Endodontic-Periodontal

Lesions

Evidence-Based Multidisciplinary
Clinical Management
Igor Tsesis
Carlos E. Nemcovsky
Joseph Nissan
Eyal Rosen
Editors

123
Endodontic-Periodontal Lesions
Igor Tsesis • Carlos E. Nemcovsky
Joseph Nissan • Eyal Rosen
Editors

Endodontic-Periodontal
Lesions
Evidence-Based Multidisciplinary
Clinical Management
Editors
Igor Tsesis Carlos E. Nemcovsky
Department of Endodontology Department of Periodontology and
School of Dental Medicine Implant Dentistry
Tel Aviv University The Maurice and Gabriela Goldschleger
Tel Aviv School of Dental Medicine
Israel Tel Aviv University
Tel Aviv
Joseph Nissan Israel
Department of Oral- Rehabilitation
School of Dental Medicine Eyal Rosen
Tel Aviv University Department of Endodontology
Tel Aviv School of Dental Medicine
Israel Tel Aviv University
Tel Aviv
Israel

ISBN 978-3-030-10724-6    ISBN 978-3-030-10725-3 (eBook)

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Contents

1 Lesions of Endodontic Periodontal Origin������������������������������������   1

Igor Tsesis, Carlos E. Nemcovsky, Joseph Nissan,
and Eyal Rosen
2 Etiology and Classification of Endodontic-Periodontal
Lesions����������������������������������������������������������������������������������������������   7
Eyal Rosen, Carlos E. Nemcovsky, Joseph Nissan,
and Igor Tsesis
3 Endodontic Considerations in the Management of
Endodontic-Periodontal Lesions���������������������������������������������������� 15
Kenneth J. Frick, Eyal Rosen, and Igor Tsesis
4 Prosthetic Considerations in the Management of
Endodontic-Periodontal Lesions���������������������������������������������������� 53
Joseph Nissan, Roberto Sacco, and Roni Kolerman
5 Endodontic-Periodontal Lesions: Periodontal Aspects���������������� 59
Carlos E. Nemcovsky, José Luis Calvo Guirado,
and Ofer Moses
6 Modern Clinical Procedures in Periodontal
Reconstructive Treatment �������������������������������������������������������������� 87
Carlos E. Nemcovsky and Jose Nart
7 VRF as an Endodontic Periodontal Lesion����������������������������������� 125
Spyros Floratos, Aviad Tamse, and Shlomo Elbahary
8 Treatment Alternatives Following Extraction of
Teeth with Periodontal-Endodontic Lesions���������������������������������� 141
Carlos E. Nemcovsky, Massimo del Fabbro, Ilan Beitlitum,
and Silvio Taschieri
9 Dental Implants Biological Complications:
Tooth Preservation Reevaluated ���������������������������������������������������� 195
Carlos E. Nemcovsky and Eyal Rosen
10 Integration of Clinical Factors and Patient Values
into Clinical Decision-Making in the Management
of Endodontic-­Periodontal Lesions������������������������������������������������ 215
Igor Tsesis, Russell Paul, and Eyal Rosen

v
 Lesions of Endodontic Periodontal
Origin
1
Igor Tsesis, Carlos E. Nemcovsky, Joseph Nissan,
and Eyal Rosen

The association of the degenerative changes in [4] suggested that endodontics is actually “peri-
the pulp tissues and periodontal disease pres- apical periodontics.” However, this term, like
ents a clinical and conceptual dilemma ever many others’ proposed definitions, has not been
since it was first described in the beginning of widely accepted.
the twentieth century by Cahn (1927) [1]. Regardless of the exact definition and
Multiple investigations on that topic were later selected characterization scheme, the etiology
on published. Being one of the earliest pub- of these endodontic-periodontal lesions derives
lished by Simring and Goldberg in 1964 [2], from the etiologies of the associated endodon-
claiming that pulpal and periodontal problems tic and periodontal diseases. The relative parts
are responsible for more than 50% of tooth of the endodontic and of the periodontal associ-
mortality [2, 3]. ated diseases in the ensuing endodontic-peri-
During the following years many possible eti- odontal lesion vary depending on the nature and
ologies, definitions, classifications, and manage- pathogenesis of the endodontic-periodontal
ment alternatives based on different paradigms lesion. It ranges from solitary endodontic
have been proposed. As a consequence, the lesions, in which most, if not the entire etiol-
understanding of this clinical scenario is a matter ogy, is of endodontic origin, to solitary peri-
for ongoing debate. odontal lesion, in which the etiology is of
Due to the close relationship between end- periodontal origin only.
odontic and periodontal diseases, Weine (1972) Root canal space infection is the main etiol-
ogy of apical periodontitis [5]. The advance of
the disease involves inflammatory reaction of the
I. Tsesis (*) · E. Rosen peri-radicular tissues and periodontal ligamental
Department of Endodontology, School of Dental space [6].
Medicine, Tel Aviv University, Tel Aviv, Israel Periodontal disease, on the other hand,
C. E. Nemcovsky involves marginal periodontium and results in the
Department of Periodontology and Implant Dentistry, progressive loss of the supportive tissues [7].
The Maurice and Gabriela School of Dental
While the etiology of both is bacterial, their clini-
Medicine, Tel Aviv University, Tel Aviv, Israel
e-mail: [email protected] cal presentation is different [8–11].
J. Nissan
Endodontic disease initiates with the involve-
Department of Oral Rehabilitation School of ment of dental pulp and clinical signs and symp-
Dental-Medicine, Tel Aviv University, Tel Aviv, Israel toms may include sensitivity to thermal stimuli
Rabin Medical-Center, Belinson Hospital,
Petah-Tikva, Israel

