Complications










12
Complications
The identication and management of complications
are integral skills for any practicing endodontist. Fur-
thermore, the importance of treatment complications
in the American Board of Endodontics (ABE) examina-
tion process cannot be overemphasized as discussion
of complications comprises one-tenth of the oral exam-
ination. Complications can range in severity from nui-
sances requiring a few extra minutes for management to
life-threatening emergencies requiring immediate medi-
cal care. In addition, complications may not affect treat-
ment prognosis or may result in the need for extraction
of an otherwise viable tooth. This chapter discusses
both intraoperative and postoperative complications.

222
Complications
12
Intratreatment Complications
Instrument separation
Instrument separation is a commonly reported complication in endodontic therapy that all
clinicians will likely encounter at some point in their careers. Though the majority of the
published literature focuses on le separations, other instruments, including burs, ultra-
sonic tips, and passively used intracanal instruments like spreaders and lentulo spirals can
separate. The introduction of nickel titanium (NiTi) instruments has increased the incidence
of instrument separation. In a retrospective clinical study of nearly 5,000 cases treated
by residents over 4 years, Iqbal et al reported a 0.25% incidence of stainless steel hand
instrument separation compared with a 1.68% incidence of NiTi rotary instrument separa-
tion (Fig 12-1). In other words, rotary instruments were seven times more likely to separate
than hand instruments. Separation was most commonly reported in the apical one-third of
canal spaces. Torque control motors and clinician experience did not affect the likelihood
of instrument separation in Iqbal et al’s study. Although Iqbal et al found that certain instru-
ments in the ProTaper system [Dentsply] were more likely to fracture than other systems,
Ankrum et al reported no difference in the likelihood of instrument separation among in-
strument systems studied, including Protaper, K3 [Kerr], and ProFile [Dentsply].
NiTi rotary instruments
1.68% incidence of
instrument separation
SS hand instruments
0.25% incidence of
instrument separation
Fig 12-1 Instrument type as a risk factor for instrument separation (Iqbal et al).
SS, stainless steel.
Both Crump and Natkin’s study on stainless steel instruments and Spili et al’s study on
NiTi instruments found that separated instruments had no statistically signicant effect on
the prognosis. However, both authors argued that the stage of treatment when the instru-
ment separation occurs, the preoperative diagnosis, and the ability to remove or bypass
the instrument fragment may inuence outcomes based on clinical empiricism. Essentially,
they suggested that greater bacterial contamination caused by the inability to disinfect the
canal space as a result of the retained instrument fragment might result in a less favorable
prognosis. A retrospective clinical study by Fu et al found that the adequacy of the root
canal lling surrounding an instrument fragment did affect prognosis following instrument
separation. Fu et al also noted a trend toward better healing in the absence of perforations
created during attempts at instrument removal. Figure 12-2 depicts the potential factors
that might affect prognosis following instrument separation.

223
Intratreatment Complications
Fig 12-2 Potential factors affecting prognosis following instrument
separation.
Adequacy of obturation following separation
Ability to bypass or remove instrument
fragment
Timing of incident
Preoperative diagnosis
Presence of perforations created during attempts
to remove instrument fragment
Orthograde
removal of
separated
fragment
Bypass
separated
fragment
Retrograde
removal or
entombment
of separated
fragment
Leave in
place and
monitor
Fig 12-3 Options for management of separated instruments (Madarati et al).
Madarati et al reviewed techniques for management of separated instrument fragments
(Fig 12-3) with the primary goal being instrument removal via a variety of techniques, most
notably ultrasonic instrumentation. If instrument fragments cannot be removed using tradi-
tional orthograde techniques, options remain to bypass the instrument, leave it in place, or
approach its removal or entombment surgically. Figure 12-4 depicts examples of different
management techniques.

224
Complications
12
Visualization with the surgical operating microscope offers an obvious advantage when
managing an instrument separation. In a clinical study, Suter et al
found that 87% of sepa-
rated instruments could be removed, and all cases of removal involved the use of a surgical
operating microscope. In the future, they predict that laser irradiation or electrochemical
dissolution techniques may be developed to remove separated instruments. Ultimately,
the primary goal should be to use caution during instrumentation to prevent separation
complications altogether.
a
c
e
b
d
f
Fig 12-4 Examples of management of separated instruments. (a and b) A lentulo spiral
was successfully bypassed. (c and d) A NiTi instrument was addressed surgically. (e and
f) A NiTi instrument was left in place.

225
Intratreatment Complications
Perforations
Iatrogenic perforations are a common complication during endodontic therapy, and recent
advances in endodontics have markedly improved clinicians’ management abilities. En-
dodontists must acknowledge that patients may arrive in their ofce with teeth that have
been previously perforated and should be prepared to diagnose and manage perforations
that occurred prior to their intervention. Signs of prior perforations, including bone loss
adjacent to the perforation site, can be recognized preoperatively, particularly with the use
of cone beam computed tomography (CBCT) imaging (Shemesh et al). For this reason,
new radiographs are always advised during treatment consultations, particularly in a pre-
viously accessed tooth. Noniatrogenic perforations due to caries or resorption are further
complicated by their respective causative pathology and contamination, and the following
recommendations may not necessarily apply in those instances.
Iatrogenic perforations can be recognized clinically by active bleeding into the canal
space, or radiographically, by close proximity of the preparation to the radicular border or
extraradicular instrument placement (Fuss and Trope). Fuss et al suggested using an elec-
tronic apex locator in the early intratreatment identication of perforations.
Early recognition and repair are keys to successful outcomes when treating perforations.
Fuss and Trope reported that size, location, and time of repair signicantly impact the prog-
nosis, as small intrabony perforations that are sealed immediately have a generally positive
prognosis. Mente et al reported that provider experience and post placement following per-
foration repair may also play a role. Seltzer et al (1970) cited both the clinician’s ability to
seal the defect and any prior microbial contamination as potential prognostic factors. These
authors described failures following unrepaired perforation due to epithelial downgrowth
and periodontal involvement followed by adjacent bone loss. Figure 12-5 summarizes the
potential factors that affect prognosis following a perforation repair. Figure 12-6 illustrates
the pathogenesis of failure for unrepaired perforations. Figure 12-7 presents an example of
failure secondary to perforation by off-angle placement of a post.
Fig 12-5 Potential prognostic factors following perforation
and repair.
Perforation location
Perforation size
Time to repair
Provider experience
Post placement following repair
Ability of clinician to seal defect
Prior microbial contamination

226
Complications
12
The development and implementation of mineral trioxide aggregate (MTA) as a repair
material has signicantly impacted practitioners’ abilities to treat iatrogenic perforations.
Early on, Lee et al (1993) recommended MTA for lateral root repairs, and Pitt Ford et al
found it effective for furcal perforation repairs. Since then, MTA has become the gold stan-
dard material in perforation repair due to its positive impact on histologic repair and treat-
ment success rates. Pitt Ford et al described cementum formation beneath MTA followed
by reformation of the periodontal ligament and normal bony architecture. These results
have been replicated by several studies in various applications of MTA use. According to
Mente et al,
the success rate of MTA perforation repair with a minimum of a 1-year follow-
up was approximately 86%. Such positive outcomes are likely related to MTAs biocompati-
bility and superior ability to seal defects. An example of a perforation successfully repaired
with MTA is shown in Fig 12-8. Further information about MTA can be found in chapter 8.
Fig 12-6 Pathogenesis of failure of unrepaired perforations
(Seltzer et al 1970).
Epithelial
downgrowth
Bacterial
contamination
Periodontal
involvement
Adjacent
bone loss
Fig 12-7 Periodontal
involvement second-
ary to a post perfora-
tion in the mesial root
of a mandibular molar.

227
Intratreatment Complications
Despite both excellent biocompatibility and positive outcomes, MTA has the limitation
of a long setting time. Consequently, in areas of heavy saliva exposure, such as adjacent to
the gingival sulcus, alternative materials have been suggested to prevent washout. Dragoo
recommended glass ionomers as an alternative to MTA for sulcular perforations. Figure
12-9 illustrates the recommended materials for management of perforations.
Fig 12-8 (a and b) Furcal perforation suc-
cessfully repaired with MTA. (c) Successful
healing was noted at a 6-month follow-up.
a b
c
Fig 12-9 Material recommendations for perforation repair.
Sulcular perforations
Glass-ionomer repair
Radicular perforations
MTA repair

228
Complications
12
Sodium hypochlorite accident
Sodium hypochlorite is an effective antimicrobial and efciently dissolves both vital and ne-
crotic tissue. As a result of its ability to dissolve tissue combined with its causticity, it poses
a risk to patients when expressed into the periapical tissues. A sodium hypochlorite acci-
dent can occur when the irrigant solution is injected beyond the apical foramen, resulting
in tissue necrosis. Sodium hypochlorite accidents are often associated with open apices or
extreme pressure during irrigation. Hulsmann and Hahn reviewed common symptoms as-
sociated with sodium hypochlorite accidents, including immediate severe pain, immediate
edema of the neighboring soft tissue with possible extension through the fascial planes,
profuse intracanal bleeding, ecchymosis, and possible taste of bleach and irritation if the
solution was injected into the maxillary sinus. Delayed ndings can include secondary in-
fection and either anesthesia or paresthesia. Vital signs can be compromised by the rapid
swelling associated with a sodium hypochlorite accident, and immediate, emergent medi-
cal attention should be sought if there are any signs of vital sign compromise. Figure 12-10
summarizes the clinical signs associated with a sodium hypochlorite accident.
Fig 12-10 Potential clinical signs of a sodium hypochlorite accident (Hulsmann and Hahn).
Secondary
infection
Paresthesia
Ecchymosis
Bad taste
and irritation
if involving
sinus
Profuse
intracanal
bleeding
Immediate
edema
Immediate
severe pain
Several case reports have been presented in the endodontic literature illustrating the po-
tential outcomes of a sodium hypochlorite accident. Sabala and Powell presented a case
involving severe immediate pain, dramatic swelling, bleeding, and ecchymosis due to inter-
stitial bleeding. Reeh and Messer described a case with a similar immediate course, in addi-
tion to postoperative infection and paresthesia lasting 15 months following the initial sodium
hypochlorite accident. Matthews and Merrill presented a case of chronic neuropathic pain
and long-lasting paresthesia 7 months following a sodium hypochlorite accident.
Several authors have described appropriate treatment regimens to address a sodium hy-
pochlorite accident (Fig 12-11). Hulsmann and Hahn recommended palliative care, including
pain control via local anesthesia and analgesics as well as initial use of cold compresses for
24 hours followed by warm compresses afterward to stimulate local circulation. They recom-
mended daily monitoring for improvement. Antibiotics are only recommended with evidence
of secondary infection or prophylactically in high-risk cases. The use of corticosteroids is con-
troversial. Any further endodontic treatment should use alternative irrigants, such as saline
or chlorhexidine.

229
Intratreatment Complications
Extrusion of materials beyond the apex
As the root canal space is continuous with the periapical tissues, the risk of overextension
of medicament or obturation material is inherent to endodontic therapy and increases in
the absence of adequate length control or in cases of open or wide apices. Although over-
extension of material can theoretically cause a foreign body reaction no matter its location,
extension into important anatomical spaces including the maxillary sinus, mental foramen,
and mandibular canal are generally considered most risky.
Calcium hydroxide (CH) is a common intracanal medicament, and though it is generally
considered safe, there are several reported cases of its overextension causing complica-
tions. Generally, extension of CH into the periapical tissues in noncritical areas does not
cause lasting defects. Although they do not advocate deliberate delivery of CH to the
periapical spaces, De Moor and De Witte presented 11 cases with CH extrusion that did
not negatively impact healing or prognosis. Similarly, a case report by Fava found no pain
or pathology resulting from extrusion of CH into the maxillary sinus following endodontic
therapy on a maxillary premolar. Figure 12-12 shows an example of CH extrusion associat-
ed with clinical healing in a case of chronic apical abscess with a sinus tract and periodon-
tal-endodontic lesion. Conversely, Lindgren et al presented a case of hemifacial ischemia
and necrosis following extrusion of CH into the mandibular canal and the surrounding cap-
illary bed of the face, palate, and ear. Similarly, Ahlgren et al presented a case of lower lip
paresthesia due to extrusion of CH into the mandibular canal. Following surgical excision
of the material and reactionary material, the paresthesia resolved.
