Contents

Introduction
Pathways of communication between the dental pulp and the periodontium
Effect of pulpal disease on periodontium
Effect of periodontal disease on pulp
Classifications
Clinical features, diagnosis and treatment of different types of endo-perio
lesions
Clinical diagnostic procedures
Differential diagnosis between pulpal and periodontal disease
Alternative treatment modalities
References
HISTORICAL REVIEW
Turner and Drew (1919) - first described effect of periodontal disease on
dental pulp.



Simring and Goldeberg (1964) - first described the relationship between
Endo and Perio.



Hiatt (1977) and Hemington (1979) - stated that there is no apparent
relationship between periodontal and pulpal disease.


ETIOPATHOGENESIS
OF
ENDO - PERIO LESIONS

5
PATHWAYS OF
ANATOMIC ORIGIN

1. APICAL FORAMEN


Apex - portal of entry of bacterial and inflammatory by- products from
pulp to the periodontium to cause periapical pathosis.


Irritants from necrotic pulp via apical foramen


Initiates an inflammatory response


Destruction of apical PDL and resorption of bone, cementum and dentin
Seltzer et al (1963)



Walton & Garnick (1986) stated that the passage of irritants from pulp was more likely
from the periapex through the inter-radicular medullary bone.

2. LATERAL AND ACCESSORY
CANALS
Potential pathway for the spread of bacterial by-products.
(Cohen 1984)

30-40% of all teeth have lateral or accessory canals.


These canals contain connective tissue and vessels that connect the circulatory
system of pulp with the periodontium.


Not visible on the x-ray films.
(Barrett 1925)


More common in posteriors. (Seltzer et al 1967)




The prevalence varies from 20% to 60% in molar furcations of permanent
teeth. (Bergenholtz and Ricucci 1969)



In deciduous molars - 23% to 30% (Winter 1962)


3. EXPOSED DENTINAL TUBULES

Due to:
Developmental defects
Periodontal Diseases
Periodontal procedures (Harrington
and Steiner 2002)


Number:
8,000 at dentinocemental junction per mm
2

57,000 at pulpal end per mm
2
(Mjor and Nordahl 1996)
15,000 at cervical area of the root per mm
2

(Harrington and Steiner 2002)


The dentinal tubules contain tissue fluid, the odontoblastic processes and
nerve fibers.



As the tooth ages, or experiences irritation, these tubules tend to reduce
in diameter or to calcify

Decreases number of patent tubules


4. DEVELOPMENTAL GROOVES


Common on maxillary lateral incisors. (Withers et al 1981)


Palatal groove formed as an anatomic variant on the crown and root of
tooth.

5. ENAMEL PROJECTION AND ENAMEL
PEARLS



Ectopic extensions of enamel that extend beyond the normal contour of
CEJ.


Favour the development of pocket.


NON-PHYSIOLOGIC
PATHWAYS
Root perforation
Vertical root fracture
Resorption
External
Internal
Poor Endodontic treatment
Poor restoration (Saunders and Saunders 1990)
Trauma

1. R1. Root Perforations1. Root P1. Root PerRoot perforation
1.forationserforatio11.ns1. Rroooot1. Root
Perforations
Etiology
Extensive carious lesions
Resorption
Operator error occurring during root canal instrumentation or post preparation


Treatment & prognosis
Depends on the size, location, time of diagnosis and treatment, degree of
periodontal ligament damage as well as the sealing ability and biocompatibility
of the repair material.


VVertical root fracture
ertical Root Fracture
Cause:
Trauma
Endodontic procedure (Chan et al 1999)

Occur in both vital and non-vital teeth
Radiographically - halo effect around the affected tooth (Meng 1999)

Incidence is higher in
Filled with lateral condensation technique
Teeth restored with intracanal posts

Produce deep periodontal pockets and localized destruction of alveolar bone.

External RootResorption

Invade cementum, dentin and pulp space.

