Do procedural errors cause endodontic

treatment failure?
LOUIS M. LIN, PAUL A. ROSENBERG and
JARSHEN LIN
J Am Dent Assoc 2005;136;187-193

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 C L I N I C A L P R A C T I C E
Do procedural errors
cause endodontic
treatment failure?
LOUIS M. LIN, B.D.S., D.M.D., Ph.D.; PAUL A.
ROSENBERG, D.D.S.; JARSHEN LIN, B.D.S., D.D.S.
ndodontic periradicular pathosis is the sequela
E of pulpal infection in the root canal system.
The classic study by Kakehashi and
colleagues1 showed that periapical inflamma-
tion developed in conventional laboratory rats
but not in germ-free rats with surgically exposed pulps.
In conventional laboratory rats, oral microorganisms
entered the pulpal cavity and caused inflammation and
necrosis, as well as subsequent peri-
radicular tissue destruction. In germ-
The primary
free rats, even when the canals were
cause of packed with sterile food debris, neither
periradicular pulpal necrosis nor periradicular inflam-
pathosis is mation developed.
In a clinical study, Sundqvist2 showed
bacterial
infection in the that bacteria could be cultured from the
canals of traumatized necrotic teeth
root canal
with intact crowns if periapical lesions
system. were present, but could not be cultured
However, from necrotic teeth if periradicular
procedural lesions were absent. Many studies have
errors impede shown that factors such as pulpal and
endodontic periradicular status, underfilling, over-
filling, root perforations, separated
therapy.
instruments and ledge formation affect
the prognosis for endodontic therapy.
However, only two factorsroot canal infection at the
time of root filling and a preoperative periradicular
lesionhave been shown clearly to have a direct impact
on the outcome of endodontic therapy.3-8
Clinicians generally believe that endodontic pro-
cedural errors, such as underfilling, overfilling, sepa-
rated instruments, root perforations and ledge forma-
tion, are the direct cause of endodontic treatment
Copyright 2005 American Dental Association. All rights reserved.
ABSTRACT
Background. This article reviews the
effect of endodontic procedural
errors, such as underfilling, A D A
J
overfilling, root perfora-
tions and separated
N
CON
instruments, on the out-
IO
come of endodontic
T
T
A
N
I
C
therapy. U
A ING EDU 4
Types of Studies
Reviewed. Filling the root
R TICLE
canal more than 2 millimeters from the
radiographic apex (underfilling) or beyond
the radiographic apex (overfilling), perfora-
tions of the root canal system and instru-
ment separation are possible complications
of endodontic therapy. Although these pro-
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cedural errors may have different causes,
they all may affect the outcome of
treatment.
Results. Endodontic procedural errors
are not the direct cause of treatment
failure; rather, the presence of pathogens in
the incompletely treated or untreated root
canal system is the primary cause of peri-
radicular pathosis. Procedural errors typi-
cally are due to several factors. Among
them is a lack of understanding of the root
canal anatomy, the principles of mechanical
instrumentation and tissue wound healing.
Clinical Implications. Procedural
errors impede endodontic therapy, thus
increasing the risk of treatment failure,
especially in teeth with necrotic pulps and
periradicular lesions. However, procedural
errors often are preventable.
Key Words. Endodontic procedural
errors; bacteria; treatment outcomes.
failure. However, procedural errors by
themselves do not jeopardize the out-
come of treatment unless a concomitant
infection is present. A procedural acci-
dent often impedes therapy or makes it
impossible for therapy to be completed
(for instance, by preventing thorough
mechanical dbridement or a bacteria-
tight seal of the root canal system). An
increased risk of failure exists when a
procedural accident occurs during treat-
JADA, Vol. 136, February 2005 187
C L I N I C A L P R A C T I C E
ment of infected teeth.9 The purpose of this
article is to review critically the effect of pro-
cedural errors on the outcome of endodontic
therapy.
UNDERFILLING OR INCOMPLETE FILLING
OF ROOT CANALS
Underfilling or incomplete filling of the root
canals (more than 2 millimeters short of the
radiographic apex) often occurs as the result of
incomplete instrumentation or ledge formation of
the root canal during mechanical instrumenta-
tion. Incomplete instrumentation commonly is
