Endo protocols

UNIVERSITY OF OSLO
FACULTY OF DENTISTRY
Department of Endodontics
Postgraduate Program in
Endodontics
Case Book
Pia Titterud Sunde
Spring Semester 2012

1
Table of Contents
Endodontic Treatment Guidelines 2
PULPITIS
Case 1 4
Treatment of the mandibular left second
molar with acute irreversible pulpitis and
cracked tooth syndrome 4
Case 2 10
Treatment of the maxillary right second
molar with irreversible pulpitis and the
mandibular right second molar with
primary infection in a patient with
myelomatosis 10
PRIMARY INFECTION
Case 3 16
Treatment of the the mandibular right
first molar with chronic apical
periodontitis in a patient with anxiety
disorders 16
Case 4 20
Treatment of the mandibular right first
molar with chronic apical periodontitis 20
Case 5 24
Treatment of the maxillary right lateral
incisor and canine in patient with
keratocystic odontogenic tumor 24
Case 6 32
Treatment of a maxillary left first molar
with iatrogenic furcal perforation 32
Case 7 38
Treatment of a mandibular right lateral
incisor with two canals 38
PERSISTENT APICAL PERIODONTITIS
Case 8 42
Retreatment of a mandibular left canine
with sinus tract and primary treatment of
a mandibular right first premolar with
acute apical periodontitis 42
Case 9 48
Retreatment of a mandibular left first
molar with post and two separated
instruments 48
Case 10 53
Non surgical - and surgical endodontic
treatment of a maxillary right central
incisor with radicular cyst 53
Case 11 61
Surgical endodontic treatment of the right
maxillary first incisor with sinus tract 61
Case 12 67
Surgical endodontic treatment of a
maxillary left canine with sinus tract 67
Case 13 72
Surgical endodontic treatment of a
maxillary right first premolar 72
Case 14 76
Non surgical retreatment and later
surgical retreatment of a mandibular right
first molar with carbon post and separated
instrument 76
RESORPTIONS
Case 15 83
Treatment of maxillary central incisors
with external inflammatory resorptions 83
Case16 88
Endodontic treatment in conjunction with
surgical treatment of maxillary right first
central, mandibular left second premolar
and first molar in patient with multiple
inflammatory cervical resorptions 88
Case 17 99
Non-surgical retreatment of the maxillary
right lateral incisor with internal
resorption 99
PAIN MANAGEMENT
Case 18 104
Patient with persistent pain maxilla left
side 104
ATYPICAL TOOTH MORPHOLOGY
Case 19 110
Endodontic treatment of a mandibular
right first molar with C-shape anatomy110
Case nr 20 113
Endodontic treatment of the immature
maxillary left lateral incisor with dens
invaginatus 113

2
Endodontic Treatment
Guidelines
Treatment of Tooth without Apical
Periodontitis:
• Preoperative radiograph.
• Anaesthesia
• Removal of plaque, caries and
leaking fillings. Tooth build-up if
required for isolation.
• Access cavity preparation.
• Localization of canal openings
• Application of rubber dam
• Disinfection of the working field
with 0.5% chlorhexidine in 70%
ethanol
• Measurement of working length,
using apex locator and working
length radiograph.
• Frequent irrigation with 0.5%
sodium hypochlorite (NaOCl).
• Final irrigation with 17%
ethylenediamine tetraacetic acid
(EDTA).
• Drying of the canals with paper
points Master point radiograph
Root filling:
• Sealers: AH Plus, Epiphany/Real
Seal Core materials: Gutta-percha,
Resilon
• Temporary IRM top filling with a 2
mm IRM plug in the canal orifice.
• Removal of rubber dam
• Final radiograph
Treatment of Tooth with Apical
Periodontitis:
• The same treatment as for teeth
without apical periodontitis, but
two-appointment treatment is the
standard procedure: 2-3 weeks
between 1st and 2nd appointment is
the standard (this is mainly for
practical reasons:
• Two-layered temporary top filling:
Cavit G and IRM
• In retreatment cases: Final irrigation
with 17% EDTA and 2%
chlorhexidine
• The periapical index (PAI) Ørstavik
et al 1986, is used for radiographic
evaluation.
Reference set of radiographs with corresponding line
drawings and their associated PAI scores (Ørstavik et al
1986).
Endodontic Surgery:
• All relevant radiographs mounted on
viewer or screen
• Anaesthesia.
• 1 minute mouth rinse with
Corsodyl®(Chlorhexidine 2mg/ml)
• full mucoperiosteal flap
• Incision: A horizontal incision
extending one to several teeth
mesial and distal of the involved
tooth and one vertical-releasing
incision, usually placed at the
mesial end of the prospective flap.
• Retraction: To hold the flap away
from the surgical site, providing
maximum access and visibility,
without causing harm to the flap or
the surrounding tissues.
•  Osteotomy: Involves removal of
cortical and cancellous bone to gain
direct access to the apical portion.
This is achieved routinely by using
rotary instruments.
• Surgical curettage: To remove all
pathologic tissue, foreign bodies,
and root and bone particles from
the periradicular area.
• Biopsy: any soft tissue lesion
removed during the surgical
procedure should be submitted for
biopsy.

3
• Microbiological sample: with paper
point directly in the periapical
smple, placed in prereduced
anaerobic transportmedium, or
periapical tissue placed in 4%
formalin for scanning electron
microscopy.
• Root end resection: by sectioning the
apical segment of the root and/or
bevelling it to the line of sight. 3
mm.
• Ultrasonic root end preparation: To
provide a clean, well-shaped class I
cavity
• Haemorrhage control
Local anaesthetic solutions possessing
vasoconstrictor properties - Xylocain-
Adrenalin® 10mg/ml + 5μg/ml
Stryphnon gauze (Adrenalonchlorid 0,33
mg/cm2)
Ferric sulfate (Fe2[SO4]3 with 15.5%
astringet and 21% stasis)
• Root-end filling: using either IRM or
MTA. Use of the MAP system
(Micro-Apical Placement) or the
MTA pellet-forming block will
ease the application of MTA.
• Cleaning of surgical site: Saline
solution to remove debris, and
tissue edges are re-approximated in
their correct position to promote
healing by primary intention.
Compression of the repositioned
tissue with a saline-moistened piece
of gauze will reduce the coagulum
to a thin fibrin layer between the
repositioned tissue and cortical
bone. Tissue margins should rest
passively in the desired place
before suturing.
• Wound closure: using non-
absorbable suture material in sizes
4-0 and 6-0. Postoperative
radiograph is taken for control of
procedures and as reference for
follow-up.
• Postsurgical care: A disposable ice
pack is covered with soft towelling,
and the patient instructed on where
and how to hold the ice pack firmly
in position against the facial tissues
approximating the surgical site.
Unless contraindicated for some
reason, the patient is instructed to
take IBUPROFEN 400 mg every 4
to 6 hours for the first 48 hours.
The patient is advised to rinse with
Corsodyl® twice daily until suture
removal.
• Suture removal: The epithelial seal at
the wound edges is evident within 2
days; suture removal can take place
earliest after 48 h but not later than
4-5 days.
• Prescription of: IBUPROFEN 400
mg. NO 30. Every 6 hours for 3
days.

4
Case 1
Treatment of the mandibular left second molar with acute irreversible pulpitis and
cracked tooth syndrome
Fig 1. Frontal view
Patient: 65 year old Caucasian male
Chief complaint: He complained about
strong pain left side. He felt sudden pain
when chewing and biting, and he had
problems with sleeping because of pain
Medical record: Non-contributory
Dental history: The patient was referred to
the post-graduate endodontic clinic from
the graduate clinic for retreatment of tooth
36 because of sudden pain.
Clinical findings 26 th
of October 2010:
Soft tissue: normal findings
Dental:
Tooth 35 MOD amalgam filling
Tooth 36 MODL composite filling
Tooth 37 occlusal and buccal amalgam
filling. Several craze lines can be seen in
the enamel (Fig. 2 , 3).
Fig 2. Tooth 37, several craze lines
are visible in the distal, lingual and
buccal aspect of the tooth
Fig 3. Occlusal view
Clinical test 26 th
of October 2010
35 36 37
EPT (0-80) 17 - 14
Cold + - +
Percussion
Vertical/horizontal
- v v and h
Palpation - - +
PPD 3 3 3
Mobility - - -
Biting +
Table 1
The patient has an intense reaction upon
coldtest and EPT on tooth 37. He could tell

5
about lingering pain that lasted about 30
seconds. Using a FracFinder on the
different cusps of tooth 37, the patient felt
sharp pain when dl cusp was tested. He felt
the pain most when he opened his mouth.
Radiographic findings 26 th
of October
2010:
Dental: Tooth 36 has an insufficient root
canal treatment and an MOD radiopaque
restauration.
Tooth 37 has a curved mesial root and
radiopaque restauration
Periodontal: 36 within normal limits,
37 attachement 2/3
Apical: 36 apical radiolcency mesial root,
(PAI 3). 37 normal PDL (PAI 2)
Fig. 4 Periapical radiograph 26.10.2010
Diagnosis 26 th
of October 2010:
Tooth 37
Pulpal: Acute irreversible pulpitis
(K04.01)
Tooth 36
Pulpal: Root filled tooth (K04.19)
Periapical: Chronic apical periodontitis
(K04.50)
Treatment plan:
Tooth 37: Treatment of inflammed pulp
Tooth 36: Retreatment of root filled tooth
Problem list:
Anatomical considerations (curved mesial
root) 37
Treatment 26 th
of October 2010
Cuspal reduction, especially dl cusp.
Access opening and location of three
canals. Bleeding from all canals. Distal
crack is visible in the pulp chamber with
extension mesially.
The patient was told that the tooth would
have a less favourable prognosis unless a
dental crown was made.
Mechanical: Bur,
NiTi hand instrumentation
-MB 17mm/R40
-ML 17mm/R40
-D16mm/R55
Chemical:1% NaOCl, 16% EDTA
Intracanal medicament: Ca(OH)2
Temporary filling: IRM
Fig. 5 Working length radiograph
Treatment 16th
of November 2010:
Less symptoms. Not tender to percussion,
but he had exsperiensed sporadic pain from
the area.
Filled with gutta-percha and AH plus,
sealed with IRM. The graduate student was
informed about the cracked tooth and the
importance of permanent rastauration with
cusp coverage.
Fig. 6 Masterpoint radiograph