Divided into two main categories:

1. Progressive inflammatory resorption

Etiology
Pulpal infection
Sulcular infection
Traumatic displacement injuries, tumours or cysts
Undue forces

2. Invasive root resorption (invasive cervical resorption)

Non-inflammatory
Due to invasion by fibro vascular tissue derived from the PDL

Clinical features
Small defect at the gingival margin
Pink coronal discoloration

Radiographic features
Well delineated or irregularly bordered radiolucency

Internal Root Resorption
Etiology
Unknown

Predisposing factors
Infected root canal
Trauma: mechanical, chemical or thermal
Bacteria
Intracoronal bleaching with 30%H
2
O
2

Clinical features
Asymptomatic

Radiographic features
Defect has a distorted outline of the root canal
A round or an oval-shaped enlargement of the root canal space


Histological features
Multinucleated giant cells


Treatment
Complete removal of the resorptive tissue
Topical application of 90% aqueous solution of trichloroacetic acid and sealing of the
defect


ETIOLOGIC FACTORS
LIVING
Bacteria
Fungi
Viruses

NON-LIVING
Extrinsic agents
o Foreign bodies

Intrinsic agents
o Cholesterol
o Epithelial rests of Malasez

LIVE PATHOGENS
1. Bacteria
A.a, T.forsythia, E.corrodens, F.nucleatum, P.gingivalis, P.intermedia, and
T.denticola. (Jansson et al 1993)
90% of microflora of necrotic pulps contained gram negative rods.
(Sandquist 1990)

2. Fungi - C.albicans
Present due to poor asepsis. (Hannula et al 1997)


3. Viruses
HS Virus, Human cytomegalo virus, Epstein-Barr virus-1

EFFECT OF PULPAL DISEASE ON THE
PERIODONTIUM
Necrosis of pulp bone resorption


Following pulp extirpation

acute inflammatory reaction may develop in periodontium

resorption of cementum and alveolar bone

27
EFFECT OF PERIODONTAL DISEASE ON
THE PULP
Periodontitis rarely produces significant changes in the dental pulp.
(Seltzer et al in 1978)


The presence of an intact layer of cementum may protect the pulp from
injurious elements produced by plaque microbiota.


The pulp has a good capacity for defense as long as the blood supply via the
apical foramen is intact. (Lang et
al 1974)



1) 1968 - Oliet and pollock classification based on different
treatment categories
2) 1972 - Simon, Glick and Frank classification based on
etiology, diagnosis, prognosis and treatment
3) 1972 Franklin S.Weine classification based on clinical
presentation strategy
4) 1975 - Guldener et al classification
5) 1977 - Hiatt WH classification
6) 1988 - Grossman classification based on treatment plan




29
1. Simon, Glick and Frank (1972)
Type 1 - Primary endodontic lesions

Type 2 - Primary endodontic lesions with secondary periodontal involvement

Type 3 Primary periodontal lesions

Type 4 Primary periodontal lesions with secondary endodontic involvement

Type 5 True combined lesions

2. Oliet and pollock (1968)
Lesions that require endodontic treatment procedures

Necrotic pulp and apical granulomatous tissue replacing the periodontium and
bone with or without a sinus tract
Chronic periapical abscess with a sinus tract
Root fractures
Root perforation
Incomplete apical root development
Teeth requiring hemisection or radisectomy

Lesions requiring periodontal treatment procedures only

Occlusal trauma causing reversible pulpitis

Occlusal trauma & gingival inflammation resulting in pocket
formation.

Suprabony or infrabony pocket formation treated with root
planing and curettage leading to pulpal sensitivity.


Lesions requiring periodontal treatment procedures only

Occlusal trauma causing reversible pulpitis

Occlusal trauma & gingival inflammation resulting in pocket
formation.

Suprabony or infrabony pocket formation treated with root
planing and curettage leading to pulpal sensitivity.