caused by inaccurate measurement of the
working length or inadequate irrigation and reca-
pitulation of canal patency and working length
during instrumentation, thus leading to the accu-
mulation of dentin filings and canal blockage.
Ledge formation can be caused by the following:
dinadequate straight-line access to the apical
portion of the canal;
dinadequate irrigation, lubrication or both;
dexcessive enlargement of a curved canal with
large files;
dpacking of debris in the apical portion of the
canal;
dskipping of sequential file sizes.10,11
Consequently, the clinician does not remove
the infected necrotic tissue remaining in the
apical portion of the root canal because of incom-
plete instrumentation or ledge formation. In teeth
with necrotic pulp and a periradicular lesion, bac-
teria colonize not only within the apical few mil-
limeters of the canal, but also at the apical
foramen. A key aspect of endodontic treatment is
the elimination of bacteria from the root canal
system.12-14 Unless this is done, persistent bacte-
rial infection in the root canal may initiate or per-
petuate periradicular inflammation after
endodontic therapy.12,13,15
Many studies have shown a poorer prognosis
for teeth with underfillings (68 percent success
rate), especially those with necrotic pulp and a
periradicular lesion, compared with teeth with
flush-fillings (94 percent success rate) and over-
fillings (76 percent success rate).3,4,6 Chugal and
colleagues16 reported that a 1-mm loss in working
length increased the chance of treatment failure
by 14 percent in teeth with apical periodontitis.
However, if the unfilled canal does not contain
irritants, such as bacteria or contaminated
necrotic tissue, underfilling by itself would not
cause periradicular inflammation.
188 JADA, Vol. 136, February 2005
Copyright 2005 American Dental Association. All rights reserved.
From about 1930 to the early 1960s, clinicians
assumed that apical percolation and subsequent
diffusion stasis of tissue fluid or blood compo-
nents in the unfilled canal space could cause per-
sistent periradicular inflammation.17 The so-
called hollow tube concept has been
disproved.18,19 Studies involving polyethylene tube
implants in animals demonstrated clearly that
blood components or tissue fluid stagnating inside
the lumen of the tubes did not induce persistent
inflammation in the tissue at the open ends of the
tubes.18,19 In contrast, if the polyethylene tubes
contained bacteria from the test animals oral
cavity, moderate-to-intense inflammation was
observed at the open ends of the tubes.20
Davis and colleagues21 demonstrated that when
the canals of vital teeth in dogs were instru-
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mented with a no. 80 file to within 1 mm of the
radiographic apex and underfilled by 3 mm, some
underfilled canal spaces became filled with viable
connective tissue that was continuous with the
periodontium one year after endodontic therapy.
Similarly, Benatti and colleagues22 reported that
when the canals of vital teeth in dogs were instru-
mented 2 mm beyond the apical foramen with
nos. 40, 60 or 80 files and underfilled 1 to 3 mm
short of the apex, the unfilled canal spaces exhib-
ited ingrowth of periodontal connective tissue 120
days after endodontic therapy.
de Souza Filho and colleagues23 demonstrated
that when the canals of teeth in dogs with peri-
radicular lesions were instrumented 2 mm
beyond the apical foramen with a no. 60 file and
underfilled by 2 to 3 mm, healing and ingrowth of
connective tissue into the root canal occurred in
67.8 percent of the animals 90 days after
endodontic treatment. This occurred because
intracanal bacteria were eliminated. The authors
believed that cases in which periradicular healing
did not occur were due to persistent root canal
infection resulting from incomplete removal of
bacteria during instrumentation.
Hrsted and Nygaard-stby24 treated patients
with vital teeth that were scheduled for extrac-
tion. They found that when pulps were extirpated
to the apical foramen and the canals were
enlarged up to 2 to 4 mm coronally to the radio-
graphic apex, the canal spaces between the root
canal fillings and the apical foramen were occu-
pied by connective tissue six to 10 months after
endodontic therapy. Several clinical studies also
have shown that if the root canals were com-
pletely dbrided of necrotic tissue and micro-
 C L I N I C A L P R A C T I C E