© Springer Nature Switzerland AG 2019 1

I. Tsesis et al. (eds.), Endodontic-Periodontal Lesions, https://doi.org/10.1007/978-3-030-10725-3_1
2 I. Tsesis et al.

and radiographic presentation of damage to the with inflammatory mediators lead to destruction
hard tissue of the tooth such as carries, trauma, or of gingival connective tissue, periodontal liga-
extensive restoration. If not treated, the pulp ment, and alveolar bone [15] (Fig. 1.2).
becomes progressively contaminated and peri-­ The transition of an endodontic disease or of a
radical bone resorption becomes evident radio- periodontal disease into a combined endodontic-­
graphically (Fig. 1.1). This process may remain periodontal disease depends on the anatomical
asymptomatic or result in purulent inflammation, communications between the root canal space
chronic or acute [12]. and of the marginal periodontium.
Infection is the main etiology for periodontal There are multiple routes of communication
disease [13, 14]. Perio-pathogenic bacterial between the root canal space and marginal peri-
plaque together with calculus accumulation on odontium [8, 11, 16–23]. The main root canal
the external root surfaces progress apically lead- opening (apical foramen) is the main pathway
ing to gingival marginal inflammation that may between the infected pulp in periodontal tissues.
progress to deeper supporting periodontal struc- In addition, open dentinal tubuli and lateral
tures. Endotoxins from bacterial plaque together canals may contain bacteria and had been

Fig. 1.1 Second maxillary premolar—the patient pre- periapical area; radiograph immediately after root canal
sented with a sensitivity to percussion: preoperative radio- treatment, resolution of the periapical lesion at the 1 year
graph—extensive coronal restoration and radiolucent follow-up

a b

Fig. 1.2 (a) Anterior mandibular teeth with severe periodontal disease: gingival recession and deep periodontal pock-
ets. (b) Following flap elevation, calculus on root surface with large loss of periodontal support is evident
1 Lesions of Endodontic Periodontal Origin 3

a b

Fig. 1.3 Central maxillary incisor with pulp necrosis and periapical lesion (a). Following root canal filling: lateral
canals communicating between the main root canal and periapical lesion are clearly seen (b)

reported as possible communication routes for ment of the periodontal disease is different, consist-
bacteria [8, 11, 16–23] (Fig. 1.3). In addition, ing on plaque and calculus elimination to render the
various pathological conditions, such as root root surface biocompatible that may be combined
fractures, perforations, resorption, or anatomical with periodontal reconstructive procedures to
anomalies, may present a pathway for the bacte- enhance periodontal support [27] (Fig. 1.4).
ria [24]. By these communications the bacteria The diagnosis of endodontic-periodontal
from the root canal space may contaminate and lesions may be intriguing, since both periodontal
infect the marginal periodontium and vice versa and endodontic diseases have similar clinical and
[2, 5, 10, 15, 25]. radiographic symptoms and may mimic each
The unique etiology and pathogenesis of the other. Moreover, the simultaneous occurrence of
endodontic-periodontal disease dictates the the pulpal and periodontal pathology can compli-
required management plan of these challenging cate diagnosis and treatment and compromise the
clinical cases and the prognosis of the affected prognosis of the involved teeth.
teeth. While in most cases the manifestation of the
The management of the pulpal disease is periodontal and endodontic diseases is clearly
almost exclusively based on the elimination of distinct, there are certain clinical scenarios when
the bacteria from the infected root canal space the signs and symptoms may be confusing, mak-
and reinfection prevention [26]. ing the final diagnosis complicated and
Unlike in endodontic disease, in periodontally ­subsequently result in the wrong treatment choice
affected teeth, bacteria reside on the exposed root [8, 23, 28, 29] (Fig. 1.5).
surfaces in the gingival sulcus and periodontal Misdiagnosis and subsequent wrong treatment
pockets [8, 9, 14, 15, 25]. Accordingly, the manage- choice may ultimately result in tooth extraction
4 I. Tsesis et al.

a b c d

Fig. 1.4 (a, b) Clinical and radiographic (respectively) appreciated in most involved teeth, note large bone fill on
aspect of lower anterior teeth shows generalized loss of distal aspect of lateral left incisor. (d) Radiograph taken
periodontal support, especially on distal aspect of lateral 3 years following periodontal surgical treatment, further
left incisor. (c) Radiograph taken 1 year following recon- enhancement of periodontal support may be appreciated
structive periodontal treatment with use of enamel matrix in most involved teeth
proteins derivative, enhanced periodontal support may be

a b

Fig. 1.5 First maxillary molar: the tooth was diagnosed using a gutta-percha cone (a), peri-radicular bone resorp-
as having a necrotic and infected pulp, chronic apical tion, and advanced periodontal disease (b)
abscess with a sinus tract traced to the disto-buccal root

[28, 30, 31]. Numerous reports in the literature involvement [4]. Besides, all root canal treated
have presented possible options for the diagnosis teeth require some type of coronal restoration,
and treatment of this condition [32]. and in cases of severe damage to the tooth hard
Following treatment of teeth with endodontic-­ tissues, there may be even needs for surgical
periodontal lesions, appropriate restorative plan treatment. In consequence, restoration of teeth
is crucial for the prognosis of the teeth. with endo-perio lesion is challenging due to
Endodontic as well as periodontal pathologies uncertain prognosis while tooth structure preser-
are closely related to the restorative aspects of vation and proper restorative materials and tech-
dentistry. Any restorative procedure may cause niques are essential for long-term success.
some degree of pulp damage, and at the same Permanent restoration, direct or indirect, should
time faulty restoration may result in periodontal be placed as soon as possible after the completion
1 Lesions of Endodontic Periodontal Origin 5