Pain control (local anesthesia and analgesia)
Initial cold compresses; warm compresses after 24 hours
Antibiotics if signs of infection
Emergency medical referral if vital signs compromised
Fig 12-11 Suggested management protocol for a sodium hypochlorite accident (Huls-
mann and Hahn).
Fig 12-12 CH extruded into a periodontal-endodontic lesion at time of pulpectomy
associated with clinical closure of prior sinus tract and periodontal pocket. Radio-
graphs taken at time of cone t (a) and postobturation (b).
a b

230
Complications
12
Overextension of obturation materials is an area of controversy in endodontics. Schilder
advocated the classic “sealer puff” for all root canal lls (Fig 12-13). This assumes that a
slight extrusion of endodontic sealer will not result in pathology. Augsburger and Peters
supported this claim when they found that eugenol-based sealers were resorbed over time.
In an animal study, Kawakami et al injected Vista-Cal [Vista Dental], a sealer consisting of
CH, iodoform, and silicone oil, into the mandibular canal and found that macrophages
phagocytosed the material, leading to time-dependent resorption. On the other hand,
Seltzer et al (1973) showed that extrusion of obturation material beyond the apex caused a
foreign body reaction, and Sjogren et al (1995, 1998) found chronic inammation and bone
resorption resulting from tissue exposure to gutta-percha (GP).
Fig 12-13 (a and b) “Puffs” of sealer are a common, usually nonpathologic occur-
rence following root canal therapy.
a b
Though controversy exists regarding overextension of obturation material into the
periapical tissues, the proximity of root apices to critical anatomical structures can make
overextension problematic. Knowles et al demonstrated that the apices of the mandibular
molars and premolars lie in close proximity to the mental foramen and mandibular nerve.
Overextension of material out of the apices of posterior mandibular teeth can put these
structures at risk. Gluskin cited possible mechanical, compression, and chemical injuries to
the mandibular nerve as potential complicating factors in overextension. Rowe reported
that extrusion of sealer into the mandibular canal could cause paresthesia due to either
direct pressure of the material on the neurovascular bundle or neurotoxicity. Tilotta-Yasu-
kawa et al presented a case series showing a correlation between proximity of obturation
materials and the mandibular canal with an increased likelihood of paresthesias.
The composition of the extruded material plays a role in the severity of any foreign body
reaction. As discussed earlier, GP can be cytotoxic, but root canal sealers are generally
considered to be the more noxious agents. Pascon, Langeland, et al reported that all sealer
materials are inherently cytotoxic in their freshly mixed state. Kozam demonstrated signif-
icant neurotoxic effects of eugenol on the sciatic nerves of bullfrogs. Presumably, similar
neurotoxicity might occur if eugenol-based sealers contact the mandibular nerve. Tamse
et al presented two cases of paresthesias following extrusion of an AH 26 [Dentsply] sealer
into the mandibular canal. Kleier and Averbach presented a case of painful dysesthesia
following extrusion of a paraformaldehyde N2-type paste into the mandibular canal.

231
Intratreatment Complications
Just as mandibular overextensions have been associated with the development of pa-
thology, so have maxillary extrusions. The proximity of the apices of the maxillary molars
to the maxillary sinus can increase the risk for development of sinus pathology. In a CBCT
study, Pagin et al showed that 22% of maxillary posterior teeth were located in close prox-
imity to the maxillary sinus, with 14% of root apices protruding into the sinus. Similarly,
Rigolone et al found that 25% of maxillary sinuses extend between the buccal and palatal
roots of maxillary molars, again based on CBCT imaging studies. Giardino et al reported
a case of Aspergillus infection in the maxillary sinus following extrusion of a zinc oxide–
eugenol sealer beyond the apex of an endodontically treated maxillary molar, presumably
related to the zinc requirement for Aspergillus metabolism. Kaplowitz presented a case of
chronic maxillary sinusitis following overextension of a GP ll in the palatal root of a maxil-
lary molar. Paraformaldehyde-containing sealers, though no longer commercially available,
are known cytotoxins. Orlay presented a case of severe pain following overextension of an
N2-type paraformaldehyde-containing sealer into the maxillary sinus.
Above all, the development of signs or symptoms of pathology, including sinusitis when
foreign materials reach the maxillary sinus or paresthesias or dysesthesias when materials
reach the mandibular nerve, should be recognized and managed or referred for proper
treatment when appropriate. Particularly in cases of nerve injury, time is of the essence.
Pogrel reported that microsurgical treatment of mandibular nerve injuries should occur
within 48 hours of the injury for maximal success.
Thermal injury
Thermal injuries to the periodontium can result from a multitude of heat-producing instruments
used during endodontic therapy. Devices—including ultrasonic and high- and slow-speed
handpieces, obturation aids including down-packing systems, and thermoplasticized GP deliv-
ery systems—create signicant amounts of heat that can traumatize living structures. In order to
prevent injury to the periodontal ligament, Eriksson and Albrektsson showed that root surface
temperatures should not increase more than 10°C (Fig 12-14). Floren et al showed that main-
taining the System B endodontic ll device [Kerr] at less than 250°C prevented said increases.
According to Lee et al (1998), the Touch ‘n Heat 5400 [Kerr] and ame-heated methods of
down-packing GP for vertical condensation provided limited temperature control and could
therefore involve root surface temperature increases of more than 10°C; this makes them less
desirable as obturation aids. Based on a clinical study on dogs, Gutmann et al reported that
thermoplasticized GP was safe in terms of its effects on the periodontium, with very little risk of
soft tissue thermal injury.
10°C increase in root surface temperature
Injury to periodontium
Fig 12-14 Threshold for thermal injury (Eriksson and Albrektsson).

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12ComplicationsThe identication and management of complications are integral skills for any practicing endodontist. Fur-thermore, the importance of treatment complications in the American Board of Endodontics (ABE) examina-tion process cannot be overemphasized as discussion of complications comprises one-tenth of the oral exam-ination. Complications can range in severity from nui-sances requiring a few extra minutes for management to life-threatening emergencies requiring immediate medi-cal care. In addition, complications may not affect treat-ment prognosis or may result in the need for extraction of an otherwise viable tooth. This chapter discusses both intraoperative and postoperative complications. 222Complications12Intratreatment ComplicationsInstrument separationInstrument separation is a commonly reported complication in endodontic therapy that all clinicians will likely encounter at some point in their careers. Though the majority of the published literature focuses on le separations, other instruments, including burs, ultra-sonic tips, and passively used intracanal instruments like spreaders and lentulo spirals can separate. The introduction of nickel titanium (NiTi) instruments has increased the incidence of instrument separation. In a retrospective clinical study of nearly 5,000 cases treated by residents over 4 years, Iqbal et al reported a 0.25% incidence of stainless steel hand instrument separation compared with a 1.68% incidence of NiTi rotary instrument separa-tion (Fig 12-1). In other words, rotary instruments were seven times more likely to separate than hand instruments. Separation was most commonly reported in the apical one-third of canal spaces. Torque control motors and clinician experience did not affect the likelihood of instrument separation in Iqbal et al’s study. Although Iqbal et al found that certain instru-ments in the ProTaper system [Dentsply] were more likely to fracture than other systems, Ankrum et al reported no difference in the likelihood of instrument separation among in-strument systems studied, including Protaper, K3 [Kerr], and ProFile [Dentsply]. NiTi rotary instruments1.68% incidence of instrument separationSS hand instruments0.25% incidence of instrument separationFig 12-1 Instrument type as a risk factor for instrument separation (Iqbal et al). SS, stainless steel.Both Crump and Natkin’s study on stainless steel instruments and Spili et al’s study on NiTi instruments found that separated instruments had no statistically signicant effect on the prognosis. However, both authors argued that the stage of treatment when the instru-ment separation occurs, the preoperative diagnosis, and the ability to remove or bypass the instrument fragment may inuence outcomes based on clinical empiricism. Essentially, they suggested that greater bacterial contamination caused by the inability to disinfect the canal space as a result of the retained instrument fragment might result in a less favorable prognosis. A retrospective clinical study by Fu et al found that the adequacy of the root canal lling surrounding an instrument fragment did affect prognosis following instrument separation. Fu et al also noted a trend toward better healing in the absence of perforations created during attempts at instrument removal. Figure 12-2 depicts the potential factors that might affect prognosis following instrument separation. 223Intratreatment ComplicationsFig 12-2 Potential factors affecting prognosis following instrument separation. Adequacy of obturation following separationAbility to bypass or remove instrument fragmentTiming of incidentPreoperative diagnosisPresence of perforations created during attempts to remove instrument fragment Orthograde removal of separated fragmentBypass separated fragmentRetrograde removal or entombment of separated fragmentLeave in place and monitorFig 12-3 Options for management of separated instruments (Madarati et al).Madarati et al reviewed techniques for management of separated instrument fragments (Fig 12-3) with the primary goal being instrument removal via a variety of techniques, most notably ultrasonic instrumentation. If instrument fragments cannot be removed using tradi-tional orthograde techniques, options remain to bypass the instrument, leave it in place, or approach its removal or entombment surgically. Figure 12-4 depicts examples of different management techniques. 224Complications12Visualization with the surgical operating microscope offers an obvious advantage when managing an instrument separation. In a clinical study, Suter et al found that 87% of sepa-rated instruments could be removed, and all cases of removal involved the use of a surgical operating microscope. In the future, they predict that laser irradiation or electrochemical dissolution techniques may be developed to remove separated instruments. Ultimately, the primary goal should be to use caution during instrumentation to prevent separation complications altogether. acebdfFig 12-4 Examples of management of separated instruments. (a and b) A lentulo spiral was successfully bypassed. (c and d) A NiTi instrument was addressed surgically. (e and f) A NiTi instrument was left in place. 