6
Fig. 7 Final radiograph 16.11.2009
Prognosis:
Endodontic: the prognosis seemed to be
good
Tooth: uncertain (a semipermanent
composite restauration was palaced i
December 2009, (one month after
endodontic therapy)
The patient had started at a private dental
practitioner.
Follow up examination 10 th
of November
2011 (12 months):
The patient had still symtoms from the
area from time to time. Retreatment of 36
was startet by general practitioner some
months ago, but the patient had canselled
the last appointment. The patient wanted to
complete root-canal treatment of tooth 36
at the postgraduate endodontic clinic.
Fig. 8 Follow up radiograph 10.11.2011
of November 2011:
Dental:
Tooth 35: MOD amalgam filling
Toth 36: composite filling, occlusal IRM
Tooth 37: composite filling with cuspal
coverage, but not covering completely at
the distal aspect. The previous buccal
amalgam filling was placed with an IRM
Fig. 9 Lingual view
Fig. 10 Buccal view
Clinical test 10 th
of November 2011
35 36 37
EPT (0-80) 23 - -
Cold + -
Percussion
Vertical/horizontal
- v v
palpation - - +
PPD 3 3 4
Mobility - - -
Biting - +
Table 2
Radiographic findings 10th
of November
2011:
Dental:
Tooth 36: insufficient root filled,
radiopaque filling MOD
Tooth 37: root filled, radiopaque filling
MO
Periodontal:
Tooth 37 attachment =2/3, bifurcation
involvement
Apical :
Tooth 36: apical radiolcency (PAI 3)
Tooth 37: normal PDL (PAI 2)

7
Diagnosis 10th
of November 2011
Tooth 36
(K04.50)
Periodontal: Within normal limits
Treatment plan:
Retreatment of root filled tooth 36
Progress notes 11th
of November 2011:
Access opening and location of three canal
orifices with guttapercha
Mechanical: Bur, IrriSafe
NiTi handinsrumentation, BioRace
-MB 20/#40
-ML 20/#40
-D 20/55#
Chemical: 1% NaOCl, 16% EDTA,
2% chlorhexidinedigluconate
Fig 11. Working length radiograph
Treatment 12th
of December 2011
Sporadic symptoms from area 37
sealed with IRM.
Fig13. Final radiograph 12.12.2011
Follow-up: The patient had an
appointment for follow-up which he
canselled. He could tell on the phone that
he still had some discomfort from the tooth
37 from time to time. Especially in the
morning, but no pain when chewing or
biting.
Discussion
The patient in the present case had an
incomplete fractured tooth.
Historically, there have been a number of
terms used to describe cracked teeth as
well as a number of different classification
schemes. The incompletely fractured tooth
has for example been defined as ‘a tooth
with a demonstrable fracture, but no
visible separation of thesegments’(1)
Cracked tooth syndrome was first
described by Cameron (2) in 1964. He
defined a cracked tooth as “an incomplete
fracture of a vital posterior tooth involving
dentin and possibly pulpal tissue.” He also
stated that these dentinal injuries may be
asymptomatic, or associated with
symptoms and even orofacial pain (2).
The American Association of Endodontists
(AAE) has identified five types of cracks
in teeth (3); craze line, fractured cusp,
cracked tooth, split tooth, and vertical root
fracture. Craze lines are visible fractures
that only involve enamel. Fractured cusps
originate in the crown of the tooth, extend
into dentin, and the fracture terminates in
the cervical region. A cracked tooth is
defined by the AAE as a crack extending
from the occlusal surface of the tooth
apically without separation of the two
segments. A split tooth is a crack that

8
extends through both marginal ridges
usually in a mesiodistal direction, splitting
the tooth completely into two separate
segments. Vertical root fractures originate
in the root, and are generally complete,
although they may be incomplete.
The diagnosis of CTS has been based in
the past exclusively on tooth symptomatol-
ogy: localized pain during chewing or
biting, unexplained sensitivity to cold, and
pain on release of pressure (2,4). A clinical
study by Rattcliff et al. (5) showed that a
larger preparation, presence of an amalgam
restoration, and parafunctional habits
increased the risk for the occurrence of
crack lines. However, in another study
60% of teeth with cracks had no
restoration (6). In a recent review of the
the literature the aim was to establish what
evidence exists regarding the risk factors
for cracked teeth and their prevention,
diagnosis, and treatment (7). They found
that there is no current evidence
demonstrating which treatment option has
the greatest success rate both from a
restorative perspective and from a pulpal
health standpoint.
Only one clinical trial conducted to support
the use of extracoronal restorations in the
treatment of cracked teeth was found in
this review of the literature. The study by
Krell and Rivera (8) reported the out-
comes of symptomatic cracked teeth that
were initially diagnosed with reversible
pulpitis and treated with full coverage
restorations. The outcomes of this study
suggest that, if a crack is identified early in
cases with a diagnosis of reversible pulpitis
and a crown is placed, root canal treatment
will be necessary in about 20% of the
cases. One hundred and twenty seven teeth
were followed after crown placement for 6
years. From a restorative standpoint, the
full coverage treatment was successful for
all 127 teeth because symptoms resolved
(with or without RCT) and the teeth were
retained. T his study did not compare
success rates of crowns versus other
restorative treatments so it is impossible to
interpret the results to say that full
coverage is the best treatment for CTS. In
another clinical study, 40 patients
diagnosed with reversible pulpitis and CTS
and treated with direct composite resto-
rations were followed for 7 years (9). The
patients were divided into two groups and
the restorations placed were either direct
composite intracoronal restorations or
direct composite cuspal overlay. After 7
years, no teeth were extracted due to
restorative failures; therefore, all treat-
ments were considered successful.
However, three patients needed RCT, 50%
of all restored teeth were still symptomatic
after 6 months, and 25% were still symp-
tomatic after 7 years. There were no
restorative failures for the group with
cuspal coverage, but the intracoronal group
did have a mean annual failure rate of
6.0%. This difference was significant.
The authors suggested that bonded
composite can be an effective treatment for
painful cracked teeth, resulting in more
than 90% of the teeth maintaining pulp
vitality.
In a study by Brynjulfsen et al.,(10), thirty-
two patients with poorly localized
orofacial pain, were finally diagnosed with
46 incompletely fractured teeth. They
found that the longer the duration of pain
before the diagnosis of an incompletely
fractured tooth was established, the more
diffuse was the distribution of pain.
Endodontic or restorative treatment
relieved the symptoms in 90% of the
patients, whilst persisting symptoms in
10% were considered part of an orofacial
pain complex of obscure aetiology.
References
1. Luebke RG. Vertical crown-root fractures in
posterior teeth. Dental Clinic of North America
1984; 28, 883– 95.
2.Cameron CE. Cracked-tooth syndrome. J Am
Dent Assoc 1964;68:405–11.
3.American Association of Endodontists. Cracking
the cracked tooth code. Endo- dontics: Colleagues
for Excellence 1997;(Fall/Winter):1–13.
4.Ratcliff S, Becker IM, Quinn L. Type and
incidence of cracks in posterior teeth. J Prosthet

9
Dent 2001;86:168–72.
5. Rattcliff S, Becker IM, Quinn L. Type and
incidence of cracks in posterior teeth.
J Prosthet Dent 2001;86:168 –72.
6. Roh BD, Lee YE. Analysis of 154 cases of teeth
with cracks. Dent Traumatol 2006;22:118 –23.
7. Lubisich EB et al. Cracked Teeth: A Review of
the Literature.jJ Esthet Restor Dent 22:158–167,
2010
8. Krell KV, Rivera EM. A six year evaluation of
cracked teeth diagnosed with reversible pulpitis:
treatment and prognosis. J Endod 2007;33:1405–
7.
9.Opdam NJ, Roeters JJ, Loomans BA, Bronkhorst
EM. Seven-year clinical evaluation of painful
cracked teeth restored with a direct composite
restoration.
J Endod 2008;34:808–11.
10.Brynjulfsen A, Fristad I, Grevstad T, Hals-
Kvinnsland I. Incompletely fractured teeth
associated with diffuse longstanding orofacial pain:
diagnosis and treatment outcome. Int Endod J
2002;35:461–6.

