ENDO-PERIO INTERRELATIONSHIP

• INTRODUCTION
• CLASSIFICATION OF ENDODONTIC-PERIODONTIC LESIONS
• PATHWAYS OF COMMUNICATION
 ANATOMIC CONSIDERATIONS
 ETIOLOGIC FACTORS AND CONTRIBUTING FACTORS
• FFECT OF PULP ON THE PERIODONTIUM
• EFFECT OF PERIODONTIUM ON THE PULP
• DIAGNOSIS
• DIFFERENTIAL DIAGNOSIS
 PRIMARY ENDODONTIC LESION
 PRIMARY PERIODONTAL LESION
 PRIMARY PERIODONTAL LESION WITH SECONDARY ENDODONTIC
INVOLVEMENT
 PRIMARY ENDODONTIC LESION WITH SECONDARY PERIODONTAL
INVOLVEMENT
 TRUE COMBINED LESION
 CONCOMITANT ENDO PERIO LESION
• TREATMENT
• CONTROVERSIES
INTRODUCTION

ENDO- PERIO LESION

An endo-perio lesion simply means that in an involved tooth both the tissues (pulp
and periodontium) are affected by the disease process.

• Pulpal and Periodontal tissues have close embryonic, anatomic and functional inter
relationships. Tissues of dental pulp and periodontium are inter linked from the embryonic
stage. The dental papilla and the dental sac are of a common mesodermal origin.

• In 1964, Simring and Goldeberg first described the relationship between endo and
perio. Pulpal and periodontal problems are responsible for more than 50% of tooth mortality
today.

• Diagnosis is often difficult since these diseases have been studied primarily as
separate entities and each primary disease may mimic clinical characteristics of the other
disease.

CLASSIFICATION

• Because of the close relationship between endodontics and periodontics, various

classifications have been suggested to divide the types of cases that may require combined or
single therapy. Much disagreement exists as to a correct classification that is consistent with
histologic and clinical situations commonly encountered.

I) Classification by Franklin. S. Weine (1972) :

The 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, which determines the type
of therapy required and the probable prognosis. The types are as follows:
 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.

II Simon J.H, Glick and Frank (1972) classified endo-perio lesions based on etiology,
diagnosis, prognosis and treatment:

 Primary endodontic lesion

 Primary endodontic lesion with secondary periodontal disease
 Primary periodontal lesion
 Primary periodontal lesion with secondarily endodontic involvement
  True combination of endodontic-periodontal lesions.

III. Stock (1988) modified Simon’s classification.

• Omitted Class V of the classification.

• He argued that both Class II and Class IV lesions in advanced stages can become
combined lesions and therefore a separate class to describe these lesions was not necessary.

CONCOMITANT PULPAL AND PERIODONTAL LESIONS

An additional classification has been proposed for lesions that may commonly be seen
clinically, and reflect the presence of two separate and distinct entities. This is referred to as
the concomitant pulpal and periodontal lesion. In essence, both disease states exist but with
different causative factors and with no clinical evidence that either disease state have
influenced the other. This situation often goes undiagnosed, and treatment is rendered to only
one of the diseased tissues in the hope that the other will respond favorably. In actuality, both
disease processes must be treated concomitantly, with the prognosis dependent on the
removal of the individual etiologic factors and prevention of any further factors that may
affect the respective disease processes.

IV) Oliet , Pollock and Grossman (1968) (Based on different treatment categories )

A) Lesions that require endodontic treatment only

 Any tooth with necrotic pulp and apical granulomatous tissues replacing periodontium
and bone, with or without a sinus tract.
 Chronic periapical abscess with a sinus tract draining through the gingival crevice.
 Root fracture longitudinal and horizontal.
 Root perforations, pathologic and iatrogenic.
 Teeth with incomplete apical root development and inflamed and necrotic pulps, with
or without periapical pathosis.
 Endodontic implants.
 Replants, intentional or traumatic.
 Transplants, autotransplants or allotransplants.
 Teeth requiring hemisections or radisections.
 Root submergence.

B). Lesions that require periodontal treatment only

 1.Occlusal trauma causing reversible pulpitis

 2. Occlusal trauma plus gingival inflammation, resulting in pocket formation.
o Reversible, but increased pulpal sensitivity caused by trauma as possibly,
exposed by dentinal tubules.
 o Reversible, but increased pulpal sensitivity caused by uncovering lateral or
accessory canals exiting into periodontium.
 3. Suprabony or infrabony pocket formation treatment with overzealous root planning
leading to pulpitis.
 4. Extensive infrabony pocket, extending beyond the root apex and sometime coupled
with lateral or apical resorption, yet with pulp that responds within normal limits to
clinical testing.

C). That require combination of treatment.

 Any group A lesion resulting in irreversible reaction in attachment apparatus and

required periodontal treatment.
 Any group B lesion resulting in irreversible reaction in pulp tissue and also requires
endodontic treatment.

V) Weine. F.S, Simring M, Goldberg, Hiatt W.H (1982)

 Pulpal disease causing periodontal disease (endodontic origin)

 Periodontal disease causing pulpal disease (periodontal origin)
 Combined periodontal and pulpal disease (concurrent)
 Endodontic failures in periodontally diseased teeth
 Vertical cracks and fractures

Another classification was recommended by the World Workshop for classification of

Periodontal Diseases (1999).

Periodontitis Associated with Endodontic Disease:

(i) Endodontic-periodontal lesion

(ii) Periodontal-endodontic lesion

(iii) Combined lesion.

von Arx and Cochran (2001) proposed a clinical treatment classification of perio‐endo
furcation lesions based on the role of membrane application in endodontic surgery.
Classification of Endodontic Microsurgical Cases by Kim and Kratchman (2006):

Pathways of Communication(developmental, pathological, iatrogenic)

Lateral and accessory canals

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. However, it seems that the prevalence of
periodontal disease associated with lateral canals is relatively low. Kirkham studied 1,000
human teeth with extensive periodontal disease and found only 2% had lateral canals located
in a periodontal pocket.
Accessory canals in the furcation of molars may also be a direct pathway of
communication between the pulp and the periodontium. These accessory canals contain
connective tissue and vessels that connect the circulatory system of the pulp with that of the
periodontium.
Seltzer et al. reported that pulpal inflammation may cause an inflammatory reaction in
the inter radicular periodontal tissues. The presence of patent accessory canals is a potential
pathway for the spread of bacterial and toxic by-products, resulting in a direct inflammatory
process in the periodontal ligament

Apical foramen

The apical foramen is the principal and most direct route of communication between the pulp
and periodontium. Bacterial and inflammatory by-products may exit readily through the
apical foramen to cause periapical pathosis. The apex is also a portal of entry of inflammatory
by-products from deep periodontal pockets to the pulp. Pulp inflammation or pulp necrosis
extends into the periapical tissues causing a local inflammatory response accompanied with
bone and root resorption. Endodontic therapy is targeted to eliminate the intraradicular
etiologic factors thus leading to healing of the periapical tissues.