of root canal therapy due to the fact that coronal infections: a molecular approach. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod. 2001;91(4):468–71.
leakage is considered as one of the important fac- 11. Simon JH, Glick DH, Frank AL. The relation-
tors that influence tooth survival during and after ship of endodontic-periodontic lesions. J Endod.
endo-perio treatment. 2013;39(5):e41–6.
From the above mentioned it is clear that the 12. Zanini M, Meyer E, Simon S. Pulp inflammation
diagnosis from clinical to inflammatory mediators: a
topic of endodontic- periodontal lesion is ulti- systematic review. J Endod. 2017;43(7):1033–51.
mately relevant to all areas of dentistry. 13. Genco RJ, Borgnakke WS. Risk factors for periodon-
The comprehensive multidisciplinary approach tal disease. Periodontol. 2013;62(1):59–94.
is of outmost importance in the diagnosis and 14. Haffajee AD, Socransky SS. Microbiology of periodon-
tal diseases: introduction. Periodontol. 2005;38:9–12.
management of the endodontic-­ periodontal 15. Loe H. The role of bacteria in periodontal diseases.
lesions in order to provide the best chance of pro- Bull World Health Organ. 1981;59(6):821–5.
viding an optimal treatment. 16. Arambawatta K, Peiris R, Nanayakkara
A simple and clinically relevant classification D. Morphology of the cemento-enamel junction in
premolar teeth. J Oral Sci. 2009;51(4):623–7.
and appropriate treatment alternatives and con- 17. Bender IB, Seltzer S. The effect of periodontal dis-
siderations together with biological perspectives ease on the pulp. Oral Surg Oral Med Oral Pathol.
of the endodontic periodontal lesions are pre- 1972;33(3):458–74.
sented in the following book chapters. 18. Gautam S, Galgali SR, Sheethal HS, Priya NS. Pulpal
changes associated with advanced periodontal dis-
ease: a histopathological study. J Oral Maxillofac
Pathol. 2017;21(1):58–63.
References 19. Gutmann JL. Prevalence, location, and patency of
accessory canals in the furcation region of permanent
1. Cahn LR. The pathology of pulps found in pyorrhetic molars. J Periodontol. 1978;49(1):21–6.
teeth. Dent Items Int. 1927;49:598–617. 20. Komabayashi T, Nonomura G, Watanabe LG, Marshall
2. Simring M, Goldberg M. The pulpal pocket GWJ, Marshall SJ. Dentin tubule numerical density
approach: retrograde periodontitis. J Periodontol. variations below the CEJ. J Dent. 2008;36(11):953–8.
1964;35:22–48. 21. Ricucci D, Siqueira JF Jr. Fate of the tissue in lateral
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endodontic treatment upon periodontal wound heal- logic conditions and treatment procedures. J Endod.
ing. J Clin Periodontol. 1997;24(7):449–56. 2010;36(1):1–15.
4. Weine F. Endodontic therapy. Saint Luis: Mosby; 22. Simon JH, Glick DH, Frank AL. The relationship
1972. of endodontic-periodontic lesions. J Periodontol.
5. Signoretti FG, Gomes BP, Montagner F, Jacinto 1972;43(4):202–8.
RC. Investigation of cultivable bacteria isolated from 23. Torabinejad M, Trope M. Endodontic and periodontal
longstanding retreatment-resistant lesions of teeth with interrelationships. In: Walton RE, Torabinejad M, edi-
apical periodontitis. J Endod. 2013;39(10):1240–4. tors. Principles and Practice of Endodontics; 1996.
6. Jakovljevic A, Knezevic A, Karalic D, Soldatovic I, 24. Tsesis I, Rosenberg E, Faivishevsky V, Kfir A, Katz
Popovic B, Milasin J, et al. Pro-inflammatory cyto- M, Rosen E. Prevalence and associated periodontal
kine levels in human apical periodontitis: correlation status of teeth with root perforation: a retrospective
with clinical and histological findings. Aust Endod J. study of 2,002 patients’ medical records. J Endod.
2015;41(2):72–7. 2010;36(5):797–800.
7. Ferreira MC, Dias-Pereira AC, Branco-de-Almeida 25. Kurihara H, Kobayashi Y, Francisco IA, Isoshima O,
LS, Martins CC, Paiva SM. Impact of periodon- Nagai A, Murayama Y. A microbiological and immu-
tal disease on quality of life: a systematic review. J nological study of endodontic-periodontic lesions. J
Periodontal Res. 2017;52(4):651–65. Endod. 1995;21(12):617–21.
8. Belk CE, Gutmann JL. Perspectives, controversies 26. Ng YL, Mann V, Gulabivala K. Tooth survival fol-
and directives on pulpal-periodontal relationships. J lowing non-surgical root canal treatment: a sys-
Can Dent Assoc. 1990;56(11):1013–7. tematic review of the literature. Int Endod J.
9. Kerekes K, Olsen I. Similarities in the microfloras of 2010;43(3):171–89.
root canals and deep periodontal pockets. Endod Dent 27. Martin-Cabezas R, Davideau JL, Tenenbaum H,
Traumatol. 1990;6(1):1–5. Huck O. Clinical efficacy of probiotics as an adjunc-
10. Rocas IN, Siqueira JF Jr, Santos KR, Coelho AM. tive therapy to non-surgical periodontal treatment of
“Red complex” (bacteroides forsythus, porphyromo- chronic periodontitis: a systematic review and meta-­
nas gingivalis, and treponema denticola) in endodontic analysis. J Clin Periodontol. 2016;43(6):520–30.
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28. Singh P. Endo-perio dilemma: a brief review. Dent 31. Rosenberg W, Donald A. Evidence based medi-
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 Etiology and Classification
of Endodontic-Periodontal Lesions
2
Eyal Rosen, Carlos E. Nemcovsky, Joseph Nissan,
and Igor Tsesis