10
Case 2
Treatment of the maxillary right second molar with irreversible pulpitis and the
mandibular right second molar with primary infection in a patient with
myelomatosis
Fig. 1 Frontal view
Chief complaint: Pain upper and lower
jaw right side. High CRP without knowing
the reason for this
Medical record: The patiend had
myelomatosis
(myeloplastic/myeloproliferating with
eosinofili and trombocytemie) that was
diagnosed in August 2010. He had been
medicated with Glyvek since then, but had
to stop this treatment because of joint
necrosis.
• He gets easily infections
• High blood pressure
• Dry mouth (frequent waterdrinking
at night)
• Dental fear
• Medicaments: Celosok 50 mg and
Atacand 4 mg
Dental history: The patient himself
contacted the dental clinic because of pain
and discomfort upper and lower jaw right
side. He had been troubled with fever for
some period of time and high CRP. The
doctors did not know the reason for this.
When he first came to the clinic, caries
removal and IRM restaurations both teeth
were made by general practitioner the day
before endodontic treatment started. He
had not visited any dentist the last years
because of dental fear.
of February 2012
Soft tissue: normal finding, pale gingiva
Poor dental hygiene upper and lower front
Dental:
Tooth 17: temporary filling
Tooth 16: MOD composite filling
Tooth 37: temporary filling
Tooth 36: MOD amalgam filling
Fig. 2 Occlusal view tooth 17
Fig. 3 Occusal view tooth 47

11
Clinical tests 28 th
of February 2012
16 17 46 47
EPT (0-80) 15 - 20 45
Cold + - + +
Percussion
Vertical/horizontal
- + - -
palpation - - -
PPD 3 3 3
Mobility - - -
Table 1
of February
2012 (the radiographs were taken before
placement of IRM)
Dental: Deep caries teeth 17 and 36.
Tooth 17 has an MO amalgam filling
Tooth 35 has an insufficient root filling
with radiopaque occlusal filling, with a gap
between tooth and filling distally.
Apical: Normal findings (PAI I)
Fig 5 Periapical radiograph 28.02.2012
Diagnosis 28 th
of February 2012
Pulpal: Tooth 17: Infected necrosis
(K04.11)
Tooth 36: Chronic irreversible pulpitis
(K04.03)
Periapical: normal
Periodontal: within normal limits
Treatment plan
Treatment of infected pulp tooth 17
Treatment of pulpitis tooth 36
Problem list
Anatomical considerations mesial and
distal roots tooth 17
Treatment 28 th
of February 2012
Tooth 17: Because of fear of bacteremia
the patient was given antibiotic
prophylaxis one hour before treatment.
Before endodontic treatment, his doctor
was contacted, who confirmed that this
was advisable because of his poor health
and risk of infections. The patient was after
endodontic treatment referred to a dentist
at the same clinic, and adviced to see a
general practitioner regularly. He was also
told about the importance of maintaining a
good oral hygiene (see discussion). He
wantet to do as much as possible in one
visit, and thought long treatment time was
better than more visits. Access cavity
opening and location of first three, then the
forth (mp) canal was located after
preparation of the mb canal.
Mb and mp had one foramen apically.
Mechanical:
Because of S shaped mb and ml canals,
extensive NiTi hand instrumentation were
performed with #06-10 files in mb and ml
canals until the files were no longer
deformed and twisted
-MB 21/30#,-MP 20/30#-DB 21/40#
-P 21/50#
chlorhexidine-di-gluconate 2%
sealed with IRM

12
Fig. 6 Working length radiographs 28.02.2012
Fig 7. Masterpoint and final radiographs
28.02.2012
Prognosis
good
Tooth: the prognosis seemed too be good
Treatment 5 th
of March 2012
Tooth 46: The patient had no symptoms
from any teeth. His general health was
better, and he had no fever.
Access opening and location of two mesial
and one distal canals. Vital tissue apically
in all canals.
Mechanical:
Bur . NiTi handinstrumentation. BioRace
-MB 21/40#, -ML 20/40#, -D 21/50#
sealed with IRM
Fig 8. Working length and masterpoint radiographs
05.03.2012.
Disussion
The patient in the present case had
myelomatosis and immunosuppressed host
defences. He was therefore given antibiotic
prophylaxis before treatment, after
consultation with his medical doctor.
The only established use of antibiotic
prophylaxis in dentistry is in the attempt to
reduce the potential consequences of
bacteremias induced by dental treatment in
certain medically at-risk patients. The
principle indication for antibiotic
prophylaxis for dental patients is the
preven-tion of infective endocarditis in
patients with specific medical conditions
that are receiving specified dental
treatments (1). Controversial indications

13
include dental patients with orthopedic
prosthetic devices, indwelling catheters
and impaired (immunosuppressed) host
defenses.
Dental patients presenting for treatment
with impaired host defenses
(chemotherapy, organ transplant or tissue
graft recipient, insulin-dependent diabetes,
alcoholics) or patients with indwelling
catheters (hemodialysis) may benefit from
antibiotic prophylaxis if their white cell
count is below 2,500 (normal = 4,000-
11,000)
The most recent published guidelines from
The American Heart Association for the
prevention of infective endocarditis in
medically at risk patients was published in
April 2007 and represent a significant
change from the previous guidelines (1).
One of the stated reasons for the
development of the current revised
guidelines was that the risk of antibiotic-
associated adverse events exceeds the
benefit, if any, from prophylactic therapy.
The host defence against bacteria in the
blood may be weakened by various
diseases and conditions, e.g., neutropenia,
asplenia, poorly controlled diabetes, end
stage of renal disease, organ transplant,
HIV infection and prosthetic joints or
implants (2).
Debelian et al. (3, 4) found that when the
root canal reamer ended 2 mm outside the
root canal, 54% of the patients had
cultivable microorganisms in the blood.
When the instrumentation ended inside the
root canal, i.e., 1 mm from the apical
foramen, only 31% of the patients had
bacteraemia. All these patients suffered
from asymptomatic apical periodontitis.
Phenotypic and genotypic profiles were
provided from the bacteria and yeast
recovered from root canal and blood. The
methods used demonstrated identity
between root canal isolates and blood
isolates, suggesting that the root canal was
the source of the blood isolates.
Savarrio et al. (5). found bacteraemia after
root canal treatment in 30%. Pulse field gel
electrophore sis showed that two pairs of
strains from blood and root canal were
identical.
The patient in the present case was advised
to improve his oral hygiene to achieve
better oral healt. An infected area is more
due to cause bacteraemia than an
uninfected area ( 6) and in the case with
periodontitis, bacteraemia may be a
common event induced by chewing and
tooth brushing.
Oral bacteria have been demonstrated in
atherosclerotic plaques, heart valves, aorta
aneurysms, brain abscesses and joints (7a,
b) .This particularly relates to periodon-
topathogens such as Aggregatibacter
actinomycetem- comitans, Treponema
denticola and Porphyromonas gingivalis.
While the main interest previously was
directed against bacteraemia after dental
surgery, authors have started to suspect
that daily events such as chewing and tooth
brushing can contribute to the cumulative
exposure over time of the cardiovascular
system to oral bacteria causing
inflammation and thereby promoting
atherosclerosis.
Both teeth in the present case were treated
in one visit each without inlay of calcium
hydroxide. The one-visit treatment in
infected teeth, especially in teeth with
apical periodontitis, is debated. The
antimicrobial effects of calcium hydroxide
have been evaluated by clinical studies
where calcium hydroxide has been shown
to successfully disinfect root canals
following 1 month dressing in 97% of
treated cases (8). In a later study by the
same group, the effectiveness was
confirmed even when the dressing was
retained in the root canal for only 1 week
(9). However, these results have not been
reproduced in other studies. Cvek et
al.,(10) Ørstavik et al.,(11) and Peters et
al.,(12) demonstrated in clinical studies
that calcium hydroxide did limit bacterial
growth but did not totally eliminate the
bacteria from the root canals. Waltimo et
al.,(13) evaluated the clinical efficacy of

14
chemomechanical preparation of the root
canals with sodium hypochlorite and
interappointment medication with cal-
cium hydroxide in the control of root canal
infection and healing of periapical lesions.
They found that calcium hydroxide
dressing between the appointments did not
show the expected effect in disinfecting the
root canal system and in treatment
outcome. Similar results had also been
shown by Tang et al. ,(14) in a clinical
study on the antimicrobial effect of
calcium hydroxide used as
interappointment dressing. Using an
infective dentine model, (15) a study by
Saleh et al.,(16) found that the use of AH
plus and Grossmans sealer in root fillings
in vitro was effective in killing E. faecalis
in experimentally infected dentinal tubules
within the zone of 300 mm around the root
canal. Other endodontic sealers, as well as
calsiumhydroxide, reduced the numbers,
but did not effectively kill bacteria in
infected dentinal tubules. Anather study by
Özcan et al.,(17)confirmed that the AH
Plus root canal sealer was effective in
rendering the test E. fae calis cells in this
ex vivo dentine infection model
uncultivable or dead, whilst GuttaFlow
was ineffective in achieving this.
An exhaustive literature search combined
with specified inclusion criteria was
performed to identify randomized or quasi-
randomized controlled trials (RCTs or
quasi-RCTs), comparing root canal
treatment in single and multiple
appointments (2 or more visits) in patients
with infected root canals (18). According
to the results from the present review, the
healing rate of single- versus multiple-visit
root canal treatment was similar for
infected teeth. They also found that the
prevalence of post-obturation pain was
significantly lower in single-visit approach
at short-term follow-up time. However,
because the number of studies included in
this review was limited, it might be
preliminary to conclude that there is no
difference between single- and multiple-
visit root canal treatments in terms of
postoperative complications for teeth with
infected root canals
References
1. Wilson W, Taubert K et al. Prevention of
Infective Endocarditis: Guidelines from the
Americam Heart Association. J Amer Heart Assoc
2007; 116:1736-54.
2. Kennedy HF, Morrison D, Tomlinson D, Gibson
BES, Bagg J, Gemmell CG. Gingivitis and
toothbrushes: potential roles in viridans
streptococcal bacteraemia. J Infect 2003;46: 67–70.
3. Debelian GJ, Olsen I, Tronstad L.
Electrophoresis of whole- cell soluble proteins of
microorganisms isolated from bacteremias in
endodontic therapy. Eur J Oral Sci 1996;104: 540–
6.
4. Debelian GJ, Eribe ER, Olsen I, Tronstad L.
Ribotyping of bacteria from root canal and blood of
patients receiving endodontic therapy. Anaerobe
1997;3:237–43.
5. Savarrio L, Mackenzie D, Riggio M, Saunders
WP, Bagg J. Detection of bacteraemias during non-
surgical root canal treatment. J Dent 2005;33:293–
303.
6. Takai S, Kuriyama T, Yanagisawa M,
Nakagawa K, Karazawa T. Incidence and
bacteriology of bacteremia associated with various
oral and maxillofacial surgical procedures. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod
2005;99:292–8.
7a Kozarov E, Sweier D, Shelburne C, Progulske-
Fox A, Lopatin D. Detection of bacterial DNA in
atheromatous plaques by quantitative PCR.
Microbes Infect 2006;8: 687–93.
7b Marques da Silva R, Caugant DA, Eribe ER,
Aas JA, Lingaas PS, Geiran O, et al. Bacterial
diversity in aortic aneurysms determined by 16S
ribosomal RNA gene analysis. J Vasc Surg
2006;44:1055–60.
8.BystromA,ClaessonR,SundqvistG.Theantibacteria
leffectof camphorated paramonochlorophenol,
camphorated phenol and calcium hydroxide in the
treatment of infected root canals. Endod Dent
Traumatol 1985;1:170-5.
9. Sjogren U, Figdor D, Spangberg L, Sundqvist G.
The antimicrobial effect of calcium hydroxide as a
short-term intracanal dressing. Int Endod J
1991;24:119-25.
10. Cvek M, Hollender L, Nord CE. Treatment of

