CONTINUING EDUCATION

Course Number: 218

Types of Endodontic Lesions:

Clinical Considerations
Lisa Germain, DDS, MScD

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 CONTINUING EDUCATION
Types of
Endodontic
Lesions: Clinical
Considerations
Effective Date: 02/01/2018 Expiration Date: 02/01/2021
Learning Objectives: After reading this article, the individual will learn:
(1) the different types and etiologies of endodontic lesions, and (2)
clinical considerations clinicians should bear in mind when determin-
ing treatment options.
About the Author
Lisa Germain, DDS, MScD, is clinical
director of DC Dental. She also is a Diplomate
of the American Board of Endodontics and a
Fellow of the International Congress of Oral
Implantologists. She can be reached via email
at lisa.germain.dds@gmail.com.
Disclosure: Dr. Germain reports no disclosures.
C
onsidering the massive amount of bacteria that colo-
nizes the oral cavity, it is amazing that any procedure
performed in the mouth can heal uneventfully. Studies
have identified more than 700 different intraoral bacterial spe-
cies, with more than 400 species being isolated from the gingi-
val sulcus around the teeth, and the remaining 300 species being
isolated from areas such as the tongue, mucous membranes, car-
ious lesions, and endodontic infections. Each person is thought
to have 100 to 200 species of intraoral bacteria, representing a
substantial diversity among different individuals.1
Infection of the root canal system is the major cause of api-
cal periodontitis2,3 (Figure 1). Scientific evidence suggests that
microorganisms are essential for the progression and perpet-
uation of various forms of apical periodontitis.4 The intent of
endodontic therapy is to eradicate the infection to prevent these
1
microorganisms from re-infecting the root canal system and
periapical tissues. Endodontic disease progresses in a coronal
to apical direction. As such, apical periodontitis occurs once the
microbes migrate into the periapical tissues through the radic-
ular portals of exit. Endodontic infections are poly-microbial
by nature. However, obligate anaerobic bacteria dominate the
microbiota in primary endodontic infections.5
When a tooth is considered nonrestorable or periodontally
compromised, or when it has a vertical root fracture, extraction
is necessary and an endosseous implant is frequently planned as a
replacement (Figure 2). Subsequent to the extraction, socket pres-
ervation is commonly performed with the placement of avascular
grafting material to scaffold the area to minimize volumetric con-
traction and maintain the dimension of the ridge.6
Placing grafting material in an area of an odontogenic infection
is often cited as a factor associated with an increased risk of infec-
tion after the placement of a dental implant.7 An entity referred to
as an implant periodontal lesion has been described in the literature,
suggesting that these bony lesions may be caused by the presence
of a pre-existing infection, residual root fragments, or foreign bod-
ies in the bone.8,9 While there is no protocol for immediate graft-
ing into sites with endodontic infections versus waiting until the
infection has cleared, a knowledge of how endodontic lesions
affect the bone is helpful in the decision-making process.
Pulp Diagnosis Without Apical Periodontitis
The diagnosis of normal pulp or reversible pulpitis indicates that
the surrounding bone is not affected. The pulp tissue is vital and
the tooth is either asymptomatic or the symptoms are not from
pulpal pathosis. Teeth with this pulpal diagnosis should only be
extracted when they are periodontally compromised or if the
tooth is not restorable. Again, if there is no pathological change
to the pulp, then there is no bacterial contamination from the
pulp to the bone.10 In turn, this endodontic state is not likely to
compromise the grafting of an extraction socket.
A diagnosis of irreversible pulpitis is more complicated, as this
pulpal status often progresses into pulp necrosis. For example, if
severe lingering cold sensitivity is present, and there is no sensi-
tivity to heat, the diagnosis is irreversible pulpitis. Changes in the
bone are unlikely. Conversely, if sharp pain to heat is present with
a lack of cold sensitivity, local foci of pulp necrosis may be present,
which will eventually progress into total pulp necrosis and pulpal
infection, with the eventual progression of this infection into the
periradicular tissues resulting in an apical periodontitis.
Apical Periodontitis
Chronic and acute apical periodontitis are biofilm-induced dis-
eases that can occur secondary to pulpal necrosis, complete root
fracture, and re-infected root canal therapy or from traumatic
 CONTINUING EDUCATION