organisms, the diseased periradicular tissues

were capable of healing even without root canal
fillings, provided that the coronal seal could pre-
vent entry of oral microorganisms into the
canal.25-28 These studies illustrate that root canal
infectionnot unfilled canal spaceis the cause
of periradicular inflammation.1
Studies also have shown that the quality of the
root canal seal influences the prognosis for
endodontic therapy. Adequate seals (that is, com-
plete root canal obturation) have been associated
with a higher success rate than have defective
seals.3,4,6 Sjgren and colleagues6 reported that
adequate root canal seals resulted in higher suc-
cess rates (67 percent) than did inadequate seals
(31 percent) in re-treatment cases. They con- Figure 1. Teeth nos. 30 and 31 underwent endodontic
cluded that bacterial infection in the root canal or

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therapy approximately three years before this radiograph
in the periradicular tissues might be the cause of was obtained. The mesiobuccal and mesiolingual canals
of tooth no. 31 were ledged and underfilled. The mesial
endodontic treatment failure in underfilled or canals of tooth no. 30 also were underfilled. Both teeth
inadequately sealed teeth. were asymptomatic and had no periradicular lesion.
16
Chugal and colleagues reported that in teeth
with a diseased periapex in which the filling den-
sity of the root canal was fair (that is, only a few torily after proper endodontic therapy.6,32,33 The
voids) or poor (many voids), 20 percent more response of the periradicular tissues to root canal
treatment failures occurred than when the filling filling materials depends on the complex interac-
density was better (no voids). Underfilling per se tion between the properties of materials (that is,
does not have a direct effect on the outcome of cytotoxicity, antigeneity and quantity) and the
endodontic therapy; rather, it is the hosts immune defenses (innate and
remaining infected necrotic tissue adapted). Root canal sealers are
in the inadequately instrumented Underfilling per cytotoxic and irritating to the peri-
and incompletely filled canal that se does not have radicular tissues.34-36 Gutta-percha
causes continuing irritation to the may act as a foreign body or hapten,
a direct effect on
periradicular tissues (Figure 1). but it is more biocompatible with
the outcome of the periradicular tissues than are
OVERFILLING OF ROOT endodontic therapy. root canal cements.37-40
CANALS
However, Sjgren and col-
Overfilling of root canals (more leagues41 demonstrated that small
than 2 mm beyond the radiographic apex) often particles of gutta-percha implanted subcuta-
occurs as a result of inflammatory apical root neously in guinea pigs induced intense tissue
resorption, an incompletely formed root apex or reaction, characterized by the presence of
instrumentation through the apical foramen macrophages and giant cells. Other animal ex-
resulting from inaccurate measurement of the periments also showed that excess root filling
working length. In such cases, creating an apical materials extruded into the periradicular tissues
stop becomes more difficult, thus leading to over- were capable of inducing periradicular inflamma-
filling. Numerous clinical studies have shown tion or necrosis of the periodontal ligament.35,42
that overfillings have a negative effect on the It is reasonable to assume that if materials
prognosis for endodontic therapy.3,4,6 These accepted for use in endodontic therapy and
studies indicate that filling materials might act extruded accidentally into the periradicular tis-
as a foreign body, causing irritation of the peri- sues were responsible for treatment failures,
radicular tissues.29-31 almost all teeth overfilled with similar materials
Nevertheless, not all overfilled teeth are would experience failure. However, clinical find-
doomed to treatment failure, because approxi- ings do not appear to completely support the his-
mately 76 percent of overfilled teeth heal satisfac- tologic findings in animal experiments of peri-