15
non-vital permanent incisors with calcium
hydroxide. VI. A clinical, microbiological and
radiological evaluation of treatment in
one sitting of teeth with mature or immature root.
Odontol
Revy 1976;27:93-108.
11. Orstavik D. Radiographic evaluation of apical
periodontitis and
endodontic treatment results: a computer approach.
Int Dent J 1991;41:89-98.
12. Peters LB, van Winkelhoff AJ, Buijs JF,
Wesselink PR. Effects of instrumentation, irrigation
and dressing with calcium hydroxide on infection
in pulpless teeth with periapical bone lesions. Int
Endod J 2002;35:13-21.
13. Waltimo T, Trope M, Haapasalo M, Orstavik D.
Clinical efficacy of treatment procedures in
endodontic infection control and one year follow-up
of periapical healing. J Endod 2005;31:863-6.
14Tang G, Samaranayake LP, Yip HK. Molecular
evaluation of residual endodontic microorganisms
after instrumentation, irrigation and medication
with either calcium hydroxide or Septo-mixine.
Oral Dis 2004;10:389-97.
15.Haapasalo M, Ørstavik D. In vitro infection and
disinfection of dentinal tubules. J Dent Res1987;
66:1375-9.
16. Saleh IM, Ruyter IE, Haapasalo M, Ørstavik D.
Survival of Enterococcus faecalis in infected
dentinal tubules after root canal filling with
different root canal sealers in vitro. Int Endod J
2004; 37:193–8.
17. Özcan E, Eldeniz AU, Arı H. Bacterial killing
by several root filling materials and methods in an
ex vivo infected root canal model. Int Endod J
2011; , 44, 1102–09.
18. Su Y, Wang C, Ye L.Healing Rate and Post-
obturation Pain of Single- versus Multiple-visit
Endodontic Treatment for Infected Root Canals: A
Systematic ReviewJ Endod 2011;37:125–132)

16
Case 3
Treatment of the the mandibular right first molar with chronic apical periodontitis
in a patient with anxiety disorders
Fig 1. Frontal view
Patient: 32 year old Asian female
The clinical photos are taken at recall, one
year later, when she felt much better than
the first visit one year earlier.
All upper front dental crown and dental
crowns 46 shown in Fig 1. are made after
the first visit to the post graduate clinic
(Fig. 1, 8 and 9)
Chief complaint: No symtoms. She says
she has has anxiety, she has dental fear,
and she feels strong discomfort in the
dental chair.
Medical record: The patient is a cathegory
Group C patient (long-time sick with home
care twice a week). She has anxiety and
bipolar disorders
Medication: Rivotril (benzodiazepine).,
Abilify (antipsychotic), Lamictal
(anticonvulsant), Remeron (tetracyclic
antidepressant), Afipran (against nausea
and vomiting)
Dental history: The patient was referred
from a specialist in pedodontics to the
post-graduate endodontic clinic from the
public dental service for treatment of tooth
46.
of September 2010
Soft tissue: Nomal findings
Dental: Tooth 48 has a composite filling
Tooth 46 has a MOD composite filling and
an occlusal amalgam filling
Tooth 45 has a dental crown (clinical
photos were not taken because of her
condition).
Clinical tests 4 th
of September2010
45 46 48
EPT (0-80) - - not
taken
Cold + - yes
Percussion
Vertical/horizontal
- both -
Palpation - yes -
PPD 3 4 3
Mobility - I -
Table 1
of September
2010
Fig. 2 Periapical radiograph

17
Dental:
Tooth 46 has an MOD radiopaque filling
material and anatomically discrepancy
distal root. The root canals seem to be
calsified apically.
Tooth 45 is insufficient root filled, and has
a dental crown
Apical: Apical radiolucencies mesial and
distal roots 46 (PAI 4) and tooth 45 has a
widened PDL
Diagnosis 04 th
of September 2010
Pulpal: Infected necrosis (K04.11)
(K04.5)
Treatment plan
Treatment of infected necrosis tooth 36
Problem list
The patient has problems having her mouth
open during long periods of time. She has
problems with vomiting during endodontic
treatment because of her medication
Treatment 13th
of October 2010
Access opening and location of three
canals. Efforts were made to calm the
patient. The canals negociated because of
calsification. The patient felt sick and had
to throw up during the endodontic
treatment.
Mechanical: Bur, Irrisafe®
Intracanal medicament:Ca(OH)2
Treatment 20 th
of October 2010
Access opening. This time the DL canal
was found just obove midroots..
The patient was calmer this time, but again
she had to throw up during treatment. The
treatment visit had to be as short as
possible. Working lengths were achieved
this time with EndoLift
Mechanical:
Irrisafe®, Endolift
NiTi handinstrumentation
MB24,5/30#, ML24,5/30#, DB 24,5/40#,
DL24/40#
Chemical:
1% NaOCl, 16% EDTA
Chlorhexidine-di-gluconate 2%
Temorary filling: IRM
Fig. 3 and 4 Working length radiographs
Treatment 09 th
of December 2010
No symptoms, not tender to percussion
filled with gutta-percha and AH plus,
sealed with IRM

18
Prognosis
Endodontic: The prognosis seemed to be
good
Tooth: The prognosis seemed too be good
of September
2011 (12 months)
Radiograph showed healing of the
periapical radiolucencies (PAI 2)
The patient was asymptomatic and
Experienced no sensitivity to percussion
or palpation tests. The PDL on 45 was
widened, but there was no progression
since last radiograph. She had new
dental crown 36 and upper front.
Fig.7 Follow- up radiograph 06.09.2011
Fig. 8 Occlusal view
Fig. 9 Buccal view
Discussion
In the present case, instrumentation of the
root canals was done with a #30 file as the
last instrument.
Mechanical instrumentation of the root
canal has been shown to reduce bacterial
count even without irrigants or dressings
(1). A combination of mechanical in-
strumentation and irrigation (2, 3) further
reduced the number of microorganisms by
100 to 1000 times.
Shuping et al. (4) and Siqueira et al. (5)
later confirmed the findings that larger file
sizes are needed to allow the irrigating
solution to reach the apex.
Larger instrumentation sizes not only
allow proper irrigation of the canals but
studies have shown a trend towards a
decrease of remaining bacteria in the canal
system. In a study by Ørstavik et al. (6)
they found that root canals instrumented to
larger-size reamers at the first appointment
appeared to be rendered bacteria-free more
easily.
Later studies confirmed this tendency (8, 9,
10,11), and Dalton et al. (7) also showed
that with increasing file size, there was an
increasing reduction of bacteria. Yared and
Dagher (12) on the other hand, reported
that a #25 file was as efficient as a #40 file
for reducing residual microorganisms.
However, in this study as well, no
statistically significant difference was
noted between the size 25 and 40 file
groups after instrumentation, and after l-
wk calcium hydroxide dressing.
Longitudinal studies have shown
instrumentation to larger files sizes doesn’t
contribute significantly to the enhanced

19
statistical success for endodontic therapy.
(13, 14, 15). However, many of these
studies do not specifically evaluate the
impact of a significant enlargement of the
canal or of apical region with regards to
clinical success.
References
1. Byström A, Sundqvist G. Bacteriologic
evaluation of the efficacy of mechanical root canal
instrumentation in endodontic therapy. Scand J
Dent Res 1981;89:321– 8.
2. Byström A, Sundqvist G. Bacteriologic
evaluation of the effect of 0.5 percent sodium
hypochlorite in endodontic therapy. Oral Surg Oral
Med Oral Pathol 1983;55: 307–12.
.3.Ingle JI, Zeldow BJ. An evaluation of
mechanical instrumentation and the negative
culture in Endodontic therapy. J Am Dent Assoc
1958;57:471– 6.
4. Shuping G, Orstavik D, Sigurdsson A, Trope M.
Reduction of intracanal bacteriausing nickel-
titanium rotary instrumentation and various
medications. J Endod 2000;26:751–5.
5. Siqueira J, Lima K, Magalhaes F, Lopes H, de
Uzeda M. Mechanical reduction of the bacterial
population in the root canal by three
instrumentation techniques. J Endod1999;25:332–5.
6. Ørstavik D. Kerekes K, Molven O. Effects of
extensive apical reaming and calcium hydroxide
dressing on bacterial infection during treatment of
apical periodontitis: a pilot study. Int Endod J
1991;24 –7.
7 Dalton BC, Orstavik D, Phillips C, Pettiette M,
Trope M. Bacterial reduction with nickel-titanium
rotary instrumentation. J Endod 1998;24:763–7.
8. Card S, Sigurdsson A, Orstavik D, Trope M. The
effectiveness of increased apical
enlargement in reducing intracanal bacteria. J
Endod 2002;28:779 – 83.
9. Rollison S, Barnett F, Stevens R. Efficacy of
bacterial removal from instrumented root canals in
vitro related to instrumentation technique and size.
Oral Surg Oral Med Oral Path Radio Endod
2002;94:366 –71.
10. Tan B, Messer H. The quality of apical canal
preparation using hand and rotary
instruments with specific criteria for enlargement
based on initial apical file size. J Endod
2002;28:658 – 64.
11. Usman N, Baumgartner JC, Marshall JG.
Influence of instrument size on root
canaldebridement. J Endod 2004;30:110 –2.
12. Yared GM, Dagher FE. Influence of apical
enlargement on bacterial infection during
treatment of apical periodontitis. J Endod
1994;20:535–7.
13. Strindberg LZ. The dependence of results of
pulp therapy on certain factors: an analytic study
based on radiographic and clinical follow-up
examination. Acta Odontol Scand
1956;14(Suppl):1.
14. Hoskinson S, Ng YL, Hoskinson A, Moles D,
Gulabivala K. A retrospective comparison of
outcome of root canal treatment using two different
protocols. Oral Surg Oral Med Oral Path Oral
Radio Endod 2002;93:705–15.
15. Friedman S, Abitbol S, Lawrence H. Treatment
outcome in Endodontics: the Toronto study. Phase
1: initial treatment. J Endod 2003;29:787–93.