Types of Endodontic Lesions: Clinical Considerations

injury. These types of endodontic complications have the poten- hybridization, and when the samples are taken directly from the
tial to affect the periradicular bone and potentially compromise bony lesions.1
grafting procedures. The asymptomatic (chronic) form of apical periodontitis is more
common. Typically, there is bony destruction secondary to the
Pulpal Necrosis spread of pulpal infection to the bone. The symptomatic form, also
When pulpal necrosis and eventual pulpal infection occurs, known as an acute apical abscess, can spread rapidly from the orig-
there is a dynamic encounter between host defenses and bacte- inal site of infection and may progress to the maxillary sinus as
rial byproducts that present at the interface of the radicular pulp well as into fascial spaces of the head and neck, which may cause
and the periodontal ligament (PDL). This results in local periapi- serious life-threatening complications. While there appears to be
cal inflammation and infection with the eventual resorption of a significantly higher diversity of bacteria in acute alveolar infec-
associated periradicular bone. The formation of various histo- tions compared to asymptomatic chronic infections, both show
pathological types of apical periodontitis are commonly referred significant quantities of microbial biofilm colonization. In addi-
to as periapical lesions.11 tion, it has been suggested that certain species of bacteria are more
Microbial culturing of the root canal space has not been suc- prominent when there are acute symptoms.13,14
cessful in accurately determining the bacterial status of the root For a tooth with a necrotic pulp, the elimination of the necrotic
canal system. Because of limitations in culturing techniques, false tissue and associated infection is the intent of endodontic therapy.
positive and false negative results often occur.12 Investigations of If performed properly, there is a high rate of success (Figure 3).
the endodontic (and periodontal) micro-flora are more accurate However, if endodontic treatment is not being considered, either
when molecular methods are used, such as DNA because of patient desires or because the tooth is non-re-
storable or periodontally compromised, extraction will
also remove the contents of the root canal space and
eliminate the source of the infection.
What happens to the infected bone becomes
the next question. Is it safe to place avascular bone
grafting materials at this time, or should grafting be
delayed? Unfortunately, there is no single answer to
these questions, and critical thinking is essential to
determine the best modality of treatment for each
individual case. Many clinical studies have shown
that with meticulous debridement of the socket, infec-
tion is unlikely to progress in a healthy patient.15-22 In
addition, premedication with antibiotics to eliminate
Figure 1. Pulp necrosis from carious exposure and Figure 2. The tooth is
the subsequent lesion of endodontic origin. unrestorable. Extraction is acute symptoms of apical periodontitis should be con-
recommended. sidered prior to any surgical procedures.20

a b c

Figure 3a. Preoperative view of a tooth with Figure 3b. Postoperative view of a tooth with Figure 3c. Healed periradicular bone, 6 months
apical periodontitis. apical periodontitis. after root canal therapy.

2
 CONTINUING EDUCATION
Types of Endodontic Lesions: Clinical Considerations
Figure 4. A J-shaped RL lesion.
a b
Figure 6a. A sinus tract Figure 6b. This radiograph shows a
high on the attached gin- widened PDL and cupping into furcation
giva of tooth No. 30. bone.
Complete Fracture and Fracture Necrosis
Teeth with vertical root fractures are not candidates for root canal
therapy, and extraction should be recommended. The alveolar
bone destruction from these fractures typically extends from
the alveolar crest to the root apex, resulting in a narrow, isolated
periodontal probing associated with the bony area adjacent to
the fracture. Bone loss may rapidly develop over time, so fracture
detection is imperative. Because root fractures present in so many
different ways, diagnosis can be challenging. Yet it is essential to
differentiate these lesions from those of apical periodontitis, and
radiographic interpretation alone is not enough.
Traditional periapical radiographs of lesions secondary to
vertical root fractures are often mistaken for apical periodontitis.
However, root canal therapy has a hopeless prognosis if performed
on these teeth. Therefore, the accuracy of diagnosis is essential. If
the radiolucency is “J-shaped” (Figure 4) or “balloons” around the
root (Figure 5), it is most likely caused by a root fracture. Often,
cupping or a significantly widened PDL space is also seen, many
times incorporating the furcation bone. Also noteworthy in form-
ing a differential diagnosis of a vertical root fracture is that if a
sinus tract is present, it is more likely to be close to the gingival
margin rather than in the mucosal area near the apices of the
3
Figure 5. A balloon-shaped RL lesion.
c
Figure 6c. A complete
vertical fracture.
tooth (Figure 6). These findings are not pathognomonic, but are
highly suggestive of a root fracture, and the patient deserves to be
informed of a potentially reduced prognosis.
CBCT images may better elucidate the bone loss that occurs
as a result of an infection secondary to a root fracture. But unless
the fracture is more than 2 voxel sizes in width, the fracture may
not be radiographically visible. When evaluating these lesions
using CBCT, they need to be aligned symmetrically with the
sagittal, frontal, and transverse planes to idealize the fracture
line with the associated osseous defect. The combination of tran-
sillumination data and periodontal probing depths, which are
associated with these defects in all 3 planes, gives the most accu-
rate information for diagnostic purposes (Figure 7). Otherwise,
a false positive diagnosis is likely because the clinician is most
likely viewing an artifact.23
If a tooth has no restoration, has a necrotic pulp, and has not
had a luxation injury, it is likely to have fracture necrosis. Micro-
scopically, there will be a longitudinal fracture extending from
the occlusal surface into the pulp and most likely extending
to an exterior surface of the root. If endodontic treatment is per-
formed on teeth with fracture necrosis, the prognosis should
be considered poor, and there is enormous potential for these
 CONTINUING EDUCATION

