Endodontic-periodontic

lesions
 INTRODUCTION

PATHWAYS OF COMMUNICATION

CLASSIFICATION

ETIOLOGY

CONTENT PATHOGENESIS
S CONTROVERSY

DIAGNOSIS

MANAGEMENT

CONCLUSION

REFERENCES
INTRODUCTION

• The endo perio lesions have been characterized by the involvement of

the pulp and periodontium in the same tooth.
• This makes it difficult to diagnose because a single lesion may present
signs of both endodontic and periodontal involvement
• Weine (1972) suggested that endodontics is actually “periapical
periodontics.”

• In 1919 Turner and Drew first described the effect of periodontal disease on
the pulp

• Simring and Goldberg, in 1964, first described the relationship between

pulpal and periodontal diseases as Pulpodontic-periodontic syndrome

• Since then, the term ‘perio‑endo lesion’ has been used to describe lesions due
to inflammatory products found in varying degrees in both periodontium and
pulpal tissues
According to Lindhe,
An “endo perio lesion” as the term implies involves a condition where
both the pulp and the periodontium are diseased simultaneously in what
appears to be a single periodontal lesion.
 RELATION BETWEEN PULP AND PERIODONTIUM

• The periodontium and pulp have embryonic, anatomic and functional inter-
relationship.

• Tissues of dental pulp and periodontium are interlinked from the embryonic
stage.

• The dental papilla (precursor of dental pulp) and dental sac (precursor of PDL)
are of a common mesodermal origin.

• At the late bell stage, epithelial root sheath separates the dental papilla and
dental follicle except at the base the future apical foramen. Therefore, it is
natural to expect that any part of periodontium can get affected by pulpal
inflammation and vice versa.(Shah N, 1974)
 PATHWAY
S
Pathways of developmental origin (anatomical pathways):

• Apical foramen, accessory canals/lateral canals

• Congenital absence of cementum exposing dentinal tubules
• Developmental grooves

A) Scanning electron micrograph of open

dentinal
tubules. (B) Higher magnification. Note
absence of
odontoblastic processes.
• Rubach and Mitchell suggested that the periodontal disease may affect
the pulp health when the accessory canal exposure occurs, allowing the
periodontopathogenic bacteria to cause inflammatory reactions followed
by pulp necrosis

• Lindhe also reported that bacterial infiltrates of the inflammatory

process may reach the pulp when there is accessory canal exposure,
through apical foramens and canaliculi of the furcation area.

• Adriaens et al. demonstrated that bacteria coming from the periodontal

pockets have the capacity of reaching the root canals towards the pulp,
suggesting that the dentinal tubules may serve as a reservoir for these
microorganisms and that a recolonization of the treated root surface may
occur.
Controversy….

• Kirkham in 1975 reported that only 2% of teeth possessed accessory

canals within the periodontal pockets among those teeth extracted for
severe periodontal disease. Thus, the likelihood that primary periodontal
infections will reach the dental pulp through accessory canals is highly
remote
Pathways of pathological origin:(non-physiological)

• Empty spaces on root created by Sharpey’s fibers

• Root fracture following trauma
• Idiopathic root resorption ‑ internal and external
• Loss of cementum due to external irritants.
Pathways of iatrogenic origin::(non-physiological)

• Exposure of dentinal tubules following root planing

• Accidental lateral root perforation during endodontic procedures
• Root fractures during endodontic procedures
Controversy…

• Root planing as part of routine periodontal therapy, for example, is

shown to decrease dentin permeability and result in the formation of a
smear layer that is acid labile.(Fogel HM, Pashley DH,1993)

• However, dentin permeability may increase on removal of the smear

layer, thus resulting in tubular penetration of oral pathogens and
subsequent pulpal irritation
Etiological and contributing factors in endo‑perio lesions
 MICROBIOLOG
Y
• In acute apical abscess, anaerobic bacteria are predominant over aerobic strains and
anaerobes, and microaerophiles were predominant in 82% of the cases studied.
(Khemaleelakul S et al,2002)

• The most prevalent isolated bacteria are Fusobacterium nucleatum, Parvimonas

micra, and Porphyromonas endodontalis.( Siqueira JF Jr, Rocas IN.2009)

• Depending on the virulence of the organisms and host resistance, a lesion that has
been chronic may exacerbate and become an acute apical abscess.
• Actinobacillus actinomycetemcomitans, bacteroides frosythus, Ekinella
corrodens, Fusobacterium nucleatum, Porphyromonas gingivalis,
Prevotella intermedia and Treponema denticola are present in both
endodontic sample as well as in teeth with chronic apical periodontitis
and chronic adult periodontitis
• Spirochetes most often isolated in root canal infections are Treponema
denticola and Treponema maltophilium.

• When comparing chronic and acute apical abscesses, Baumgartner and

colleagues found a significantly higher incidence of spirochetes in acute
abscesses and cellulitis than in asymptomatic infected root canals.

• Treponema socranskii was the most frequently encountered species.