20
Case 4
Treatment of the mandibular right first molar with chronic apical periodontitis
Fig. 1 Frontal view
Patient: 52 year old Caucasian female
Chief complaint: Episodes of dull pain and
discomfort when chewing.
Medical record: Non contributory
Dental history: The patient is referred to
the post-graduate endodontic clinic by her
general dental practitioner for
endododontic treatment of tooth 46.
of January 2010:
Dental: Tooth 45 has an MOD composite
filling. Tooth 46 has an MODBL
composite builtup and caries can bee seen
and along the composite margins.
Tooth 47 has a dental crown
Fig. 2 Buccal view
Fig.3 Lingual view
of January 2010
45 46 47
EPT (0-80) 14 - -
Cold + - +
Percussion
Vertical/horizontal
- v +h v
palpation - - -
PPD 3 4 4
Mobility - - -
Table 1
of January
2010:
Dental: Tooth 46 has an MOD radiopaque
filling material and calsified canals in the
apical 1/3 of the root.
Apical: Tooth 46 has apical radiolucencies
mesial and distal roots (PAI 5) and lateral
radiolucency mesial root
Fig 4. Periapical radiograph

21
Diagnosis 20 th
of January 2010:
(K04.50) and chronic lateral periodontitis
(K.04.51)
Treatment plan:
Remove caries and composite restauration
Treatment of infected pulp/apical
periodontitis
Problem list:
Negotiating calcified root canals
Treatment 29 th
of January 2010:
Removal of old composite filling and
caries revealed that not much tooth
substance was left. Access opening and
location of three canals. It was not possible
to access optimal working length because
of calsified canals.
The patient was told that the endodontic
treatment and tooth would have a poor
prognosis. She did not want to extract the
tooth before trying treatment.
Mechanical:Bur,Irrisafe®
NiTi handinstruments
MB: #40/13 mm, ML: #40/13 mm
D: #55/ 15 mm
Chlorhexidine- di-gluconate 2%
Treatment 03 rd
of February 2010:
Still pain and tender to percussion.
Instrumentation of lateral
canal in the mb canal to #25 with
preconturated stainless steel instrument;
pus when patency
Fig.6 instrument in lateral canal
Treatment 05 th
of May 2010:
sealed with IRM

22
Prognosis:
poor
Tooth: The prognosis seemed too be poor
of September
2011 (16 months):
experienced no sensitivity to percussion or
palpation tests. She had got a dental crown
restauration.
Radiograph showed evidence of
healing of the periapical radiolucencies
apically both roots and lateral radiolucency
mesial root (PAI 2). Radiograph shows
placement of post in the distal root.
Fig. 6 Follow up radiograph 16.09.2011 (16
months)
Discussion
Strindberg (1) stated in 1956 that the
highest success rate is obtained when the
root filling is confined to 1 mm from the
radiographic apex. In the study by Sjögren
et al in 1990 (2) they found that the
outcome in teeth with preopertive apical
periodontitis was 68% when the root filling
was more than 2 mm short of the
radiographic apex, compared to 94% when
the filling reached within 2 mm of the
apex. Subsequently, most prognosise
studies confirmed the practice of staying
short of the apex to obtain the best
treatment outcome.(3-9) In a study by
Åkerblom et al (10), looking at the
outcome of obliterated root-filled teeth that
were rootfilled only one third of the
rootlength,. Cinical and radiographic
follow-up examinations were performed
for 2 to 12 yr. The criteria for obliteration
were: (a) The root canal was not patent for
more than one-third of the root length. (b)
No root canal lumen was visible on the
radiographs apical to the instrumented
portion. In teeth with preoperative
periapical radio-lucencies, a success rate of
62.5% was noted..
An accessory canal is any branch of the
main pulp canal that communicates with
the external surface of the root. A lateral
canal is an accessory canal located in the
coronal or middle third of the root, usually
extending horisontallyfrom the main root
canal (11).
Ramifications can be observed anywhere
along the length of the root, but they occur
more commonly in the apical portion and
in posterior teeth (12). In 73.5% of the
cases, ramifications are found in the apical
third of the root, in 11% in the middle
third, and in 15% in the coronal third (13).
Ricucci et al. (14) reviews and reports on
the histopathologic and histobacteriologic
status of the tissue in lateral canals and
apical ramifications (LC/AR) in diverse
clinical conditions as well as in response to
endodontic treatment. Serial sections from
493 human tooth specimens obtained by
extraction or apical surgery. They found
that LC/AR were observed in about 75%
of the teeth. Chemomechanical preparation
partially removed necrotic tissue from the
entrance of LC/AR, whereas the adjacent
tissue remained inflamed, sometimes
infected, and associated with periradicular

23
disease. In cases in which lateral canals
appeared radiographically ‘‘filled,’’ they
were actually not obturated, and the re-
maining tissue in the ramification was
inflamed and enmeshed with the filling
material.
References
1. Strindberg LZ. The dependence of the results of
pulp therapy on certain factors. An analytic study
based on radiographic and clinical follow-up
examinations. Acta Odontol Scand 1956; 14(Suppl
21).
2. Sjögren U, Hägglund B, Sundqvist G, Wing K.
Factors affecting the long term results of
endodontic treatment. J Endod 1990;16:498-504.
3. Smith CS, Setchell DJ, Harty FJ. Factors
influencing the success of conventional root canal
therapy—a five year retrospective
study. Int Endod J 1993;26:321-33.
4. Friedman S, Löst C, Zarrabian M, Trope M.
Evaluation of success and failure after endodontic
therapy using a glass ionomer cement sealer. J
Endod 1995;21:384-90.
5. Sjögren U, Figdor D, Persson S, Sundqvist G.
Influence of infection at the time of root filling on
the outcome of endodontic treatment of teeth with
apical periodontitis. Int Endod J 1997;30:297-306.
6. Ng YL, Mann V, Gulabivala K. A prospective
study of the factors affecting outcomes of
nonsurgical root canal treatment: part 1: periapical
health. Int Endod J 2011; 44: 583–609.
7. RicucciD, Russo J, Rutberg M,Burleson JA,
Spångberg L. A prospective cohort study of
endodontic treatments of 1,369 root canals: results
after 5 years. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 2011;112:825-842
8. Ricucci D. Apical limit of root canal
instrumentation and obturation: part 1. Int Endod J
1998;31:384-93.
9. Ricucci D, Langeland K. Apical limit of root
canal instrumentation and obturation: part 2—A
histological study. Int Endod J 1998;31:394-409.
10. Akerblom A, Hasselgren G. The Prognosis for
Endodontic Treatment of Obliterated Root Canals J
Endod 1988; 14: 565-567.
11.DeDeusQD.Frequency,location,and direction of
the lateral,secondary,and accessory canals. J Endod
1975;1:361–6.
.
12.VertucciFJ. Rootcanal anatomy of the human
permanent teeth.Oral Surg Oral Med Oral Pathol
1984;58:589–99.
13. Vertucci FL. Root canal morphology and its
relationship to endodontic procedures. End topics
2005; 10: 3-29.
14.Ricucci D, Siqueira JF. Fate of the Tissue in
Lateral Canals and Apical Ramifications in
Response to Pathologic Conditions and Treatment
Procedures. J Endod 2010;36:1–15

24
Case 5
Treatment of the maxillary right lateral incisor and canine in patient with
keratocystic odontogenic tumor
Fig 1. Frontal view
Chief complaint:
Pain and discomfort maxilla right side after
surgery and removal of keratosystic
odontogen tumor 2 months ago. Complains
about palatal swelling right side
Medical record: Albyl E 160 mg
Dental history: first referred from private
practinioner for implant treatment.
Radiolucent area was observed maxilla
right of postgraduate student in
orthodontics September 2009. Tooth 12
did not respond to sensitivity test and the
patient was referred to the Department of
Oral Surgery and Oral Medicine.
CT scan showed a radiolucent area from
tooth 11 to 15, expanding into the nasal
floor and into sinus maxillaris. No buccal
bone was evident. The patient was
operated in October 2009, and histology
confirmed the diagnosis odontogenic
keratocystic tumor.
In December 2009 the patient had still
symptoms and was referred to the post -
graduate endodontic clinic for endodontic
treatment of tooth12.
of December 2009:
Soft tissue: Palatal, fluctuating, soft
swelling region 12,13
Dental:
Tooth 12: mesial composite filling
Tooth 13: sound
Tooth 14: amalgam filling
Tooth 15: MOD composit filling
Teth 16,17: dental crowns
Fig 2. Buccal view
Fig 3. Palatal view: palatal swelling region 13
of December 2009
11 12 13 14
EPT (0-80)
cold
-
-
-
-
-
-
15
-
Percussion
Vertical/horizontal
- h - -
palpation - + + -
PPD 3 4 4 3
mobility - - - -
Table 1
of December
2009
Dental: Tooth 12 has a mesial radiopaque

25
filling material
Tooth 13 is sound, Tooth 14 has an MO
amalgamfilling , while tooth 15 has an
MOD radiopaque filling material
Periodontal: Attachment 2/3-1/2
Apical : radiolucency from midline to
mesially tooth 15, with extension to the
nasal floor and into the maxillary sinus
(PAI 5) (see description below)
Radiological description (in Norwegian) from the Department of Maxillofacial Radiology
Fig. 4 Periapical radiographs taken at the post graduate clinic 15.12.2009