2.1 Introduction tributing to a periodontal disease, or preventing

healing of a periodontal disease [2]. Simiring
The periodontium and the dental pulp are and Goldberg [2] also explained that these two
closely associated, sharing embryonic, func- processes generally exist side by side, and may
tional, and anatomical interrelationships. A have the same signs and symptoms. Thus, they
century ago, Turner and Drew [1] described for may be difficult to distinguish [2].
the first time the effect of periodontal diseases The traditional classifications of endodontic-­
on the pulp tissue. Then, in 1964 Simiring and periodontal lesions are usually based on the
Goldberg [2] described a disease of the peri- origin of the infection, i.e., primary endodontic
odontium caused by a pulpal disease, termed lesions, primary periodontal lesions, and differ-
“Retrograde periodontitis.” They stated that ent combinations of the above. However, due to
unlike marginal periodontitis, in which the dis- the interrelationships of these two entities it had
ease proceeds from the gingival margin as the been claimed that these classifications are too
source of infection toward the tooth apex, in academic and theoretical and may not be clini-
“retrograde periodontitis” the pulp is the source cally practical.
of the pathogens affecting the periodontium, This chapter will review the etiological fac-
potentially causing a periodontal disease, con- tors of endodontic-periodontal lesions, the
common classifications of these pathologies,
and will suggest a novel and clinically practi-
cal classification for these intriguing clinical
E. Rosen · I. Tsesis (*) scenarios.
Department of Endodontology, School of Dental
Medicine, Tel Aviv University, Tel Aviv, Israel
C. E. Nemcovsky
Department of Periodontology and Implant Dentistry, 2.2 Pulpal-Periodontal Routes
The Maurice and Gabriela Goldschleger School of of Communication
Dental Medicine, Tel Aviv University,
Tel Aviv, Israel
Although it may seem that the dental pulp and
e-mail: [email protected]
the periodontium are two distinct tissues, there
J. Nissan
Department of Oral-Rehabilitation School of Dental
are many potential routs in which these tissues
Medicine, Tel Aviv University, Tel Aviv, Israel can communicate [3–7], such as the apical fora-
Rabin Medical-Center, Belinson Hospital, men [2, 8]; exposed dentinal tubules [3]; lateral
Petach-Tikva, Israel and accessory canals [4]; certain anatomical

© Springer Nature Switzerland AG 2019 7

I. Tsesis et al. (eds.), Endodontic-Periodontal Lesions, https://doi.org/10.1007/978-3-030-10725-3_2
8 E. Rosen et al.

variations [9, 10]; or pathological conditions 2.3  he Etiology of Endodontic-­

T
such as root perforations and fractures [11, 12]. Periodontal Lesions
The apical foramen is the main route of com-
munication between the pulp and the periodon- Both endodontic and periodontal diseases are
tal tissues. In case of pulp infection, the bacteria multifactorial with many demographic [13, 14],
and their by-products may exit through the api- anatomical [4, 5, 9, 10, 15], genetic [16, 17], sys-
cal foramen causing periapical inflammation. temic [18, 19], behavioral [20, 21], and other
In certain cases, the associated periapical tissue potential contributing factors. However, since
destruction can spread coronally and involve the both endodontic [22] and periodontal diseases
marginal periodontium. On the other hand, in [23] are primarily associated with infection, even
case of severe periodontal disease with deep peri- in the presence of these contributing factors, a
odontal pockets the vice versa may happen [2, 8]. disease will develop mainly in the presence of
Dentinal tubuli are another possible route for infection [22, 23].
the communication between the root canal system In 1965, Kakehashi et al. [24] evaluated the
and periodontium. Between 13,700 and 32,300 pathological changes resulting from untreated
dentinal tubules per square millimeter may be experimental pulp exposures in germ-free rats
present in the cervical dentin [5]. Therefore, peri- as compared with conventional rats with normal
odontal disease and procedures such as scaling oral flora. In the normal rats, pulp necrosis and
and root planning may lead to exposed dentin [3], abscess formation occurred in all specimens. In
and allow the pulp tissue to communicate with contrast, no devitalized pulps or abscesses were
the external root surface and the periodontium. found in the germ-free animals, thus demonstrat-
Lateral and accessory canals can be present ing that bacterial infection is necessary for the
along the root including the cervical areas of development of an endodontic periapical disease
the tooth. Gutmann [4] studied the external root [24]. In accordance, numerous studies have dem-
surface of molars to determine patent accessory onstrated that the basic etiology of periodontal
canals, and reported that accessory canals were diseases is also a bacterial infection [25, 26].
demonstrated in the furcation region in 28% of However, even when the conditions devel-
the teeth. The presence of such patent accessory oped allow the progression of an endodontic-­
canals is a potential pathway for the spread of periodontal disease, for example, following root
bacteria and toxic substances resulting in inflam- perforation or development of root originated
matory process in the periodontal tissues [6]. fracture, it may take time until bacteria colonize
Anatomical variations such as palatogingival the pulpal-periodontal communication site, and
groove [9], a relatively common developmental additional time until an associated pathology
anomaly in maxillary incisors, or the presence develops [27].
of gaps between the enamel and cementum with Traditionally, one of the most intriguing ques-
exposed dentin [10], may provide favorable con- tions has been how endodontic and periodontal
ditions for communication between the periodon- microorganisms link together to form an end-
tal and the pulpal tissues, for plaque retention, odontic-periodontal disease. Zehnder et al. [28]
and for periodontal disease progression toward claimed that although the periodontal pocket
the apical areas of the root that may eventually presents a greater variety of microorganisms than
involve the pulp [9, 10]. the infected pulp, when an endodontic infection
Treatment complications such as root per- is caused by severe periodontitis, all bacterial
forations or root originated fractures open up a species found within the root canals are also pres-
significant communication passage between the ent in the periodontal pocket. These similarities
root canal system and the periodontal tissues. in the microflora of these two niches were also
In case of infection, these complications can reported by Kerekes and Olsen [29], supporting
lead to the formation of endodontic-periodontal the concept that infection may spread from one
lesions [11, 12]. niche to the other.
2 Etiology and Classification of Endodontic-Periodontal Lesions 9