225Intratreatment ComplicationsPerforationsIatrogenic perforations are a common complication during endodontic therapy, and recent advances in endodontics have markedly improved clinicians’ management abilities. En-dodontists must acknowledge that patients may arrive in their ofce with teeth that have been previously perforated and should be prepared to diagnose and manage perforations that occurred prior to their intervention. Signs of prior perforations, including bone loss adjacent to the perforation site, can be recognized preoperatively, particularly with the use of cone beam computed tomography (CBCT) imaging (Shemesh et al). For this reason, new radiographs are always advised during treatment consultations, particularly in a pre-viously accessed tooth. Noniatrogenic perforations due to caries or resorption are further complicated by their respective causative pathology and contamination, and the following recommendations may not necessarily apply in those instances. Iatrogenic perforations can be recognized clinically by active bleeding into the canal space, or radiographically, by close proximity of the preparation to the radicular border or extraradicular instrument placement (Fuss and Trope). Fuss et al suggested using an elec-tronic apex locator in the early intratreatment identication of perforations. Early recognition and repair are keys to successful outcomes when treating perforations. Fuss and Trope reported that size, location, and time of repair signicantly impact the prog-nosis, as small intrabony perforations that are sealed immediately have a generally positive prognosis. Mente et al reported that provider experience and post placement following per-foration repair may also play a role. Seltzer et al (1970) cited both the clinician’s ability to seal the defect and any prior microbial contamination as potential prognostic factors. These authors described failures following unrepaired perforation due to epithelial downgrowth and periodontal involvement followed by adjacent bone loss. Figure 12-5 summarizes the potential factors that affect prognosis following a perforation repair. Figure 12-6 illustrates the pathogenesis of failure for unrepaired perforations. Figure 12-7 presents an example of failure secondary to perforation by off-angle placement of a post. Fig 12-5 Potential prognostic factors following perforation and repair. Perforation locationPerforation sizeTime to repairProvider experiencePost placement following repairAbility of clinician to seal defectPrior microbial contamination 226Complications12The development and implementation of mineral trioxide aggregate (MTA) as a repair material has signicantly impacted practitioners’ abilities to treat iatrogenic perforations. Early on, Lee et al (1993) recommended MTA for lateral root repairs, and Pitt Ford et al found it effective for furcal perforation repairs. Since then, MTA has become the gold stan-dard material in perforation repair due to its positive impact on histologic repair and treat-ment success rates. Pitt Ford et al described cementum formation beneath MTA followed by reformation of the periodontal ligament and normal bony architecture. These results have been replicated by several studies in various applications of MTA use. According to Mente et al, the success rate of MTA perforation repair with a minimum of a 1-year follow- up was approximately 86%. Such positive outcomes are likely related to MTA’s biocompati-bility and superior ability to seal defects. An example of a perforation successfully repaired with MTA is shown in Fig 12-8. Further information about MTA can be found in chapter 8. Fig 12-6 Pathogenesis of failure of unrepaired perforations (Seltzer et al 1970).Epithelial downgrowthBacterial contaminationPeriodontal involvementAdjacent bone lossFig 12-7 Periodontal involvement second-ary to a post perfora-tion in the mesial root of a mandibular molar. 227Intratreatment ComplicationsDespite both excellent biocompatibility and positive outcomes, MTA has the limitation of a long setting time. Consequently, in areas of heavy saliva exposure, such as adjacent to the gingival sulcus, alternative materials have been suggested to prevent washout. Dragoo recommended glass ionomers as an alternative to MTA for sulcular perforations. Figure 12-9 illustrates the recommended materials for management of perforations. Fig 12-8 (a and b) Furcal perforation suc-cessfully repaired with MTA. (c) Successful healing was noted at a 6-month follow-up. a bcFig 12-9 Material recommendations for perforation repair.Sulcular perforations• Glass-ionomer repairRadicular perforations• MTA repair 228Complications12Sodium hypochlorite accident Sodium hypochlorite is an effective antimicrobial and efciently dissolves both vital and ne-crotic tissue. As a result of its ability to dissolve tissue combined with its causticity, it poses a risk to patients when expressed into the periapical tissues. A sodium hypochlorite acci-dent can occur when the irrigant solution is injected beyond the apical foramen, resulting in tissue necrosis. Sodium hypochlorite accidents are often associated with open apices or extreme pressure during irrigation. Hulsmann and Hahn reviewed common symptoms as-sociated with sodium hypochlorite accidents, including immediate severe pain, immediate edema of the neighboring soft tissue with possible extension through the fascial planes, profuse intracanal bleeding, ecchymosis, and possible taste of bleach and irritation if the solution was injected into the maxillary sinus. Delayed ndings can include secondary in-fection and either anesthesia or paresthesia. Vital signs can be compromised by the rapid swelling associated with a sodium hypochlorite accident, and immediate, emergent medi-cal attention should be sought if there are any signs of vital sign compromise. Figure 12-10 summarizes the clinical signs associated with a sodium hypochlorite accident. Fig 12-10 Potential clinical signs of a sodium hypochlorite accident (Hulsmann and Hahn).Secondary infectionParesthesiaEcchymosisBad taste and irritation if involving sinusProfuse intracanal bleedingImmediate edema Immediate severe painSeveral case reports have been presented in the endodontic literature illustrating the po-tential outcomes of a sodium hypochlorite accident. Sabala and Powell presented a case involving severe immediate pain, dramatic swelling, bleeding, and ecchymosis due to inter-stitial bleeding. Reeh and Messer described a case with a similar immediate course, in addi-tion to postoperative infection and paresthesia lasting 15 months following the initial sodium hypochlorite accident. Matthews and Merrill presented a case of chronic neuropathic pain and long-lasting paresthesia 7 months following a sodium hypochlorite accident. Several authors have described appropriate treatment regimens to address a sodium hy-pochlorite accident (Fig 12-11). Hulsmann and Hahn recommended palliative care, including pain control via local anesthesia and analgesics as well as initial use of cold compresses for 24 hours followed by warm compresses afterward to stimulate local circulation. They recom-mended daily monitoring for improvement. Antibiotics are only recommended with evidence of secondary infection or prophylactically in high-risk cases. The use of corticosteroids is con-troversial. Any further endodontic treatment should use alternative irrigants, such as saline or chlorhexidine. 229Intratreatment ComplicationsExtrusion of materials beyond the apex As the root canal space is continuous with the periapical tissues, the risk of overextension of medicament or obturation material is inherent to endodontic therapy and increases in the absence of adequate length control or in cases of open or wide apices. Although over-extension of material can theoretically cause a foreign body reaction no matter its location, extension into important anatomical spaces including the maxillary sinus, mental foramen, and mandibular canal are generally considered most risky. Calcium hydroxide (CH) is a common intracanal medicament, and though it is generally considered safe, there are several reported cases of its overextension causing complica-tions. Generally, extension of CH into the periapical tissues in noncritical areas does not cause lasting defects. Although they do not advocate deliberate delivery of CH to the periapical spaces, De Moor and De Witte presented 11 cases with CH extrusion that did not negatively impact healing or prognosis. Similarly, a case report by Fava found no pain or pathology resulting from extrusion of CH into the maxillary sinus following endodontic therapy on a maxillary premolar. Figure 12-12 shows an example of CH extrusion associat-ed with clinical healing in a case of chronic apical abscess with a sinus tract and periodon-tal-endodontic lesion. Conversely, Lindgren et al presented a case of hemifacial ischemia and necrosis following extrusion of CH into the mandibular canal and the surrounding cap-illary bed of the face, palate, and ear. Similarly, Ahlgren et al presented a case of lower lip paresthesia due to extrusion of CH into the mandibular canal. Following surgical excision of the material and reactionary material, the paresthesia resolved. Pain control (local anesthesia and analgesia)Initial cold compresses; warm compresses after 24 hoursAntibiotics if signs of infectionEmergency medical referral if vital signs compromisedFig 12-11 Suggested management protocol for a sodium hypochlorite accident (Huls-mann and Hahn).Fig 12-12 CH extruded into a periodontal-endodontic lesion at time of pulpectomy associated with clinical closure of prior sinus tract and periodontal pocket. Radio-graphs taken at time of cone t (a) and postobturation (b). a b 230Complications12Overextension of obturation materials is an area of controversy in endodontics. Schilder advocated the classic “sealer puff” for all root canal lls (Fig 12-13). This assumes that a slight extrusion of endodontic sealer will not result in pathology. Augsburger and Peters supported this claim when they found that eugenol-based sealers were resorbed over time. In an animal study, Kawakami et al injected Vista-Cal [Vista Dental], a sealer consisting of CH, iodoform, and silicone oil, into the mandibular canal and found that macrophages phagocytosed the material, leading to time-dependent resorption. On the other hand, Seltzer et al (1973) showed that extrusion of obturation material beyond the apex caused a foreign body reaction, and Sjogren et al (1995, 1998) found chronic inammation and bone resorption resulting from tissue exposure to gutta-percha (GP). Fig 12-13 (a and b) “Puffs” of sealer are a common, usually nonpathologic occur-rence following root canal therapy. a bThough controversy exists regarding overextension of obturation material into the periapical tissues, the proximity of root apices to critical anatomical structures can make overextension problematic. Knowles et al demonstrated that the apices of the mandibular molars and premolars lie in close proximity to the mental foramen and mandibular nerve. Overextension of material out of the apices of posterior mandibular teeth can put these structures at risk. Gluskin cited possible mechanical, compression, and chemical injuries to the mandibular nerve as potential complicating factors in overextension. Rowe reported that extrusion of sealer into the mandibular canal could cause paresthesia due to either direct pressure of the material on the neurovascular bundle or neurotoxicity. Tilotta-Yasu-kawa et al presented a case series showing a correlation between proximity of obturation materials and the mandibular canal with an increased likelihood of paresthesias. The composition of the extruded material plays a role in the severity of any foreign body reaction. As discussed earlier, GP can be cytotoxic, but root canal sealers are generally considered to be the more noxious agents. Pascon, Langeland, et al reported that all sealer materials are inherently cytotoxic in their freshly mixed state. Kozam demonstrated signif-icant neurotoxic effects of eugenol on the sciatic nerves of bullfrogs. Presumably, similar neurotoxicity might occur if eugenol-based sealers contact the mandibular nerve. Tamse et al presented two cases of paresthesias following extrusion of an AH 26 [Dentsply] sealer into the mandibular canal. Kleier and Averbach presented a case of painful dysesthesia following extrusion of a paraformaldehyde N2-type paste into the mandibular canal. 