1. Ann Periodontol 1999; 4:84-89.
Periodontic-Endodontic Lesions
Huan Xin Meng
Beijing Medical University, Beijing. China.
Lesions of the periodontal ligament and adjacent alveolar bone may originate from
infections of the periodontium or tissues of the dental pulp. This review focuses on the
relationship of lesions of endodontic origin with lesions of periodontal origin and their
classification.
KEY WORDS
Dental pulp diseases/classification; dental pulp diseases/etiology; periodontal
diseases/classification; periodontal diseases/etiology; lesions/endodontic:
lesions`periodontic.
Pulpal infection may cause a tissue- destructive process that proceeds from the apical
region of a tooth toward the gingival margin. The term 'retrograde peri-odontitis" was
succested in order to differentiate this from marginal periodontitis in which the infection
spreads from the gingival margin toward the root apex.1'2 Another term. pulpodontic-
periodontic syndrome, has been used to define a syndrome involving inflammation or
degeneration of the pu!p with a periodontal pocket adjacent to the same tooth. This
syndrome can be initiated by either pulpal or periodontal disease and may manifest pulpal
and periodontal symptoms, in general. Pulpal infection has the potential to initiate
inflammatory changes in the alveolus at both apical and non-apical locations of teeth.3
Combined lesions (previously referred to as "true" combined lesions) are those that occur
where an endodontically induced periapical lesion exists on a tooth that is also
periodontally involved.4 Al of these conditions can be placed under the general term
periodontitis associated with pulpa disease. This review focuses on the relation of lesions
of endodontic origin with lesions of periodontal origin and their classification.
COMMUNICATION BETWEEN ENDODONTIC AND PERIODONTAL LESIONS
The periodontium, communicates with pulp tissues through many channels or pathways.
These channels may be involved in extending pulpal infections to the periodontium, and
vice versa.
Lateral and Accessory Canals and Foramina
Studies of human teeth have shown that lateral and accessory canals and foramina are
present in great numbers, especially in the bifurcation and trifurcation regions of molars.
Some investigators found accessory canals in molar furcations in 20% to 60% of
permanent teeth, 6 and in 23% of deciduous molars examined.7 In a study of 1,140
extracted adult human teeth lateral canals were found in 27% of the teeth, and distributed
at various levels of the root.8 The lateral canals were filled with capillaries, pulp cells,
ground substance, and connective tissue fibers that were continuous with the pulp tissue.
In many cases the width of the accessory foramina or lateral canals was exceedingly

2. small, permitting the presence of only small caliber vessels and their supporting stroma.3 In
another report, 2% of the 100 teeth studied had accessory canals located within a
periodontal pocket and 23% had 1 or 2 accessory canals.9
A fairly high prevalence of lateral canals in posterior teeth that communicate with the floor
of the pulp chamber and the periodontal ligament has been reported in anirnals.10-11 Thus,
there is ample evidence to indicate that infection of the pulp can potentially communicate
with the perodontium at locations other than the apex of the tooth.
Apical Foramen and Other Communications
It has been shown that when apical granulomas from necrotic pulps are extensive, the
granulomatous tissue can be present along the lateral aspects of roots, which may cause
extensive resorption of the alveolar crest.3 Other communications between the
periodontium and pulp may include dentinal tubules and common vasculolymphatic
drainage.1, 12
Although communication between pulp and periodontium can be focused on the vascular
route, many other possible avenues exist. The following anatomical entities or pathways
have also been mentioned in the literature as possible causes of periodontally derived
endodontic lesions: lingual grooves, root/tooth fractures, cemental agenesis,/hypoplasia,
root anomalies, intermediate bifurcation ridges, fibrinous communications, and trauma-
induced root resorption.13
Effect of Pulpal Diseases on the Periodontal Tissues
Pulpal disease is known to cause periodontal changes in both animals 3,10,11,14 and humans
1,3,4,15,16
through lateral canals, accessory foramina, and crestal extension of
granulomatous lesions.