However, other reports suggested that there ferent characteristics of the pathological
are fundamental differences between the micro- process, such as: classifications that were
flora recovered from infected root canals and based on the diagnosis, prognosis, and treat-
from periodontal pockets, perhaps because coc- ment of these lesions [7]; classifications that
cus and rods predominate within infected root were based on pathologic relationship [37]; or
canals while spirochetes and rods predominate classifications that were based on treatment
within periodontal pockets [30, 31]. [38].
Rôças et al. [32] assessed the occur- Simon et al. [7] were the first to suggest a clas-
rence of the so-called “red complex bacteria” sification of endodontic-periodontal lesions that
(Porphyromonas gingivalis, Bacteroides for- was mainly based on diagnosis, prognosis, and
sythus, and Treponema denticola) that may be treatment. This classification included primary
associated with severe periodontal diseases, in endodontic lesions, primary periodontal lesions,
root canal infections. They found that at least one primary endodontic lesions with secondary peri-
member of the red complex was found in 33 of odontal involvement, primary periodontal lesions
50 cases, and concluded that since the “red com- with secondary endodontic involvement, and true
plex” bacteria are known oral pathogens, their combined lesions.
manifestation in root canal infections suggests According to Simon et al. [7], Primary end-
that they may play a role in the pathogenesis of odontic lesions clinically manifest with a pos-
periradicular diseases [32]. sible drainage from the gingival sulcus, swelling
Nevertheless, in recent years as our under- in attached gingiva, and some discomfort. The
standing of the ecology of biofilms improved, necrotic pulp may be associated with a sinus tract
these traditional controversies seem to become extending from the root apex along the root sur-
redundant. Despite the commonly held percep- face, to exit at the cervical line. The radiographic
tion of oral bacteria as solitary surviving micro- examination would usually show bone loss,
organisms, in the different oral niches, bacteria appearing as a radiolucency along the entire root
form complex biofilm communities. These bio- length. Other clinical presentations are also pos-
films are specialized ecological communities, sible such as in multi-rooted teeth, were the sinus
where the bacteria use different mechanisms tract may drain into the bifurcation area with an
to align their activity within the community in associated radiographic appearance of periodon-
order to adopt to the constantly changing envi- tal involvement [39].
ronmental conditions. These adaptations include After some time plaque accumulates at the
dynamic changes in the biofilm species compo- gingival margin which could result in marginal
sitions and proportions within the community periodontitis, and then this primary endodontic
[33–36]. Thus, exposure of a specific biofilm disease may become secondarily involved with
to a different ecological niche, like exposure of periodontal destruction. Simon termed this condi-
endodontic biofilm to the periodontium and vice tion as Primary endodontic lesions with second-
versa, would initiate these adaptation processes, ary periodontal involvement [7, 39]. When this
altering these two communities to align together occurs, both endodontic and periodontal therapy
and to spread from one niche to the other. are required and the tooth prognosis depends
mainly on the success of the periodontal treat-
ment, assuming that the endodontic procedures
2.4 Traditional Classifications are usually more predictable [7, 39].
of Endodontic-Periodontal Simon et al. [7, 39] classified Primary peri-
Lesions odontal lesions as lesions that are caused by a
periodontal disease that gradually progresses
Many classifications were suggested along the along the root surface toward the apical region.
years to describe the versatility of these clini- The diagnosis is based on common periodontal
cal scenarios. Each of these was based on dif- examinations such as probing depth m ­ easurement.
10 E. Rosen et al.

Pulp vitality examination should confirm that the evidence that either disease has influenced the
pulp is vital. Thus, since the pulp in still vital, the other [42].
prognosis in this scenario primarily depends upon Then in 1996 Torabinejad and Trope [38] sug-
the efficacy of the periodontal treatment [7, 39]. gested another classification that was based on
According to Simon et al. [7, 39], as the periodon- the treatment point of view: endodontic origin,
tal pocket progresses toward the apical areas of periodontal origin, combined endo-perio lesions,
the root, lateral canals and eventually the apical separate endodontic and periodontal lesions,
foramen may become exposed to the periodon- lesions with communication, lesions with no
tal microflora which can lead to pulp necrosis. communication.
This condition was termed Primary periodontal Most of these classifications agreed on the pos-
lesions with secondary endodontic involvement sible origins of these lesions as some of these are
[7, 39]. Simon et al. pointed out that diagnosti- of endodontic origin, some are of periodontal ori-
cally, these lesions may cause a dilemma as they gin, and some are different combinations of the
may be indistinguishable from primary endodon- above [7, 37, 38]. However, there are significant
tic lesions with secondary periodontic involve- disagreements among the traditional classifica-
ment. It should be noted that the exact association tion schemes as to how these pathologies should
between the progression of a periodontal disease be further subdivided into additional subgroups as
and its effect on the condition of the dental pulp is the pathology progresses.
a matter of long-lasting debate [40, 41]. However, Accurate diagnosis of the exact nature of the
modern studies reveled that in the presence of lesion is crucial for an effective treatment, and to
a significant chronic periodontal disease, pulp assess the tooth prognosis [8, 43, 44]. Generally,
inflammation and necrosis do occur [41]. when it is a lesion of purely endodontic origin,
According to Simon’s classification [39] True the treatment of choice would be endodontic, and
combined lesions may develop when an endodon- the prognosis would mainly depend on the abil-
tic periapical lesion progresses in a tooth that ity to endodontically treat the disease. When the
is also periodontally involved, until these two lesion is purely of periodontal etiology, a peri-
pathologies merge along the root surface. Again, odontal treatment is the main treatment of choice
this condition may also pose a significant diag- and the feasibility of this periodontal treatment
nostic dilemma as its clinical and radiographic would determine the tooth prognosis. In all other
presentations are indistinguishable from other cases, both endodontic and periodontal treat-
previously mentioned lesion types. From the ments are required and the ability to control and
treatment and prognosis aspects, periapical heal- treat both diseases would determine the tooth
ing is probable following endodontic treatment. prognosis [8, 43, 44].
However, the periodontal disease may or may not In this context, the diagnosis of primary end-
respond to periodontal treatment, depending on odontic lesions without periodontal involvement
the severity of the periodontal disease [39]. and primary periodontal lesions without end-
Following the publication of Simon’s classifi- odontic involvement is usually straightforward
cation, in 1982 Guldener and Langeland [37] sug- and feasible. In primary endodontic lesions, the
gested a new classification that was based on the pulp is non-vital and infected, and on the other
pathologic relationship: endodontic-­ periodontal hand, in a tooth with primary periodontal lesion,
lesion, periodontal-endodontic lesion, and com- the pulp is vital. However, a combined disease
bined lesions. such as primary endodontic lesion with second-
In 1990 Belk and Gutmann [42] suggested to ary periodontal involvement, primary periodontal
add to the previously presented Simons’s clas- disease with secondary endodontic involvement,
sification an additional classification, termed concomitant lesions, or true combined lesions
Concomitant pulpal-periodontal lesion. In this may all radiographically and clinically look
clinical scenario, both endodontic and periodon- alike, especially in advanced stages of the disease
tal diseases coexist in the same tooth, with no [43, 44]. Thus, it seems that from the treatment
2 Etiology and Classification of Endodontic-Periodontal Lesions 11