FUNGI (YEASTS)

• Yeast colonization associated with periradicular 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

• The majority of the recovered fungi were Candida albicans

• It’s been suggested that the reduction of specific strains of bacteria in the
root canal during endodontic treatment may allow fungi overgrowth in
the remaining low-nutrient environment
VIRUSES

• The presence of viruses in the dental pulp was first reported in a patient
with AIDS

• Sabeti et al. suggested that human cytomegalovirus and the Epstein–Barr

virus play a role in the pathogenesis of symptomatic periapical lesions

• Herpesvirus activation in periapical inflammatory cells may impair the

host defense mechanisms and give rise to overgrowth of bacteria, as seen
in periodontal lesions
 A vital pulp is very resistant to microbial invasion.

Penetration of the surface of a healthy pulp by oral bacteria is relatively

slow or may be blocked entirely.

In contrast, a necrotic pulp is rapidly invaded and colonized by bacteria.

When the pulp becomes necrotic, inflammatory byproducts of pulpal origin
may leach out through these pathways and initiate/trigger an inflammatory
vascular response in the periodontium, cause destruction of periodontal
tissue fibers, resorption of adjacent alveolar bone and cementum
• Nature and extent of periodontal destruction depends on various factors
such as

 virulence of microorganisms,

duration of the disease and

 the host defense mechanism

Classification of endodontic-periodontal
lesions

• Simon, Glick and Frank (1972)

• Based on etiology and progression of the disease:

• Primary endodontic lesions

• Primary endodontic lesions with secondary periodontal
involvement
• Primary periodontal lesions
• Primary periodontal lesions with secondary endodontic
involvement
• True combined lesions.
 Primary endodontic lesion

• 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 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.
Combined diseases
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.
• 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.

• In molar teeth the prognosis may be better.

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 .

• The degree of attachment loss in this type of lesion is invariably large

and the prognosis guarded(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.
Though Simon et al. have classified these lesions into five types but actually
three, four and five can be considered as combined lesions.

 There have been many classifications suggested by several other authors such
as “independent periodontal and endodontic lesions” (Harrington GW,2002)or

 “concomitant pulpal and periodontal lesions”(Ammons WF,2002) to describe

endo‑perio lesions

concomitant pulpal and periodontal lesions reflect the presence of two separate
and distinct disease states with different causative factors and with no clinical
evidence that one disease state has influenced other
According to Weine 1982: based on clinical and radiological symptoms

• Class I : tooth in which symptoms clinically and radiographically simulate

periodontal disease but are infact due to pulpal inflammation or necrosis.

• Class II : Tooth that has both pulpal 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

disease but infact has periodontal disease.

• Guldener and Langeland (1982)
Based on possible pathologic relationships:
• Endodontic – periodontal lesions:
• Periodontal – endodontic lesions
• Combined lesions
• Grossman I (1991)

Based on therapy into three groups,

1. Teeth that require endodontic therapy alone

2. Teeth that require periodontal therapy alone

3. Teeth that require endodontic as well as periodontal treatment.

Torabinejad and Trope (1996)

Based on the origin of the periodontal pocket,

1. Endodontic origin

2. Periodontal origin

3. Combined endo-perio lesion

4. Separate endodontic and periodontal lesions

5. Lesions with communication

6. Lesions with no communication.

World workshop for classification of periodontal diseases (1999)

Periodontitis associated with endodontic disease:

1. Endodontic-periodontal lesion

2. Periodontal-endodontic lesion

3. Combined lesion
von Arx and Cochran proposed a classification of endo-perio lesion based on
the clinical treatment with the employment of a membrane (2001)

Class I: Periapical bone defect without marginal lesion

- Ia Lingual/palatal cortex not eroded
- Ib Lingual/palatal cortex eroded (with a buccal surgical approach, this will
result in a transosseous or through-and-through bone defect)

Class II: Periapical lesion (with or without lingual erosion) and concomitant
marginal lesion
- IIa No communication between the separate lesions
- IIb The two lesions are fused = communicating apico-marginal or
endodontic-periodontic lesion

Class III: Lateral or furcational lesion (with or without marginal lesion)

- IIIa No communication to alveolar crest/marginal periodontium
- IIIb Communication to alveolar crest/marginal periodontium
Kim and Kratchman (2006)

a. Absence of periradicular lesion, no mobility, normal pocket depth, but

unresolved symptoms after non-surgical therapies have been exhausted.

b. Presence of a small periradicular lesion in the apical quarter, clinical

symptoms such as discomfort/sensitivity to percussion as sinus tract, normal
periodontal probing depths, and no mobility.

c. Large periradicular lesions progressing coronally but without periodontal

pockets and/or mobility.

d. Clinically similar to those in Class C but with periodontal pockets >4 mm and
no communication of the pocket and the endodontic lesion.

e. Deep periradicular lesions with endodontic-periodontal communication to the

apex, but no obvious fracture.

f. Apical lesion and complete denudement of the buccal plate but no mobility.
In 2009, PV Abott and JC Salgado proposed that those teeth that have both
endodontic and periodontal diseases occurring at the same time should be
called ‘‘concurrent diseases’’ rather than ‘‘combined endo-perio lesions’’.