26
Fig 5 Panoramic view shows expansion of osteolytic process into the nasal floora and sinus maxillaris
20.10.2009.
Fig. 6 Axial CT scan demonstrates destruction of
alveolar bone region 12-15
Fig. 7 Axial CT scan demonstrates expanded and
thinned buccal and palatal cortex, with the buccal
cortex being perforated (more cranial view than Fig
6)

27
Fig. 8 Coronal CTscan demonstrates corticated
process occupying part of maxillary sinus
Fig. 9 Sagittal CT scan shows expansion of the
tumor in maxillary sinus
Diagnosis 15 th
of December 2009:
Pulpal: necrosis (K04.11)
tooth 12 (K04.50).
Keratocystic odontogenic tumor (K.09.0)
Periodontal: Chronic marginal
periodontitis (K05.03)
Treatment plan:
Treatment of necrotic pulp tooth 12 and
observation; especially tooth 13
Treatment 15 th
of December 2009:
Access opening and location of one canal
12. No bleeding, but pale pink liquid in the
canal (cystic liquid?). Length measurment
on radiograph only.
Mechanical: Bur, Irrisafe®, NiTi hand
instrumentation- 22 corr 22,5/#45
Chemical: 1% NaOCl,16% EDTA
Temporary filling:IRM
Treatment 20 th
of January 2010:
sealed with IRM
Fig. 11 Masterpoint radiograph tooth 12

28
Treatment 10 th
of February 2010:
The patient had an appointment regarding
control tooth 13. This time it did not
respon to sensivity tests.
of February 2010
11 12 13 14
EPT (0-80)
cold
35
-
-
-
-
-
50
-
Percussion
Vertical/horizontal
- - - -
palpation - - + -
PPD 3 3 3 3
mobility - - - -
Access opening and location of one canal
tooth 13. No bleeding, but like 12; pale
pink liquid in the canal
Mechanical:
Bur and IrriSafe
Stainless steel hand instrumentation
27,5mm/ #50
Chemical:1% NaOCl,16% EDTA
Fig. 13 Working length radiograph tooth 13
Treatment 04 th
of March 2010
No symptoms, not tender to percussion, the
palatal swelling has dissapeared.
sealed with IRM
Follow up examination 02nd
of February
2011 and 12th
of April 2012 (13 and 27
months):
After 13 months: The patient
was asymptomatic and experienced no sen
sitivity to percussion or palpation tests.
healing of the periapical radiolucency (PAI
3), although a mottled appearance in the
bone structure can be seen.
After 27 months: Continuous PDL (PAI 2),
and the Department of Oral Surgery and
Oral Medicine confirm healing after
resurgey 6 months earlier (Fig. 21).

29
The patient have had 6 months recalls at
the department of oral and maxillofacial
surgery, and in March 2011 a recidiv was
observed in the same region. A CT scan
was taken. Biopsi was taken during
surgery and histology confirmed that the
radiolucency was a recidive of the
odontogenic keratocystic tumor.
Fig. 17 Panoramic view; before re-surgery in
March2011
Fig. 18 Panoramic view; After re-surgery October
2011
Fig. 19 Follow up radiograph
12.04.2012
Fig 20: Follow up radiograph
12.04.2012

30
Fig. 21 Panoramic view shows healing of the lesion, most likely with scar tissue12.04.2012
Discussion
The odontogenic keratocyst has been one
of the most controversial pathological
entities of the maxillofacial region since
Philipsen first described it in 1956 (1).The
World Health Organization recent
classification of Head and Neck Tumors
reclassified the keratocyst as a benign
neoplasm, recommending the term
‘‘keratocystic odontogenic tumor”
(KCOT) (2).
The surgical treatment method for KCOT
is categorized as conservative or
aggressive. Conserva-tive treatment is
cyst-oriented and includes marsu-
pialization or enucleation with or without
curettage. Its advantage is preservation of
anatomical structures, including teeth,
which is advocated because KCOTs
commonly present in younger patients. It
has been asserted that a conservative
approach is applicable to all age.
Aggressive treatment addresses the
―neoplastic nature‖ of KCOT and
includes peripheral ostectomy, chemical
curettage with Carnoy’s solution or en
bloc resection. The aggressive modalities
have been recommended for large KOCTs
and recurrent lesion (3).
In a clinopathological study (4), three
hundred and twenty-two patients (192
male and 130 female) with cystic lesions
of the jaw were successfully diagnosed and
treated. One hundred and fifty-five (48%)
were radicular cysts, 80 (25%) were
dentigerous cysts, 23 (7%) were
odontogenic keratocyst (=keratocystic
odontogenic tumor), 19 (6%) were
eruption cysts, 16 (5%) were traumatic
bone cysts, and 29 (9%) were non-
odontogenic cysts. The angiogenesis was
assessed in KCOT, DC, and normal oral
mucosa using CD-105 antigen . It was
demonstrated that CD-105 antigen is
strongly expressed in microvessels of
KCOT compared to DC and normal oral
mucosa, suggesting that the cyst wall of
KCOT plays a role in the neoplastic
behavior of the lesion. These finding can
further support the WHO decision (3)
recommending the term KCOT, as it better
reflects its neoplastic nature.
Although prognostic factors based on
clinico-pathologic and
immunohistochemical findings for deter-

31
mining the potential for recurrence of
KCOT still remains unclear, its use for
determining the potential for recurrence of
KCOT after surgical treatment may
become important to successfully manage
this neoplasm’s aggressive behavior.
The key element for future management of
KCOTs will probably be based on
thorough knowledge of the biological basis
of this tumor, thereby enabling a more
tailored treatment approach (5).
KCOTs are benign but locally aggressive,
it is generally accepted that they arise from
the remnants of the dental lamina which
persist in subepithelial tissues including
bone after the completion of odontogenesis
(6).
Since the KCOT is a relatively uncommon
lesion, epidemiological data vary
considerably. KCOTs probably account for
between about 2% and 11% of all jaw
cysts and can occur at any age; many data
suggest a bimodal age distribution around
the third and sixth decades (7).
One of the clinical features of the KCOTs
that causes difficulty in management is
their tendency to recur after treatment.
Reported rates of recurrence range from
3% to 60% (7). Many theories have been
proposed to account for the high level of
recurrence of these lesions. Firstly, the
cyst lining is delicate and remnants can be
left behind after surgical removal, satellite
cysts (from odontogenic epithelial
residues) or daughter cysts (from out
pouching’s of the main cyst lining) may
develop into new cysts after removal.
A Cochrane systematic review (8) sought
high level evidence on the effectiveness of
managing keratocystic odontogenic
tumours by comparing the effectiveness of
surgical interventions and adjuncts for
their treatment. No eligible studies for
inclusion were found.
References
1.Philipsen HP. Om keratocystedr (kolesteratomer)
and kaeberne. Tandlaegebladet 1956;60:963–71.
2.Barnes L, Eveson JW, Reichart P, et al. World
Health Organization classification of tumors.
Pathology and genetics of head and neck tumors.
IARC Press: Lyon; 2005.
3. Morgan TA, Burton CC, Qian FA. A
retrospective review of treatment of odontogenic
keratocyst. J Oral M axillofac Surg 2005;63:960-3.
4. Esther Manor 1, Leonid Kachko 2, Max B.
Puterman 3, George Szabo 4, Lipa Bodner 9Cystic
Lesions of the Jaws – A Clinicopathological Study
of 322 Cases and Review of the Literature Int. J.
Med. Sci. 2012; 9(1):20-26.
5. Mendes RA, Carvalho JFC, van der Waal I.
Characterization and management of the
keratocystic odontogenic tumor in relation to its
histopathological and biological features. Oral
Oncology 2010; 46: 219–225.
6. Soskolne WA, Shear M. Observations on the
pathogenesis of primordial cysts. British Dental
Journal 1967;123(7): 321–6.
7. Shear M, Speight PM. Odontogenic keratocyst.
In: Shear M, Speight PM editor(s). Cysts of the
Oral and Maxillofacial Regions. 4th Edition.
Oxford: Blackwell Munksgaard, 2007:6–58.
8. Sharif FNj, Oliver R, Sweet C, Sharif
MO.Interventions for the treatment of keratocystic
odontogenic tumours (KCOT, odontogenic
keratocysts (OKC)). Cochrane Database Syst. Rev.
2010

32
Case 6
Treatment of a maxillary left first molar with iatrogenic furcal perforation
Fig. 1 Frontal view
Patient: 47 year old Central Asian male
Chief complaint: Episodes of dull pain
the student clinic for endododontic
treatment of tooth 26 and treatment of
furcal perforations
Clinical findings April 29 th
2010
Soft tissue: Gingival recession mandibular
firs centrals
Dental: Tooth 24: amalgam filling
Tooth 25 is sound
Tooth 26 has a temporary filling and distal
composite filling.
Fig. 2 Buccal view
Fig. 3 Palatal view
of April 2010
24 25 26
EPT (0-80) 26 16 -
Cold + + -
Percussion
Vertical/horizontal
- - v + h
palpation - - -
PPD 3 3 4
Mobility - - I
of April 2010
Dental: Tooth 25 is sound
Tooth 26 has a radiopaque filling material
Periodontal: Attachment is 2/3
Apical: Tooth 25 has continuous PDL
while 26 has widened PDL apically and
mesially along the mesial root (PAI 3)

33
Radiographic findings: history (graduate
clinic)
Fig. 5 Periapical radiograph before
treatment at graduate clinic17.03.2009
Fig. 6 Instruments in perforation in
the furcal area 01.02.2010
Diagnosis 29 th
of April 2010
(K04.50)
Treatment plan:
periodontitis and closure of perforations
with MTA
Problem list : Perforations
Treatment 29 th
of April 2010:
Access opening and location of mb and mp
canals. These canals were previously not
instrumented. Perforations were seen two
places in the furcal area close to the mesial
canals. These perforations had happened
during instrumentation and not access
preparation, and the perforations were
discovered when the student should
obturate the tooth at the last visit.
Bleeding from both perforations was
stopped with Ca(OH)2 . MTA was placed
over both perforations. A moist cotton
pellet was placed over the MTA for 15
min., so the cement could set.
Mechanical: Bur, Pre RaCe, Irrisafe® ,
NiTi handinstrumentation
MB: #40/20 mm, MB2: #40/19 DB:
#40/19 (corr. from 20)mm
P: #50/ 19 (corr. from 20)mm
Fig. 7 Working length radiographs