231Intratreatment ComplicationsJust as mandibular overextensions have been associated with the development of pa-thology, so have maxillary extrusions. The proximity of the apices of the maxillary molars to the maxillary sinus can increase the risk for development of sinus pathology. In a CBCT study, Pagin et al showed that 22% of maxillary posterior teeth were located in close prox-imity to the maxillary sinus, with 14% of root apices protruding into the sinus. Similarly, Rigolone et al found that 25% of maxillary sinuses extend between the buccal and palatal roots of maxillary molars, again based on CBCT imaging studies. Giardino et al reported a case of Aspergillus infection in the maxillary sinus following extrusion of a zinc oxide– eugenol sealer beyond the apex of an endodontically treated maxillary molar, presumably related to the zinc requirement for Aspergillus metabolism. Kaplowitz presented a case of chronic maxillary sinusitis following overextension of a GP ll in the palatal root of a maxil-lary molar. Paraformaldehyde-containing sealers, though no longer commercially available, are known cytotoxins. Orlay presented a case of severe pain following overextension of an N2-type paraformaldehyde-containing sealer into the maxillary sinus. Above all, the development of signs or symptoms of pathology, including sinusitis when foreign materials reach the maxillary sinus or paresthesias or dysesthesias when materials reach the mandibular nerve, should be recognized and managed or referred for proper treatment when appropriate. Particularly in cases of nerve injury, time is of the essence. Pogrel reported that microsurgical treatment of mandibular nerve injuries should occur within 48 hours of the injury for maximal success. Thermal injuryThermal injuries to the periodontium can result from a multitude of heat-producing instruments used during endodontic therapy. Devices—including ultrasonic and high- and slow-speed handpieces, obturation aids including down-packing systems, and thermoplasticized GP deliv-ery systems—create signicant amounts of heat that can traumatize living structures. In order to prevent injury to the periodontal ligament, Eriksson and Albrektsson showed that root surface temperatures should not increase more than 10°C (Fig 12-14). Floren et al showed that main-taining the System B endodontic ll device [Kerr] at less than 250°C prevented said increases. According to Lee et al (1998), the Touch ‘n Heat 5400 [Kerr] and ame-heated methods of down-packing GP for vertical condensation provided limited temperature control and could therefore involve root surface temperature increases of more than 10°C; this makes them less desirable as obturation aids. Based on a clinical study on dogs, Gutmann et al reported that thermoplasticized GP was safe in terms of its effects on the periodontium, with very little risk of soft tissue thermal injury. 10°C increase in root surface temperatureInjury to periodontiumFig 12-14 Threshold for thermal injury (Eriksson and Albrektsson). 232Complications12Ultrasonic instruments, including those used to remove posts or create apical prepa-rations during surgical endodontic therapy, create heat, particularly when used without adequate coolant. Davis et al suggested that post removal with ultrasonic instruments is particularly risky due to the relatively short amount of time during which increases to root temperature can occur that are high enough to cause periodontal damage. They found that only 20 seconds of dry ultrasonic instrumentation raised external root surface tem-peratures 10°C. Gluskin et al suggested that the use of adequate water or air coolant could prevent damaging temperature increases. Suggestions for methods to reduce the risk of thermal injury by ultrasonic instrumentation are summarized in Fig 12-15.Short duration drillingReduction of thermal injuryWater or air coolantFig 12-15 Methods to reduce thermal injury with the use of ultrasonic instruments.Root-end surgery involves ultrasonic root-end preparations and osteotomy creation with either ultrasonic handpieces or high-speed burs. Nicoll and Peters reported that water irrigation protected slabs of dentin from temperature increases with ultrasonic scaling. This work was applied to surgical endodontics, and consequently, coolants are recommended during ultrasonic or high-speed drill manipulation of bone and surrounding tissues. Like surgical endodontics, delivery of intraosseous anesthesia requires osteotomy prepa-ration. Woodmansey et al reported a case of osteonecrosis following osteotomy prepara-tion for intraosseous anesthesia without coolant. Although this particular case may have involved increased risk for nonhealing due to surgical access to remove a separated per-forator and medical compromise of the patient, the authors suggested that short-duration use of the perforator could minimize the frictional heat production and therefore the risk of thermal injury to the periodontium. Air emphysemaAir emphysema can occur during endodontic treatment when air is forced through the root canal space into the periapical tissue and beyond, creating swelling and crepitus. Classically, Shovelton presented 13 cases of air emphysema secondary to endodontic therapy, including one case in which a clarinet player introduced air via an open endodontic access. Eleazer and Eleazer found that air syringes created signicant air pressure in periapical spaces in an in vitro model. A review by Hulsmann and Hahn found that air emphysema was self limiting and generally resolved without intervention. However, dramatic sequelae including fatal pneu-momediastinum can result. An et al presented a case of orbital, cervicofacial, and mediastinal emphysema following endodontic retreatment of a mandibular premolar. 233Intratreatment ComplicationsAs swelling involving the fascial planes is commonly noted immediately following end-odontic procedures, a differential diagnosis should include postoperative are-up, necro-tizing fasciitis, allergic reactions, angioedema, hematoma, or air emphysema (Fig 12-16). Fig 12-16 Differential diagnoses for swelling noted postoperatively.Allergic reactionsAngioedema HematomaAir emphysemaNecrotizing fasciitisPostoperative are-upBrain abscessA brain abscess is perhaps one of the most feared complications following untreated or recurrent endodontic disease. Periapical abscesses are generally considered encapsulated, with little risk of associated bacteremia unless overinstrumentation occurs during treatment (Bender et al). However, Li et al, reviewed the direct and indirect pathways for spread of root canal pathology to the brain (Fig 12-17). Direct extension can occur via fascial planes, hema-togenous spread via the valveless facial veins or systemic circulation, or lymphatic spread. Indirect extension can occur via seeding from secondary extraoral infections; for example, a secondary brain abscess can develop following bacterial endocarditis of dental origin. Fig 12-17 Proposed pathways for brain abscess from endodontic infection (Li et al).Direct extensionHematogenousIndirect extensionLymphatic 234Complications12AllergyAllergic hypersensitivity reactions can occur to materials used in endodontic therapy. These reactions can be classied into four types (Fig 12-18). Types I and IV create the traditional allergic reactions experienced secondary to contact and ingested allergens commonly en-countered in endodontics. Type I hypersensitivity reactions occur immediately on exposure to the allergen and result in varying physiologic responses dependent on the target tissue. Type I reactions can include urticaria, bronchospasm, vomiting, diarrhea, and anaphylaxis. Type IV hypersensitivity reactions are delayed and usually occur between 48 and 72 hours postexposure. These represent an antibody response to an allergen to which the patient had been previously exposed. Contact dermatitis is the classic type IV hypersensitivity reaction. For a full review of allergies, please review a textbook on inammation, such as Trowbridge and Emling’s Inammation: A Review of the Process.Fig 12-18 The hypersensitivity reactions (Trowbridge and Emling). • Immediate• Anaphylaxis, hives, broncho-spasm, vomiting/diarrhea• Antibody- dependent cytotoxicity• Autoimmunelike tissue destruction• Immune complex formation• Pathology due to systemic deposits• Delayed-type• Cell-mediated immune memory response• Contact dermatitisTypeITypeIITypeIIITypeIVDuring any new patient encounter, any history of allergy must be recorded. Certain aller-gies, such as to latex rubber and certain antibiotics, are relatively common and are relevant in the diagnosis and treatment planning of endodontic disease. Less common allergens may still be relevant, including other pharmacologic agents (eg, analgesics and anesthet-ics) and certain types of dental materials. Knowledge of medication sensitivities, especially in patients who have had particularly adverse reactions to certain medications or materials in the past, is also relevant and should be accounted for in patient-specic planning. In some cases, it may be necessary to coordinate treatment with a patient’s physician to mit-igate allergy-associated risks. Allergies to endodontic dental materials are rare, but several have been reported in the literature. Case reports exist of more severe reactions than anticipated given the exposure. Gazelius et al presented a case report of conrmed contact allergy with GP in a patient with latex skin allergy, resulting in prolonged pain following obturation that resolved once the offending GP was removed. Barkin et al presented a case of severe allergic reaction to eugenol in an endodontic sealer. These reports, however, appear to be the exception rather than the norm. Although la-tex rubber allergies are relatively common, the risk of cross-allergenicity with commercially available GP is low. Costa et al investigated this cross-reactivity and found only potential cross-allergenicity between latex rubber and raw GP, which is only rarely added to commer-cial GP products. As a result, they advise that clinicians should avoid the use of GP only in patients with a type I hypersensitivity reaction to natural rubber latex. If the patient exhibits a type IV hypersensitivity to latex, avoidance of GP is not necessary. 235Intratreatment ComplicationsAdverse reactions to local anesthesiaBesides the rarely reported allergic reaction, administration of local anesthesia for end-odontic therapy does pose several risks to patients. Infections and paresthesia can occur following the injection of local anesthetics in the oral cavity. The introduction of any material in violation of the oral mucosa introduces the risk of infection, and needle tract infections are a risk following administration of local anesthesia. Connor and Edelson presented a case report of a facial cellulitis attributed to the introduc-tion of pathologic oral bacteria via local inltration dental anesthesia. Reports exist in the literature of long-lasting paresthesias following administration of local anesthetics, potentially due to physical trauma or neurotoxicity. Pogrel and Thamby reported a low incidence of permanent paresthesia following inferior alveolar nerve block anesthesia. Because paresthesia represents an immensely unfavorable reaction and occurs in response to a commonly performed injection, efforts to reduce this incidence based on risk factors are of interest. Haas and Lennon as well as Gaffen and Haas found a ve-fold increase in paresthesias when articaine was implemented for IAN blocks. More recently, Garisto et al reported that prilocaine and articaine used for dental local anesthesia were associated with an increased risk of paresthesia at 7.3 and 3.6 times, respectively (Fig 12-19). Most cases in-volved paresthesia of the lingual nerve following inferior alveolar nerve block anesthesia. The authors proposed that this increased risk of paresthesia may be due to the 4% concentration of commercially available prilocaine and articaine, which is higher than that of other commer-cially available local anesthetics like lidocaine, bupivacaine, and mepivacaine, resulting in greater potential for neurotoxicity. In addition, they proposed that the lingual nerve generally has simpler architecture at the level at which the mandibular block is