Dentinal tubules

Exposed dentinal tubules in areas of denuded cementum may serve as communication

pathways between the pulp and periodontal ligament. Exposure of dentinal tubules may occur
due to developmental defects, disease, or periodontal procedures.
These tubules may be denuded of their cementum coverage as a result of periodontal disease,
surgical procedures or developmentally when the cementum and enamel do not meet at the
cemento-enamel junction (CEJ) thus leaving areas of exposed dentin. Patients experiencing
cervical dentin hypersensitivity are an example of such a phenomena.
Furthermore, the same tooth may have different CEJ characteristics with dentin exposure on
one side while the other sides are covered with cementum. This area becomes important in
assessing the progression of endodontic pathogens, as well as the effect of root scaling and
planing on cementum integrity, and bleaching-induced root resorption following the use of
30% hydrogen peroxide. Other areas of dentinal communication may be through
developmental grooves, both palatogingival and apical.

Palatogingival grooves

Palatogingival grooves are developmental anomalies of the maxillary incisor teeth, with
lateral incisors more often affected than central incisors (4.4% versus 0.28%, respectively).
These usually begin in the central fossa, cross the cingulum, and extend apically with varying
distances. Generally the incidence of palatogingival grooves ranges from 1.9% to 8.5%.
Everett and Kramer reported that 0.5% of the teeth examined had a palatogingival groove
extension to the root apex, thus contributing to an endodontic pathologic condition.
Enamel projections and pearls
Enamel projections are ectopic deposits of enamel that extends into root furcations. Master
D.H reported that these projections extend to furcations of 28.6% of mandibular molars and
17% of maxillary grooves and may favour development of pocket. Moskow and Martinez
(1990) reported that the presence of such developmental anomalies, favour pocket formation
in these regions.

PATHWAYS OF PATHOLOGICAL ORIGIN

Empty spaces created by Sharpey’s fibres

Sharpey’s fibres become mineralized during the process of gradual apposition of cementum.
However, sometimes only the periphery of Sharpey’s fibers in the cellular cementum gets
calcified leaving a central uncalcified core. These fibres if destroyed, leave a “SIEVE-LIKE”
porous surface full of canals, which in case of microbial invasion increases the feasibility of
the inflammatory extension into the tubules.

Perforations

Perforation of the root creates a communication between the root canal system and the
periodontal ligament.
This may occur as a result of over-instrumentation during endodontic procedures, internal or
external root resorption, or caries invading through the floor of the pulp chamber.
The prognosis for teeth with root perforation is usually determined by the location the
perforation, the chance of building new attachments, and the accessibility of the remaining
root canals.
Teeth that have perforations in the middle or apical third of the root have the greatest chance
of healing. The closer the perforation is to the gingival sulcus, particularly into the coronal
third of the root or the furcation region, the greater the likelihood of apical migration of the
gingival epithelium in initiation of a periodontal lesion. In general, smaller perforations
appropriately managed do not cause long-term periodontal inflammation.

Vertical root fractures

A vertical root fracture can produce a “halo” effect around the tooth radiographically. Deep
periodontal pocketing and localized destruction of alveolar bone are often related to long-
standing root fractures. The fractured site provides a portal of entry for irritants from the root
canal system to the surrounding periodontal ligament.
Vertical root fractures have contributed to the progression of periodontal destruction in the
presence of apparently successful endodontic tooth therapy and overall periodontal site
stability.

Resorption

 Internal Resorption: In most cases, the condition is painless and so tends to be

diagnosed during routine radiographic examination. If untreated, the lesion is
progressive and will eventually perforate the wall of the root, and then the pulp will
become non-vital. The prognosis is poor once there is occurrence of root perforation.
(Ingle 1994).
  External Resorption: Chronic inflammatory tissues developing in periodontal
pockets probably is the causative factor. If sulcular epithelial lining of pocket is
missing and chronic inflammatory tissues contact the cementum, the process of
decalcification begins. When external resorption destroys enough dentin to reach the
pulp, pulp inflammatory changes begin. Andreasen (1981) has proposed a
classification of those external root resorptions that have a known
– Surface resorption
– Replacement resorption associated with ankylosis
– Inflammatory resorption associated with inflammation in the periradicular tissues
adjacent, to the resorption site.
Subforms are:
 Peripheral inflammatory root resorption (PIRR)
 External inflammatory root resorption (EIRR)

PATHWAYS OF IATROGENIC ORIGIN

Exposure of dentinal tubules following root planning:

Root surface treatment increases the number of exposed dentinal tubules, there is enhanced
opportunity of fluid movement, resulting in pulpal sensitivity. During pulpal death however
degeneration of odontoblastic process and collagen fibres occur further increasing the
permeability of tubules and easing the transfer of toxins from pulp into the attachment
apparatus.

Accidental lateral perforation during endodontic therapy:

May occur during preparation of the access cavity, root canal space or post space. Results in
undesirable communication between the pulp space and external tooth surface at any level in
the pulp chamber or along the length of the pulp space.

ETIOLOGIC FACTORS- LIVE PATHOGENS/ NON-LIVING/ CONTRIBUTING

FACTORS

Live pathogens

• Among the live pathogens encountered in a diseased pulp and periapical tissues are:
– Bacteria
– Fungi and
– Viruses
 Jansson et al. concluded in a study that pathogens in necrotic root canals may
stimulate epithelial downgrowth along denuded dentin surfaces with marginal
communication and thus augment periodontal disease.
 The same group of investigators, 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 found that endodontic infection in mandibular molars was
associated with more attachment loss in the furca. These authors suggested that
 endodontic infection in molars associated with periodontal disease may enhance
periodontitis progression by spreading pathogens through accessory canals and
dentinal tubules.
• Proteolytic bacteria predominate in the root canal microbiota.
• Specific PCR methods were used to detect Actinobacillus actinomycetem comitans,
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 (adult) periodontitis.
• Spirochetes are another type of microorganism associated with both endodontic and
periodontal diseases.

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
 The majority of the recovered fungi were Candida albicans. C. albicans has been
detected in 21% of infected root canals .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.
 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.
 Another possibility is that fungi may gain access from the oral cavity during treatment
as a result of poor asepsis

VIRUSES

• There is increasing evidence to suggest that viruses play an important role in both
endodontic and periodontal diseases. In patients with periodontal disease, herpes
simplex virus is frequently detected in gingival crevicular fluid and in gingival
biopsies of periodontal lesions.
• Human cytomegalovirus 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 samples .
• 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. 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.
• Sabeti et al. Suggested that human cytomegalovirus and Epstein– Barr virus play a
role in the pathogenesis of symptomatic periapical lesions.
• Herpes virus activation in periapical inflammatory cells may impair the host defense
mechanisms and give rise to overgrowth of bacteria as seen in periodontal lesions.
• Herpes virus-mediated immune suppression may be detrimental in periapical
infections due to already compromised host responses in the granulomatous tissue.
Alterations between prolonged periods of herpes virus latency interrupted by periods
of activation may explain some burst-like symptomatic episodes of periapical disease
Frequent reactivation of periapical herpes virus may support rapid periapical
breakdown. Absence of herpes virus infection or viral reactivation may be the reason
that some periapical lesions remain clinically stable for extended periods of time.

NON-LIVING ETIOLOGIC AGENTS

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

EXTRINSIC AGENTS

Foreign bodies

 Foreign bodies are frequently found to be associated with inflammation of the

periradicular. 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 these substances and the clinical reaction
may either acute or chronic. Therefore, such conditions may be either symptomatic or
asymptomatic. Microscopically, these lesions demonstrate the presence
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.