and prognosis aspects it is not practical to use the odontal disease, it is usually impossible to ini-
traditional categorization schemes. tially assess the contribution of the endodontic
Two major groups of endodontic-periodon- infection to clinical manifestation of this com-
tal lesions may be identified according to the bined disease. On the other hand, the endodon-
etiological origin: pathological endo-perio tic treatment is considered more predictable than
lesions—resulting from the disease of the pulp the periodontal. Thus, it is advised to initially
or periodontium—and iatrogenic endo-perio perform a root canal treatment, and only initial,
lesions—representing a complication of the treat- nonsurgical periodontal procedures such as scal-
ment that results in an artificial communication ing and root planing. Following, it is advised to
between the root canal space and marginal peri- control healing for 3–4 months to monitor resolu-
odontium. Classical example of iatrogenic endo-­ tion of the endodontic infection and its effect on
perio lesion can be iatrogenic root perforation or the tooth periodontal status. Provided endodon-
iatrogenic root fractures. tic improvement, based on the more specific and
Thus, we suggest to use a three-component accurate understanding of the periodontal status
categorization scheme of endodontic-periodontal of the tooth, a comprehensive periodontal treat-
lesions: ment strategy may be planned.
In cases involving teeth with previous end-
1. Purely endodontic lesion: when the pulp is odontic treatment, the diagnosis and classifica-
necrotic and infected, and there is a draining tion can be challenging. In these cases, since
sinus tract coronally through the periodontal pulp vitality tests cannot be performed, it is
ligament into the gingival sulcus. more difficult to clinically assess the condition
2. Purely periodontal lesion: when a deep peri- of the pulp space and its involvement in the dis-
odontal lesion involves most of the root sur- ease. Therefore, in case of a doubt, when it is
face, and the dental pulp is vital. suspected that the root canal treated pulp space
3. Endodontic-periodontal lesion: when the pulp is infected, the cases should be endodontically
is necrotic and infected, and there is a deep retreated.
periodontal pocket.

For lesions of purely endodontic origin, the 2.5 Conclusions

clinical manifestation and the diagnosis is usu-
ally consistent with chronic or acute apical • A close anatomical association between end-
abscess. The proper management of the disease odontic and periodontal tissues may lead to
will include eradication of the bacterial infection spread of the infection between the root canal
by a root canal treatment, and the tooth prognosis and marginal periodontium.
will depend mainly on the efficacy of the end- • Classification of the endodontic-periodontal
odontic treatment. lesions should be based on the primary etio-
Purely periodontal lesions are clinically con- logical factor of the pathology and clinical
sistent with severe periodontal disease, involving presentation as purely endodontic, purely
a great part of the root/s surface. The manage- periodontal or endodontic-periodontal lesions.
ment of these lesions is by periodontal treatment
and there is no need for endodontic treatment.
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 Endodontic Considerations
in the Management of Endodontic-
3
Periodontal Lesions

Kenneth J. Frick, Eyal Rosen, and Igor Tsesis

Objectives multiple health conditions that may influence

1. Understand endodontic diagnosis and how it their oral health, such as diabetes, cardiovascular
relates to periodontal lesions. disease, and cancer. Patients with diabetes melli-
2. Understand the pulpodentinal complex and tus have been associated with increased risk to
how its dynamics can influence the develop- periodontal disease and may also be at greater
ment of endo-perio lesions. risk of developing apical periodontitis [1]. Recent
3. Become familiar with a variety of endo-perio evidence has also been presented suggesting
related lesions and their clinical presentation. patients with periodontal disease may have
delayed healing after endodontic therapy [2]. The
presence of cardiovascular disease, from a clini-
3.1 Endodontic Diagnosis: cal study in Sweden, was found to increase the
Getting to the “Root” odds of having apical periodontitis by a factor of
of the Problem 3.8 [3]. Many patients being treated for cardio-
vascular disease also have hypercholesterolemia
3.1.1 Medical and Dental History and are most likely taking a statin drug. As a
result, they may be at risk of developing pulp
Medical History: The age of the patient and cur- canal obliteration over time [4], which may make
rent medical conditions can influence both the the tooth more susceptible to developing apical
diagnosis and course of treatment. Younger periodontitis. Even cancer, such as lymphomas,
patients often present with good health and are may mimic periodontal and periapical conditions
taking few oral medications that may affect their [5]. So it is important to be aware of these possi-
teeth. However, older patients can present with bilities when assessing the patients’ medical his-
tory and any possible link to their current chief
complaint.
K. J. Frick (*) Dental History: The dental history as reported
Department of Endodontics, University of Missouri, by the patient is a critical element. It is a detailed
Kansas City, MO, USA review of the history of the patient’s chief com-
e-mail: [email protected] plaint and can be a key to the diagnosis, although it
E. Rosen · I. Tsesis is a subjective history, and is influenced by the
Department of Endodontology, patient’s memory and current emotional status or
School of Dental Medicine,
Tel Aviv University, stress level. At times patients are very poor histori-
Tel Aviv, Israel ans of their oral health! Questions to the patient