JADA, Vol. 136, February 2005 189

Copyright 2005 American Dental Association. All rights reserved.
C L I N I C A L P R A C T I C E
Figure 2. Tooth no. 10 underwent endodontic therapy
more than 10 years before this radiograph was obtained.
The canal was overfilled with silver point. The tooth was
asymptomatic and had no periradicular lesion.
radicular inflammation in all overfilled teeth;
approximately 76 percent of overfilled teeth heal
satisfactorily without clinical signs and/or symp-
toms after proper endodontic therapy.3,4,6,32
Clinically successful endodontic treatment does
not necessarily imply histologic periapical
healing.43-45 Extruded root canal filling materials
may cause localized periradicular inflammation
and a delay in periradicular healing that may not
result in treatment failure, as would be mani-
fested by clinical symptoms or signs or by radio-
graphic evidence of periradicular destruction.43-45
In an endodontic re-treatment study, Bergen-
holtz and colleagues46 reported that root filling
material was not the immediate cause of unsuc-
cessful treatment; rather, treatment failures were
caused by a persistent root canal infection or by
reinfection in the apical area resulting from
overinstrumentation. Halse and Molven33 demon-
strated that apical overfilling per se had little
influence on the healing results of endodontic
therapy, regardless of the preoperative periradic-
ular status. They concluded that treatment fail-
ures were related closely to infection.
Sjgren and colleagues6 also demonstrated that
190 JADA, Vol. 136, February 2005
Copyright 2005 American Dental Association. All rights reserved.
slight overfilling (< 2 mm beyond the radio-
graphic apex) appeared to have no influence on
the treatment outcome, even in teeth with apical
periodontitis. Lin and colleagues47 reported that
although the apical extent of root canal fillings
had no correlation with endodontic treatment
failure, intraradicular infection was a critical
factor.
Overinstrumentation frequently precedes over-
filling, which inevitably poses the risk of forcing
infected root canal contents into the periradicular
tissues, thereby impairing the healing pro-
cess.23,46,48 Endodontic treatment failures asso-
ciated with overfilled teeth usually are caused by
concomitant intraradicular infection, extraradic-
ular infection, or both.9,13
Noiri and colleagues49 used the scanning elec-
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tron microscope to examine extruded gutta-
percha cones retrieved from teeth that had under-
gone failed endodontic treatment. They
demonstrated that biofilms had formed and
attached to the extruded gutta-percha cones.
Therefore, they believed that biofilms were the
cause of persistent periradicular inflammation.
Biofilm is an accumulation of microorganisms
embedded in a self-produced extracellular
polysaccharide matrix, adherent to a solid organic
or inorganic surface.50,51 Biofilms constitute a pro-
tected mode of bacterial growth that enables
organisms to survive in a hostile environment.
Bacteria embedded within biofilms are resistant
to both acquired immunological and nonspecific
antimicrobial defenses, as well as to antimicrobial
therapy.52
Phagocytes are unable to effectively engulf bac-
teria growing within a complex polysaccharide
matrix adhering to a solid surface. Consequently,
biofilms are remarkably resistant to phagocytes.53
Overfilling per se is not as irritating to the peri-
radicular tissues as are intraradicular micro-
organisms (Figure 2). Nonetheless, overfilling is
not encouraged, because the filling material may
cause foreign-body giant cell reaction31 or may act
as a foreign body that supports the formation of
biofilms.51
SEPARATED INSTRUMENTS
Instrument separation or breakage usually is
caused by improper use or overuse of the instru-
ments, as well as by excessive force applied to the
instruments in curved or calcified canals during
instrumentation. A limited number of studies per-
tain to the influence of instrument separation on
 C L I N I C A L P R A C T I C E

the outcome of endodontic therapy. Crump and

Natkin54 analyzed 53 endodontically treated teeth
with separated instruments in the canals. They
found no statistically significant difference in
failure rates between root-filled teeth that had or
had not experienced instrument separation. How-
ever, Frostell55 and Strindberg3 showed that root-
filled teeth in which instruments had separated
experienced failed endodontic treatment 14 per-
cent more frequently than did those in which
instruments had not separated.
Seltzer and colleagues56 reported that peri-
apical repair could occur in endodontically treated
teeth with separated instruments if vital pulps Figure 3. Tooth no. 31 underwent endodontic therapy
approximately two years before this radiograph was
were present in the teeth before therapy. In con- obtained. An instrument was separated in the canal of
trast, instrument separation in root-filled teeth the mesial root. The tooth was asymptomatic and had no
periradicular lesion.
with necrotic pulps resulted in a less favorable