INTRINSIC AGENTS

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%. 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.
However, it is possible that all of these factors may contribute to the accumulation,
concentration and crystallization of cholesterol in a periapical lesion

Russell bodies

 Russell bodies can be found in most inflamed tissues throughout the body including
the periradicular tissues. 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 prevalence of Russell bodies, the mechanisms of their production, and their exact
role in pulpal inflammation have not yet fully elucidated.

Rushton hyaline bodies

 The presence of Rushton hyaline bodies (RHB) is a feature unique to some

odontogenic cysts. 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. Some authors suggested that RHB are material left
behind from a previous surgical operation It is not clear why the RHB form mostly
within the epithelium.

Charcot-Leyden crystals

 Charcot-Leyden crystals (CLC) are naturally occurring haexagonal 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.
Recent findings support the theory that activated macrophages have a role in the
formation of CLC. In addition, the presence of CLC can be detected within a
periapical lesion that failed to resolve after conventional endodontic treatment.
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.

Epithelium

 Epithelial rests of Malassez remains in rest, if 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.

CONTRIBUTING FACTORS

Poor endodontic treatment:

Correct endodontic procedures and techniques are key factors for treatment success.
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.

Poor restorations

• Coronal leakage is an important cause of failure of endodontic treatment. Root canals

may become recontaminated by microorganisms due to delay in placement of a coronal
restoration and fracture of the coronal restoration and/or the tooth.
• Teeth in which both the root fillings and restorations were adequate had only 9%
failure, while teeth in which both root fillings and restorations were defective had about 82%
failure

Trauma

• Trauma to teeth and alveolar bone may involve the pulp and the periodontal
ligament. Both tissues can be affected either directly or indirectly. Treatment of traumatic
dental injuries varies depending on the type of injury and it will determine pulpal and
periodontal ligament healing prognosis.

Resorptions

• Root resorption is a condition associated with either a physiologic or a pathologic

process resulting in a loss of dentin, cementum and/or bone. 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.

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 due to the
failure of the tooth germ to form another root. As long as the epithelial attachment remains
intact, the periodontium remains healthy.

EFFECT OF PERIODONTIUM ON THE PULP

 A considerable portion of the literature has been devoted to a discussion of the effect
of periodontal disease on the pulp. Among the papers are those by Cahn; Henrici and
Hartzell; Seltzer, Bender, and Ziontz; Bender and Seltzer; Siani; Mazur and Massler;
Rubach and Mitchell (two papers); Stahl; and many others.

 Of all these papers, only those by Mazur and Massler and Czarnecki and Schilder,
disclaim any relationship of periodontal disease as a causative factor in pulpal disease.
The others all state either that a relationship appears possible or that a definite
correlation was found. Since the greater evidence appears to be on the positive side,
until further and more definitive work to the contrary is published, it may be assumed
that the interrelationship exists and must be taken into consideration in the treatment
of patients with periodontal problems.

 Periodontal disease may lead to infection of the root canal system through these
channels
lateral root canals
dentine tubules
furcation canals
resorption lacunae (external root resorption).

INFLUENCE OF PERIODONTAL INFLAMMATION / LESION ON THE PULP

Degenerative changes in the pulps of periodontally involved teeth were first demonstrated by
Cahn (1927) and later by Sicher (1936). Sauerwein (1955) and Mazur and Massler (1964)
found that periodontal disease had no influence on the pulp and suggested that systemic
factors were the cause of pulp degeneration. Under light and scanning electron microscope
studies by Seltzer et al 1963, pulps of periodontally involved teeth free of caries or
restorations were found to be atrophic. A high percentage (37%) exhibited inflammatory
pulpal changes, and approximately 10% had totally necrotic pulps.

Lateral canals and accessory foramina-

The size of the foramina in the pulpal floor ranges from 4 to 250 μ (koenings et al,
1974; perlich et al 1981) Especially in the distal roots of lower molars and in the
palatal roots of upper molars, many anomalies in the size and shape of the root canals
are found. Frequently in these teeth, the canals fan out towards the apex in a “canoe
shaped” arrangement. In some instances chronic inflammation may be found in the
canoe and not in the remainder.

Studies revealed that the lateral canals are filled with capillaries, pulp cells, ground
substance, and fibers. In many teeth however the width of accessory foramina or
lateral canals are exceedingly small, permitting the presence of only small caliber
vessels and their supporting stroma.
 Deep periodontal lesions were frequently found exposing the lateral canals along the
sides of the root, thereby interfering with the nutritional supply of the pulps. Small
regions of necrosis or infarction occur.

Atrophic changes

The effect of periodontal lesions on pulp presumably comes out through interference
with nutritional supply, inducing atrophic and other degenerative changes, such as
decrease in number of pulp cells, dystrophic mineralisation, fibrosis, reparative dentin
formation, inflammation and resorption. Because of impaired nutrition,
nutrition, some pulp
cells do not come into equilibrium with the available blood supply and hence
degenerate. The pulps of periodontally involved teeth have smaller than normal cells,
with greater than normal collagen deposition. Pressure atrophy can occur because of
mobility of teeth.
The increased pressure from movement of teeth affects blood vessels and decreases
blood supply to the tissues resulting in vascular atrophy. A small area of infarction
takes place, with resultant coagulation necrosis.
necrosis. The death of cells and their
subsequent mineralisation are a natural sequence of deprivation of nourishment.

Inflammatory changes

In severe periodontal lesions,

lesions, apical granulomas and root resorptions are produced by
extension of granulation tissue from the pocket. Inflammatory cells may also
occasionally be detected infiltrating the apical pulp tissues, thereby causing apical
pulpitis. Inflamed or necrotic pulps, produced from periodontal lesions, are then
instrumental in perpetuating periodontal lesion.
Toxic products are discharged into periodontal tissues through the same lateral canals
or other means of ingress. Thus a viscious cycle is established.
These may be responses to toxic products entering through canal openings normally
covered with bone and periodontal ligament, but now exposed to oral fluids .

Resorptions

Root resorption is consistently associated with both pulp-induced and periodontally –

induced inflammatory lesions. Resorptions of the side of the roots are frequently
found subjacent to the granulation tissue overlying the roots.
roots. When the periodontal
lesions are deep, resorptions are also found within the root canals, often opposite
lateral canals and at the apical foramina.