traditionally adminis-tered, differentiating it from the main branch of the inferior alveolar nerve at that location. As a result of these ndings, as well as the lack of evidence to support superior effectiveness of these higher concentrations, Garisto et al suggested that local anesthetics in concentrations of 4% might be avoided for inferior alveolar block anesthesia. Fig 12-19 Prilocaine and articaine have an increased risk of paresthesia when used for local anesthesia, particularly for inferior alveolar nerve blocks (Garisto et al).Prilocaine: 7.3Articaine: 3.6Paresthesia following root-end surgeryElevation of a soft tissue ap for any dentoalveolar surgical procedure involves severance of supercial nerves, and short- or long-duration paresthesia can result, depending on the extent of injury. According to Kim et al, as long as complete severance of a major nerve bundle has not occurred, normal sensation should recur in approximately 4 weeks, or in rare cases, within a few months. Wesson and Gale reported that transient paresthesia is a 236Complications12common complication in mandibular molar surgery, with 20% of patients experiencing some sensory disturbance. The majority of patients experienced resolution over time, as only 1% of patients reported a permanent decit. Post-Treatment ComplicationsFlare-upsThe American Association of Endodontists (AAE) Glossary of Endodontic Terms denes a are-up as “an acute exacerbation of periradicular pathosis after initiation or continu-ation of root canal treatment.” In a meta-analysis, Tsesis et al reported the incidence of postoperative are-up as relatively low at 8.4%. The authors proposed that the etiology is likely multifactorial, comprising chemical, mechanical, and microbial factors inherent in the endodontic disease and treatment (Fig 12-20). Despite this proposal, no consensus on causation has been achieved, and the heterogeneity of data included in the meta-analysis made statistical analysis impossible. Siqueira reviewed the potential causes of are-up and proposed that the altered apical environment created by endodontic therapy might allow for a changed balance in host defenses, facilitating increased microbial aggression. Chemical MicrobialFlare-upMechanicalFig 12-20 Potential etiologies of are-up (Tsesis et al).The literature is replete with potential predictors for are-ups. In a retrospective chart review, Torabinejad et al found that age greater than 40 years old, female sex, mandibular teeth, allergies, preoperative pain, and analgesic use, as well as retreatment, were associ-ated with an increased risk of are-ups. Although Torabinejad et al found that the absence of periapical lesions was associated with an increased risk of are-up, Iqbal et al found the opposite and associated preoperative periapical radiolucencies with an increased risk of are-up. The presence of preoperative pain and analgesic use seems to be the most reported risk factor in the literature, with additional support in studies by Imura and Zuolo as well as Walton and Fouad. Figure 12-21 summarizes potential risk factors for are-ups. Several authors proposed that multiple-visit therapy and the use of an antimicrobial intraca-nal medicament might reduce the incidence of are-up in necrotic, infected teeth. In a prospec-tive study, Trope reported an increased incidence of are-ups when retreatment procedures were performed on teeth with apical periodontitis in a single visit. However, a systematic review by Sathorn et al found no evidence to support an increased incidence of are-up in single- ver-sus multiple-visit therapy. Eleazer and Eleazer actually reported a lower incidence of are-up in single-visit compared with multiple-visit treatment in a retrospective analysis of necrotic teeth. 237Post-Treatment ComplicationsClinically, Walton dened a are-up as an in-crease in pain or swelling, usually within a few hours to a few days following treatment, that prompts an unscheduled visit to the treating clini-cian. He suggested that treatment should involve psychologic management to reassure the patient that the condition is treatable and should not affect the prognosis, localized treatment to reclean and medicate the canal or incise and drain swelling, and pharmacologic management (Fig 12-22). Phar-macologic management might involve the use of long-acting local anesthetics, such as bupivacaine (Dunsky and Moore), or systemic drugs, including analgesics, steroids, and antibiotics, where indicat-ed. For a review of relevant medications as well as their indications for use, please see chapter 5. Some have proposed the use of prophylactic antibiotics to prevent the occurrence of postoperative are-ups. Abbott et al reported that preoperative antibiotics reduced the incidence of are-ups following treatment of asymptomatic necrotic, infected teeth. This study was awed, however, as it used an outside control group. Other literature has failed to support the practice of routine prophylactic antibiotic prescription. A prospective ran-domized controlled trial by Pickenpaugh et al found no reduction in the incidence of are-up by prophylactic amoxicillin in asymptomatic, necrotic teeth. Similarly, a prospective study by Walton and Chiappinelli found no effects with preoperative penicillin. Thankfully, the occurrence of a are-up does not affect the overall prognosis. Sjogren et al and Friedman et al each found no statistically signicant effect of postoperative are-ups on the overall prognosis of nonsurgical root canal therapy. Fig 12-21 Risk factors for are-up (Torabinejad et al).Preoperative analgesic useAgeTooth type RetreatmentsPreoperative painSexFig 12-22 Management of are-ups (Walton).Pharmaco-therapeuticsLocalized treatmentPsychologic 238Complications12FailuresThough not traditionally thought of as a complication, failure of endodontic therapy, either in the short or long term, is an adverse event that both the provider and patient hope to avoid. Failures occur for a multitude of reasons but can be generally classied as persistent infections or secondary reinfection of a previously cleaned space (Fig 12-23). Fig 12-23 Possible etiologies of failing endodontic therapy.Persistent infectionsReintroduction of bacteriaIntraradicular biolmsInfection introduced during initial therapyExtraradicular biolmsCoronal leakageFracturePersistent infections may result from intraradicular or extraradicular factors. Siqueira et al dened persistent infections as those due to the originally infective microbes. This may be due to persistent intradicular or extraradicular biolms that both the antimicrobial treat-ment methods and immune system could not completely address. Happonen also sug-gested that extraradicular periapical actinomycosis may be a causative agent for persistent infections due to its particular resistance to traditional treatment modalities. Happonen recommended surgical removal of the apical lesion to treat persistent periapical actino-mycosis. Although true cysts and foreign bodies are theoretically nonmicrobial, Siqueira et al raised skepticism that an intraradicular or extraradicular biolm component could ever be completely ruled out as a contributor to persistent pathology in these cases. Similarly, they ruled out that procedural errors such as instrument separation or overlling directly resulted in failure without a persistent intraradicular or extraradicular infection as the more likely etiologic agent. Secondary infections, unlike persistent infections, occur due to reintroduction of bac-teria from the oral cavity. Siqueira et al dened secondary infections as those occurring due to microbes different from those present with the inciting endodontic disease. These microbes may be introduced during endodontic therapy, as when adequate rubber dam isolation is not used, or due to breakdown of the coronal seal following treatment. Swan- 239Post-Treatment Complicationsson and Madison performed an in vitro study of coronal leakage and showed that only 3 days of saliva exposure following loss of a temporary lling led to signicant microbial contamination. The AAE glossary described fractures as a pathway for recurrent infection and failure of root canal therapy. Vertical root fractures in particular most often occur in pre-viously endodontically treated teeth and provide a direct pathway for reinfection. Figures 12-24 and 12-25 depict examples of failures attributed to caries and vertical root fracture, respectively. Fig 12-24 Failure due to coronal leakage. (a) The patient failed to have a permanent restoration placed following root canal therapy. (b) The result was recurrence of symp-toms 1 year later due to lost temporary ll and recurrent caries. a bFig 12-25 Failure due to vertical fracture in the distal root of the mandibular right second molar. The vertical fracture and resultant bone loss is less apparent in the periapical radio-graph (a) than in either the axial (b) or coronal (c) CBCT images.a b cPersistent painSimilar to failures, persistent pain following endodontic therapy is something both the provider and patient prefer to avoid. Short-term pain following endodontic treatment is rel-atively common. Law et al found that 19% of patients reported severe pain following end-odontic therapy lasting an average of 2 days. Long-term pain, however, is relatively uncom-mon. In a systematic review, Nixdorf et al (2010a) found that 5% of patients experienced persistent pain more than 6 months following endodontic therapy. Polycarpou et al found that female sex, a history of chronic pain, preoperative mechanical allodynia (measured by percussion tenderness), and preoperative pain were all risk factors for persistent pain. 240Complications12Persistent pain may be of endodontic origin or in other cases may arise from other sources. Using the same data from their earlier systematic review, Nixdorf et al (2010b) found that, of the 5% of patients with long-term discom-fort, 3.4% of patients’ pain was of non-odontogenic origin (Fig 12-26). Put an-other way, the frequency of long-term odontogenic pain was 1.6%. Sources of nonodontogenic pain included mus-culoskeletal or neuropathic pain, head-aches, and pathology related to nearby structures such as the maxillary sinuses, salivary glands, vasculature, brain tumors, angina, or throat cancer (Nixdorf et al 2010b). Unfortu-nately, many episodes of nonodontogenic persistent pain may indicate that the original endodontic treatment may have been performed due to a misdiagnosis. Odontogenic causes of persistent pain may be difcult to ascertain and can include refractory infections, infraction, periodontal disease, and traumatic occlusion among other sources. For more information on non-endodontic pain, please refer to chapter 7.Whether odontogenic or not, persistent pain oftentimes comprises a grab bag diag-nosis, and a denitive diagnosis may elude the provider. In a study that also found a 5% frequency of persistent pain, Vena et al found that two-thirds of those patients reporting pain did not have an identiable cause. Obviously, a lack of denitive diagnosis comes with its own psychosocial consequences as well as a high likelihood of ineffective treatment. 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Eur J Oral Sci 1995;103:313–321.Spili P, Parashos P, Messer HH. The impact of instrument fracture on outcome of endodontic treatment. J Endod 2005;31:845–850.Suter B, Lussi A, Sequeira P. Probability of removing fractured instruments from root canals. Int Endod J 2005;38:112–123.Tamse A, Kaffe I, Littner MM, Kozlovsky A. Paresthesia following overextension of AH-26: Report of two cases and review of the literature. J Endod 1982;8:88–90.Tilotta-Yasukawa F, Millot S, El Haddioui A, Bravetti P, Gaudy JF. Labiomandibular paresthesia caused by endodontic treatment: An anatomic and clinical study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:e47–e59.Trowbridge HO, Emling RC. Inammation: A Review of the Process, ed 5. Chicago: Quintes-sence, 1997.Wesson CM, Gale TM. Molar apicectomy with amalgam root-end lling: Results of a prospective study in two district general hospitals. Br Dent J 2003;195:707–714.Woodmansey KF, White RK, He J. 