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prognosis.3,4,56-58 If a separated instrument can be
bypassed and incorporated into the root canal
filling, the prognosis for endodontic therapy is
favorable.59,60
Torabinejad and Lemon11 suggested that the
prognosis is best when separation of a large
instrument occurs in the later stages of canal
instrumentation close to the working length. The
prognosis is poor for teeth with undbrided canals
in which a small instrument is separated short of
the apex or beyond the apical foramen early in
instrumentation, because the prognosis depends
on the extent of undbrided infected canal space
apical to the separated instrument.
Strindberg3 cautioned that instruments sepa-
rated in the root canals should be considered a
serious problem, because the practitioner does not
know whether an infection was present apical to
the separated instrument at the time of the acci-
dent. Accordingly, instrument separation is not the
direct cause of endodontic therapy failure; rather,
the separated instrument impedes the mechanical
instrumentation of the infected root canal apical to
the instrument, and that is the primary cause of
treatment failure (Figure 3).
ROOT PERFORATIONS
Root canal walls may become perforated as a
result of iatrogenic causes, resorptive processes or
caries. Iatrogenic perforations often are due to a
lack of attention to the details of the internal
anatomy of the root canal system and a failure to
consider anatomical variations.61 Strip perfora-
tions (that is, perforation of canal walls resulting
from excessive removal of canal dentin) may
result from excessive enlargement of the coronal
Figure 4. Endodontic therapy was performed on tooth
no. 30 approximately three years before this radiograph
was obtained. The mesiobuccal canal was perforated
close to the furcation area and was repaired immediately
with mineral trioxide aggregate. The tooth was
asymptomatic and had no osteolytic lesion at the perfora-
tion site.
third of small curved canals, which has been
described as a danger zone.62 Perforations also
can be caused by an inability to maintain canal
curvature because of ledge formation.
The prognosis for endodontically treated teeth
with root perforations depends on several factors,
such as the time that has elapsed before the den-
tist repairs the defect, the location of the perfora-
tion (its proximity to the gingival sulcus), the ad-
equacy of the perforation seal and the size of the
perforation.61 All of these factors are related
closely to bacterial infection.63-65 Root perforations
often prevent negotiation through the canal, as
well as treatment of the original root canal apical
to the perforations. Although dentists may treat a
root perforation as a lateral canal in vital teeth
with irreversible pulpitis, the often-neglected bac-

JADA, Vol. 136, February 2005 191

Copyright 2005 American Dental Association. All rights reserved.
C L I N I C A L P R A C T I C E
terial contamination still plays an important role
in the prognosis for endodontic therapy.
Therefore, root perforations are not the direct
cause of endodontic treatment failure. Rather, the
primary cause of periradicular inflammation is
the remaining infected tissue in the uninstru-
mented portion of the canal apical to the perfora-
tion (Figure 4).
CONCLUSION
The primary cause of periradicular pathosis is
bacterial infection in the root canal system.1
Without the presence of bacteria, periradicular
inflammation will not develop or persist, unless
cytotoxic filling materials have been forced into
the periradicular tissues.32,35 Endodontic pro-
cedural errors are not the direct cause of treat-
ment failure. Rather, they increase the risk of
failure because of the clinicians inability to elimi-
nate intraradicular microorganisms from the
infected root canals.
Dr. Louis Lin is a professor and director of the Advanced Education
Program in Endodontics, Department of Endodontics, New York Uni-
versity College of Dentistry, 345 E. 24th St., New York, N.Y. 10010,
e-mail lml7@nyu.edu. Address reprint requests to Dr. Lin.
Dr. Rosenberg is a professor and chair, Department of Endodontics,
and associate dean for graduate programs, New York University Col-
lege of Dentistry, New York City.
Dr. Jarshen Lin is an instructor and a director of the predoctoral
endodontic program, Department of Restorative Dentistry and Bioma-
terials Sciences, Harvard School of Dental Medicine, Harvard Univer-
sity, Boston.
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