Several experimental animal studies have assessed the effect of pulpal injury on the
periodontium.3,10,11 It has been noted that interradicular periodontal lesions can be initiated
by inflamed or necrotic pulps after mechanical pulp exposures in posterior teeth of kittens,
dogs, monkeys,3,10,11 and rats.14 In most instances, lateral canals were found to be
associated with the production of the periodontal lesions and led to destruction of much of
the interradicular bone and bone in bifurcations.3,10
Periodontal lesions induced by pulp diseases have also been noted in humans.1.3-5.15-17 In a
case series of 109 teeth considered to have a hopeless periodontal prognosis. 89% of the
teeth were successfully retained after endodontic therapy.1 These results suggest that the
cases were affected by a retrograde periodontitis. In another study, 80% of the teeth
(42/53) subjected to pulpal and periodontal irritants had a greater incidence of
inflammatory reactions than those teeth with periodontal disease alone.' Several recent
retrospective clinical studies have shown a correlation between degree of marginal
periodontal breakdown and presence of periapical pathology in periodontitis- prone
patients. 18-20 In an experimental study in monkeys, an intra-canal infection with endodontic
pathogens stimulated epithelial down growth along denuded dentin surfaces.21 Based on
his finding it has been suggested that endodontic infections in periodontitis-prone patients
may contribute to the progression of periodontitis.21
Periodontal damage of pulpal origin has the potential to occur in the early stages of pulpal
disease. Furthermore, an apical endodontic lesion may also extend and drain along the
periodontium (previously referred to as retrograde períodontitis). In molar teeth this

3. pathway usually follows a track to the furcation, but may reach the crevice on any aspect
of the tooth.22 The inflammation from inflamed and necrotic pulps can readily spread
through lateral canals and accessory foramina into the periodontal ligament.
EFFECT OF PERIODONTAL INFLAMMATION ON THE PULP
Although dental plaque bacteria have the potential to induce pathologic changes in the
pulp along the same pathways as en endodontic infection can affect the periodontium in
the opposite direction, the effect of periodontal disease on the pulp is not as c!ear-cut as
the effect of pulpal disease on the periodontium. It has been found that inflammatory
alterations or localized necrosis of pulp tissue were adjacent to lateral canals in roots
exposed by periodontal disease. 5 The direct inflammatory extension of periodontal
inflammation through the apical foramen or lateral canals to the pulp, including subsequent
pulpal necrosis, has been demonstrated.23.24 However, normal pulps have also been
observed in teeth with advanced periodontal disease.25.26
The initial effect of periodontal inflammation on the pulp may be degenerative. Fibrosis,
calcifications, and collagen resorption have been reported in pulps of teeth with long-
standing periodontal disease. 24, 27 Irregular or reparative dentin formation has also been
found with some resorption of dentin in periodontally diseased teeth.23
During scaling and root planing, cementum and superficial dentin are removed from the
root surface by instrumentation. In one study, chronic pulpitis with bacterial penetration of
dentinal tubules was found adjacent to roots of teeth that had been scaled and root
planed.28
MICROBIOLOGY
Early microbiological studies29 that assessed the microflora associated with acute
suppurative dental infections implicated streptococci or staphylococci as the causative
microorganisms, but more recent studies suggest that the microbiota of an acute
dentoalveolar abscess is usually polymicrobial 6,29 30 similar to periodontal disease.
Fusobacterium, Prevotella, Porphyromonas, Peptostreptococcus, and Streptococcus are
the predominant genera that have been isolated.30-34 Spirochetes also reside in infected
root canals.35,36 Acute exacerbations of chronic periapical infections are frequently
associated with specific anaerobes, particularly Porphyromonas gingivalis and
Porphyromonas endodontalis.30
The microbiota in necrotic pulps are not as complex as those in deep periodontal pockets.
The former is usually comprised of a limited number of bacterial species of which one or
two may predominate 6 such as blackpigmented Bacteroides.37, 38 Depending on the
microbiota and capacity of the host to resist the infection, an acute abscess or a chronic
inflammatory reaction may develop at any site along the periodontium, where there are
direct communications with the pulpal chamber.6
CLINICAL FEATURES
In contrast to superficial periodontal lesions extending from gingivitis, pulpal diseases have
the potential to initiate inflammatory changes deep in the alveolus at both apical and non-
apical locations of involved teeth.