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See American Board of Endodontics.Abscess(es)apical, 97brain, 233, 233fcharacteristics of, 20, 75historical description of, 11immunoglobulin levels in, 54microabscesses, 52periapical, 233Abscess theory, of cyst formation, 57, 57fAccessory canals, 34, 34fAcetaminophen, 73–74, 74tAcetylcholinesterase, 28Actinomyces, 14Actinomycosis, 14, 238Acute apical abscess, 97Adaptive immunity, 51, 51fAδ bers, 27, 39, 51–52, 85, 106Adjunctive irrigation techniques, 130–131, 131fAdrenergic nerves, 28Aggregatibacter actinomycetemcomitans, 11Aging, 30, 31fAir emphysema, 232–233, 233fALARA principle, 90Allergyhypersensitivity reactions, 234, 234flatex, 234local anesthetics, 69Allodynia, 87Allografts, 143, 143fAlloplasts, 143, 143fAlveolar fractures, 89, 180, 182, 187Amalgam, 141, 142tAmeloblastomas, 113American Academy of Oral and Maxillofacial Radiology, 93, 94fAmerican Association of Endodontistsapexication as dened by, 148apexogenesis as dened by, 146avulsions and, 194Colleagues for Excellence, 69cone beam computed tomography indications, 93, 94fcracked tooth versus cracked tooth syndrome, 97diagnostic terminology, 96, 96fare-ups as dened by, 236fracture classication, 97, 97f, 99f, 182f, 239implants and, 156pulp capping as dened by, 146pulp polyp as dened by, 100pulp sensitivity testing and, 181pulpotomy as dened by, 147radiographic examination guidelines, 183rubber dams, 123silver points, 137, 137fsplinting recommendations, 185, 185fsurgical operating microscope, 124American Board of Endodontics, 1American Dental Association code of ethics, 157, 157fτ-Aminobutyric acid, 74Amoxicillin, 71t, 237Anachoresis, 10, 50Analgesics, 73–74, 74tAnemia, 75, 116Anesthesia. See also Local anesthesia.adjunctive techniques, 122–123, 123fintraosseous, 232mandibular, 121–122maxillary, 121pain source identied using, 88palatal, 121pulpal, 121supplemental, 123Ankylosis, 181, 194Anterior superior alveolar nerve, 38Antibiotic pastes, 151Antibioticsafter avulsion injuries, 189bacterial resistance to, 69commonly used, 71tcontraindications for, 70fdosage of, 70, 71tdrug interactions with, 71tare-up prevention and, 69indications for, 69, 70fpathogen susceptibility to, 69prophylactic use of, 72f, 72–73, 144, 237Anticurvature lling technique, 126, 126fAnxiolytics, 74–75Apexication, 148–149, 148f–149f, 188, 215Apexogenesis, 146, 215fApical abscesses, 97Apical diagnoses, 96f, 96–97Apical foramenage-related changes in, 30anatomy of, 33–34arterial structures in, 29constriction of, 34electronic apex locator for location of, 125major, 33–34minor, 33–34Apical periodontitisasymptomatic, 97bacteria and, 53, 53f, 55f, 179Page numbers followed by “f” indicate gures; those followed by “t” indicate tables 246IndexAbiologic medications for, 76bone resorption in, 55cardiovascular disease and, 76cellular responses in, 54cytokines in, 54–55diabetes and, 76humoral responses in, 54–55lymphocytes in, 54nonsurgical root canal therapy outcome affected by, 210outcomes affected by, 210, 212pathology of, 53, 53fpost-retreatment, 212, 212fpost-treatment, 211fprevalence of, 6pulpal disease progression to, 179pulpal necrosis and, 8f, 53frecurrent, 136requirements for, 179, 179fsmoking and, 77symptomatic, 96Apical radiolucencies, 58, 58f, 211fApical surgery, 141, 144, 213Apical tissue, 96Archaea, 14Articaine, 68, 68t, 121–122, 235, 235fAs low as reasonably achievable principle. See ALARA principle.Asaccharolytic, 13Aspergillus, 14Asymptomatic apical periodontitis, 97Atypical facial pain, 108–109, 109fAtypical odontalgia, 109Atypical species, in endodontic infections, 14f, 14–15Augmentin, 71tAutogenous grafts, 143, 143fAutotransplantation, 145–146Avulsionsdescription of, 183in immature teeth with closed apex, 191–192in mature teeth with closed apex, 191periodontal ligament maintenance in, 189radiographic ndings in, 185replantation of, 189, 191–192storage of tooth, 189, 189f, 191treatment of, 186t, 189–192, 190fBBacteremia, 72–73Bacteriaantibiotic resistance by, 69apical periodontitis and, 53, 53f, 55f, 179carious, 45gram-negative, 9, 16gram-positive, 9, 16isolated species of, 12f, 12–13multiple-visit therapy effects on, 132in periapical lesions, 55–56, 56fBay cysts, 57–58Beam-hardening artifacts, 93, 93f, 98ß agonists, 29Bioactive cements, 142, 142tBiolms, 11f, 11–12, 128, 238, 238fBiologic width, 154, 154fBisphosphonate-related osteonecrosis of the jaw, 75Bitewing radiographs, 89, 90fBiting pain, 87Black-pigmented bacteroides, 13, 13fBleachinginternal, 152intracoronal, 203nonvital, 216Blood owto maxillary teeth, 36–37, 37fpulpal, 28–30, 48, 52, 52fBone resorption, 55. See also Resorption.Borrelia burgdorferi, 77Brain abscess, 233, 233fBridge abutments, 47BRONJ. See Bisphosphonate-related osteonecrosis of the jaw.Brown tumor, 117Buccal inltrations, 121–123Buccal nerve, 39Buccal object rule, 91Buccal space, 17Buccal vestibule, 17Bupivacaine, 68t, 121, 144Burs, 141CC bers, 27–29, 39, 51–52Calcications, pulpal, 112, 112fCalcitonin gene-related peptide, 25, 29, 48, 51Calcium hydroxideapexication using, 148, 148fdescription of, 12, 194extrusion of, in periapical areas, 229intracanal uses of, 132–133stem cells affected by, 151Calcium hydroxide liners, 47Calcium sulfate, 139Candida albicans, 14Canine space, 17Canines, 32t–33tCardiac pain, 110Cardiovascular disease, 76Cariespathophysiology of, 45, 46fpulpal inammation caused by, 45–46Carrier-based obturation systems, 134, 138Case reports, 3Case-control studies, 3Cause and effect, 3Cavernous sinus thrombosis, 20Cavit, 135CBCT. See Cone beam computed tomography.CDJ. See Cementodentinal junction.CEJ. See Cementoenamel junction.Cell(s)apical periodontitis responses by, 54in periapical granulomas, 56–57periapical pathology responses by, 54, 54fpulpal irritant responses by, 52Cementodentinal junction, 33–34, 125, 135, 141Cementoenamel junction, 31, 94, 124, 152 Index247DCemento-osseous dysplasia, 116, 116fCementumage-related changes in, 30tears of, 110, 111fCentral incisors, 32t–33tCephalexin, 71tCGRP. See Calcitonin gene-related peptide.CH. See Calcium hydroxide.Chemotherapeutics, 76Chief complaint, 83Children, traumatic dental injuries in, 178Chlorhexidine gluconate, 129–131, 130f, 133, 133fChondroitin sulfate, 27Chronic apical abscess, 97CHX. See Chlorhexidine gluconate.Clark’s rule, 91Clindamycin, 71tClinical examinationelements of, 83fobjective examination. See Objective examination.subjective examination, 83t, 83–84CMV. See Cytomegalovirus.Cohort studies, 2Cold testing, 84–85Collagen, 27Collagen brils, 26Common carotid artery, 36Complicated fractures, 182, 184fComplicationsair emphysema, 232–233, 233fallergy, 234brain abscess, 233, 233fendodontic surgery, 144extrusion of materials beyond apex, 229f–230f, 229–231failures, 238–239are-ups, 236–237. See also Flare-ups.instrument separation, 222–224, 222f–224fintraoperative, 94intratreatment, 222–227local anesthesia adverse reactions, 235, 235fperforations, 225–227, 225f–227fpost-treatment, 236–240regenerative endodontics, 152, 152fsodium hypochlorite accident, 228–229, 228f–229fthermal injuries, 231f, 231–232traumatic dental injuries, 193–194, 195fComprehensive medical history, 84Concussion, 182, 184f, 186t, 187Condensing osteitis, 97, 115Cone beam computed tomographyadvantages of, 92, 93fartifacts on, 93, 93fbeam-hardening artifacts on, 93, 93f, 98computer algorithms, 91costs of, 92description of, 6, 39, 89disadvantages of, 92–93, 93fendodontic failures evaluated with, 240eld of view, 92, 92timage interpretation, 94–95, 95findications for, 90f, 93–94, 94fintraoperative complications diagnosed using, 94maxillary sinus mucositis on, 95fmechanism of action, 91–92nonsurgical root canal therapy outcomes evaluated using, 211previously treated teeth imaged using, 94radiation dosages with, 92, 92troot fracture evaluations, 94, 185two-dimensional dental radiographs versus, 92vertical root fracture diagnosis using, 98, 98fworking length determination using, 124–125Condentiality of patient records, 157Contact dermatitis, 234Coronal discoloration, 201Coronal aring, 127, 127fCoronal fractures, 46, 99Coronal leakage, 239Coronary artery disease, 76Cracked tooth, 97, 156Cracked tooth syndrome, 46, 97, 156, 156fCraze lines, 97Crown fractures, 182, 182f, 184f, 186tCrowned teeth, 47, 47fCrown/root fractures, 182, 182f, 186t, 187C-shaped root canals, 35–36, 36fCyclooxygenases, 74Cystsnasopalatine duct, 113, 113fperiapical, 57f, 57–59, 90Cytokinesin apical periodontitis, 54–55in bone resorption, 55Cytomegalovirus, 15Cytotoxic T cells, 54DDanger space, 20DE. See Dens evaginatus.Deafferentation pain, 109Decoronation, 194, 205DEJ. See Dentinoenamel junction.Dens evaginatus, 35, 151fDens invaginatus, 35, 94Dental history, 83Dental pulp. See Pulp.Dentinanatomy and physiology of, 25–26caries penetration into, 46fclassication of, 26, 26fdehydration of, 47dysplasia of, 112embryology of, 25–26facts about, 26fodontoblast secretion of, 25radicular, 216sensitivity of, 28fDentinal hypersensitivity, 106Dentinal tubules, 25–26, 28, 52, 141Dentinoenamel junction, 25–26Dentinogenesis, 24–25, 30 248IndexDDentition. See also Teeth; specic teeth.arterial supply to, 36–37neural pathways to, 38f, 38–39primary. See Primary dentition.Dermatan sulfate, 27DI. See Dens invaginatus.Diabetes, 76–77Diagnosisapical, 96f, 96–97clinical examination for. See Clinical examination.fractures. See Fractures.periapical lesions, 90periodontal-endodontic lesions, 99–100, 100fpulpal, 96, 96fradiographic examination for. See Radiographic examination.Diazepam, 75Digital radiography, 90DNA techniques, 9Doxycycline, 189Drug interactionswith analgesics, 74twith antibiotics, 71tEEAL. See Electronic apex locators.EBV. See Epstein-Barr virus.Ectodermal cells, 24EDTA, 125, 129, 150Ehlers-Danlos syndrome, 112, 112fEIRR. See External inammatory root resorption.Electric pulp testing, 48, 84–86, 87f, 181Electronic apex locators, 124–125, 125fEmbryology, of teeth, 24–25, 25fEmphysema, air, 232–233, 233fEnamelembryology of, 24inner epithelium of, 24–25outer epithelium of, 24–25Endo Ice, 85Endocarditis, 72, 72fEndodontic diseasein primary dentition, 217radiographic entities that resemble, 111–117Endodontic are-ups. See Flare-ups.Endodontic infectionsanatomical distribution of, 17–20atypical species in, 14f, 14–15consequences of, 20historic perspectives on, 50–51isolated species in, 12f, 12–13overview of, 10pathways of, 19, 19tpatterns of spread for, 18, 18f, 19tpolymicrobial, 10primary, 16f, 16–17secondary, 16f, 16–17viruses, 15, 15fEndodontic lesions, 99Endodontic microbiology. See Microbiology, endodontic.Endodontic surgeryblood loss during, 138calcium sulfate use in, 138complications of, 144follow-up care after, 153grafts, 143healing after, 144–145, 145fhemostasis for, 139, 139findications for, 138membranes, 143–144nonsurgical retreatment versus, 138outcomes of, 213–214, 214fpostoperative management of, 144resection, 141retrolling, 141–142, 142tretropreparation, 141soft tissue healing after, 144surgical site exposure, 140suturing, 142tools and techniques used in, 138unconventional approaches, 145–146Endodontic treatmentapexication, 148–149, 148f–149f, 215bacteremias after, 72digital radiography uses in, 90failure of, 238–239follow-up care, 153implants versus, 155–156internal bleaching, 152local anesthesia for, 121–123, 123fnonsurgical retreatment, 136–138, 137f–138f, 212, 212fnonsurgical root canal therapy. See Nonsurgical root canal therapy.persistent pain after, 239–240, 240fpulp capping, 146, 147f, 214–215pulpal necrosis treated with, 188pulpotomy, 147, 147f, 215regenerative endodontics, 149–152, 150f–152f, 216fin restored teeth, 47, 47fsuccess rates for, 208surgery. See Endodontic surgery.Endodontically treated teeth. See also Previously treated teeth.nonsurgical retreatment in, 136–138, 137f–138f, 212, 212fperiodontal disease effects on, 100restoration ofbiologic width, 154, 154fimplants for, 155–156indications for, 153posts, 154–155, 155freasons for, 153, 154fsuccess rates for, 209Endotoxin, 9, 9fEnterococcus faecalis, 12, 13f, 17, 129, 133Epidemiology, 5–6Epinephrine, 68t, 69, 139Epithelial rests of Malassez, 57Epstein-Barr virus, 