© Springer Nature Switzerland AG 2019 15

I. Tsesis et al. (eds.), Endodontic-Periodontal Lesions, https://doi.org/10.1007/978-3-030-10725-3_3
16 K. J. Frick et al.

should include: How long has the condition been What is the level of oral hygiene? Is there gen-
present? Does the area feel swollen? What is the eralized gingivitis, perhaps even hyperplastic
pain like? What brings on the pain? Does the pain tissue? This may point to a periodontal verses
linger? What does not affect the pain? Has the con- endodontic assessment; consider the side effect
dition prevented sleep? These questions are of calcium channel blocking agents causing gin-
designed to determine the nature of the problem, as gival hyperplasia [8]. Radiographs should
endodontic symptoms (history of spontaneous include two periapical and one bitewing projec-
pain, lingering pain to cold, pain to biting) usually tion, as it has been shown that radiographs
develop over a period of weeks or months, but peri- exposed from multiple angulations are more
odontal related symptoms (sore gums, bleeding diagnostic [9]. It also may be prudent to con-
gums, foul odor) may linger for months to years. sider a 3D CBCT scan. Depending on the results
Another important question to consider pertains to of the periapical radiographs, CBCT scans may
the possibility of a history of trauma. Were there be indicated, as they are more accurate in reveal-
any events with the patient that may have led to this ing apical pathologies and root morphological
current condition? This last question may be impor- anomalies as compared to 2D periapical images
tant to ask of the younger patients (or their guard- [10, 11]. In reviewing the radiographs, special
ian). Dental trauma, although not the scope of this attention is given to cortical bone height and
chapter, is another possible etiology of gingival and bone loss associated with the roots of the tooth
dental conditions. The reader is referred to the pub- in the area of interest pointed out by the patient,
lications of the International Association of Dental as well as the condition of the root canals. The
Traumatology for further information regarding the clinician must be aware of possible indications
topic of dental trauma [6]. of horizontal or vertical bone defects that may
Another important question to ask as part of suggest periodontal disease and will need to be
the dental history involves previous endodontic probed in the mouth. Other questions the clini-
treatments. Could the current condition be related cian must consider regarding the radiographs
to a recently completed root canal procedure? Or are whether canals are visible in the roots, do
has the patient had root canal therapy years ago, the canals appear calcified, are there areas of
but currently periodontal disease has flared up, resorption, and has the tooth had endodontic
and now an issue has developed around one of therapy, as well as, what is the condition and
these previously treated root canals. In a retro- type of any present restorations. Lastly, what is
spective cohort study, Ruiz et al. has shown that the condition of the PDL space and is it trace-
the risk of developing apical periodontitis in end- able on the radiograph next to the lamina dura?
odontically treated teeth is 5.19 times greater for These are all questions to be considered when
patients with periodontal disease compared to viewing the radiographs.
patients without the disease [7]. Extraoral Exam: The purpose of the extra-
oral exam is twofold. First, it should be done as
an oral cancer screening, checking lymph nodes,
3.1.2 Clinical Exam thyroid gland, and muscles of mastication for
signs of abnormalities and asymmetry; second, as
Radiographs: In order to determine an accurate a means to see any evidence of odontogenic
diagnosis, three areas must be considered: the swelling of the face. Depending on the informa-
history of the problem, current radiographs (and tion derived from the dental history, the clinician
historical ones if available), and a thorough clin- might suspect temporomandibular disease
ical exam. The first part of this, the medical and (TMD) as part of the differential diagnosis, espe-
dental history, was presented above. The next cially if no direct soft tissue or endodontic lesion
step is to obtain radiographs of the affected area is found to explain the chief complaint. TMD has
and complete the clinical exam. Although this is been shown to be one of the most common causes
a problem-focused exam, do not ignore the of non-odontogenic pain that is mistaken for
overall presentation of the patient’s mouth. toothache [12].
3 Endodontic Considerations in the Management of Endodontic-Periodontal Lesions 17

Intraoral Exam: It is during this portion of (PDL), or is it from dentinal sensitivity due to
the examination process that most causes of the caries or a cuspal fracture. Percussion sensitivity
chief complaint will be revealed. Periodontal that is present no matter where the tooth is tapped
probing, palpation, percussion, and sensibility (buccal, occlusal, or lingual) is most probably
testing (Cold test and Electric Pulp Test (EPT)) from an inflamed PDL and apical periodontitis.
of the suspected area will all need to be carefully Isolated areas of percussion sensitivity on the
considered. Most likely the patient will direct same tooth suggest a dentinal issue, such as a
you to the area of concern, but before exploring fracture, caries, or possible occlusal trauma.
that area, the clinician must do an intraoral sweep Endodontic etiologies tend to be more percussion
of the mouth as part of the oral cancer screening sensitive than periodontal ones [14, 15].
process, and to gauge the overall periodontal Sensibility Testing: Testing a tooth’s response
health (and oral hygiene) of the patient. Then, a to cold or heat has often been called vitality test-
periodontal probing survey of the mouth can be ing, but this is actually an inaccurate use of the
done, ending in the suspected problem area. term. Vitality testing measures the level of vascu-
Periodontal Probing: With the completion of larity of a tissue, and is more of a histological
the periodontal probing in multiple areas of the term. Sensibility testing measures the neural
mouth, the clinician should be aware of the gen- response of a tissue, and how the subject
eral periodontal health of the patient. With this responds. The level of the response can be defined
knowledge, careful probing of the affected tooth as the sensitivity of the test. Thus, when a cold or
is completed, paying particular attention to the heat test is conducted on a tooth, the sensibility is
pattern of probing depths around the tooth. A gin- tested, with the level of response being the sensi-
gival abscess of periodontal origin would com- tivity [14]. Endodontically involved teeth that
monly have wide areas of pocketing compared to have not become necrotic will usually have an
those from an endodontic origin, which tend to exaggerated and delayed and/or lingering
be narrower. Harrington published a classic illus- response. The clinician should not be surprised
tration of this in 1979 [13] and a similar illustra- by this response if the patient reported lingering
tion based on it is shown in Fig. 3.1. and spontaneous pain as part of their dental his-
Palpation: Documentation of the sensitivity tory. A negative response to the thermal tests
of the alveolar gingival tissues, both buccal and would indicate a necrotic pulp, especially if it
lingual, is an important part of the examination also tested negative (no response, i.e., 80 reading)
process. Areas of palpation sensitivity and or to an electric pulp test (EPT). The combination of
swelling should be noted and recorded. these negative responses to both tests has a high
Percussion: This test often identifies the sensitivity and specificity in providing an accu-
offending tooth, especially if there is an end- rate diagnosis of pulpal necrosis [16, 17].
odontic component responsible. However, com- Regarding the concept of sensitivity and specific-
plications to this test exist. It is important to ity, terms that are sometimes confusing to the
discern whether the percussion sensitivity is average clinician, consider this simple illustra-
coming from an inflamed periodontal ligament tion as an example. Figure 3.2 shows a photo of a

