases, root canal treatment was done followed by periodontal therapy with the use of
platelet-rich fibrin (PRF) as the regenerative material of choice. PRF has been a breakthrough in the
stimulation and acceleration of tissue healing. It is used to achieve faster healing of the intrabony
defects. Absence of an intraradicular lesion, pain, and swelling, along with tooth stability and
adequate radiographic bone fill indicative of successful outcome.

FUTURE DIRECTIONS
Although the current research in regenerative therapy is very promising, complete biological
regeneration of periodontal and endodontic tissues is not yet predictably obtained. Bone grafts
generally result in repair rather than regeneration. GTR is a sound principle, but it does not always
regenerate the lost tissues predictably and completely. EMDs and growth and differentiation factors
have a short biological half-life limiting their use for complete regeneration.

SCs possess great potential for complete regeneration but still needs to be demonstrated as effective
in human clinical trials. Future directions involve the fabrication of vehicles and scaffolds that are
able to have a sustained release of growth factors and SCs with the aim of complete and true
biological regeneration to restore the original tissues.49

EXTRACTION - the last option

Extraction may be indicated, if treatment can be simplified without loss of function and aesthetics.
Teeth which are frequently sacrificed are those with advanced periodontal disease or crown-root
fractures.

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SUMMARY

120
 SUMMARY
It is known that both the pulp and the periodontium is closely linked between each other, through
the apical foramen, accessory canals, and dentinal tubules of the root, and one can interfere on the
integrity of the other. Although there is the existence of these communication routes, the
mechanism of direct transmission of the periodontal infection to the pulp is still controversial.51
The periodontal-endodontic lesion develops by extension of either periodontal destruction apically
combining with an existing periapical lesion or an endodontic lesion marginally, combining with an
existing periodontal lesion. From the diagnostic point of view, it is important to realize that as long
as the pulp remains vital, although inflamed or scarred, it is unlikely to produce irritants that are
sufficient to cause pronounced marginal breakdown of the periodontium.21

Inflammatory processes in the periodontium associated with necrotic dental pulp and periodontal
disease have an infectious etiology. The essential difference between the two disease entities is their
respective source of infection. Rarely will established endodontic lesions involve the marginal
periodontium, unless they are developing close to the bone margin. A potential pathway for
infectious elements in the root canal in such instances may be lateral canals. 21

Acute manifestations of root canal infections can result in rapid and extensive destruction of the
attachment apparatus. Abscesses may drain off in different directions, either through a sinus tract
along the periodontal ligament space or through extra osseous fistulation into the gingival sulcus or
pocket. Following proper endodontic therapy, these lesions should be expected to heal without a
persistent periodontal defect. 21

Taking into consideration, the facts about the classification, diagnosis and the therapy of endo-perio
lesions, it appears that diagnosis of pulpal lesion is comparatively more complicated than
diagnosing a periodontal lesion. Because pulpal response to various vitality tests is not reliable
always. For example, the vital pulp of a concussed tooth may respond negatively to the vitality test
and espcialy in multirooted teeth due to partial necrosis the pulp vitality tests may fail. The pulp
may give false negative or false positive response. The entire dentition should be examined for
possible causes of pain before commencing treatment. Some periodontal lesions of endodontic
origin can heal following root canal treatment alone.52

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The diagnosis of periodontal lesions, degenerative, or combined can be complicated by the presence
of pulpal inflammatory lesions. A moderately deep periodontal furcation (Class II) involvement can
lead to the exposure of furcation canals to the oral environment. Through this, a portion of pulpal
tissue can become inflamed with resultant pain. A combined lesion of this type presents a
diagnostic dilemma of considerable dimensions. Case of pocket in the furcation, plus pain and
positive clinical signs of pulpal involvement in a caries-free tooth, our diagnostic acumen leads to
the safe conclusion that, in this instance, the pulpal involvement was caused by periodontal
recession which led to pulpal exposure through a furcal canal.

With a similar clinical condition, that is a periodontal pocket in the furca and signs of pulpal
inflammation, the presence of a deep restoration, and new or recurrent caries, our suspicious
become aroused as to which of the lesions came first. We now wish to determine whether the
reverse is true, or if the lesions were coincidental and unrelated in their presence. The latter would
be rare indeed in the area such as the described.

The first step to the solution of the problem best described, as a common lesion with possible
etiology of either origin is to recognize that no tooth is a separate entity in a patient with full or
partial dentition. If there are other teeth, their condition must be considered in the examination and
diagnosis of the tooth in question. With a mouth relatively free of periodontal pockets and with a
tooth, which manifests a pulpal periodontal inflammatory lesion in the presence of suspicious
carious activity, we first lay the responsibilities of etiology of the common lesion to the caries. This
is done in the full realization that we may be in error, but with a relatively periodontally free mouth,
caries must be considered a suspect with regard to the etiology of this lesion.