Lesions requiring combined endodontic-periodontic treatment procedures

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

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

3. Franklin S.Weine in 1972
Class I- symptoms clinically and radiographically stimulate periodontal
disease but are due to pulpal inflammation or necrosis
Class II tooth that has both pulpal and periodontal disease concomitantly.
Class III no pulpal problem but the tooth requires endodontic therapy to
gain periodontal healing
Class IV tooth that clinically and radiographically stimulates
pulpal/periapical disease but infact has periodontal disease.


4. Guldener et al, 1975
Class I: primary endodontic lesion
I(a) Accidental Perforations
I(b) Chronic periradicular lesion

Class II: primary periodontal lesion
II(a) Advanced periodontal disease with or without extension into
apical area.
II(b) Secondary endodontic involvement

Class III: combined lesion

5. Hiatt WH, 1977
Pulpal lesions with secondary periodontal disease of short duration

Pulpal lesions with secondary periodontal disease of long duration

Periodontal disease of short duration with secondary pulpal disease

Periodontal disease of long duration with secondary pulpal disease

Periodontal disease treated with hemisection/ root amputation
Complete and incomplete crown fractures
Independent pulpal and periodontal lesions which merge into a combined
lesion
Pulpal lesion which evolve into periodontal lesion following treatment
Periodontal lesion which evolve into pulpal lesion following treatment

6. Grossman classification (1988)
Type 1 Requiring endodontic treatment only

Type II Requiring periodontal treatment only

Type III Requiring combined endo-perio treatment

CLINICAL FEATURES, DIAGNOSIS
AND TREATMENT OF
DIFFERENT TYPES OF
ENDO-PERIO LESIONS

1. PRIMARY ENDODONTIC LESIONS
Causes
Deep carious lesion
Large restoration approximating the pulp
History of a pulpotomy
Pulp capping
Poor root canal treatment

Symptoms
Mobility
Localized bone loss
Narrow pocket
Tenderness to percussion
Sinus tract
Swelling of marginal gingiva

Radiographic features
Osseous destruction involves one tooth only
No associated generalized bone loss


Treatment
Conventional root canal therapy (Paul and Hutter 1997)


Prognosis
Excellent
Rapid healing - 3 to 6 months

2. Primary endodontic lesions with
secondary periodontal involvement
Pulp vitality tests are negative.


Treatment
First endodontic therapy
After 1-2 months - periodontic therapy
Periodontal therapy scaling and root planing.
(Paul and Hutter 1997)


Prognosis
Depends on the severity of periodontal involvement.
Efficacy of the periodontal therapy.

3. Primary Periodontal Lesions
Characteristics
Caused by periodontal pathogens
Teeth are vital
Presence of generalized bone loss
Calculus/plaque & soft tissue inflammation
Broad based pockets
Mobility
Minimal or no pain
Periodontal abscess during acute phase of the disease
Develops over a longer period of time

Treatment
Periodontal therapy, Root amputation, Guided tissue regeneration
Root canal therapy is not indicated


Prognosis
Depends on the extent of the periodontitis.
Most teeth with periodontitis resulting in attachment loss to the apex do
not have a favorable prognosis.


4. Primary periodontal lesion with
secondary endodontic involvement
Characteristics
History of extensive periodontal procedures
Presence of deep periodontal pockets
Generalised bone loss
Retroinfection of the pulp tissue


Symptoms
Sensitivity to temperature
Tenderness on percussion
Sometimes severe pain is there
Presence of mobility and swelling

Treatment
Periodontal therapy, Root amputation, Guided tissue regeneration.
Conservative root canal therapy


Prognosis
Dependent on the periodontal therapy.
In single-rooted teeth the prognosis is usually poor, as the periodontal
breakdown is very severe, necessitating extraction


5. True combined lesions

Characteristics
Due to - failed Endodontic treatment, plaque & calculus deposits
Have significant periodontal involvement.
Pulp testing gives negative results


Causes
Vertical root fracture
Perforations
Root resorption

Treatment
Endodontic therapy
Periodontal therapy, hemisection, bicuspidization & root amputation
Periodontal therapy can be performed during or immediately after the
endodontic treatment
Advanced endodontic surgical intervention may also be required


Prognosis
Depends totally on the outcome of periodontal therapy.
The greater the periodontal involvement, the poorer the prognosis is.