Toxic products

Inflammatory lesions in the pulp may also be responses to toxic products entering
through canal openings that are normally covered with bone and periodontal ligament
but are exposed to oral fluids.
 Pulp inflammation in periodontal involved teeth can occur from extension of
periodontal connective tissue. Just as products from inflamed pulpal tissue can cause
periapical or inter-radicular inflammation, periodontal disease can cause pulpitis. In
severe periodontal lesions, not only are apical granulomas and root resorptions
produced through extensions of the granulomatous tissue from the pocket, but also
inflammatory cells can also be detected infiltrating the apical tissues. The coronal
pulp tissue may, for a time, remain uninflammed.
In turn, inflamed or necrotic pulps, produced from periodontal lesions, are
instrumental in perpetuating the periodontal lesion by elaborating toxic products that
invade the periodontal tissues through the same lateral canals or other means of
ingress. Thus, the vicious cycle is established. In terms of treatment, it is difficult to
visualize an effective cure without concurrent elimination of both the pulpal and
periodontal lesions.
The microorganisms present in periodontal lesions may be capable of producing
necrosis of cells and fiber degeneration by action of metabolic products, destructive
enzymes or other mechanisms. Toxic products from microorganisms in the oral cavity
can also affect the pulp through the denuded dentinal tubules

Deep scaling

Deep scaling and curettage in periodontal treatment may possibly be instrumental in

causing pulpal damage. Both in vitro and in vivo experiments by Stallard (1968)
showed that intact cementum acted as a barrier to the inward penetration of the dye
(2% aqueous solution of tryphan blue) into the dentin. Such protection is lost when
cementum is removed by root planing. Sensitivity of teeth after deep scaling and
curettage may be due not only to denudation of the roots of the teeth but also to the
production of inflammatory changes or hemorrhages in the pulps of the teeth.
Deep scaling may severe blood vessels, especially in the furcation regions of the
molars. The consequent loss of blood supply to a small region of the pulp can produce
a pain spasm and ultimately the death of pulp cells supplied by the affected
capillaries. Death of cells, with subsequent calcification, is the usual sequel of blood
deprivation. However, not all periodontal instruments terminate in pulpal
inflammation and necrosis. A productive response may occur in the pulps of
periodontally involved teeth when the disease progresses slowly or there are fewer or
narrower lateral canals. Cementum deposition appears to obliterate these canals,
thereby retarding or preventing ingress of pulp irritants

Local medication

It is another possible cause for injury and necrosis of pulp cells. The use of drugs such
as Formalin, zinc chloride, and sodium fluoride for desensitization of the necks of
teeth, especially when root surfaces have been exposed by loss of bone and an
epithelial downward proliferation, is potentially damaging. In these circumstances,
irritating chemicals may enter the pulp tissue through accessory or lateral foramina,
thereby causing injury to the pulp cells as well as the vessels that supply them with
nutrients.
For example, formalin, in relatively low concentrations, exerts a lethal effect on the
cells. Other cells may cause destruction of cells by derangement of osmotic
 equilibrium. However, few drugs used to treat hypersensitive dentin have been
reported to induce dentinal sclerosis, with no adverse pulp effects
Bergenholtz and Lindhe, in an animal study, found that 70% of root specimens
examined showed no pathologic changes, despite the fact that 30% to 40% of the
periodontal attachment was lost. The remaining 30% of roots displayed only small
inflammatory cell infiltrates or formation of reparative dentin or both in areas where
pulp was adjacent to root exposed through periodontal destruction. These tissue
changes were frequently associated with root surface resorption, suggesting that
dentinal tubules must be uncovered before irritation can be transmitted.
These observations suggest that the presence of an intact cementum layer is important
for the protection of the pulp from toxic elements produced by the plaque microbiota.
Hence, periodontal disease and periodontal treatments should be regarded as potential
causes of pulpitis and pulpal necrosis. It has also been reported that the pulps of teeth
with long-standing periodontal disease develop fibrosis and various forms of
mineralization.
During the course of periodontal therapy, it behooves the dentist to watch for telltale
signs of pulpal inflammation and to take whatever measures are needed to avoid pulp
damage whenever possible. Such cautions should include the following:
o Avoiding use of irritating chemicals when contact with root surfaces is
unavoidable. Minimizing use of ultrasonic and rotary scaling instruments
when there is a strong possibility of less than 2 mm of dentin thickness
remaining, particularly after removal of considerable depth of necrotic
cementum and dentin.
o Allowing minor pulpal irritations to subside before employing further
procedures, which might cause more damage.
o Recognizing the need for and instituting endodontic therapy when an
irreversible condition has resulted.

EFFECT OF PERIODONTAL THERAPY ON THE PULP

Once it is determined that periodontal disease is present, some type of therapy is

required. Among the instruments used to remove deposits from tooth surfaces are
ultrasonic vibrations, scalers and curettes. Stanley has stated that if as little as a 2
mm of remaining dentin thickness exists between the pulp and an irritating
stimulus, there is little chance of any pulp damage occurring.
occurring.
However, in some cases tooth configuration together with removal of a portion of
the protective barrier, such as by crown preparation or curetting of necrotic
cementum and dentin, may bring pulpal irritants well within the 2 mm limit.
Common sites of such intrusion are the proximal surfaces of the roots of
mandibular anterior teeth, which are normally thin mesio-distally, and the furcation
and buccal areas of the roots of maxillary and mandibular molars.
Bender and Seltzer have reported that teeth with periodontal disease plus extensive
restorations disclosed a greater degree and more frequent examples of pulpal
inflammation than those with either condition singly. If teeth with some degree of
pulpal inflammation are further insulted by the irritational effects of some aspects
of periodontal therapy, an irreversible condition may result.
INFLUENCE OF PULPAL PATHOLOGIC CONDITION ON THE PERIODONTIUM

Inflamed or necrotic pulps can produce periodontal lesions by the passage of

inflammatory or degenerative products through lateral canals that communicate
between pulp and periodontal ligament. Other avenues of communication between the
pulp and periodontal ligament, such as the dentinal tubules, may also be responsible
for the extension of inflammatory lesions.

Another mechanism through which periodontal structure become involved is as

follows: When periapical granulomas resulting from necrotic pulps are extensive, the
granulomatous tissue extends along the lateral aspects of the roots, causing extensive
bone resorptions. Periapical inflammation tends to spread towards furcation area.

After pulp inflammation has been induced, an inflammatory infiltrate may be detected
in molars near alveolar crest, mainly in vicinity of lateral canals. Separation of
alveolar crest periodontal fibers by edema occurs. The inflammation may then be
followed by resorption of cementum and dentin of teeth in furcation regions and
resoption of crestal alveolar bone. This crestal bone resorption occurs in some
instances without apparent presence of bifurcation canals, which may be present but
undetected. With passage of time, these resorptions may be repaired or occasionally,
they may persist. If inflammation persists, cell rests of malassez may be stimulated to
proliferate, eventually resulting in pocket formation
Pulpal pathology as a cause of periodontal disease has received much attention during
the last decade. Pulpal degeneration results in necrotic debris, bacterial byproducts,
and other toxic irritants that can move toward the apical foramen, causing periodontal
tissue destruction apically and potentially migrating toward the gingival margin.
Simring and Goldberg termed this “retrograde periodontitis” to differentiate the
process from “marginal periodontitis” in which the disease proceeds physically from
the gingival margin toward the root apex. When pulpal disease progresses beyond the
confines of the tooth, inflammation extents and affects the adjacent periodontal
attachment apparatus. This inflammatory process often results in dysfunction of the
periodontal ligament, as well as resorption of alveolar bone, cementum, and even
dentin. The endodontic infection has been regarded as local modifying risk factor for
periodontitis progression if left untreated.

In addition, the medicaments (e.g., high concentrations of calcium hydroxide,

corticosteroids, antibiotics) used for root canal therapy can also irritate the periodontal
attachment apparatus. However, the nature and extent of periodontal destruction is
dependent on several factors, including virulence of the irritating stimuli present in
the root canal system (e.g., microbiota, medicaments, foreign-body reactions),
duration of the disease, and host defense mechanisms.