3 3 9 3 3
a 3 6 9 6 3 b

Fig. 3.1 (a) The probing depths of a wide periodontal pocket. (b) The probing depths of a narrow periodontal pocket
(Illustration courtesy of Molly S Kaz Frick, 2018)
18 K. J. Frick et al.

Fig. 3.2 Sign on door

not intended to be used
as an example of a
specificity test

Fig. 3.3 Routes of

Primary endodontic lesions
endodontic infection
through the apex or
lateral canals of a tooth
(Courtesy Dr. Riley,
UMKC School of
Dentistry)

doorway with two doors. One of the doors is ruled out if the offending tooth responds nor-
marked with a sign that says, “use other door.” So mally to those tests. Figure 3.3 presents an illus-
in this example, if the presence of disease would tration of the typical routes of infection of
be identified by going through the correct door, endodontic lesion, such as from apical foramina
the sign on the door identifying where you should or lateral and furcal canals.
not go, i.e., no disease, would be the specificity
test. If instead, however, a sign was on the door
intended to be opened said “use this door,” that 3.1.3  ndodontic Only or
E
sign would be the sensitivity test. So sensitivity Periodontic Only Lesions
are tests that identify a condition, response, or
disease, and specificity tests identify the lack of In this next section several cases representing
the presence of a condition, response, or disease. either only endodontic or only periodontic lesions
Results of sensibility tests are a critical ele- are shown. Figure 3.4 shows an example of a
ment in determining whether the diseased condi- purely endodontic in orgin lesion. Figures 3.5,
tion of the tooth is periodontal or endodontic 3.6, and 3.7 show an example of a case that tested
origin. An etiology of endodontic origin is easily normal to pulp testing and was diagnosed as a
3 Endodontic Considerations in the Management of Endodontic-Periodontal Lesions 19

a b

Fig. 3.4 (a) shows tooth #31, initially referred to a perio- Sensibility testing revealed no responses from both cold
dontist for treatment of a periodontal abscess. Deep pock- and EPT. A diagnosis of pulpal necrosis and chronic api-
eting (9 mm +) was found on the buccal furcation, but all cal abscess were made and the tooth was treated endodon-
other areas around the tooth had normal probings (3 mm tically. (b) shows osseous healing 9 months after
or less). The patient was not in pain but had some minor endodontic treatment and restoration with a crown
buccal swelling of the gingival tissue near the furcation. (Radiographs courtesy Dr. Stephanie Mullins)

tion of the pulp is not always accurately predict-

able, as discussed in Seltzer and Bender’s classic
paper [18]. The terminology used at the time of
Seltzer’s paper included terms such hyperemia,
acute serous pulpitis, and acute suppurative pul-
pitis, and it were these diagnostic terms that were
not correlated to the histological status of the
tooth in their paper. The study at the time called
into question the accuracy of pulpal sensibility
Fig. 3.5 Clinical photograph of symptomatic gingival testing for diagnostic purposes. However, the
abscess buccal to tooth #19. Note the swelling on the validity of clinical sensibility testing has been
lower right side as indicated by the arrow. Gentle palpa-
tion of the swelling was sensitive and produced suppura- more recently demonstrated. In an evaluation of
tion from a broad 6 mm pocket, mesial buccal and 150 patients receiving endodontic therapy,
midbuccal areas of the tooth. Subgingival calculus was Weisleder et al. compared the clinical ability of
clinically detectable. Sensibility testing with cold was cold and electric pulp testing (EPT) to predict
normal (responded, no lingering) on this and all control
teeth (Image courtesy Dr. Rex Livingston, UMKC School tooth vitality or necrosis via direct observation of
of Dentistry) the status of the pulp after initiation of endodon-
tic therapy. Ninety-seven percent of the teeth
periodontal abscess. Another case illustrating this responding positively to both cold and EPT were
is shown in Fig. 3.8, where the patient was ini- found to be vital, and 90 percent of the teeth
tially referred for endodontic therapy on tooth responding negatively to both were found to be
#14 due to chewing pain and buccal swelling. necrotic [17]. In another study, Ricucci et al.
Pulp sensibility tests indicated the tooth was evaluated 95 human extracted teeth and com-
vital, so periodontal therapy with osseous surgery pared their clinical diagnosis to the histological
and grafting was completed. presentation of the tooth. Using current American
Regarding sensibility testing, it is important to Board of Endodontics terminology of normal
note, however, that the actual histological condi- pulp, reversible pulpitis, and irreversible pulpitis,