6. Concomitant Endo-Perio Lesion

Belk and Gutmann 1990


This condition often goes undiagnosed.

Both diseases are treated concomitantly with removal of individual
etiologic factors.

Prognosis
Dependent on removal of individual etiologic factors and prevention of any
further factors of the respective diseases.


CLINICAL DIAGNOSTIC
PROCEDURES
CLINICAL DIAGNOSTIC PROCEDURES
Visual examination
Palpation
Percussion
Mobility
Radiographs
Pulp vitality testing: Cold test, electric test, blood flow test, cavity test,
restored teeth testing
Pocket probing
Fistula tracking
Cracked tooth testing: Transillumination, wedging, staining.
Selective anesthesia test

1. Visual examination


Soft tissue
Presence of inflammation, ulcerations or sinus tracts.


Hard tissue
Examined for dental caries, defective restorations, erosions, abrasions, cracks
or fractures.
Developmental anomaly
A discolored permanent tooth represents necrotic pulp.
Pink spot in crown - internal resorption


2. Palpation
Done with firm digital pressure to the mucosa covering the roots and
apices.

To detect the presence of periradicular abnormalities

Cannot differentiate between endodontic and periodontal lesion


3. Percussion

Tapping on the incisal or occlusal surfaces

The tooth crown is tapped vertically and horizontally.

Pain on vertical percussion - presence of pulpal disease.

Pain on horizontal percussion - infection of periodontal origin.


4. Mobility
Loss of periodontal support

Fractured roots

Periradicular abscess

5. Radiographs
Carious lesions
Extensive or defective restorations
Previous root canal treatments
Root fractures
Periradicular radiolucencies
Thickened periodontal ligament
Alveolar bone loss

6. Pulp vitality testing
Designed to assess the response of the pulp to different stimuli.

Differentiate between pulpal and periodontal disease.

Abnormal response Degenerative changes
No response Pulp necrosis
Moderate transient response Normal vital pulp
Quick painful response Reversible pulpitis
Lingering painful response Irreversible pulpitis




a)- Cold test
Agents
Ice sticks
Ethyl chloride
Co
2
(dry ice at -78
0
C)
Dichloro-difluoro-methane (DDM at -50
0
C)


Sharp brief pain that does not last more than a few seconds - Vital pulp
Intense and prolonged pain response - irreversible pulpitis
Lack of response - pulp necrosis

b)- Electric test
No response- pulp necrosis.

Positive response - vital pulp or partially necrotic pulp.

False-positive responses - partial pulp necrosis, patient anxiety,
ineffective isolation or inadvertent contact with metallic restorations.

False-negative responses - obliterated root canals, recently traumatized
teeth, teeth with immature apices, patient taking drugs that elevate the
pain threshold and poor electrode-tooth contact.

c)- Blood flow test
Determine the vitality of the pulp by measuring its blood flow.

Sensors are applied to the external surfaces of the crown and the pulp
blood flow is recorded and compared to controls.



Non-invasive
Painless
Not used routinely

d)- Cavity test
Highly reliable in determining the vitality


Positive response - vital pulp tissue
Negative response - pulp necrosis


7. Pocket probing
Blunt calibrated periodontal probe


Probing depth
Clinical attachment level
Sinus tracking



8. Fistula tracking
Inflammatory exudates may often travel through tissues and structures of
minor resistance and open anywhere on the oral mucosa or facial skin.