Periodontal lesions induced by root perforations

Perforations of side of root or of floor of pulp chamber made during course of root
canal treatment may cause formation of periodontal pockets. The severity of
inflammation induced in periodontal ligament by perforating bur is related to amount
 of tissue destruction and to rapidity with which perforated areas are sealed.
Subsequent repair is also related to salivary and microbial contamination of wound.

Beavers et al (1986) found that after the roots of monkey teeth were intentionally
perforated and sealed under aseptic conditions with either hard setting calcium
hydroxide cement or with sterile Teflon discs, several phases of tissue reactions
occurred. Initially, there was an acute inflammatory reaction and necrosis of a portion
of periodontal ligament. This was followed by an intermediate phase in which
granulation tissue formed and necrotic debris, bone, cementum, and dentin fragments
were resorbed. In a late phase, (42 days), the inflammation subsided. The connective
tissue matured and bone and cementum were elaborated.

In studies by Seltzer (1970), when furcation perforations in monkey teeth were sealed
off immediately with ZOE or amalgam, the inflammatory response was mild and
repair ensued. When such perforations were left open for 6months-1yr, however,
severe periodontal destruction occurred. Downward epithelial proliferation ensued
with deep pocket formation. In more advanced cases, severe bone resorption caused
complete denudation of the roots

Prognosis for retention of perforated teeth depends on location and size of perforation,
ability of operator to seal off the perforated regions and speed with which the
perforation is closed. Large perforations and those which cannot be effectively be
closed which have been contaminated by saliva stimulate the formation of periodontal
pockets and enhance bone resorption. Generally, root perforations in the middle and
apical thirds of the root canal have a better prognosis than those in cervical third of
root or in floor of pulp chamber.

Periodontal lesions induced by root fractures in endodontically treated teeth

Partial or complete fractures of roots may occur during or after root canal treatment.
Periodontal pockets develop with accompanying bone destruction. The pockets are
generally narrow with normal sulcus depth on either side. The causes of such fractures
have been ascribed to wedging and/or corrosion of posts or pins or to excessive forces
generated during condensation or root canal fillings. Bacteria, necrotic tissue, food
and unidentified amorphous debris and root canal filling materials were found in
fracture spaces. They postulated that the source of bacteria was from colonies in the
root canals, which were not removed during preparation.

Endodontic failures in periodontally-involved teeth

Failures of endodontic treatment are apparently enhanced in the presence of

periodontal disease. Failure of endodontic treatment in anterior teeth relate to
periodontal disease is around 36% and that in posterior teeth 72.9%. There is
tendency towards increased incidence of endodontic failures in periodontally involved
crowned teeth.
 DIAGNOSIS

1. Dental history to elicit signs and symptoms

2. Visual examination

Swelling caused by endodontic infections occur in the mucobuccal fold and

periodontal infections occur in the attached gingiva
Teeth are examined for any caries, defective restoration, erosions, abrasions, cracks,
fractures and discoloration
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.

3. Swelling

The location of swelling often aids in the differentiation between pulpal and
periodontal lesions. In teeth with pulpal involvement, the swelling manifests in the
mucobuccal fold, whereas in periodontal disease the swelling involves the region of
the alveolar or palatal mucosa.

4. Fistula Tracking
Presence of a sinus tract allows for a proper diagnosis & radiograph with a gutta-
percha within the orifice of the fistula leads us to the source.
 If the gutta-percha point goes to the apex of the tooth, the fistula is of endo origin,
when the point goes to midroot or furcation a periodontal problem is diagnosed

5. 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.

6. 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.
7. Vitality Test:

Periodontally involved teeth usually respond within normal limits, while pulpally
involved teeth gives a negative response
Pulp test findings

If the patient complains of pain and the test produces a normal reaction indicating a
vital pulp, periodontal treatment should be done first.
On other hand, if the test findings are abnormal, with or without pain, endodontic
treatment should be done first.

8. Probing
Its an important test to differentiate endodontic and periodontal lesions
In periodontal lesions probing defects are usually wide and do not usually extend to
the apex of the involved teeth, in contrast probing defects from endodontic lesions are
usually narrow and extent to the apices.
9. Radiographs

Periodontal lesions are usually associated with bone loss extending from cervical
region towards the apex.
While in pulpal lesions the bone loss is confined to the involved tooth which extends
coronally to the Cemento enamel junction
Often, the initial phases of periradicular bone resorption from endodontic origin is
confined only to cancellous bone.
For purposes of differential diagnosis, periapical and bitewing radiographs should be
taken from several angles.

Cracked tooth is tested by – transillumination, wedging, staining by methylene blue

DIFFERENTIAL DIAGNOSIS

• During the course of treatment, clinicians are frequently presented with the dilemma
of accurately assessing the contribution of endodontic and periodontal lesions.
• These lesions may be totally separate from each other and present no extraordinary
therapeutic consideration. In a few other situations, there is no obvious demarcation between
the two lesions, which both radiographically and clinically appear as one.
For differential diagnostic purposes the ‘‘endoperio lesions’’ are classified as:
– Primary endo disease,
– Primary perio disease,
– Primary endo disease with secondary perio involvement,
– Primary perio disease with secondary endo involvement,
– True combined diseases.

PRIMARY ENDODONTIC DISEASES

Causes
Deep carious lesion
Large restoration approximating the pulp
History of a pulpotomy, pulpcapping
Poor root canal treatment
Considerable diminution of pulp canal space
Deep carious lesion involving pulp

Symptoms
Tenderness to percussion
 Swelling
Mobility
Narrow periodontal pocket
Localized bone loss
Signs

Presence of sinus tract

The suppurative process may cause a sinus tract along the periodontal ligament space
or through patent channels (including the apical foramen and lateral accessory canals)
This usually results in a narrow opening of the sinus tract into the gingival sulcus and
pocket that can be easily traced with a gutta-percha cone or a periodontal probe. Such
a tract can readily be probed down to the tooth apex, where no increased probing
depth would otherwise exist around the tooth.
In multirooted teeth, a periodontal ligament sinus tract can drain off into the furcation
area and resemble a Grade III, “through and-through” furcation defect resulting from
periodontal disease
Treatment
Complete resolution is usually anticipated after conventional endodontic therapy.

Prognosis
Excellent

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
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.

EFFECT OF PULP ON PERIODONTAL TISSUES DEVELOPMENT OF CLASS I

ENDODONTC-PERIODONTAL LESION IN MOLARS

Pulpal inflammation begins within the coronal portion of the pulp and extends apically,
the products of inflammation can cause damage in the periodontal ligament of the furca
adjacent to such canals long before they reach the tissues at the root apex.

• Such a reaction would give the typical radiographic appearance of the Class I
endodontic-periodontal problem, where the furca is involved, as distinguished by a definite
radiolucency in that are, whereas the periapical region shows little or no deviation from
normal.
• Rubach and Mitchell demonstrated histologically that auxiliary canals in the area of
the furca led directly into the tissues of the periodontal ligament. Vertucci and Williams
reported that 46% of mandibular first molars had auxiliary canals in the furcation region
 The greater thickness of bone in the periapical region of mandibular molars compared
with that in the area of the furca also tends to mask any radiographic visualization of bone
loss in the former while emphasizing the destruction in the thinner bone.