Concurrent endodontic and periodontal diseases Without communication

Concurrent endodontic and periodontal diseases with communication

Singh 2011 classified endo‑perio lesions based on the pathogenesis and,
usually endodontic lesions produced as a result of treatment modalities

1.Endodontic lesions: an inflammatory process in the periodontal tissues

resulting from noxious agents present in the root canal system of the tooth.

2.Periodontal lesions: an inflammatory process in the pulpal tissues resulting

from accumulation of dental plaque on the external root surfaces.

3.True-combined lesions: both an endodontic and periodontal lesion developing

independently and progressing concurrently which meet and merge at a point
along the root surface.

4.Iatrogenic lesions: usually endodontic lesions produced as a result of

treatment modalities.
A classification by Khalid S Al-Fouzan, 2014based on the primary disease
with its secondary effect New classification based on the primary disease
with its secondary effect:
1. Retrograde periodontal disease: It could be of two types
a. Primary endodontic lesion with drainage through the PDL
b. Primary endodontic lesion with secondary periodontal involvement.
2. Primary periodontal lesion.
3. Primary periodontal lesion with secondary endodontic involvement
4. Combined endodontic-periodontal lesion
5. Iatrogenic periodontal lesions.
a. Root perforations
b. Coronal leakage
c. Dental injuries or trauma
d. Chemicals used in dentistry
e. Vertical root fractures.
Primary Endodontic Lesion with
Drainage through the Periodontal
Ligament.
• A deep narrow probing defect is noted on just one aspect of the tooth
root.
• 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 diagnostic 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. Primary
endodontic diseases usually heal following root canal treatment.
Primary Endodontic Lesion with
Secondary Periodontal Involvement.

• There is a more extensive periodontal pocket which has occurred as a

result of the drainage from noxious agents present in an infected root
canal system. Long-term existence of the defect has resulted in deposits
of plaque and calculus in the pocket with subsequent advancement of
the periodontal disease. The integrity of the periodontium will be
reestablished if root canal treatment is done properly
Primary Periodontal Lesion.

• The periodontal disease has gradually spread along the root surface
towards the apex.

• The pulp may remain vital but may show some degenerative changes
over time. In such cases, it is advisable to treat the periodontal tissues
only
Primary Periodontal Lesion with
Secondary Endodontic Involvement.

• Progression of the periodontal disease and the pocket leads to pulpal

involvement via either a lateral canal foramen or the main apical
foramen. The pulp subsequently becomes necrotic and infected. In such
cases, it is advisable to treat both tissues
Combined Endodontic-
Periodontal Lesion.
• The tooth has a pulpless, infected root canal system and a coexisting
periodontal defect

• An attempt should be made to identify the primary cause of a combined

lesion but this may not always be possible. In such cases, it is not
essential to determine which disease entity occurred first as the treatment
will involve both endodontic and periodontal management.

• It is generally advisable to treat both tissues concurrently in order to

create the most favourable environment for healing.
 Iatrogenic periodontal lesion.

• Root perforations, root fracture, coronal leakage and chemical injuries to

the periodontium due to endodontic or conservative procedures may lead
to they are likely to cause necrosis of the cementum, in ammation of the
periodontal ligament, and subsequently root resorption.

Ray and Trope reported that defective restorations with adequate root
fillings had a higher failure rate in comparison to teeth with inadequate root
fillings but with adequate restoration
David Herrera, Belén Retamal‐Valdes.2 017 WORLD WORKSHOPJ Clin
Periodontol. 2018;45(Suppl 20):S78–S94.
PATHOGENESIS
EFFECT OF PULPAL DISEASE ONTO
PERIODONTAL TISSUES
• Local invasion of the cariogenic bacteria or a shift in the bacterial
content of biofilm can lead to inflammatory changes in the dental pulp.

• This frequently happens in the absence of caries extension into the pulp
chamber.

• Bacterial by products relevant to pulpitis include lactic acid, ammonia,

urea, lipopolysaccharide, and lipoteichoic acid.

• It is notable that the dental pulp is capable of managing numerous

microbial insults because of its extensive intra pulpal lymphatic system.

• However, an overwhelming pulpal inflammatory response may be

induced through various mechanisms and numerous microbial
challenges.
•  Endodontic lesions

the pulp becomes inflamed/infected,

localized oedema and a resulting increase in intra-pulpal pressure and cell

death.

Increased damage associated with an inflammatory exudate cause local

collapse of the venous part of the local microvasculature.

local tissue hypoxia and anoxia

localized necrosis, the chemical mediators of which cause further localized

oedema.

an inflammatory response of the periodontal ligament at the apical

foramen and/or adjacent to openings of accessory canals.
 A periapical lesion may perforate the cortical bone close to the apex, elevate the
periosteum and overlying soft tissues, and drain into the gingival sulcus, and form
pseudopockets that simulate periodontal disease without necessarily permanent
damaging of the cementum and its fibres

• If the acute periapical drainage becomes chronic and drainage through the
gingival sulcus continues a downgrowth of epithelium along the tract can
result in a periodontal pocket in which secondary periodontal disease may
complicate the lesion.
Mo K. Kang, Kenneth C. Trabert, Shebli Mehrazarin. Newman and
Carranza’s Clinical Periodontology.
Lipopolysaccharide and lipoteichoic acid bind Toll-like
receptors(present on the surface of some immune cells in
the pulp)

induce the release of inflammatory

mediators(prostaglandins, cytokines, and chemokines). In
particular, tumor necrosis factor alpha, interleukin-1 (IL-
1), IL-8, IL-12, and chemokines CCL2 and CXCL2