15EPT. See Electric pulp testing.Ethics, 157, 157f Index249IEugenol, 135, 135f, 230Evidence, levels of, 2fExpert opinions, 3External apical root resorption, 194External carotid artery, 36External inammatory root resorption, 204–205, 205fExternal jugular vein, 37External root resorptioninammatory, 204–205, 205forthodontic treatment and, 48–49Extracellular connective tissue, 27Extraradicular infections, 11Extremophiles, 14Extrusive luxation, 183, 184f, 186t, 187FFacial artery, 36Failure of endodontic therapy, 238–239Falls, 178False negative, 5, 5tFalse positive, 5, 5tFascial spaces, 17–18, 19t, 20, 39Federal laws, 157Ferrule effect, 154FISH. See Fluorescent in situ hybridization.Fisher exact test, 4Flaps, 142Flare-upsantibiotics for prevention of, 69denition of, 236–237in diabetes, 77factors associated with, 236fincidence of, 59, 236local anesthetics for, 237management of, 237, 237fpredictors for, 236risk factors for, 237fFluorescent in situ hybridization, 9Focal infection theory, 8, 50Focused examination, 84Foramen ovale, 39Foramen rotundum, 38Foreign body reaction, 230Formaldehyde, 136, 147Formocresol, 147Fracture(s)alveolar, 89, 180, 182, 187categories of, 97–98, 97f–98fcoronal, 46, 99crown, 182, 182f, 184f, 186tcrown/root, 182, 182f, 186t, 187denition of, 239diagnostic testing for, 88as pulpal irritant, 46radiographic ndings, 184f, 184–185root. See Root fractures.staining of, 88types of, 97–98, 97f–98fvertical root, 97–99, 98f, 239, 239fFractured cusps, 97Fungal infections, 14Furcation, 87, 87f–88fFusobacterium nucleatum, 11GGAGs. See Glycosaminoglycans.Glass-ionomer cements, 135, 204Glycosaminoglycans, 27Grafts, 143Gram-negative bacteria, 9, 16Gram-positive bacteria, 9, 16Granulomas, 56–57, 57f, 59, 90Greater palatine nerve, 38Growth factors, 24, 150Gutta-percha, 85, 134, 136, 142, 230–231, 234HHand instruments, 126–127Hank’s Balanced Salt Solution, 189, 191Head and neck lymphatic drainage, 38Headaches, 107f, 107–108Healingafter pulp capping, 146after root fractures, 187fsoft tissue, 144surgical, 144–145, 145fHealth Insurance Portability and Accountability Act, 157Heat testing, for pulp sensitivity, 85Helper T cells, 54, 54fHemostasis, 139, 139fHepatitis, 77Herpes simplex virus, 15Herpes zoster, 116HERS. See Hertwig’s epithelial root sheath.Hertwig’s epithelial root sheath, 25, 34, 148HHV. See Human herpesvirus.HIPAA. See Health Insurance Portability and Accountability Act.HIV. See Human immunodeciency virus.Hodgkin lymphoma, 77Hollow tube theory, 50–51Horizontal incisions, 140, 140fHSV. See Herpes simplex virus.Human herpesvirus, 15Human immunodeciency virus, 15Hyaluronate, 27Hypercementosis, 115Hyperparathyroidism, 117Hyperplastic pulpitis, 100Hypersensitivity reactions, 234, 234fHypothesis testing, 3IIADT. See International Association of Dental Traumatology.Iatrogenic perforations, 225–227Ibuprofen, 73–74, 74t, 84ICD. See Implantable cardiac debrillators.ICRR. See Invasive cervical root resorption.Immature necrotic teeth, 215–216, 216fImmunoglobulinsin apical periodontitis, 54in periapical cysts, 57Immunologic theory, of cyst formation, 57, 57fImplantable cardiac debrillators, 125Implants, 155–156 250IndexIIncidence, 5f, 5–6Incisions, 140, 140fIncisive nerve, 39Incisors, 32tInfectionendodontic. See Endodontic infections.historic perspectives on, 50–51non-endodontic, 110–111persistent, 238primary, 16f, 16–17secondary, 16f, 16–17, 238Zones of Fish for containment of, 8, 8fInfective endocarditis, 72, 72fInferior alveolar artery, 36–37Inferior alveolar nerveanesthetic block of, 75, 121–122description of, 39radiographic images of, 95fInferior alveolar vein, 37Inltrations, 121Infraorbital artery, 37Inhalational anxiolytics, 75Innate immunity, 51, 51fInner enamel epithelium, 24–25Instruments/instrumentationdescription of, 126–128irrigation with, 128f, 128–130master apical le, 127nickel titanium, 222, 222frotary, 127, 222separation of, 222–224, 222f–224fsmear layer created by, 127–128stainless steel, 222ultrasonic, 232Intentional replantation, 145Interleukin-1α, 55Interleukin-1ß, 52, 55Interleukin-6, 55Interleukin-10, 55Internal bleaching, 152Internal carotid artery, 36Internal jugular vein, 38Internal root resorption, 100, 193–194, 200–201, 201fInternational Association of Dental Traumatology, 185International Classication of Headache Disorders, 107Intracanal medicaments, 132–133, 133f, 150Intracoronal bleaching, 203Intraoperative complications, 94Intraoral examination, 84Intraosseous anesthesia, 232Intrapulpal nerves, 27f, 27–28Intrasulcular incisions, 140, 140fIntrusive luxation, 183, 184f, 186t, 187–188, 188fInvasive cervical root resorption, 194, 201–204, 202f–203fIrreversible pulpitis, 51, 53, 69, 75, 96, 156Irrigationadjunctive techniques for, 130–131, 131firrigants used in, 128f, 128–130, 150passive ultrasonic, 131sodium hypochlorite for, 128–129, 129f–130fIrritants, pulpal. See Pulpal irritants.Isolated species, in endodontic infections, 12f, 12–13JJawbisphosphonate-related osteonecrosis of, 75malignancies of, 114, 114fradiolucencies of, 115, 115fradiopacities of, 115–116, 116fLLactobacillus, 45Lateral canal, 34, 34fLateral condensation, 134Lateral incisors, 32t–33tLateral luxation, 183, 184f, 186t, 187Lateral pharyngeal space, 20Latex allergy, 234Laws, 157Left subclavian vein, 38Lesser palatine nerve, 38Leukocytes, 52Levels of evidence, 2fLidocaine, 68t, 121Lingual nerve, 39, 235Lipopolysaccharide, 9, 52–53, 55Local anesthesia. See also Anesthesia.adjunctive techniques, 122–123, 123fadverse reactions to, 235, 235fagents used in. See Local anesthetics.mandibular anesthesia, 121–122maxillary anesthesia, 121Local anestheticsallergies to, 69duration of action, 68–69are-ups managed with, 237hemostatic uses of, 139indications for, 68lipid solubility of, 68paresthesias after, 235properties of, 68types of, 68tLPS. See Lipopolysaccharide.Ludwig angina, 20Luxation-type injuriesfollow-up of, 189radiographic ndings in, 185treatment of, 186t, 187–189types of, 182–183Lyme disease, 77Lymph nodes, 38, 38fLymphaticsmaxillofacial, 38, 38fpulpal, 30Lymphocytes, 54Lymphoma, 77MMAF. See Master apical le.Magnication, 124, 124fMalignancies, 114, 114f Index251NMandibular anesthesia, 121–122Mandibular nerve, 39Mandibular osteomyelitis, 111fMandibular teethcanines, 33tinfections of, 18, 19tinnervation of, 39surgical anatomy of, 39venous drainage from, 37Masserann technique, 137Master apical le, 127Masticatory muscles, 38Maxillary anesthesia, 121Maxillary artery, 36–37Maxillary nerve, 38Maxillary sinusmaxillary root protrusion into, 39mucositis of, 95fsurgical anatomy of, 39Maxillary teethanesthesia for, 121arterial supply to, 36–37, 37fcanines, 32tincisors, 32tinfections of, 18, 19tinnervation of, 38molars, 32tpremolars, 32troot canal anatomy in, 32troot protrusion into maxillary sinus by, 39, 95venous drainage from, 37Maxillary vein, 37Maxillofacial regionanatomy of, 36–37arterial supply to, 36–37, 37flymphatics of, 38, 38fneuroanatomy of, 38–39surgical anatomy of, 39venous drainage, 37Measuresof statistical signicance, 3–4of validity, 4–5, 4f–5fMedical history, 84Medications. See Pharmacology; specic medication.Membranes, 143–144Mental foramen, 39, 89, 94–95, 95fMental nerve, 39Mental space, 18Mepivacaine, 68tMesenchymal cells, crest-derived, 24Meta-analyses, 2Metastases, 114, 114fMethylene blue dye, 141Metronidazole, 69, 71tMicroabscesses, 52Microbiology, endodontichistory of, 8overview of, 7research methods, 9Microbiome, 10MicroCT, 92–93Microscope, surgical operating, 124, 124f, 224Middle superior alveolar nerve, 38Migraine headaches, 107–108Mineral trioxide aggregateapexication using, 148, 149f, 215, 216fperforating resorptive defects treated with, 201perforation repair using, 226–227, 227fproperties of, 142tpulp capping using, 146, 215pulpal healing promoted with, 47pulpotomy using, 147, 147f, 217retrolling uses of, 141–142, 213sealers using, 135Minocycline, 151Mobility assessments, 87, 88fMolars, 32t–33tMolecular research, 10Molecular techniques, 9Mouth guards, 195MTA. See Mineral trioxide aggregate.Multiple myeloma, 77Multiple-visit therapy, 131f, 131–132, 236Myofascial pain, 106NNasopalatine duct cysts, 113, 113fNegative predictive value, 4f, 5Neuralgia-inducing cavitational osteonecrosis, 109Neurobromatosis, 116–117Neurokinin A, 29Neuropathic pain, 108, 108fNeuropeptide Y, 25, 29Neuropeptides, 51Neurovascular pain, 109–110Nickel titanium alloys, 127Nickel titanium instruments, 222, 222fNICO. See Neuralgia-inducing cavitational osteonecrosis.Nitrous oxide, 75NMDA receptors, 75Non-endodontic diseasesheadaches, 107f, 107–108pain. See Pain.Non-endodontic infections, 110–111Non-Hodgkin lymphoma, 77Noninfectious swelling, 111Nonodontogenic pain, 240Nonresorbable membranes, 143Nonsteroidal anti-inammatory drugsdrug interactions, 74tmechanism of action, 73Nonsurgical retreatment, 136–138, 137f–138f, 212, 212fNonsurgical root canal therapyaccess preparation, 124instrumentation, 126–128intracanal medicaments, 132–133, 133firrigation, 128–131isolation, 123magnication, 124, 124fmultiple-visit therapy, 131f, 131–132, 236obturation, 134f, 134–135, 137 252IndexNoutcomes of, 209t, 209–211, 211fpatency, 125–126, 126fprognostic rates for, 209t, 209–211, 211fsingle-visit therapy, 131f, 131–132, 236temporary restorations, 135working length determination, 124–125, 125fNonvital bleaching, 216NPY. See Neuropeptide Y.NSAIDs. See Nonsteroidal anti-inammatory drugs.Nutritional deciency theory, of cyst formation, 57, 57fOObjective examinationcold testing, 84–85electric pulp testing, 84elements of, 83t, 84focused examination, 84intraoral examination, 84periodontal examination, 87, 87f–88fperiodontal ligament assessment, 87pulp sensitivity tests, 84–86Obturationnonsurgical root canal therapy uses of, 134f, 134–135, 137overextension of materials used in, 230, 230fOcclusal adjustment, 49–50, 50fOcclusal forces, 49–50Occupational Health and Safety Administration, 157OCEBM. See Oxford Centre for Evidence-Based Medicine.Ochsenbein-Luebke technique, 140Odontoblasts, 25, 205Odontoclasts, 199Odontogenesis, 24Odontogenic pain, 73, 84Oehler’s dens invaginatus classication, 35, 35fOHSA. See Occupational Health and Safety Administration.Ophthalmic vein, 37Opioid receptors, 73Oral cancer screening, 84Orofacial trauma, 178Orthodontic treatmentinternal cervical root resorption caused by, 202pulpal tissue affected by, 48f, 48–49root resorption and, 48–49Osteoblasts, 55Osteocalcin, 25Osteoclasts, 55Osteoconductive grafts, 143Osteogenic grafts, 143Osteoinductive grafts, 143Osteomyelitis, mandibular, 111fOsteonecrosisbisphosphonate-related osteonecrosis of the jaw, 75neuralgia-inducing cavitational, 109Osteosarcoma, 114fOsteotomy, 140, 232Outcomesapexication, 215, 216fapical periodontitis effects on, 210, 212endodontic surgery, 213–214, 214ffactors that affect, 208nonsurgical retreatment, 212, 212fnonsurgical root canal therapy, 209t, 209–211, 211fvital pulp therapy, 214–215Outer enamel epithelium, 24–25Oxford Centre for Evidence-Based Medicine, 2–3PPacemakers, 86Painanalgesics for, 73atypical facial, 108–109, 109fbiting, 87cardiac, 110deafferentation, 109hydrodynamic theory of, 28myofascial, 106neuropathic, 108, 108fneurovascular, 109–110nonodontogenic, 240odontogenic, 73, 84persistent, 239–240, 240fphantom tooth, 109postoperative, 73psychogenic, 110referred, 106selective anesthesia testing for, 88sinus, 106–107Palatal anesthesia, 121Panoramic radiographs, 89, 90fPapilla-based incision, 140Paraformaldehyde-containing sealers, 231Paresthesias, 235–236Paroxysmal hemicrania, 108Passive step-back technique, 126, 126fPassive ultrasonic irrigation, 131Patency, 125–126, 126fPatient record condentiality, 157PCO. See Pulp canal obliteration.PCOD. See Periapical cemento-osseous dysplasia.PCR. See Polymerase chain reaction.PDL. See Periodontal ligament.Peer-reviewed journals, 1–2Penicillin VK, 69, 71tPercocet, 74tPercussion tenderness, 87Perforations, 225–227, 225f–227fPeriapical abscess, 233Periapical actinomycosis, 14, 238Periapical cemento-osseous dysplasia, 113, 114f, 116Periapical cysts, 57f, 57–59, 90Periapical granulomas, 56–57, 57f, 59, 90Periapical index score, 153Periapical inammation, 9, 9fPeriapical lesionsbacteria