• MANDIBULAR FIRST MOLAR WITH SEVERE INFLAMMATORY PROCESS IN

FURCATION, MINIMAL APICAL DESTRUCTION IS NOTED. AFTER
ENDODONTIC TREATMENT, AREA HAS HEALED. PULPAL FLOOR IS PACKED,
BUT NO FURCATION CANAL IS PICKED UP WITH THE SEALER.

• Moss et al, studied histologically the pulpal floor of primary infected and noninfected
molars. They found that the floor of an infected molar was more permeable to methylene blue
dye than was that of noninfected tooth. They therefore concluded that there was a constant
flow of material directly through the pulpal floor between the pulp and the adjacent tissues.
No study has been made of permanent molar pulpal floors, and the greater thickness as
compared to that in primary teeth might be sufficient barrier to prevent constant interchange.
However, such a possibility does exist and might explain some of the Class I lesions where
no furcal auxiliary canal is demonstrable.

• In view of these facts, the Class I endodontic-periodontal lesion in molars, which has
caused so much confusion and misunderstanding for the dental population, becomes clear.
The radiographic appearance of the furcation results from a pericanicular radiolucency of an
auxiliary canal in the region or results from inflammatory products extending through the
pulpal floor. The lesion suggests an inflammation of severe intensity due to the thinness of
the bone and the normal presence of marrow spaces, which are susceptible to invasion in that
area

The periapical area may appear normal radiographically because the inflammation has not
yet extend through the tooth to that region and/or because a greater thickness of bone is
present to mask the destruction. Following endodontic therapy, with the toxic products
removed from the pulp canal space, the dynamic healing potential of the bone brings
about a return to normal.

• OTHER TYPES OF CLASS I ENDODONTIC-PERIODONTAL PROBLEMS

• On occasion a recall radiograph will show a radiolucency on a lateral surface or in the
furca of the treated tooth where no defect was present preoperatively. This lesion has the
same features as the typical Class I endodontic-periodontal lesion, except that the root canals
are filled, usually adequately. Those who are not in agreement with the pulpal etiology
suggested for Class I lesions point to the cases of this type in repudiation.

Invariably the diagnosis at that time was some type of pulpitis, indicating that most of the
root canal was filled with vital tissue. By way of canal enlargement and frequent
irrigation with hypochlorite, the inflammed pulp was removed from the canal proper and
a dense root canal filling placed. However, inflamed tissue might have remained in any
auxiliary canals present, relatively unaffected by the instrumentation and irrigation. After
the canal filling, the remaining inflamed tissue undergoes necrosis and causes breakdown
of the surrounding periodontal structures.

This type of failure is analogous to the root canal filling that does not seal an
insufficiently debrided apex and allows for the development of a periapical radiolucency
due to the breakdown of the tissue remaining within the canal

The type of failure described may be successfully re-treated if the canal filling material
adjacent to the radiolucency can be removed and retreatment done.

PRIMARY ENDODONTIC DISEASE WITH SECONDARY PERIODONTAL

INVOLVEMENT

Characteristics
Long standing pulpal pathosis leads to destruction of periodontal apparatus through apical
foramen/ lateral canals.
Accumulation of plaque and calculus results in further apical migration of the epithelial
attachment.
Leads to periodontal destruction, pocket formation.

Diagnosis

Radiographs which show periodontal disease with angular defects at the initial site of
the endodontic involvemen
Pulpal vitality test (necrotic pulp) negative respons
Periodontal status – accumulation of plaque and calculus, periodontal pocket
It is a common clinical observation that in multirooted teeth, vital tissue can be found
in canals adjacent to ones containing completely necrotic pulp tissue. Breakdown
products from necrotic uninfected pulps do not seem to be sufficient to cause
periapical pathosis (Bergenholtz 1974,Sundqvist 1976, Möller et al. 1981). In
addition, there does not seem to be much breakdown from dead, uninfected tissue. In
contrast, breakdown products from the cell walls of Gram-negative bacteria found in
 infected root canals (Dahle´n & Bergenholtz 1980) can cause inflammatory alterations
in the periapical area (Dwyer & Torabinejad1981).
Hence, infected necrotic pulps will always lead to periapical tissue reactions if not
treated (Sundqvist 1976,Möller et al. 1981). The location of this inflammation is most
often at the apex of the tooth. However, periodontal tissue breakdown due to
endodontic infection not infrequently occurs around the opening of an accessory canal
on lateral root surfaces or in the furcation region of multirooted teeth. Such lesions
can mimic marginal periodontal pathology, and have been termed ‘retrograde
periodontitis’ (Simring & Goldberg1964).

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 local deepening 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.

PRIMARY PERIODONTAL DISEASES

Characteristics

Teeth vital
Generalized/localized bone loss
Generalized/localized plaque/calculus
Soft tissue inflammation
Deep periodontal pockets
Mobility
Diagrammatic representation showing angular bone loss

Diagnosis
History
Visual examination
Probing – periodontal pocket formation
Pulp testing – positive response
Radiographs – generalized/localized vertical or horizontal bone loss

Treatment
---Periodontal therapy
---Pulp space therapy (advance cases)
---Treatment depends on the extent of the periodontitis and on patients ability to
comply with potential long term treatment and maintenance therapy.
Prognosis

Depends on the outcome of periodontal therapy.

PRIMARY PERIODONTAL DISEASE WITH SECONDARY ENDODONTIC

INVOLVEMENT

This situation exists when the apical progression of periodontal disease is sufficient to
open and expose the pulp to the oral environment through dentinal tubules, lateral
canal or both.
These lesions present the most difficult diagnostic problem
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 .

Characteristics
Deep periodontal pockets present on other teeth as well also
 History of extensive periodontal procedures
Irreversible pulpal pathosis

Symptoms
Dentinal Sensitivity
Tenderness to percussion
Mobility
Swelling
Diagnosis
History of disease progression
Probing
Pulp testing
Radiographic changes

Treatment
Periodontal therapy
Pulp space therapy

Prognosis
Depends on continuing periodontal treatment subsequent to endodontic therapy
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 planing 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.

TRUE COMBINED LESIONS

Pulpal and periodontal disease may occur independently or concomitantly in and

around the same tooth. Once the endodontic and periodontal lesions coalesce, they
may be clinically indistinguishable. The prognosis of multirooted teeth with combined
pulpal and periodontal lesions depends largely on the extent of the destruction caused
by the periodontal disease component. A necrotic pulp or a failing endodontic
treatment, plaque, calculus, and periodontitis will be present in varying degrees.

Horizontal attachment loss, even an optimal endodontic result may not be sufficient to
retain the tooth as a functioning member of the dentition. If the periodontal lesion is
an advanced, multiwalled bony defect, the success of therapy likely depends on the
ability to fill or regenerate attachment to obliterate the defect.

Therefore the decision to treat and retain teeth with combined periodontal and
endodontic lesions should be carefully considered in regard to the overall dental
treatment plan as the time and cost of combined defect treatment may be
considerable.
 Teeth with vertical root fractures also belong in this category, and have been found to
have radiolucencies involving the periodontal ligament in 75% of the cases (Meister
etal. 1980). If apical foramina and accessory canals are referred to as avenues of
communication for bacteria between pulpal and periodontal tissues, vertical root
fractures should be called bacterial highways. As a result of bacterial growth in a
fracture space, the adjacent periodontal ligament and (in vital cases) pulp tissue will
become the seat of an inflammatory lesion, causing breakdown of connective tissue
fibers and alveolar bone.