IL-1 responsible for bone resorption

APICAL PERIODONTITIS
 Goldberg stated that,
leakage of
Pulpal Necrosis of Bacterial
Degeneration pulp byproducts &
toxins

Periodontal
Migrates toward
destruction
gingival margin
apically

Retrograde
Periodontitis
(SimringM, Goldberg M. The pulpal pocket approach: Retrograde
periodontitis. J Periodontol 1964;35:22-48. )
Effect of periodontal disease on pulp
•  Periodontal lesions
• Plaque and calculus initiate periodontal lesions.

• Inflammatory mediators cause destruction of gingival connective tissue, periodontal

ligament and alveolar bone.

• Alteration of the root surface occurs by loss of the outer cementoblast layer and
results in shallow resorptive lesions of cementum.

• Endotoxins produced by plaque bacteria also have an irritant effect on overlying soft
tissue, preventing repair.

• Although periodontal disease has been shown to have a cumulative damaging effect
on the pulp tissue, total disintegration of the pulp will only be a certainty if bacterial
plaque involves the main apical foramina, compromising the vascular supply.
 According to Selzer et al,

Exposure of Interfere with

Deep Pdl lesions
lateral canals nutritional supply

Fatty Pulp tissue Localized area of

degeneration breakdown inflammation

Deep pdl lesions were found exposing the lateral

Atrophic
canals thereby interfering with nutritional supply to
changes in
the pulp
the pulp
- Selzer 1998
• The presence of an intact cementum layer is important for the protection
of the pulp from pathogenic agents produced by the plaque
bacteria. Therefore, the exposure of dentinal tubules by the removal of
cementum due to rigorous scaling and root-planing for the treatment of
periodontal disease will allow bacterial invasion of the tubules. This
would increase the likelihood of cumulative damage to the pulp.

• Results from microbiological and immunological studies support the

suggestion that the source of endodontic infection in perio-endo lesions
with periodontal origin is the periodontal pocket bacteria.
• Combined lesions

• The pathogenesis of a true-combined lesion is identical to the pathogenesis

of primary endodontic and periodontal lesions.

• These lesions are often indistinguishable from an advanced primary

endodontic lesion with secondary periodontal involvement and/or a primary
periodontal lesion with secondary endodontic involvement.

• True combined endodontic-periodontal disease occurs with less frequency. It

is formed when a coronally progressing endodontic disease joins an infected
periodontal pocket progressing apically.
 Iatrogenic lesions
Root perforations  At the site of perforation, an inflammatory reaction in
periodontal ligament produces a degradation of surrounding tissues and
formation of a lesion which can progress as a conventional primary
endodontic lesion.
The overfilling of root canals produces a lesion in exactly the same way as
the lesion originating adjacent to the apical foramen rather than the lateral
wall or pulpal floor.
Coronal leakage is the leakage of bacterial elements from the oral
environment along the restoration's margin to the endodontic filling.
Certain chemicals used in dentistry have the potential to cause root
resorption. Clinical reports have shown that intracoronal bleaching with
highly concentrated oxidizing agents, such as 30-35% hydrogen peroxide,
can induce root resorption.
The irritating chemical may diffuse through the dentinal tubules and when
combined with heat, they are likely to cause necrosis of the cementum,
inflammation of the periodontal ligament, and subsequently root resorption.
PERIODONTAL – ENDODONTIC CONTROVERSY

• Two questions have been raised and

continue to be matters of dispute.

• 1) Is periodontal disease a cause of

pulpal necrosis?

• 2) Can a pulpless tooth be cause of

periodontal disease?
Periodontal disease

• the pulp has a quite sophisticated vasculature system with a network of

capillary beds, precapillary sphincters and arteriovenous shunts, which
provides a significant capacity for the pulp to survive

• ‘periodontal disease’ is a ‘direct cause of pulpal atrophy and necrosis’,

• ‘periodontal disease’ is ‘more deleterious to the pulp than both caries and
restorations combined’ (Petka K,2001), and

• ‘periodontal disease and periodontal treatments should be regarded as

potential causes of pulpitis and pulpal necrosis’(Wang HL,2002).
• (Mandi FA.1972, Langeland K,1974) have also suggested that periodontal
disease is degenerative to pulpal tissues and results in continued calcification,
fibrosis, collagen resorption, and inflammation
• Dentin thickness also contributes to the protection of the pulp.