4. Effect of Acute Endodontic Lesions on the Marginal Periodontium
Acute manifestations of root canal infections can result in rapid and extensive destruction
of the attachment apparatus.5 Dental abscesses can form at any level of the periodontium,
from the tooth neck to the apex and may drain anywhere along this path: i.e., a sinus tract
along the periodontal ligament space or an extra-osseous fistula into the gingival
sulcus/pocket. Trans-alveolar abscesses may be caused by seeping of purulent exudate
from an adjacent periapical abscess into the empty tooth socket 39 and in deciduous
molars; dental abscesses frequently develop at bifurcation areas.17 The periodontium can
be extensively damaged at sites of periapical infection. Following proper endodontic
therapy, such lesions frequently heal without a persistent periodontal defect.6
Endodontic and periodontal abscesses may resemble each other clinically, differing only in
the point of origin and specific path of infection. In most instances, periapical abscesses
occur singly, the involved teeth may be extruded and exhibit tenderness to percussion and
hyper mobility. Marked lymphadenopathy is common, as is facial swelling and extension of
the infection along tissue planes to points of drainage (either intraoral or extraoral). Fever
and malaise commonly occur, which may be due to the action of the endogenous pyrogen
interleukin-1, which is found in high levels in exudates from periapical abscesses. A range
of significant complications may arise from untreated endodontic abscesses.40 Persistent
fever has been reported due to an occult dental abscess.41
Root Perforations
lnflammatory lesions in the marginal periodontium as manifested by increased probing
depth, suppuration, increased tooth mobility, and loss of fibrous attachment may result
from an undetected or unsuccessfully treated root perforation.6, 42 A periodontal abscess
may also occur in the absence of any previous periodontal disease, following perforation of
the lateral wall of the root during endodontic therapy.1, 33
Vertical Root Fracture
In general, vertical root fractures occur most often on endodontically treated teeth.
However, spontaneous vertical root fractures of non-endodontically treated teeth can also
occur and more than 500 cases have been reported in the Chinese population.43-52 The
clinical features of vertical root fractures in non-endodontically treated teeth can
sometimes appear as combined endodontic and periodontal lesions.45.46.52-54 Pain during
occlusion or mastication is the principal symptom. Thermal sensitivity, gingival swelling,
and periodontal abscess or sinus tracts are also common. Upon clinical examination pulps
of fractured teeth may or may not be responsive to electric pulp testing. 50, 52-54 Narrow or
localized deep pockets are usually detected by periodontal probing. Widening of the root
canal space and periapical and/or periodontal radiolucencies are radiographic
characteristics which may aid in diagnosis.46,50,54 One study indicated that vertical root
fractures are often associated with traumatic occlusal contacts or severe abrasion which
increased the occlusal load during chewing. Another study found that most of the fractures
passed along incremental fines in dentine, and fractures frequently occurred on flat roots
with 2 canals, 51 suggesting that they may be related to developmental or anatomic
defects.
Root fractures frequently occur on endodontically treated teeth and are associated with a
deep pocket on a surface of the tooth which may or may not be abscessed. 6 Symptoms
and signs associated with vertical root fractures show a variety of characteristics and are

5. difficult to distinguish from these associated with periodontal and endodontic lesions. Pain
on selective loading of cusps may be an indication of a root fracture.
Combined Lesions
This lesion occurs as the result of the interaction between diseases of endodontic and
periodontal origin, on the same tooth, irrespective of the sequence in which they occur.
The clinical and radiographic examinations do not permit identification of the primary
cause of the lesion.
DIAGNOSIS
The diagnosis of periodontal lesions associated with pulpal diseases may be relatively
simple if a patient has been monitored over a period of time and records (e.g.,
radiographs) are available. The diagnosis becomes more difficult when a complete history
is unavailable. A growing periapical area with secondary formation of a deep periodontal
pocket may be similar in clinical and radiographic appearance to a long-standing
periodontal lesion that has progressed to the root apex. 2
The radiographic image of bone resorption, including the apical and furcal or marginal
regions, may confuse rather than aid in making a diagnosis.
However, if radiographs taken during the progression of bone resorption reveal it to be
extending from the apex to the crest, the apical region can be positively identified as the
origin of the infection.55 In general, it is easier to determine the origin of the lesion when a
vital pulp test is obtained, because the test results usually will rule out an endodontic
etiology. However, pulp tests may not always be reliable.56
This consideration is particularly relevant when challenges to pulpal status arise from
periodontal diseases.57
Partial necrosis of a pulp, especially in a multirooted tooth, may be a result. 5, 23.58 This
may allow for positive responses to pulp testing suggesting vitality, despite the existence
of a combined lesion. 59 It has been suggested that when doubt exists about a pulp's
status, a test cavity can be made.2 However; this may not always provide a more exact
determination of pulpal status once partial pulpal necrosis has occurred.
A non-vital or endodontically-treated tooth associated with a combined lesion presents a
greater diagnostic problem.2, 4 In this situation, pulpal necrosis is frequently associated
with inflammatory involvement of the periodontal tissue. The location of these pulpal
lesions is most often at the apex of the tooth, but they may also occur at any site where
lateral and furcal canals exit into the periodontium.