Radioopaque material
Gutta percha points
Silver cones


9. Cracked tooth testing
Transillumination

Wedging

Staining


10. Selective anesthesia test
Useful when source of pain cannot be attributed to a specific arch.

DIFFERENTIAL DIAGNOSIS
BETWEEN PULPAL AND
PERIODONTAL DISEASE
PULPAL PERIODONTAL
Cause

Pulp infection Periodontal infection
Vitality Non vital Vital
Restoration Deep or extensive Not related
Inflammation Acute Chronic
Root surface Smooth Rough
Pockets Single , narrow Multiple, widespread
Ph value Acid Alkaline
Microbial Few Complex
Plaque / calculus Not related Primary cause
1. CLINICAL
68
2. RADIOGRAPHICAL
PULPAL PERIODONTAL
Pattern Localised Generalised
Bone loss Wider apically Wider coronally
Periapical Radiolucent Not related
Vertical bone loss No Yes
69
3. HISTOPATHOLOGICAL
PULPAL PERIODONTAL
JUNCTIONAL EPITHELIUM No apical migration Apical migration
GRANULATION TISSUE Apical Coronal
GINGIVA Normal Some recession
70
4. THERAPY
71
PULPAL PERIODONTAL
Root canal therapy

Periodontal treatment

THERAPEUTIC MANAGEMENT OF
PULPAL
AND PERIODONTAL DIS EASE
ENDODONTIC LESION PRIMARY
Patients with pulpal disease present only diagnostic and treatment decisions
relative to the endodontic lesion.
Debridement of the pulp chamber and canal, as well as the completion of
appropriate endodontic therapy, are sufficient to result in healing of the
lesion.
Pulpal abscesses and apical lesions generally resolve with conventional
therapy, although apical surgery may be required in certain instances.
Periodontal treatment is not required in the absence of any periodontal
involvement.
Occasionally, an abscess of pulpal origin, through an apical or lateral canal,
may establish drainage through the periodontal ligament and erupt into the
furcation or the gingival sulcus.
The signs and symptoms of this process are identical to the initial signs and
symptoms of abscesses establishing a path in a more horizontal direction,
with the exception that a fistula is not evident.
Therefore it becomes necessary to separate the signs and symptoms of pulpal
disease from those associated with a periodontal abscess.
The patient's history, periodontal probing, radiographs, and pulpal testing are
therefore consistent with pulpal disease.
Root canal treatment resolves any tract or stoma that is present.
INDEPENDENT PERIODONTAL AND
ENDODONTIC LESIONS
Patients with pulpal disease may also present with inflammatory periodontal
disease. Gingivitis or early periodontitis, other than tenderness, bleeding on
brushing, or probing, commonly results in little discomfort.
Pulpal disease, however, is associated with more noxious signs and symptoms. The
progress of periodontitis is slow, with the exception of acute disease such as
periodontal abscesses or necrotizing ulcerative gingivitis.
Therefore the prompt management of the pulpal lesion is the primary concern.
Pulpal extirpation and filling of the canals is the proper course of therapy, since
extirpation of the pulp usually leads to the elimination of the patient's acute
symptoms.
Although residual sensitivity to percussion or movement of the tooth may persist
for a period, therapy for gingivitis or early periodontitis may be delayed until the
acute symptoms of pulpal disease are alleviated.
A different scenario may result if a patient with chronic periodontitis
experiences a loss of pulpal vitality.
Such a patient may simultaneously have the clinical signs and symptoms of
both periodontitis and apical periodontitis.
The extent to which each can affect the tooth is both independent and
variable. The involvement of the apical periodontium by a pulpal lesion may
obscure the symptoms of periodontitis.
Therefore the ability to determine the independence of the two lesions on
any tooth or area is a key consideration in the sequence of therapy. Most
commonly the lesions are independent and do not communicate
Rarely a patient may present with abscesses of both pulpal and periodontal
origin.
As the apical lesion tends to be the most painful lesion, endodontic therapy is
normally initiated before or at the same appointment at which the
periodontal abscess is drained.
Again, the patient's history and thorough probing allows a determination of
the extent of each problem and the independence of the two defects.
Endodontic therapy results in the resolution of the endodontic lesion.
It will, however, have little or no effect on the periodontal pocket, and
appropriate periodontal therapy will be required for a successful result.
COMBINED LESIONS (PERIO-ENDO)
The true combined lesion results from the development and extension of an
endodontic lesion into an existing periodontal lesion (pocket).
Such lesions may present with the characteristics of both diseases, which may
complicate diagnosis and treatment sequencing.
A thorough history and careful clinical and radiographic examinations are
required to identify and accurately assess the contribution of each lesion to
the patient's dental problems and to derive a treatment sequence that is
likely to produce an optimal therapeutic result.
Usually the developing periapical lesion extends coronally to connect with a
preexisting, chronic, widebased periodontal pocket. On rare occasions a
developing periodontal lesion, associated with a developmental groove, may
extend apically to connect with an apical or lateral endodontic lesion.
It also has been suggested that if periodontitis progresses to involve a lateral
canal or the apex of a tooth, then a secondary pulpal infection may be
induced. This is referred to as retrograde pulpitis.
Retrograde pulpitis, if it exists, is quite rare.
The pain from the loss of pulpal vitality is the most common presenting
complaint of patients with combined lesions.
The symptoms reported are those most commonly found with pulpal disease.
Thermal pulp testing provides information relative to the status of the pulp,
and dental radiographs can confirm the presence of apical changes and the
extent of bone loss.