• Stanley stated that if a 2-mm thickness of dentin remains between the pulp and
an irritating stimulus, little chance of pulpal damage exists.
• Acid etching: During periodontal regenerative therapy, root conditioning
using citric acid helps to remove bacterial endotoxin and anerobic 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. Application of citric acid may have a detrimental effect on the
dental pulp
• Weine summarized the precautions that can be taken during the course of
periodontal therapy:

(1) avoid using irritating chemicals on the root surface,

(2) minimize the use of ultrasonic scalers when less than 2 mm of dentin
remains, and
(3) allow minor pulpal irritations to subside before completing additional
procedures.
When these precautions are not followed and the microvasculature of the pulp
is damaged during periodontal procedures that involve deep curettage or
periodontal surgical efforts to save the tooth, necrosis may result
• Unless the microvasculature of the pulp is compromised during aggressive
periodontal procedures or excessively deep curettage severs the apical
vessels, most periodontal interventions result in only a localized pulpal
response and dentin hypersensitivity(Vandenwijngaert S, Vanlerberghe
K,2000)
• Tagger & Smukler 1977 removed roots from molar teeth so extensively
involved with periodontal disease that root amputation was required, and
found that none of the pulps of the resected roots showed inflammatory
changes.
• Haskell et al.1980 also removed roots from maxillary molars with total or
nearly total periodontal involvement and found no inflammatory cells or very
few inflammatory calls present in the pulps of the periodontally involved
resected roots.
• Czarnecki & Schilder 1979 performed a histological study of intact, caries-
free teeth and compared the pulps of teeth which were periodontally within
normal limits with teeth which had periodontal disease.
The pulps in the intact, caries-free, periodontitis group were all histologically
within normal limits regardless of the severity of the periodontal disease.
In the same study they found that only teeth with extensive decay or extensive
restorations showed evidence of pulp pathosis.
• A case report by Torabinejad & Kiger of a patient with extensive
periodontal disease supports the position that advanced periodontal disease
has little or no effect on the pulps of humans.
• Excessive root planing and curettage that remove the cementum and dentin
from the root surface encourage narrowing of the pulp canals. This process
is thought to be reparative rather than inflammatory.(Bender IB, Seltzer
S,1972)
• periodontal disease has no effect on the pulp, unless it extends all the way
to the tooth apex, the dental pulp is capable of surviving significant insults
and that the effect of periodontal disease as well as periodontal treatment
on the dental pulp is negligible(Czarnecki RT,1979)
• Jaoui L(1995), Torabinejad M(1985), Bergenholtz G(1984) et al.
periodontal disease or sequelae of periodontal treatment does not affect
the pulp
 The effects of endodontically
involved teeth on periodontal
health and healing

• pulpless tooth with a periapical lesion promotes the initiation of periodontal

pocket formation, promotes the progression of periodontal disease, and
interferes with healing of a periodontal lesion after periodontal treatment.

Jansson, Ehnevid, Lindskog and Blömlof

The periodontal- endodontic controversy. Perio 2000. 2002;30: 123-130.

• Jansson et al. assessed the effect of endodontic pathogens on marginal
periodontal wound healing of denuded dentinal surfaces surrounded by
healthy periodontal ligament. Their results showed that in infected teeth,
the defects were covered by 20% more epithelium while the noninfected
teeth showed only 10% more connective tissue coverage. They concluded
that pathogens in necrotic root canals may stimulate epithelial downgrowth
along denuded dentin surfaces with marginal communication and thus
augment periodontal disease
• Jansson et al. stated that teeth with periapical lesion had lost more
proximal bone .
0.19 mm of bone loss\ year vs 0.06mm\ year for teeth with no periapical
lesion
To summarize necrotic pulp or tooth with periapical lesion has impact on
periodontium and having being cause for inititiation of periodontitis

The periodontal- endodontic controversy. Perio 2000. 2002;30: 123-130.

• One credible human study in the literature supports the position that
endodontically obturated teeth may interfere with the effectiveness of
attachment regeneration procedures.

• Sanders et al. reported in 1983 that after the use of freeze-dried bone
allografts 65% of the teeth that did not have root canal treatment showed
complete or greater than 50% bone-fill in periodontal osseous defects, while
only 33% of the teeth which had root canal treatment prior to the
periodontal surgical procedure had complete or greater than 50% bone-fill.
• Lesions of only endodontic origin had a success outcome of 95.2%,
whereas teeth with combined lesions had a success outcome of only
77.5%. This finding suggests that bone healing and tissue healing are
negatively affected after endodontic surgery for lesions of combined
origin(Kim E, Song JS,2008)
 Effects of Endodontic Pathosis on Development of
Retrograde Peri-implantitis

• Persistence of endodontic bacteria and inflammatory cells commonly

facilitates the development of retrograde peri-implantitis or a
radiographically evident periapical lesion at the apex of an osseointegrated
implant, accompanied by swelling, pain, tenderness, and sinus tract
formation(Ayangco L, Sheridan PJ,2001)
Under circumstances where complications arise during implant placement,
such as
• overheating of bone during preparation of the implant osteotomy,
• placement of the implant too close to the adjacent tooth,