Diagnosis
Probing – wide periodontal pockets
Radiographs - crestal bone loss and periapical lesion of pulpal form
Pulpal testing – no response to vitality test

Treatment
Endodontic therapy
Periodontal therapy.
Hemisection
Bicuspidization
Root amputation

Prognosis

Depends on the each individual factor.

Adequate root canal therapy resulted in resolution of the periapical lesion, prognosis
of the affected tooth then depends totally on the outcome of periodontal therapy.
This situation often goes undiagnosed, and treatment is rendered to only one of the
diseased tissues in the hope that the other will respond favorably. In actuality, both
disease processes must be treated concomitantly, with the prognosis dependent on the
removal of the individual etiologic factors and prevention of any further factors that
may affect the respective disease processes.

CONCOMITANT PULPAL AND PERIODONTAL LESIONS

An additional classification has been proposed for lesions that may commonly be seen
clinically, and reflect the presence of two separate and distinct entities. This is
referred to as the concomitant pulpal and periodontal lesion. In essence, both disease
states exist but with different causative factors and with no clinical evidence that
either disease state have influenced the other
 TREATMENT OF ENDO-PERIO LESIONS

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.
Appropriate diagnosis is critical. The clinician must be able to identify the clinical
characteristics of a lesion, determine whether or not root canal treatment has the
potential to resolve the lesion, and establish a reasoned prognosis.

TREATMENT AND PROGNOSIS OF ENDO-PERIO LESIONS

Treatment decision-making and prognosis depend primarily on the diagnosis of the specific
endodontic and/or periodontal disease. The main factors to consider are pulp vitality and the
type and extent of the periodontal defect.
Patients with pulpal disease may have a healthy periodontium, gingivitis, or varying amounts
of attachment loss (periodontitis) on the affected or adjacent teeth.
A host of other dental problems may also exist. Therefore, appropriate treatment varies with
the presence, nature, and extent of involvement of the diseases.
Primary endodontic lesions
– Because these lesions are initiated and perpetuated by toxins within the canal system
through the periapex and are not true periodontal pockets, adequate cleaning and
shaping as well as obturation ordinarily results in resolution.
– Probing defects and mobility often disappear quickly. These lesions do not require
any adjunctive periodontal treatment and should not be curetted before the results of
root canal treatment are evaluated.
– Prognosis is good and depends on the success of the root canal treatment
Primary periodontal lesions
– Should be treated only by periodontal therapy.
– Prognosis depends on the severity of the periodontal disease, efficacy of periodontal
therapy and patient response; however, prognosis of primary periodontal lesions is not
as favorable as primary endodontic lesions.
– Primary periodontal lesions should be treated by non-surgical phase therapy in the
first instance.
– Subsequently, poor restorations and developmental grooves that are involved in the
lesion must be removed.
– Periodontal surgery should be performed after the completion of non-surgical phase
therapy if deemed necessary.
Primary endodontic with secondary periodontal lesions
– The prognosis for treatment of primary endodontic disease with secondary periodontal
involvement depends primarily on the severity of periodontal involvement.
– Should first be treated with endodontic and simple hygiene phase therapy.
 – In this case, multi-visit endodontics should be practiced and the placement of
intracanal medicament was found to be very useful in reducing inflammation and
favoring repair.
– Treatment results should be evaluated in 2-3 months and only then further periodontal
treatment should be considered. This sequence of treatment allows sufficient time for
initial tissue healing and better assessment of the periodontal condition.
– But in cases where healing with only endodontic therapy does not occur then both
endodontic and periodontal treatments should be carried out since with endodontic
treatment alone, only part of the lesion may heal up to the level of the secondary
periodontal lesion.
– May also occur as a result of iatrogenic damage such as root perforation or fracture
during root canal treatment or placement of pins or posts.
– 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 mineral trioxide aggregate, reinforced zinc oxide-eugenol
cementglass ionomer cements and Vitremer have been recommended to seal root
perforation.
– 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.
Primary periodontal secondary endodontic lesion and true combined lesions
– Require both endodontic and periodontal regenerative procedures.
– The success rate of the endodontic-periodontal combined lesion without a
concomitant regenerative procedure has been reported to a range from 27% to 37%.
– Combined lesions can be classified into three types, first, tooth with two separate
lesions, one endodontic usually periapical and one periodontal with no
communication, second, teeth with a single lesion that involves both endodontic and
periodontal pathoses and third, teeth with endodontic and periodontal lesions that
were once separate but now communicate
– True-combined lesions should be treated initially as primary endodontic lesions with
secondary periodontal involvement. Prior to surgery, palliative periodontal therapy
should be completed and root canal treatment carried out.
– The prognosis of true combined lesion is often poor or even hopeless, especially when
periodontal lesions are chronic and extensive.
– The prognosis of combined diseases mainly rests with the efficacy of periodontal
therapy.
– When traditional endodontic and periodontal treatments prove insufficient to stabilize
an affected tooth, the clinician must consider treatment alternatives.
– Alternate treatments often consist of resective or regenerative approaches
– Resective methods involve removal of affected roots or extraction of involved teeth.
When a tooth requires extraction, the option for restoring occlusal function should
include placement of dental implants with hybrid prostheses.
 – Root amputation, hemisection or separation may allow the root configuration to be
changed sufficiently for part of the root structure to be saved.
– Bone replacement grafts using guided tissue and bone regeneration techniques are
ways to reestablish biologic structures that were lost during this disease process.
– Root resection is the removal of a root with accompanying odontoplasty, before or
after endodontic treatment.
– The indications for root resection often include (but are not limited to) - tooth
fracture, perforation, root caries, dehiscence, fenestration, external-root resorption
involving one root, impaired endodontic treatment of a particular root, severe
periodontitis affecting only one root, and severe Grade II or III furcation involvement.
Contra indication:
– When loss of bone involves more than 1 root and the remaining root would have
inadequate support
– Fused roots

Factors to be considered before root resection:

The operator need to consider various factors before root resection such as tooth function,
root filling, anatomy, restorability, bone support around the healthy root and patient’s
compliance.
(i) Functional tooth→ tooth should be a functional member of dentition.
(ii) It should be possible to provide pulp space therapy, which has a good prognosis
(iii) Sufficient tooth structure must remain to allow the tooth to be restored
(vi)The roots should be separate with some inter-radicular bone so that removal on one root
will not hamper the remaining roots
(v) Patient must be a suitable candidate for the lengthy operative procedures and able to
maintain high standard of oral cleanliness
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 (GTR).
These regenerative procedures with the aid of the microscope, in the treatment of combined
lesions have been found to have a success rate of 77.5%. (Kim E 2008)

Treatment and prognosis

Because these lesions are initiated and perpetuated by toxins within the canal system
through the periapex and are not true periodontal pockets, adequate cleaning and
shaping as well as obturation ordinarily results in resolution. Probing defects and
mobility often disappear quickly. These lesions do not require any adjunctive
periodontal treatment and should not be curetted before the results of root canal
treatment are evaluated. Prognosis is good and depends on the success of the root
canal treatment

NON SURGICAL PERIODONTAL THERAPY –

• Successful periodontal therapy is dependent on anti infective procedures aimed at

eliminating pathogenic organisms found in dental plaque associated with the tooth
surface and within other niches in the oral cavity
 •
ROLE OF MECHANICAL THERAPY: MANUAL, SONIC AND
ULTRASONIC SCALERS
• When manual instrumentation or sonic/ultrasonic scalers are used for the treatment of
the subgingival pockets, profound shifts in the composition of the microbial flora are
observed.