in, 55–56, 56fborders of, 89cysts, 57f, 57–59diagnosis of, 90frequency of, 59 Index253Pgranulomas, 56–57, 57f, 59, 90histologic evaluation of, 56types of, 58, 58fPeriapical pathologyapical periodontitis, 53, 53fcellular responses to, 54, 54fhumoral responses to, 54–55Periapical radiographs, 89, 90f, 92t, 94, 95f, 183Periapical radiolucencies, 113–114, 117fPeriapical tissues, 54, 54fPeriodontal diseaseorofacial infections caused by, 110pulpal tissue affected by, 49Periodontal examination, 87, 87f–88fPeriodontal ligamentaccessory canals and, 34, 34fassessment of, 87calcium hydroxide effects on, 133luxation-type injuries, 185odontoclasts in, 199surgical healing and, 144traumatic dental injury effects on, 194widening of, 113Periodontal pocket depths, 87Periodontal-endodontic lesions, 99–100, 100fPeriodontitisapical. See Apical periodontitis.pulpal tissue affected by, 49, 49fPeriorbital space, 17, 20Periosteal necrosis, 145Persistent idiopathic facial pain, 108–109Persistent infections, 238Persistent pain, 239–240, 240fPhantom tooth pain, 109Pharmacologyanalgesics, 73–74, 74tantibiotics. See Antibiotics.anxiolytics, 74–75local anesthetics, 68t, 68–69Phentolamine mesylate, 69PHI. See Protected health information.Photodynamic therapy, 130, 130fPIFP. See Persistent idiopathic facial pain.Plasma cells, 52, 77Platelet-rich brin, 147PMN. See Polymorphonucleocyte inltrate.Polymerase chain reaction, 9Polymorphonucleocyte inltrate, 145Polymyalgia rheumatica, 110Porphyromonas spp.description of, 13, 13fP. gingivalis, 11Positive predictive value, 4f, 5Post(s)in endodontically treated teeth, 154–155, 155fperforation of, 226fremoval of, 136Posterior superior alveolar nerve, 38Posterior superior alveolar vein, 37Predentin, 48Predictive values, 4f, 5Premolars, 32t–33tPressure resorption, 206, 206fPrevalence, 5f, 5–6Previously initiated therapy, 96Previously treated teeth. See also Endodontically treated teeth.cone beam computed tomography of, 94denition of, 96Prevotella melaninogenica, 13Prevotella nigrescens, 13Price, Weston, 8, 50Prilocaine, 68t, 235, 235fPrimary dentin, 26, 26fPrimary dentitionendodontic disease in, 217necrosis in, 217traumatic dental injuries in, 192Primary infections, 16f, 16–17Primary intention, 142Prions, 15Prognosis, 6Prognostic rates. See Success rates.Prostaglandins, 54Prosthetic joints, 72f, 72–73Protected health information, 157Proton pump, 12Psychogenic pain, 110Pterygoid venous plexus, 37Pterygomandibular space, 17, 20PUI. See Passive ultrasonic irrigation.Pulpadrenergic nerves of, 28age-related changes in, 30, 31fanatomy of, 27arterial structures in, 29autonomic nerves of, 28bacterial contamination of, 10, 10fblood ow in, 28–30, 48, 52, 52fcalcication of, 112, 112fcollagen composition of, 27composition of, 27description of, 96diagnoses associated with, 96, 96fdirect visualization of, 85embryology of, 25extracellular connective tissue of, 27, 27fimmunology of, 52–53lymphatics of, 30necrosis of. See Pulpal necrosis.orthodontic treatment effects on, 48f, 48–49periodontitis effects on, 49, 49fsensory nerves of, 27f, 27–28stimulation of, 29, 29f, 46vasculature of, 29–30, 30fvasodilation of, 29vital pulp therapy. See Vital pulp therapy.Pulp canal obliteration, 193Pulp capping, 146, 147f, 214–215Pulp chamber anomalies, 112Pulp polyp, 100Pulp revascularization therapy, 188Pulp sensitivitydescription of, 28, 28f, 76loss of, 86testing forbaseline, 181cold testing, 84–85 254IndexPelectric pulp testing, 84–86, 87f, 181epidemiology of, 86tuid changes caused by, 85fheat testing, 85, 87fin luxation-type injuries, 188radiation therapy and, 76Pulp stones, 76, 112, 112fPulp vitality testing, 86–87, 87f, 181, 188Pulpal anesthesia, 121Pulpal healingpulpal necrosis and, 11restorative materials and, 47Pulpal inammationcaries as cause of, 45–46development of, 52leukocytes in, 52posttraumatic, 179Pulpal irritantscaries as, 45–46cellular responses to, 52fractures as, 46humoral responses to, 52immune responses activated by, 51, 51fneurovascular responses to, 51–52occlusal forces as, 49–50orthodontic treatment as, 48–49periodontal disease as, 49, 49frestorative treatment as, 46–47thermal insults as, 48Pulpal necrosisapical periodontitis and, 8f, 53fdenition of, 96in endodontic lesions, 99herpes zoster and, 116pulpal healing and, 11pulpal irritants as cause of, 51after traumatic dental injuries, 193Pulpal pathologydescription of, 51fractures as cause of, 46histology of, 53neurovascular responses to, 51–52signs and symptoms, 53Pulpectomy, 229fPulpitishyperplastic, 100irreversible, 51, 53, 69, 75, 96, 156reversible, 53, 96Pulpotomy, 147, 147f, 215, 217P value, 3–4, 4fPyrosequencing, 16QQuorum sensing, 11RRadiation therapy, 76Radicular dentin, 216Radiographic examinationbitewing radiographs, 89, 90fcone beam computed tomography. See Cone beam computed tomography.digital radiography, 90panoramic radiographs, 89, 90fperiapical radiographs, 89, 90f, 92t, 94, 95f, 183radiographic changes, 89radiology principles, 88systematic approach, 88, 89ftraumatic dental injuries, 183two-dimensional dental radiography, 90–92, 91fRadiology, 88Randomized controlled trials, 2RANKL. See Receptor activator of nuclear factor kappa-B ligand.Ratner bone cavities, 109Reactionary dentin, 26Receptor activator of nuclear factor kappa-B ligand, 55Rectangular ap, 140Referred pain, 106Refrigerant spray, 85Regenerative endodontics, 149–152, 150f–152f, 216fReparative dentin, 26, 47Replacement resorption, 194, 205, 205fReplantation, of avulsed teeth, 191–192Research, 9–10Resection, 141Resilon, 134Resin-modied glass ionomers, 47Resorbable membranes, 143–144Resorcinol, 136Resorptionin apical periodontitis, 55cytokine involvement in, 55description of, 199external apical root, 194external inammatory root, 204–205, 205finternal root, 193–194, 200–201, 201finvasive cervical root, 194, 201–204, 202f–203fmalignancies as cause of, 114, 114forthodontic therapy and, 48–49pathogenesis of, 199, 200fpressure, 206, 206freplacement, 194, 205, 205fafter traumatic dental injuries, 193–194types of, 100, 200fResource-intensive studies, 2Restorative treatmentsendodontic therapy after, 47, 47fpulpal tissue affected by, 46–47quality of, 210temporary, 135, 153, 156Retrolling, 141–142, 142t, 213Retropreparation, 141Reversible pulpitis, 53, 96Rheumatoid arthritis, 76Root apex, 33Root canal(s)accessory, 34anatomy of, 31–36conguration of, 31, 32t–33tC-shaped, 35–36, 36fmaxillary, 32tvariants of, 35–36Vertucci classication system for, 31, 31fRoot canal lling materials, 155 Index255TRoot canal space, 35Root fracturescharacteristics of, 182, 182fcone beam computed tomography detection of, 94healing after, 187, 187fhorizontal, 184fradiographic ndings of, 184ftreatment of, 186t, 186–187vertical, 97–99, 98f, 185, 239, 239fRoot resorption. See Resorption.Root ZX apex locator, 125, 125fRoot-end surgery, 232, 235–236Rotary instruments, 127, 222Rubber dams, 123“Russian Red” removal, 136–137, 137fSSaccharolytic, 13Scalloped submarginal incisions, 140Scleroderma, 113Sealer, 135, 230, 230fSecond order neurons, 39Secondary canal, 34, 34fSecondary dentin, 26, 26fSecondary infections, 16f, 16–17, 238Semilunar aps, 140Sensitivity, 4f, 5Sensory nervesof pulp, 27f, 27–28stimulation of, 29, 29fSeparated instruments, 222–224, 222f–224fSialophosphoprotein, 25Sickle cell anemia, 116Signaling molecules, 24Silver points, 137, 137fSimvastatin, 55, 146Single-unit implants, 156Single-visit therapy, 131f, 131–132, 236Sinus pain, 106–107Smear layer, 127–128Smoking, 77Sodium hypochloriteaccidents involving, 228–229, 228f–229fantimicrobial uses of, 150chlorhexidine gluconate and, 130fproperties of, 128–129, 129fSodium perborate walking bleach technique, 152Soft tissue healing, 144SP. See Substance P.Specicity, 4f, 5Spirochetes, 14Splinting, 185, 185f, 186tStainless steel instruments, 222State laws, 157Statisticsmeasures of statistical signicance, 3–4measures of validity, 4–5, 4f–5fStem cells, 151Step-down technique, 126, 126fStreptococci, 12Streptococcus spp.S. epidermidis, 17S. mitis, 12S. mutans, 45Stressed pulp syndrome, 46Study design, 2–3Subclavian vein, 37Subjective examination, 83t, 83–84Sublingual space, 18, 20Subluxation, 182, 184f, 186t, 187Submandibular space, 18, 20Submarginal incisions, 140, 140fSubmental space, 18, 20Subodontoblastic capillary plexus, 29Substance P, 25, 29, 49, 51Success ratesfor endodontic surgery, 213–214for endodontic treatment, 208factors that affect, 208for nonsurgical retreatment, 212, 212ffor nonsurgical root canal therapy, 209t, 209–211, 211ffor pulpotomy, 215for vital pulp therapy, 214–215Sulcular perforations, 227Sulfur granules, 14Super EBA, 141, 142tSuperoxol, 152Supplemental anesthesia, 123Suppressor T cells, 54, 54fSurgeryendodontic. See Endodontic surgery.maxillofacial anatomy, 39unconventional approaches, 145–146Surgical endodontics. See Endodontic surgery.Surgical operating microscope, 124, 124f, 224Surgical root canal therapy. See Endodontic surgery.Surgical site exposure, 140Suturing, 142Swelling, noninfectious, 111Symptomatic apical periodontitis, 96Systematic reviews, 2TT cells, 54, 54fTA. See Temporal arteritis.Talon cusp, 35Tannerella forsythia, 11, 16Teeth. See also Mandibular teeth; Maxillary teeth; Primary dentition; specic teeth.arterial supply to, 36–37avulsed. See Avulsions.embryology of, 24–25, 25fmicrocracks in, 179neural pathways to, 38f, 38–39thermal sensitivity of, 46Temporal arteritis, 109–110Temporary restorations, 135, 153, 156Tension-type headaches, 108Tertiary dentin, 26, 26fTest outcomes, 5tTetracalcium aluminoferrite, 141, 142tTetracycline, 69Thermal injuries, 231f, 231–232Thermal insults, 48Thermal sensitivity tests, 86 256IndexTThird order neurons, 39Thoracic duct, 38Tissue engineering, 149TN. See Trigeminal neuralgia.Tooth preparation, 46–47Tooth stiffness, 153Trabeculae, 145Transillumination, 88Traumatic dental injuriesacute priority, 180, 180fage of patient and, 178, 179favulsionsdescription of, 183in immature teeth with closed apex, 191–192in mature teeth with closed apex, 191periodontal ligament maintenance in, 189radiographic ndings in, 185replantation of, 189, 191–192storage of tooth, 189, 189f, 191treatment of, 186t, 189–192, 190fin children, 178complications of, 193–194, 195fdelayed priority, 180, 180fdescription of, 100diagnosis ofclinical examination, 181clinical ndings, 182–183, 182f–183fdata necessary for, 180periradicular testing, 181primary survey in, 179secondary survey in, 179systematic approach for, 180, 181fepidemiology of, 178external inammatory root resorption and, 204falls as cause of, 178fracturesradiographic ndings, 184f, 184–185types of, 182guidelines for, 177incidence of, 178luxation-type injuriesfollow-up of, 189radiographic ndings in, 185treatment of, 186t, 187–189types of, 182–183mouth guards for prevention of, 195pathophysiology of, 179postoperative instructions for, 192prevention of, 195in primary dentition, 192prioritization of, 180, 180fprognosis for, 192, 193tpulpal inammation after, 179pulpal necrosis after, 193radiographic examination, 183radiographic ndings, 184f, 184–185resorption after, 193–194risk factors for, 178fsplinting of, 185, 185f, 186tsubacute priority, 180, 180ftreatment of, 185–192, 186tTreponema spp., 14Triangular ap, 140Triazolam, 75Trichloroacetic acid, 204Trigeminal autonomic cephalalgias, 108Trigeminal ganglion, 39Trigeminal nerve, 38–39Trigeminal neuralgia, 108Triptans, 107True cysts, 57–58Tumor necrosis factor-α, 55Two-dimensional dental radiography, 90–92, 91fUUltrasonic instruments, 232Ultrasonic retropreparations, 141Ultrasonic vibration, 136–137Uncomplicated fractures, 182, 184fVValidity, 4–5, 4f–5fVaricella zoster virus, 15Vasculature, pulpal, 29–30, 30fVenous drainage, 37Vertical condensation, 134Vertical releasing incision, 140Vertical root fractures, 97–99, 98f, 185, 239, 239fVertucci’s root canal classication system, 31, 31fVicodin, 74tViruses, 15, 15fVital pulp therapypulp capping, 146, 147f, 214–215pulpotomy, 147, 147f, 215purpose of, 146success rates for, 214–215VZV. See Varicella zoster virus.WWorking lengths, 124–125, 125fXXenografts, 143, 143fZ“Zones of Fish,” 8, 8f

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