• or altering of the blood supply of the adjacent tooth during implant surgery,

• the implant placement itself may result in devitalization of the adjacent

tooth and subsequent development of peri-implantitis

• presence of existing or recurrent periapical disease from an endodontically

treated tooth resulting in contamination of the adjacently placed implant
• Brisman and colleagues demonstrated several cases in which implants
placed adjacent to asymptomatic, endodontically treated teeth exhibiting
no clinical or radiographic signs of periapical disease resulted in peri-
implantitis, which resolved with surgical intervention.
• MANAGEMENT
• conventional root canal therapy- to resolve underlying symptomatic or
radiographic endodontic and periapical disease,
• Endodontic retreatment should be performed to address failure of endodontic
therapy.
• Delaying the placement of an implant after completion of endodontic treatment
on an adjacent tooth or
• increasing the distance between the implant and the adjacent endodontically
treated tooth may reduce the likelihood of peri-implantitis.
• The use of nonmachined surfaced implants may also decrease the chances of
implant failure because machined-surfaced implants placed adjacent to or at the
site of previous endodontic infection are more likely to result in the development
of retrograde periimplantitis(Quirynen M,2005)
• Under circumstances where endodontic infection results in periimplantitis,
• surgical debridement and disinfection of the implant surface and resolution of
the endodontic pathosis are critical to continued success of the implant.
 Affected implants exhibiting poor stability require removal of the implant,
 debridement of granulation tissue within the implant osteotomy site, and
 either placement of bone graft and subsequent implant or immediate
placement of a longer or wide implant.

• Stable implants exhibiting radiographic evidence of periapical pathosis may

be surgically debrided and the implant surface disinfected using chlorhexidine
or tetracycline while ensuring that it is not damaged and that systemic

antibiotics are administered upon successful debridement.

• Brisman and associates demonstrated a case in which an implant placed at
the site of the mandibular incisor succumbed to retrograde periimplantitis
and fistula that, on removal of the implant, was found to lead to the
adjacent mandibular canine, which had been endodontically treated several
years earlier. Subsequent apicoectomy of the adjacent tooth and placement
of a new implant prevented further implant apical inflammation and failure
Visual examination
Palpation
Fistula tracking
Percussion
Mobility
Radiograph
Pulp vitality testing
- Cold test
- Heat test
- Electric test
Blood flow test
Cavity test
Cracked tooth testing
-Transillumination
-Wedging
-Staining
DIAGNOSIS

• Cohen S, Burns RC. Pathways of the Pulp.

• 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.
• 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)
Clinical examination
• Visual examination

• Visual examination includes the examination for the presence of inflammation

ulcerations or sinus tract in alveolar mucosa and attached gingiva.The necrotic pulp
is associated with sinus tract.

• Periodontal pathology is indicated by changes in color, texture, and architecture of

the gingival tissues.

• The teeth are examined for abnormalities such as caries, defective restorations,
erosions, abrasions, cracks, fractures, and discolorations.

• 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
• 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 peri radicular abnormalities or ‘‘hot’’
zones that produce painful response to digital pressure.

• A positive response to palpation may indicate active peri radicular

inflammatory process.

• does not indicate whether the inflammatory process is of endodontic or

periodontal origin.
• Percussion

• Finger or blunt instrument can be used by tapping on the tooth surfaces.

• An abnormal positive response indicates inflammation of the periodontal

ligament that may be either from pulpal or periodontal origin.

• Although this test does not disclose the condition of the pulp, it indicates
the presence of a periradicular inflammation.

• The sensitivity of the proprioceptive fibers in an inflamed periodontal

ligament will help identify the location of the pain.

• This test should be performed gently, especially in highly sensitive teeth.

 • Swelling caused by pulpal infections
often occurs in the mucobuccal folds or
spreads to the facial planes.
• Muscle attachments and root length
Swelling determine the route of drainage.
• Swelling caused by periodontal infection
is usually found in the attached gingival
and rarely spreads beyond the
mucogingival junction and usually does
not cause facial swelling
 • Acute or "blow-out" lesions
• When a patient presents with a localized swelling
that involves the gingival sulcus, it may be
difficult to determine whether the swelling is due
to a periodontal abscess or an abscess of
endodontic origin.
PERIODONTAL • The swelling is usually on the labial side of the
PROBING tooth but may occasionally be on the lingual
side. As the sulcus is probed, there is usually
normal sulcus depth all the way around the tooth
until the area of the swelling is probed.
• At the edge of the swelling the probe drops
significantly to a level near the apex of the
tooth and the probing depth remains the full
width of the swelling.
• At the opposite edge of the swelling, probing is
once again within normal limits.
• The width of the detached gingiva can be as broad as the entire buccal
or lingual surface of the tooth. This swelling can be characterized as
having "blown-out" the entire attachment on that side.

• Endodontic treatment only is indicated. As the result of endodontic

management of the swelling, complete periodontal reattachment
occurs within 1 week in most cases
 • Suppuration can occur with either pulpal or
periodontal pathosis.
• If associated with periodontal disorders, it
Suppuration may be linked with an acute periodontal
or abscess abscess, a chronic periodontal disease, or an
acute exacerbation of a chronic disorder.
formation • Suppuration associated with pulpal pathosis
may be with either an acute or chronic
condition such as an acute alveolar abscess
or a chronic alveolar abscess draining
through a fistula.
 • 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
Fistula tracking mucosa or facial skin.
• Intraorally, the opening is usually visible on the
attached buccal gingiva or in the vestibule.
• Fistula tracking is done by inserting a semirigid
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, which reveals the course of the
sinus tract and the origin of the inflammatory
process
• Mobility
• one is with two ends of blunt instrument and
• other is through finger and a blunt instrument,
• the pressure of application is in both horizontal
and vertical component and score is assigned.
• Tooth mobility is directly proportional to the
integrity of the attachment apparatus or to the
extent of inflammation in the periodontal
ligament.
• Hypermobility is quite common in cases of
primary endodontic involvement and should not
be confused with true mobility caused by
periodontal destruction.
• In cases of primary endodontic pathology, the
mobility resolves within a week of initiating
endodontic therapy.
 • Carious lesions, extensive or defective
restorations, pulpotomies, previous root
Radiographic canal treatment and possible mishaps,
examination canal obliteration, root resorption, root
fractures, and periradicular
radiolucencies are all determined by
radiographic examination.
• Thus, it is important to focus on specific entities on a radiograph.