Types of Endodontic Lesions: Clinical Considerations

a b c

Figure 7a. Tooth No. 18, Figure 7b. A misdiagnosis of Figure 7c. Nine months later, the
without a restoration or history apical periodontitis, and a root patient returns with symptoms.
of luxation. canal was performed.

d e

Figures 7d and 7e. Extraction of the tooth, confirming fracture

necrosis.

Figure 8. Transillumination of a tooth with a complete fracture. Figure 9. Replacement

resorption after traumatic
injury.

fractures to cause extensive and rapid periradicular bone loss
(Figure 8). Early diagnosis is imperative.
There is good news and bad news when ridge preservation
is considered for post-extraction sites, whereby a tooth was
extracted because of a vertical root fracture. The good news is
that this type of infection is now a periodontal lesion, not an end-
odontic lesion. The host response to bacteria and the formation
of osteolytic lesions are common to both endodontic and peri-
odontal lesions. Both lesions exhibit inflammation that appears
to inhibit bone formation.
However, lesions of endodontic origin pose a particular chal-
lenge since the bacteria exist in a protected reservoir that is not
readily accessible to immune defenses (ie, the fracture site).
Leakage from the fracture site creates an egress for bacteria, and,
therefore, the infection source is no longer contained within the
unyielding tooth structure.24,25 The bad news is that grafting
is more challenging because the socket is now a 4-wall defect
instead of a 5-wall defect.
Previously Treated Teeth
Endodontic therapy has a predictable success rate. However,
endodontic failure and a resulting secondary infection can occur
because of procedural errors or from bacterial invasion due to
microleakage from inadequate coronal restorations.26 Microbiota