Careful probing confirms the presence and morphology of any periodontal
pocket and permits the location of the communication with the apical lesion.
The periodontal portion of the defect commonly has plaque, calculus, and/or
root roughness as a finding. This contaminated root surface and the
associated osseous defect is the major complication to treatment of
combined lesions.
The extent to which the periodontal lesion contributes to the loss of bone is
a key consideration in diagnosis and treatment planning. Endodontic
treatment is highly predictable, and when appropriately performed, the
alterations in radiographic appearance and clinical probing disappear.

The periodontal component of a combined lesion is a more difficult problem.
It cannot resolve as long as the endodontic lesion is present, yet effective
endodontic treatment cannot eliminate the periodontal pocket. Even with
periodontal treatment, the periodontal defect commonly does not resolve to
the same extent that the endodontic lesion does.
The ability to eliminate the periodontal component of the defect ultimately
dictates treatment of the tooth. If the majority of the bony support has been
lost from periodontitis, regardless of the predictability of endodontic therapy,
the tooth may have a hopeless prognosis.

ROOT AMPUTATION
Farrar 1884

To eliminate a weak, diseased root.


ADVANTAGE:
To retain a portion of this strategic tooth and to avoid extraction of the entire
tooth

INDICATIONS:
When endodontic treatment of one root is technically impossible or when
such treatment has failed.

When untreatable furcation involvement is present and removal of the root
will facilitate oral hygiene in that area.

When extensive loss of bone has occurred around one root of an upper molar.

When a fractured root of an upper molar is present.

When a root has been perforated and cannot be treated endodontically.

When a root has been destroyed by extensive decay.

HEMISECTION
Refers to sectioning of the crown of a molar tooth, with either the removal of
half the crown and its supporting root structures or retention of both the
halves to be used after reshaping as two premolars.

Indications:
When periodontal involvement of one root is severe.
When loss of bone is extensive in the furcation area.
When the root has been destroyed by extensive decay.


REFERENCES
Clinical textbook of Periodontology; Carranza, 10
th
Edition
Clinical periodontology and implant dentistry: Jan Lindhe, 5
th
edition.
Pathologic interactions in pulpal and periodontal tissues. J Clin Periodontol 2002; 29:663-
671.
Diagnosis, prognosis and decision making in the treatment of combined periodontal
endodontic lesions. Periodontology 2000, Vol. 34, 2004, 165 203.
Detection of localized tooth related factors that predispose to periodontal infections.
Periodontology 2000, Vol. 34, 2004, 136-150.
The influence of endodontic treatment upon periodontal wound healing. J Clin Periodontol
1997; 24:449-456.
The periodontal-endodontic controversy Periodontology 2000, Vol. 30, 2002, 123 130.
The chicken or the egg? Periodontal-endodontic lesions. Quintessence International
2007;4(1):15-21.
The pathogenesis and treatment of endo-perio lesions. CPD Dentistry 2001;2(3):91-95.