• These should include the coronal status, crestal bone height and shape, presence
of an apical or lateral radiolucency, bony trabeculation, integrity of the lamina
dura, and careful evaluation of the obturation of the root canal if present.

• apical lesions originating from a primary pulpal infection lead to retrograde

periodontitis that migrates from the root apex in a cervical direction. On the
contrary, periodontal infections lead to the loss of crestal bone from the cervical
area of the tooth in an apical direction.

• For example, radiographic lesions representing severe periodontitis appear wider

at the cervical end than the apical portion of the lesion.

• Apical or lateral radiolucencies may also result from differences in trabeculation

patterns not associated with pulpal infection.

• A break in the lamina dura accompanied by an apical or lateral radiolucency is

usually indicative of a chronic or acute pulpal infection.
• Pulp
Pulp vitality testing
sensibility testing
• They check the pulpal response on application of
stimuli. It also helps to differentiate between
pulpal or periodontal origin. It can be interpreted
based on the response obtained
• Cold test
• Ice sticks, ethyl Chloride, carbon dioxide,
dichlorodifluoromethane are the agents used for
this purpose.
• Electric pulp test
• Electric stimulus is applied to tooth with the help
of special pulp tester device. Most of the
available devices work on similar principal and
they are effective. Stimulation of the sensory
nerve fibers of the pulp to produce a response is
the purpose of the test. Intact pulp is elicited by
positive response and pulp necrosis through
negative response.
 • The normal response of a healthy pulp to
heat is pain that increases in intensity
and decreases immediately once the heat
Heat test is removed. Lingering pain indicates an
irreversible inflamed pulp.
• In case of periodontally involved teeth,
persistence of pain even after removal of
stimulus indicates an endodontic
involvement.
 • Determination of the vitality of pulp
through measuring blood flow is the
purpose of the test.
Blood flow • Oxyhemoglobin is measured through
different systems such as
test • dual wavelength spectrophotometry,
pulse oximetry, and laser Doppler.
• These are relatively new tests which are
not commonly practiced and are non-
invasive and painless.
 • Test cavity is considered to be the most
reliable test in determination of pulp.
• It involves making a cavity without
anesthesia.
Test cavity • Vital pulp tissue shows a positive
response; pulp necrosis is indicated by
negative response.
• Endodontic treatment is initiated by
extending the cavity when the pulp
shows no response.
• Selective anesthesia test
• This test specifies the area of pain when the source is not so clear. It is
observed that area of pain disappears when appropriate side block is
given. This test has limited use in differentiating the pulpal and
periodontal disease.
 CRACKED TOOTH TESTING
Transillumination:
A fiberoptic connected to a high-power light source is used to illuminate the
crown

Wedging:
During the test, wedging forces are created as the patient is instructed to chew
on a cottonwood stick or other firm material.

Staining:
• Methylene blue dye is swabbed on the occlusal surface of the tooth
• 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.
• Parolia, et al.: Endo ‑ perio:A dilemma from 19th until 21st century.
Journal of Interdisciplinary Dentistry. 2013;3(1):1-10
 DIFFERENTIAL DIAGNOSIS OF PULPAL AND
PERIODONTAL LESIONS :
Pulpal Periodontal
Clinical

Cause Pulp infection Periodontal infection

Vitality Nonvital Vital
Restorative Deep or extensive Not related
Plaque / calculus Not related Primary cause
Inflammation Acute Chronic
Pockets Single, narrow Multiple,wide coronally
pH value Often acid Usually alkaline
Radiographic Pulpal Periodontal

Pattern Localized Generalized

Bone loss Wider apically Wider coronally
Periapical Radiolucent Not often related
Vertical bone loss No Yes
Histopathology

Junctional epithelium No apical migration Apical migration

Granulation tissues Apical (minimal) Coronal (Larger)
Gingival Normal Some recession
Therapy

Treatment Root canal therapy Periodontal treatment

TREATMENT
• The decisions and treatment strategy for the application of the regenerative
procedures are made at various levels such as pre-surgical, post-root canal
treatment, intra-surgical, and post-surgical.
• Factors influencing treatment outcome should also be considered at each
level under patient-specific, defect-specific, and healing categories.