Many studies in the literature indicate that combined periodontal and endodontic therapy is
essential for successful healing of a periodontal-endodontic lesion. It has been said that either
endodontic or periodontic treatment alone would not lead to a satisfactory prognosis, if both disease
entities are present and that both must be considered together. Hiatt and Amen claimed that
persistent periodontal disease may clear up only after definitive periodontal therapy is followed by
successful endodontic treatment. Most authors agree that both forms of therapy are essential for
successful healing of combined lesions.

However, the problem arises over which lesion came first and which caused or perpetuated the
clinical problem. It is generally agreed that pulpal disease could initiate or perpetuate periodontal
disease; the opposite theory is controversial.

122
Johnson and Orban6 showed that periodontal disease that remained after unsuccessful endodontic
therapy cleared up after successful endodontic therapy. Several authors have also shown the
remission of severe periodontal bone loss after endodontic therapy alone. Simring and Goldberg
postulated that endodontic therapy is indicated in the treatment of terminal periodontal disease that
does not respond to periodontal therapy. 21

The effect of periodontal inflammation on the pulp is controversial and conflicting. It has been
suggested that periodontal disease has no effect on the pulp, at least until it involves the apex. On
the other hand, several studies suggested that the effect of periodontal disease on the pulp is
degenerative in nature including an increase in calcifications, fibrosis and collagen resorption, as
well as a direct inflammatory effect. However, it seems that the pulp is not directly affected by
periodontal disease, until recession has opened up an accessory canal to the oral environment.
Therefore, treatment of combined lesions should aim at eliminating both the problems.21

Treatment and prognosis of primarily endodontic and primarily periodontal disease is very
straightforward. However, prognosis of combined forms of the lesions is more difficult to predict.
Endodontic therapy is more predictable and completion of this therapy before periodontal
procedures has a positive effect on periodontal healing. The most guarded prognosis is given for
true combined lesions. In general, assuming that endodontic therapy is adequate, what is of
endodontic origin will heal. However, in cases of combined disease, the prognosis of combined
diseases rests with the severity and extent of the periodontal lesion and the efficacy of periodontal
therapy.9

It is essential to understand that in perio-endo lesions, the endodontic treatment is the more
predictable of the two. However the success of endodontic therapy is dependent on the completion
of periodontal therapy. The complete treatment of both aspects of perio-endo lesions is essential for
successful long-term results. Due to the complexity of these affections, an interdisciplinary
approach with a good collaboration between endodontists, periodontologists and microbiologists, is
recommended.21

123
CONCLUSION

124
 CONCLUSION
A perio-endo lesion can have a varied pathogenesis which ranges from quite simple to relatively
complex one. Having enough knowledge of these disease processes is essential in coming to the
correct diagnosis. It is important to remember that the recognition of pulp vitality is essential for a
differential diagnosis and for the selection of primary measures for treatment of inflammatory
lesions in the marginal and apical periodontium.

Diagnosis of teeth with necrotic pulps can be difficult to establish. The entire dentition should be
examined for possible causes of pain before commencing treatment. Some periodontal lesions of
endodontic origin can heal following root canal treatment alone.77 The endodontic treatment can be
completed before periodontal treatment is provided when there is no communication between the
disease processes. However, when there is a communication between the lesions of the two
diseases, then the root canals should be medicated until the periodontal treatment has been
completed and the overall prognosis of the tooth has been reassessed as being favorable.

The use of non-toxic intracanal therapeutic medicaments is essential to destroy bacteria and to help
encourage tissue repair.78 Because the primary aetiology is infection, endodontic treatment is
directed at control and elimination of the root canal flora by working in a sterile way. Based on
current knowledge, the best available method for obtaining clean, microbe-free root canals is
instrumentation with antimicrobial irrigation reinforced by an intracanal dressing with calcium
hydroxide.79 

The presence of a combined endodontic-periodontal lesion will always result in a compromised

situation following treatment. Even with apparently successful treatment, the tooth will still be
compromised as there is likely to be some gingival recession and loss of periodontal attachment and
bone support. It is of utmost importance that the patient maintains good oral hygiene and obtains
regular professional care for this region. The tooth anatomy and the etiology of endodontic-
periodontal lesions offer a strong base for establishing a correct diagnosis.

125
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.

 Thus it can be concluded that it is of extreme importance that the dentist should know how to
differentiate between the origins of the periodontal-endodontic lesions, including all the routes of
communication between the pulp and the periodontium which act as possible “bridges” for the
microorganisms, thereby enabling the dissemination of the infection from one site to another.

Through this knowledge, the dentist will achieve the correct diagnosis and adequate treatment,
resulting in greater chances of obtaining success in the treatment of the periodontal-endodontic
lesions.

Due to the complexity of these infections, an interdisciplinary approach with a good collaboration
between endodontists, Periodontist, and microbiologists is recommended.

126
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