Differential Diagnosis
Determination of pulp vitality is essential for a differential diagnosis and for selection of
primary measures for treatment of inflammatory lesions in the marginal and apical
periodontium. Deep restorations, dental trauma, endodontic treatment, previous pulp
capping, and pulp vitality testing are factors to be considered when assessing the peed for
endodontic treatment as a part of overall periodontal therapy.6
Location and extent of pockets, probing depth, and furcation invasions are also essential
for the differential diagnosis.60 If the pulp reacts clinically normal, but a periodontal pocket

6. can be located, then periodontal tissues should be suspected as the origin of either the
acute or chronic inflammatory process. On the other hand, when the pulp is found to test
non-vital, the inflammatory process which passes through a lateral canal or the apical
foramen will cause a lesion of endodontic origin. When pulpitis is clinically recognized in a
tooth with pre-existing periodontal disease, the pulpitis may be secondary to the
periodontal disease, particularly in the absence of any other obvious cause of pulpitis. The
presence of subgingival calculus deposits and the degree and location of inflammation are
important to note in determining the primary source of the disease.
When severe or angular localized lesions of the periodontium are detected, the differential
diagnosis between pulpal and periodontal origins should be made. Severe localized
periodontal lesions are well documented periodontal consequences of pulpal pathoses.22
However, destruction of the periodontium near or about the apical area of a tooth does not
necessarily indicate that the lesion is of pulpal origin. Large and diffuse areas of
radiographically evident periapical destruction can occur without compromising the health
of the pulpal tissues.61 Such lesions can occur in the following circumstances: 1) direct
extension of an active periodontal lesion; 2) interproximal channel lesion, generally seen in
the mandibular cuspid area: 3) cystic Iesions derived from epithelial remnants of tooth-
forming-tissues; 4) localized sites of rapidly advancing periodontitis; or 5) localized lesions
of osteomyelitis involving the periodontium.61
It has been suggested that the percentage of spirochetes as seen by darkfield microscopy
might be of value in the differential diagnosis of periodontal and endodontic abscesses.62
In this study it was reported that, in periodontal abscesses, spirochetes were the
predominant cell (mean, 40.6 ± 10.9%) with coccoid cells present in significantly lower
numbers (mean, 19.7 ± 10.9%). In endodontic abscesses the reverse was true, where
coccoid cells dominated (mean, 44.3 ± 19.7%) and only few spirochetes were present
(mean, 5.6 ± 4.7 %).62 The clinical value of this observation has not yet been determined.
CONCLUSION
Pulpal disease may cause periodontal chances in both animals and humans through
lateral canals, accessory canals, accessory and apical foramina, and gingival extension of
endodontic lesions. Periodontal diseases may cause pulpal changes trough
communications between the pulp and the root surface. These pathologies (i.e.,
endodontic or periodontal) may exist independently of each other on the same tooth. lt is
proposed that the combined lesion is where there is an interaction between diseases of
endodontic origin and periodontal diseases on a tooth. Thus the combined lesion is the
lesion to be classified.
ACKNOWLEOGMENT
The author expresses her appreciation to Dr. Esmonde Corbet for his generous assistance
in the preparation of this paper.

7. Consensus Report: Periodontic-Endodontic Lesions
The group accepted the review paper written prior to the workshop. Infections of
periodontal or endodontic origin may result in increased periodontal probing depths
adjacent to the root surface, swelling, bleeding on probing, suppuration, fistula formation,
tenderness to percussion, increased tooth mobility, angular bone loss, and pain. These
signs and symptoms are usually due to plaque-associated periodontitis which begins at
the margin of the gingiva and proceeds apically. However, these signs and symptoms may
also be caused by endodontic infections that enter the periodontal ligament at the apical
foramen or through lateral or accessory canals and proceed coronally. These signs and
symptoms may also be the result of a root fracture. With the exception of root fractures,
when the endodontic lesion is the chief cause of the clinical infection, endodontic therapy
may lead to its complete resolution.
The group acknowledged that some periodontal-endodontic lesions are primarily of
endodontic origin. In other instances, bacteria from chronic or aggressive forms of
periodontitis can gain access to pulpal tissues through accessory canals or the tooth apex
and lead to pulpal infection. In those cases where dire is any coalescence of endodontic
and periodontal lesion, the group agreed that these situations should be termed,
`Combined Periodontal-Endodontic Lesions." This classification is not based on the inicial
etiology of the lesion. Either the periodontal or endodontic lesion may be the cause or the
result of the other or both may develop independently. Therefore, the group recommended
the following classification:
VII. Periodontitis Associated With Endodontic Lesions
A. Combined periodontal-endodontic lesions
GROUP MEMBERS
Nicklaus Lang, Group Leader Huan Xin Meng
W.A. Soskolne. Chair Michael Newman
Gary Greenstein, Secretary M. John Novak
David Cochran Howard Tenenbaum Esmonde Corbet