• The pre-surgical assessment includes

- establishing and verifying the non-vital status of the pulp,

- the extent and severity of the periodontal destruction, and
- therapeutic prognosis of the planned regenerative procedure.
The intra-surgical assessment should include
- morphology of the periodontal defect,
- defect type,
- material of choice to fill the defect and augment healing,
- control of patient's oral hygiene, and
- wound stabilization
Treatment protocol according to Abott is as follows:

Initial management
Longer-term
Remove management
existing restorations and caries
Defer root
Chemo filling untilprepare
mechanically after canals

Need for periodontal

Medicate surgery
canals (depends onassessed
symptoms)
Surgery completed with satisfactory outcome
Follow-up management

Change intracanal dressing after 3–4 weeks

Provide initial periodontal treatment

Review healing after 3 months

Reassess need for further periodontal treatment

If more periodontal treatment (e.g., surgery) is required,

Change intracanal medication again

If healing response is favourable,

Complete root canal filling

Treatment decision-making and prognosis

• The main factors to consider are pulp vitality and type and extent of the
periodontal defect.

• The prognosis and treatment of each endodontic– periodontal disease type

varies.

 Primary endodontic disease should only be treated by endodontic therapy

and has a good prognosis.

Primary periodontal disease should only be treated by periodontal therapy.

prognosis depends on severity of the periodontal disease and patient
response.
• The prognosis of primary periodontal lesions is poorer than that of primary
endodontic lesions and the treatment choice should be decided due to defect
and root morphology.

• In the case of deep (≥ 4 mm intrabony component) and narrow (≤ 45°)

intrabony defects regenerative techniques such as Guided Tissue Regeneration
(GTR) or the use of biologically active substances such as Enamel Matrix
Derivatives (EMD), Platelet Rich Fibrin (PRF), growth factors and Bone
Morphogenetic Proteins (BMP) should be considered. (Oh SL 2012,
Karunakar P 2017)

• However if the defect morphology is shallow (< 4 mm) and wide (> 45°),
resective surgical treatment options should be taken into consideration.(Oh
SL, Fouad AF 2009)
• Primary endodontic disease with secondary periodontal
involvement should first be treated with endodontic therapy.
Treatment results should be evaluated in 2– 3 months and only then
should periodontal treatment be considered. Prognosis of primary
endodontic disease with secondary periodontal involvement depends
primarily on the severity of periodontal involvement, periodontal
treatment and patient response
The prognosis of primary periodontal disease with secondary endodontic
involvement and true combined diseases depends primarily upon the
severity of the periodontal disease and the response to periodontal
treatment.
Cases of true combined disease usually have a more guarded prognosis
than the other types of endodontic–periodontal problems. From
periodontal point view, the prognosis of combined lesions is usually poor
or hopeless if severe attachment loss exists.( Simring M,2011)
Therefore, hemisection or extraction may also be the treatment of choice
due to periodontal reasons
In general, assuming the endodontic therapy is adequate, what is of
endodontic origin will heal. Thus the prognosis of combined diseases rests
with the efficacy of periodontal therapy
• Iatrogenic lesions like perforation during root canal instrumentation or
preparation of the canal for post and core, require a surgical approach or
sealing through an access cavity with a zinc oxide eugenol, glass ionomer
or mineral trioxide aggregate sealing material immediately.
• 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.

• Treatment depends on the tooth type, extent, duration and location of

fracture, for example, single rooted tooth with lesions caused by vertical
root fracture has a hopeless prognosis and should be extracted while molars
can be treated by root resection or hemisection

• Case reports showed that after the root resection, complete healing occurs
between 15 to 20 months.(Oh SL. 2012)
 Endodontic therapy done prior to periodontal therapy bacause,

• Early initiation of endodontic treatment ensures that the cementum layer is kept
intact until root canal infection is completely eliminated.
• Because there would be no exposed dentine on the root surface, there is reduced
chance of root resorption and improved periodontal healing.
• Also, if periodontal therapy is done prior, there is possible chance of extrusion of
toxic medicaments and necrotic debris during pulpal debridement thereby
increasing risk for secondary infection
 ALTERNATIVE TREATMENT MODALITIES :

When traditional endodontic and periodontal treatments prove insufficient to

stabilize affected teeth, the clinician must consider other treatment
alternatives like

• Root amputation :refers to removal of one or more roots of multirooted

tooth while other roots are retained.

• Hemisection :denotes removal or separation of root with its accompanying

crown portion
Parolia, et al.: Endo ‑ perio:A dilemma from 19th until 21st century. Journal of
Interdisciplinary Dentistry. 2013;3(1):1-10
• conclude that periodontal healing in terms of improvement in
periodontal parameters after 6 months of ET in immediate surgical
periodontal treatment was comparable to healing after 9 months of ET
in delayed surgical treatment in endodontic- periodontal apically
communicating lesions which suggested that there may not be need to
wait for 3 months after endodontic treatment for definitive
periodontal therapy
CONCLUSION

• A perio‑endo lesion can have a varied pathogenesis which ranges from quite
simple to relatively complex one. To make a correct diagnosis the clinician
should have a thorough understanding and scientific knowledge of these
lesions. Despite the segmentation of dentistry into the various areas of
specialization, a clinician needs to perform restorative, endodontic or
periodontal therapy, either singly or in combination. Therefore, to achieve the
best outcome for these lesions, a multi‑disciplinary approach should be
involved
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