4
 CONTINUING EDUCATION
Types of Endodontic Lesions: Clinical Considerations
from primary infected root canals with apical periodontitis
differ in number and species from secondarily infected canals.
In addition, Enterococcus faecalis has been shown to be the most
prevalent species associated with endodontic failures and may
be more difficult to eradicate.27,28 While this might not affect
grafting in a healthy patient, delayed grafting should be consid-
ered in a patient with adverse risk factors.
Traumatic Injury
While many forms of root resorption are idiopathic, there is
strong evidence that ankylosis, a form of replacement resorption,
occurs as a result of traumatic injury to teeth. The highest risk
of ankylosis occurs after subluxation and avulsion injuries due
to the severity of damage to the PDL. An intrusion injury is par-
ticularly destructive because it crushes not only the PDL (and its
associated blood supply), but the alveolar bone as well.
While no single observation or test is diagnostic for ankylosis,
some of the signs include a lack of mobility, a sharp and solid
sound when the tooth is percussed, infra-position of the tooth
compared to adjacent teeth, and the radiographic absence of a
PDL. Replacement resorption does not usually affect the surround-
ing bone. The resorption process typically continues over time,
replacing the root structure with the invading bone at a variable
and unpredictable rate29 (Figure 9).
The first inclination may be to extract these teeth, though this
decision is decidedly multidisciplinary. The actual treatment
decision should be based on the age of onset as well as prosthetic
and surgical implications that would be present if the tooth is
extracted. When ankylosis begins before the patient has finished
growing, the growth of the alveolar bone can be arrested. If the
patient has finished growing, and if the tooth is in a favorable
position, extraction may not be necessary for many years.
While the pulp may be necrotic due to the injury, the resorp-
tion is caused by the disruption in the PDL and will not be
arrested with root canal therapy. The necrotic pulp is caused by
infection. The resorption is inflammatory in nature. If extraction
is the treatment of choice, the challenge will be removing the
tooth as atraumatically as possible. Care must be taken to sepa-
rate the bone from the tooth to prevent removal of the attached
and ankylosed cortical plate. In addition, decortication of the
bony socket is essential to induce bleeding if the ankylosed
tooth has compromised the blood supply in the area.
CONCLUSION
Root canal therapy is a very predictable procedure if done cor-
rectly. If the tooth is severely periodontally involved, is nonrestor-
able, or has a vertical root fracture, extraction is recommended to
prevent further destruction of the associated bone.
5
Grafting protocols in areas of endodontic lesions must be
made on a patient-by-patient basis. Identification of the cause
of the lesion and its influence on the surrounding bone is essen-
tial for appropriate decision making. If grafting is performed
immediately post-extraction, meticulous debridement of the
socket is paramount.
Ultimately, for the patient’s best interest, treatment planning
in dentistry should be multidisciplinary. All specialists should
offer pertinent information with regard to their particular area
of expertise to maximize the predictability and success of the case.
Since it is important to determine the cause of the alveolar bone
loss, a comprehensive endodontic evaluation is imperative.F
References
1. Paster BJ, Olsen I, Aas JA, Dewhirst FE. The breadth of bacterial diversity in the human
periodontal pocket and other oral sites. Periodontol 2000. 2006;42:80-87.
2. Narayanan LL, Vaishnavi C. Endodontic microbiology. J Conserv Dent. 2010;13:233-239.
3. Siqueira JF Jr. Microbiology of apical periodontitis. In: Ørstavik D, Pitt Ford T, eds. Essen-
tial Endodontology: Prevention and Treatment of Apical Periodontitis. 2nd ed. Oxford,
England: Blackwell Munksgaard; 2008:135-139.
4. Kakehashi S, Stanley HR, Fitzgerald RJ. The effects of surgical exposures of dental
pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol.
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5. Bammann LL, Estrela C. Microbiological aspects in endodontics. In: Estrela C. Endodon-
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6. Misch CE. Bone augmentation for implant placement: keys to bone grafting. In: Misch
CE, ed. Contemporary Implant Dentistry. 2nd ed. St. Louis, MO: Mosby; 1999.
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10. Berman LH, Hartwell GR. Diagnosis. In: Hargreaves KM, Cohen S, eds. Cohen’s Pathways
of the Pulp. 10th ed. St. Louis, MO: Mosby Elsevier; 2011:2-39.
11. Nair PN. Pathogenesis of apical periodontitis and the causes of endodontic failures. Crit
Rev Oral Biol Med. 2004;15:348-381.
12. Sathorn C, Parashos P, Messer HH. How useful is root canal culturing in predicting
treatment outcome? J Endod. 2007;33:220-225.
13. Sakamoto M, Rôças IN, Siqueira JF Jr, Benno Y. Molecular analysis of bacteria in
asymptomatic and symptomatic endodontic infections. Oral Microbiol Immunol.
2006;21:112-122.
14. Tronstad L, Barnett F, Riso K, Slots J. Extraradicular endodontic infections. Endod Dent
Traumatol. 1987;3:86-90.
15. Santos AL, Siqueira JF Jr, Rôças IN, Jesus EC, Rosado AS, Tiedje JM. Comparing
the bacterial diversity of acute and chronic dental root canal infections. PLoS One.
2011;6:e28088.
16. Chrcanovic BR, Martins MD, Wennerberg A. Immediate placement of implants into
infected sites: a systematic review. Clin Implant Dent Relat Res. 2015;17(suppl
1):e1-e16.
17. Casap N, Zeltser C, Wexler A, Tarazi E, Zeltser R. Immediate placement of dental implants
into debrided infected dentoalveolar sockets. J Oral Maxillofac Surg. 2007;65:384-392.
18. Lindeboom JA, Tjiook Y, Kroon FH. Immediate placement of implants in periapical
infected sites: a prospective randomized study in 50 patients. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 2006;101:705-710.
19. Lazzara RJ. Immediate implant placement into extraction sites: surgical and restorative
advantages. Int J Periodontics Restorative Dent. 1989;9:332-343.
20. Novaes AB Jr, Novaes AB. Immediate implants placed into infected sites: a clinical
report. Int J Oral Maxillofac Implants. 1995;10:609-613.
21. Waasdorp JA, Evian CI, Mandracchia M. Immediate placement of implants into infected
sites: a systematic review of the literature. J Periodontol. 2010;81:801-808.
22. Novaes AB Jr, Vidigal Júnior GM, Novaes AB, Grisi MFM, Polloni S, Rosa A. Immediate
implants placed into infected sites: a histomorphometric study in dogs. Int J Oral Maxil-
lofac Implants. 1998;13:422-427.
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Types of Endodontic Lesions: Clinical Considerations