34
Fig 9 shows two perforations (arrows) close to the
mb and mp canals
Fig. 10 MTA in perforations (arrows)
Fig. 11 MTA over perforations and Cavit in mb, mp
and db canals
Treatment 10 th
of June 2010
sealed with IRM
Fig 13. Final radiograph 10.06.2010
Prognosis
good
Tooth: the prognosis seemed too be poor
because of large perforations near the
crestal bone, time delay before
restauration, (see discussion) and little
remaining tooth substance.
Follow up examination 10th
of June 2011
and 10th
of April 2012 (12 and 22 months)
Radiograph showed periapical healing
mesial root. (PAI 2)
palpation tests. The tooth had been
restored with a composite filling

35
(12 months)
months)
Discussion
Over a period of 11 years, 55 root
perforations were recorded at the
Department of Cariology and Endodontics,
School of Dentistry, University of Bergen
(1). Forty-four of these perforations were
diagnosed during endodontic or
prosthodontic treatment, seven during
routine endodontic recall and four prior to
endodontic retreatment. Perforations
occurred in all tooth groups, but were more
common in the maxilla than in the
mandible. Of the perforations occurring
during endodontic treatment, nine were
located in the midroot level and 11 in the
apical third of the roots. Further analysis of
specific procedures related to perforations
demonstrated that attempts to negotiate
calcified canals accounted for 11 out of 26
perforations (42%). Nine out of 26 (35%)
occurred during root canal instrumentation,
and the remaining six (23%) resulted from
attempts to locate calcified canal orifices.
Factors that affect treatment prognosis of
perforation repair include the level,
location and size of the perforation, the
time delay before perforation repair and
the material used to seal the
perforation.(2). According to Tsesis and
Fuss (3) the prognosis of old and large
crestal perforations is questionable.
Perforations near the crestal bone are
susceptible to epithelial migration and
rapid pocket formation and treatment of
these has a low success rate.(4,1).
Pitt Ford et al (5) were the first
investigators who used MTA for repair of
furcal perforations. They showed that
cementum was generated underneath the
material in most treated teeth, in contrast to
the teeth whose furcation perforation sites
were repaired with amalgam. These
authors reported that when a perforation is
left untreated for a period of time and
becomes contaminated, the healing rate
after perforation repair with MTA is
significantly reduced.
Mineral trioxide aggregate (MTA) has
later been successfully used to repair
perforations (6,7,8,9).
MTA has not only been shown to be
biocompatible but has also demonstrated
the ability to allow regeneration of dental
hard tissues (10,11). Main et al (7) showed
that MTA had the ability to promote
regeneration of cementum, thus facilitating
regeneration of the periodontal apparatus.
Torabinejad et al (12) claimed that the
reduction of bacterial leakage when MTA
was used as the repair material was result
of its sealing ability rather than an
antimicrobial property of the material.
However, Eldeniz et al.,(13) evaluating the
antibacterial activity of leachable
components from selected root- end filling
materials, found that set samples of
ProRoot MTA cement completely
inhibited Pseudomonas aeruginosa and
delayed or limited growth of Enter. faeca-
lis. Similar results were obtained in other
studies where the antimicrobial properties
of MTA were evaluated.(14,15).

36
In a dye leakage study, Lee et al (16)
investigated the sealing ability of MTA in
lateral perforations and reported that MTA
allowed significantly less leakage than
IRM or amalgam. In a study by Lodiene et
al., (9), the percentage of leaking samples
was significantly higher in resin composite
than in the other groups and the negative
control group (p <0.05). SEM inspection
revealed the presence of bacteria in all
leaking specimens. Bacteria were observed
along the filling-dentine interface as well
as in dentinal tubules at some distance
from the filling. They concluded that the
resin composite material leaked
significantly more than the MTA and glass
ionomer cements when used to repair large
furcation perforations. Bacteria could
penetrate into dentine even at a distance
from the perforation filling. Bacterial con-
tamination may occur through furcation
canals or dentinal tubules as well as along
the material-dentine interface.
A recent case series investigated the
prognosis of teeth with perforations in the
furcation or within the cervical third of
roots repaired with GMTA. They reported
that 9 of 10 teeth healed after 5 years (17).
A two year follow-up in the present case
shows satisfactory conditions, both
clinically and radiographically. It appears
that MTA repair in the furcal area has
made a bacteria-tight seal, so no
reinfection has taken place.
References
1. Kvinnsland I, Oswald RJ, Halse A,
Grønningsæter AG. A clinical and roentgenological
study of 55 cases of root perforations. Int Endod J
1989; 22: 75-84
2. Tsatsas D V, Meliou H A, Kerezoudis N P.
Sealing effectiveness of materials used in furcation
perforation in vitro. Int Dent J 2005; 55: 133–141.
3. Tsesis I, Fuss Z. Diagnosis and treatment of
accidental root perforations. Endod Topics 2006;
13: 95–107.
4. Petersson K, Hasselgren G, Tronstad L.
Endodontic treatment of experimental root
perforations in dog teeth. Endod Dent Traumatol
1985; 1: 22–28.
5. Pitt Ford TR, Torabinejad M, Mc Kendry DJ,
Hong CU, Kariyawasam SP. Use of mineral
trioxide aggregate for repair of furcal perforations.
Oral Surg Oral Med Oral Pathol Oral Rad Endod
1995; 79: 756-763
6. Arens DE, Torabinejad M. Repair of furcal
perforations with mineral trioxide aggregate. Oral
Surg Oral Med Oral Pathol Oral Rad Endod 1996;
82: 84-88
7. Main C, Mirzayan N, Shabahang S, Torabinejad
M. Repair of root perforations using mineral
trioxide aggregate: A Long-term study. J Endod
2004; 2: 80-83
8. Schwarts RS, Mauger M, Clement DJ, Walker
WA. Mineral trioxide aggregate: a new material for
endodontics. J Am Dent Assoc 1999; 130: 967-975
9. Lodiene G, Kleivmyr M, Bruzell E, Ørstavik D.
Sealing ability of mineral trioxide aggregate, glass
ionomer cement and composite resin when
repairing large furcal perforations
10. Koh ET, Torabinjead M, Pitt Ford TR, Brady K,
Mc Donald F. Mineral trioxide aggregate stimulates
biological response in human osteoblasts. J Biomed
Mater Res 1997; 37: 432-439.
11. Koh ET, Mc Donald F, Pitt Ford TR,
Torabinejad M. Cellular response to mineral
trioxide aggregate. J Endod 1998; 24: 543-547
12. Torabinejad M, Hong CU, Pitt Ford TR,
Kettering JD. Anti bacterial effect of some root
filling materials. J Endod 1995; 21: 403-406
13.Eldeniz A U, Hadimli H H, Ataoglu H, Orstavik
D. Antibacterial effect of selected root-end filling
materials. J Endod 2006; 32: 345–349.
14. Sipert C R, Hussne R P, Nishiyama C K, Torres
S A. In vitro antimicrobial activity of Fill Canal,
Sealapex, Mineral Trioxide Aggregate, Portland
cement and EndoRez. Int Endod J 2005; 38: 539–
543.
15. Tanomaru-Filho M, Tanomaru J M, Barros D B,
Watanabe E, Ito I Y. In vitro antimicrobial activity
of endodontic sealers, MTA-based cements and
Portland cement. J Oral Sci 2007; 49: 41–45.
16. Lee SJ, Monsef M, Torabinejad M. Sealing
ability of a mineral trioxide aggregate for repair of
lateral root perforations. J Endod 1993; 19: 541-544
18. Nakata TT, Bae KS, Baumgartner JC.

37
Perforation repair comparing mineral trioxide
aggregate and amalgam using an anaerobic
bacterial leakage model. J Endod 1998; 24: 184-186
17. Pace R, Giuliani V, Pagavino G. Mineral
trioxide aggregate as repair material for furcal
perforation: case series. J Endod 2008;34:1130–3.

38
Case 7
Treatment of a mandibular right lateral incisor with two canals
Fig. 1 Frontal view
Patient: 42 year old Asian female
Chief complaint: No complains
the post-graduate endodontic from the
graduate clinic for endododontic treatment
of tooth 41. Teeth 31,32 and 33 were
endodontically treated in 2007.
of September 2011:
Soft tissue: Normal findings
Dental: Dental crowns all teeth upper and
lower jaws and teeth 31, 32,33 had
occlusal composite fillings
Fig. 2 Buccal view. Tooth 41 blue arrow
of September 2011
41 42 31
EPT (0-80) - - -
Cold - - -
Percussion
Vertical/horizontal
- - -
palpation - - -
PPD 4 4 4
Mobility II II I
of September
2011
Dental: Tooth 42 has a dental crown, the
root canal appears to be calsified. Teeth
41, 31,32 are all root filled
Periodontal: attachment is 2/3-1/2
Apical: Tooth 42 has an apical
radiolucency (PAI 4)
Teeth 32,31 have widened PDL (PAI 2)
Radiographic findings: history
Teeth 31, 32 and 33 were endodontically
treated in 2005 by post graduate student.
Old radiographs show that the periapical
radiolucensies have healed (PAI 3 in 2005
and PAI 2 in 2007). In the radiograph from
2007, it is evident that tooth 41 has
widened PDL apically.