TOPICAL ANTIMICROBIAL AGENTS

• The term anti-infective therapy was first referred to when topical antimicrobial agents
such as chlorhexidine, hydrogen peroxide, baking soda or povidone iodine were
applied professionally as an adjunct to mechanical debridement.

• ROLE OF SUSTAINED LOCAL DELIVERY ANTIMICROBIAL AGENTS

• In disease sites that are more difficult to control, local drug delivery devices such as
chlorhexidine chips (PerioChipTM) or 10% doxycycline gel (AtridoxTM) may be
placed directly adjacent to the infected site. Pathogenic organisms that were not
accessible to mechanical removal by hand or power-driven instruments can be
reduced or eliminated.

• ROLE OF SYSTEMIC ANTIBIOTICS IN NONSURGICAL THERAPY

• While periodontal debridement with or without locally applied chemotherapeutic

agents is usually affective in controlling early to moderate periodontal lesions, more
advanced cases may require antibiotics following periodontal debridement if the sites
• have not responded as well as expected.

ROLE OF HOST-MODULATING DRUGS

 Subantimicrobial dose of doxycycline (PeriostatA) that targets tissue breakdown by
blocking bacterial and host-derived enzymes associated with loss of alveolar bone and
connective tissue.
It was also shown to augment and maintain clinical attachment level gains and probing
depth reductions, reduction of bleeding on probing and prevention of loss of alveolar
bone height.

TREATMENT ALTERNATIVES
• When traditional endodontic and periodontal treatments prove insufficient to stabilize
an affected tooth, the clinician must consider treatment alternatives.
• Alternate treatments often consist of resective or regenerative approaches

• Resective methods involve removal of affected roots or extraction of involved teeth.

When a tooth requires extraction, the option for restoring occlusal function should
include placement of dental implants with hybrid prostheses.
• Bone replacement grafts using guided tissue and bone regeneration techniques are
ways to reestablish biologic structures that were lost during this disease process.

RESECTIVE TECHNIQUES
• Root resection is the removal of a root with accompanying odontoplasty, before or
after endodontic treatment.
• Its indications are restricted to multirooted teeth where one or more roots cannot be
saved.
• The indications for root resection often include (but are not limited to) - tooth
fracture, perforation, root caries, dehiscence, fenestration, external-root resorption
involving one root, impaired endodontic treatment of a particular root, severe
periodontitis affecting only one root, and severe Grade II or III furcation involvement.
•
• The final restoration of root-resected teeth will depend significantly on the nature of
the resection the amount of remaining tooth structure, periodontal status, and the
patient’s occlusion.
• Controversy has also existed regarding the benefits and need for endodontic therapy
before root resection. Instances develop, however, where exploratory surgery is
necessary, and should the periodontal problem be more extensive than that determined
presurgically, the removal of a root should be carried out at that time. In these
instances, a removal of the involved root without endodontic treatment would be
acceptable, but root canal therapy should be performed as soon as possible after root
removal

Contra indication:
• When loss of bone involves more than 1 root and the remaining root would have
inadequate support
• Fused roots

Factors to be considered before root resection:

• (i) Functional tooth→ tooth should be a functional member of dentition.
• (ii) It should be possible to provide pulp space therapy, which has a good prognosis
• (iii) Sufficient tooth structure must remain to allow the tooth to be restored
• (vi)The roots should be separate with some inter-radicular bone so that removal on
one root will not hamper the remaining roots
• (v) Patient must be a suitable candidate for the lengthy operative procedures and able
to maintain high standard of oral cleanliness

Hemisection:
Indications: Multirooted teeth in which there are isolated areas of extensive bone loss on
a root or bone loss exposing the furcation.
Perforation into furcation resulting in severe bone destruction
Caries involving much of the root.

The Perio Endo Relationship – Controversies

Does periodontal disease cause pulp necrosis?

Does periodontal therapy cause pulp changes?
Do severely periodontally involved teeth with normal vitality response, still require RCT
as a prophylactic measure?
What is the effect of pulpless teeth on periodontal tissues?

Do endodontically treated teeth respond differently to periodontal therapeutic procedures?

Can periodontal regenerative techniques be attempted on endodontically treated teeth?
The Perio Endo Relationship – The Facts
Many of the reports published in the early 60’s and 70’s describing pulpal changes in
periodontally involved teeth were inaccurate & suffered from histological artifacts.
Well framed recent studies have not found any evidence of periodontitis causing pulp
necrosis.
Even teeth with severe periodontitis reaching the apical third of the root were found to
have normal pulps.
Only when the blood supply to the pulp at the apical foramen was affected, the pulp
showed changes.
Pulpal insults through exposed lateral canals/patent dentinal tubules have relatively
insignificant effects on the ability of the pulp to survive.
This is more so for teeth not serving as abutments.
There is no evidence that teeth with moderate to severe periodontitis necessarily require
RCT as a prophylactic measure.
Periodontal therapy has not found to have any effect on pulp.

Periodontally affected tooth vis a vis Endodontic status – Position

Unless periodontal disease extends all the way to the tooth apex, the weight of evidence
in the literature suggests that the dental pulp is capable of surviving significant insults &
that the effect of periodontal disease as well as periodontal treatment on the dental pulp is
negligible.
The relationship of periodontal disease & pulp has been exaggerated in historical
literature.

Endodontically involved teeth & Periodontal health & healing – The Facts
Various studies have reported wide ranging findings on the effect of pulp disease on
periodontal health & healing.
A tooth with a necrotic pulp or that has RCT may pose a risk factor for periodontal
disease.
Significantly increased P.D & CAL were found in pulpless teeth than normal ones.
The rate of bone destruction in teeth with periapical lesion appeared to be statistically
more albeit clinically marginal.
In one study, use of DFDBA in endodontically treated teeth showed less bone fill than
normal teeth.
However well controlled studies, where endodontic treatment was judged adequate, these
teeth responded in the same way as others.
Well controlled studies have shown that prognosis is good even for molars treated by
RCT.

Endodontically involved teeth & Periodontal health - Position

The periodontal prognosis is not affected if a satisfactory, adequate endodontic treatment
is done.
Although there might be some statistical difference, clinically endodontically treated teeth
respond similarly to periodontal therapy as compared to vital teeth.

• Conclusion
• Interrelationship between pulpal and periodontal disease have been both confirmed
and denied for over 100 years. The most intimate and demonstrable relationship between the
two tissues is by means of the vascular system. The similarities between the endodontic-
periodontal microfloras suggest that cross-infection between the root canal and the
periodontal pocket can occur. An in depth understanding of the mechanisms by which these
diseases processes interact, together with a thorough diagnostic examination, usually will
help direct the proper course of treatment.

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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