23. Montoya-Salazar V, Castillo-Oyagüe R, Torres-Sánchez C, Lynch CD, Gutiérrez-Pérez JL,
Torres-Lagares D. Outcome of single immediate implants placed in post-extraction
infected and non-infected sites, restored with cemented crowns: a 3-year prospective
study. J Dent. 2014;42:645-652.
24. Pannkuk T. Fracture detection of endo treated teeth with CBCT scan. Clinical Endo.
2009;35:719-722.
25. Berman LH, Kuttler S. Fracture necrosis: diagnosis, prognosis assessment, and treat-
ment recommendations. J Endod. 2010;36:442-446.
26. Gajan EB, Aghazadeh M, Abashov R, Salem Milani A, Moosavi, Z. Microbial flora of root
canals of pulpally-infected teeth: Enterococcus faecalis a prevalent species. J Dent Res
Dent Clin Dent Prospects. 2009;3:24-27.
27. Graves DT, Oates T, Garlet GP. Review of osteoimmunology and the host response in
endodontic and periodontal lesions. J Oral Microbiol. 2011 Jan 17;3.
28. Gomes BP, Pinheiro ET, Gadê-Neto CR, Sousa EL, Ferraz CC, Zaia AA, Teixeira FB, Sou-
za-Filho FJ. Microbiological examination of infected dental root canals. Oral Microbiol
Immunol. 2004;19:71-76.
29. Flores MT, Andersson L, Andreasen JO, Bakland LK, MalmgrenB, Barnett F, Bourguignon
C, DiAngelis A, Hicks L, Sigurdsson A, Trope M, Tsukiboshi M, von Arx T; International
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injuries. I. Fractures and luxations of permanent teeth. Dent Traumatol. 2007;23:66-71.

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 CONTINUING EDUCATION

Types of Endodontic Lesions: Clinical Considerations

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POST EXAMINATION QUESTIONS

1. Infection of the root canal system is the major cause of 4. The diagnosis of “normal pulp” or “reversible pulpitis” indicates
apical periodontitis. that the surrounding bone is not affected. The pulp tissue is
a. True. vital, and the tooth is either asymptomatic or the symptoms are
b. False. not from pulpal pathosis.
a. The first statement is true, the second is false.
2. Endodontic disease progresses in a coronal to apical direction. b. The first statement is false, the second is true.
Apical periodontitis occurs when microbes migrate into the c. Both statements are true.
periapical tissues through the radicular portals of exit. d. Both statements are false.
a. The first statement is true, the second is false.
b. The first statement is false, the second is true. 5. If severe lingering cold sensitivity is present and there is no
c. Both statements are true. sensitivity to heat, the diagnosis is:
d. Both statements are false. a. Reversible pulpitis.
b. Pulpal necrosis.
3. An “implant periodontal lesion” has been described in the litera- c. Irreversible pulpitis.
ture and may be caused by the presence of: d. None of the above.
a. A pre-existing infection.
b. Residual root fragments. 6. Chronic and acute apical periodontitis are biofilm-induced dis-
c. Foreign bodies in the bone. eases that can occur secondary to:
d. All of the above. a. Pulpal necrosis.
b. Complete root fracture.
c. Re-infected root canal therapy.
d. All of the above.

7
 CONTINUING EDUCATION

Types of Endodontic Lesions: Clinical Considerations

7. The asymptomatic (chronic) form of apical periodontitis has
bony destruction secondary to the spread of pulpal infection
to the bone. The symptomatic form is also known as an acute
apical abscess.
a. The first statement is true, the second is false.
b. The first statement is false, the second is true.
c. Both statements are true.
d. Both statements are false.
9. On a periapical radiograph, if a radiolucency is J-shaped and
“balloons” around the root, it is most likely caused by a root
fracture. Often, cupping or a significantly widened PDL space is
also seen.
a. The first statement is true, the second is false.
b. The first statement is false, the second is true.
c. Both statements are true.
d. Both statements are false.

8. Teeth with vertical root fractures are candidates for root canal 10. When diagnosing ankylosis, which of the following signs indi-
therapy, and extraction should be a treatment of last resort. cate ankylosis?
a. True. a. Lack of mobility.
b. False. b. Sharp, solid sound upon percussion.
c. Radiographic absence of a PDL.
d. All of the above.

8
 CONTINUING EDUCATION

Types of Endodontic Lesions: Clinical Considerations

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