39
31.05.2005
29.01.2007
Diagnosis 07 th
of September 09.2011
(K04.50)
Periodontal: Normal
Treatment plan
periodontitis
Problem list
Negotiating calcified root canals
Treatment 07 th
of September 2011
Access opening and location of one canal.
The canal is necrotic.The lingual canal was
localised with preconturaed #15 after full
instrumentation of the first canal. Working
length was achived with EndoLift
#08.Care was taken not to remove too
much tooth substance because of fragile
root and overextended crown.
Mechanical:
Burs, Irrisafe® ,EndoLift, NiTi
handinstruments, BioRace B: #30/14 mm,
L: #30/13 mm
Fig 6 and 7. Working length radiographs, working
length not achieved in lingual canal in Fig. 6.
Treatment 28 th
of September 2011
sealed with IRM
Fig 9. Masterpoint radiograph

40
Fig 10. Final radiograph 28.09.2011
Prognosis
good
Tooth: The prognosis seemed too be good
of April 2012
(6 months)
Radiograph showed widened PDL 41, but
there was evidence of healing (PAI 2)
The patient was asymptomatic
And experienced no sensitivity to
percussion or palpation tests.
Fig. 11 Follow up radiograph 17. 04.2012
Discussion
Several methods have been used to investi-
gate the anatomy of root canals, for
example, direct observation with the aid of
a microscope (1), sectioning techniques (2)
filling with an inert material and then
decalcifying (3), and the examination of
radiographs (4).
The incidence oftwo canals in the case of
mandibular incisors has been reported to
be as low as 4 per cent (5), and as high as
41.4 per cent (6), with an average value of
approximately 30 percent. Madeira and
Hetem found the incidence to be 11.5%.
(7),Vertucci found it to be 25.7% (8a, b),
Green 20% (9) and Kartal and Yanikuglo
45%(10) . In the study by Kartal and
Yanikuglo (10) , it was found that two
canals connect in the apical third in 37% of
the cases and reach the apex as one canal.
In the present case the mandibular 41 had a
type III (1-2-1) in Vertuccis classification.
In the study by Kartal and Yanikuglo (10),
the found central and lateral mandibular
incisiors with this classification in 20% of
their samples.
Four hundred and fifty-five extracted
mandibular incisor and 340 extracted
mandibuiar premolar teeth were
radiographed to assess the incidence of
twin canals as visualized on radiographs
taken in the mesio-distal direction. The
ability to detect the presence of these twin
canals by viewing radiographs taken in the
sundard bucco-lingual direction was then
assessed. Using the guideline that
'disappearance or narrowing infers
division' when viewing these radiographs
resulted in a failure to diagnose one-third
ofthe twin canals (11).
In a study on two hundred extracted
mandibular inisors undertaken to
determine the most effective horizontal
beam angulation for the diagnosis of twin
canals, it was found that the 20° right and
30° left horizontal beam angulations
showed significantly more accurate
diagnosis of twin canals than the ortho-
radial view (0°) (12).
References
1. Ainamo, J. & LoE, H. A stereomicroscopic
investigation of the anatomy of the root apices of
910 maxillary and mandibular teeth Odontologist
Tidskrift. 1968: 16; 411-426.

41
2. Green, D .Double canals in single
roots.OralSurgery. OralMedicine and
OralPathology,1973; 35; 689-696.
3. Hess W . Anatomy ofthe Root Canals of the
Teeth of the Permanent Dentition. Part I, 1025 pp.
27-29. William Wood and Co., New York
4. Rankie-Wilson, R.W. & Henry P. The bifurcated
root canal in lower anterior teeth. J Am Dent Ass.
1965:70; 1162-1165.
5. Ingle J.I. Endodontics.1965 p. 130. Lea and
Febiger, Philadelphia.
6. Benjamin KA and Dawson J. Incidense of two
root canals in human mandibular incisor teeth. Oral
Surg 1974; 38: 122-6.
7. Madeira M and Hetem S. Incidense of
bifurcations in mandibular incisors. Oral Surg
1973; 36: 589-91.
8a. Vertucci FJ. Root canal anatomy of the human
permanent teeth. Oral surg 1984; 53: 589-99.
8b.Vertucci FJ. Root canal anatomy of the
mandibular anterior teeth. J Am Dent Assoc 1974;
89: 369-71.
9. Green D. A stereomicroscopic study of the root
apices of 400 maxillary and mandibular anterior
teeth. Oral Surg 1956; 91: 1224-8.
10. Kartal N, Yanikoğlu FC.
Root canal morphology of Mandibular Incisors. J
Endod. 1992 Nov;18(11):562-4.
11. Nattress BR, Martin DM. Predictability of
radiographic diagnosis of variations in root canal
anatomy in mandibular incisor and premolar teeth.
Int Endod J 1991; 24: 58-62.
12. Klein RM, Blake SA, Nattress BR, Hirschmann
PN. Evaluation of X-ray beam angulation for
successful twin canal identification in mandibular
incisors Int Endod J 1997; 20: 58-63

42
Case 8
Retreatment of a mandibular left canine with sinus tract and primary treatment of
a mandibular right first premolar with acute apical periodontitis
Fig. 1 Frontal view
Patient: 55 year old South American male
Chief complaint
Episodes of strong pain left side.
Medical record: Allergic to pollen.
Ulcerus
Medication: Nexium
the graduate clinic for surgical treatment of
tooth 43. This tooth was treated at the post-
graduate clinic 18.11. 2009 and the root-
filling seemed dense and good.
The patient had been at a dental emergency
clinic 01.05 2012 (three days before)
because of pain and swelling in the same
area. He got Apocilling 660 mg
prescription for one week. No endodontic
treatment was done.
of May 2011
Soft tissue: Sinus tract buccaly region 43
Dental: Tooth 43 has lost part of the
occlusal filling.
Tooth 44 has a temporary filling IRM
Teeth 41 and 42 have composite fillings
incisally
All teeth have erosive occlusal damages
and dental crowns in upper jaw.
Fig. 3 Buccal view; gutta-percha point in sinus tract
of May 2011
42 43 44
EPT (0-80) 23 - 54
Cold + - no
Percussion
Vertical/horizontal
- both -
palpation - yes -
PPD 3 4 3
Mobility - I -

43
Radiographic history
Fig. 4 Periapical radiograph before endodontic
treatment 22.09.2009
Fig. 5 Periapical radiograph after endodontic
treatment 18.11.2009
of May 2011
Dental: Tooth 43 is root filled, lack of top
filling. Tooth 44 has a radiopaque filling
material filling that appears to be close to
the pulp.
Apical: Apical diffuse radiolucency tooth
43 that extend masially towards the
marginal bone (PAI 5). The radiopaque
guttapercha point can be seen in the lesion
Fig. 6 Periapical fistulogram 04.05.2011
Diagnosis 04 th
of May 05.2011
Pulpal: root filled tooth (K04.19)
with sinus tract (K04.62)
Treatment plan:
Retreatment tooth 43
Problem list:
Most likely a persistent infection
Treatment 04 th
of May 2011:
Access opening and location of one canal.
Pus in the canalspace
Mechanical: Bur, Irrisafe®, BioRace ,
NiTi handinstrumentation 24/60#
Chemical: 1% NaOCl, 16% EDTA

44
Fig 7. Working length radiograph tooth 43
The patient had since last visit
(16.05.2011) had an episode of acute pain
in the same region. Another post graduate
student had diagnosed tooth 44 with acute
apical periodontitis (K.04.4). The
radiograph that date showed apical
radiolucency 44 (PAI 3). The tooth still
tested positive on EPT (68). It was
irrigated with 16% NaOCl, placement of
eugenolpellet and IRM.
Treatment 31st
of May 2011:
Mechanical:
Bur, Irrisafe®, BioRace
19 mm adjusted to18,5/50#
Fig. 8 Working length radiograph tooth 44
Treatment 15th
of June 2011:
Teeth 43 and 44 were filled with gutta-
percha and AH plus, sealed with composite
Fig. 9 Masterpoint radiographs 15.06.2011
Prognosis:
good for 44 and uncertain for 43
Teeth: The prognosis seemed too be good
for booth teeth if permanent restaurations
are made, most preferably dental crown
because of erosion problems.
Thee graduate student was informed about
extensive erosions, further treatment and
refunds
of October
2011 and 13th
of March 2012 (4 and 9
months):
The patint had not experienced pain, the
sinus tract was closed and he had achieved
dental crowns on all teeth lower jaw.

45
healing of the periapical radiolucency 43
(PAI 2 after 9 months) and healing of the
periapical radiolucency 44 (PAI 1)
palpation tests.
Fig. 13 Buccal view 13.03.2012
Discussion
Discussion
One of the species of bacteria frequently
retrieved from previously root-filled canals
is Enterococcus faecalis, which is a Gram-
positive facultative anaerobe. In previous
studies, the prevalence of E. faecalis in
failed endodontic cases ranged between 24
and 70%, when culture-based techniques
were used (1-6).
Numerous studies demonstrate the hardy
nature of enterococci, which are able to
resist various intracanal medications and
adapt to harsh environmental conditions
(7). In a recent study (8), The genetic
relationship between E. faecalis from root
canals and isolates from the different host
sources was determined using pulsed-field
gel electrophoresis. In 16% (8⁄50) of the
patients, enterococci were collected from
the root canal samples. The genetic
analysis showed that the isolates from the
root canals were not related to those from
the normal gastrointestinal microflora.
None of these patients had enterococci in
their saliva samples. They concluded that
endodontic infections with E. faecalis are
probably not derived from the patient’s
own normal microflora, which indicates
that these infections are of exogenous
origin.
Bacteria associated with persistent apical
infections such as E faecalis are often
more challenging to eradicate. Several
studies have reported that calcium
hydroxide is not effective in eliminating E
faecalis, which is often associated with
persistent endodontic infections.(9-
13).Such bacteria can proficiently invade
the dentinal tubules and have the ability to
survive and buffer the high pH produced
by calcium hydroxide.(14)
Kuruvilla and Kamath (15) compared the
separate and combined effects of 2.5%
NaOCl and 0.2% chlorhexidine in vivo.
Teeth treated with chlorhexidine and
NaOCl combined showed the greatest
reduction in the number of micro-
organisms. In a clinical study, it was
reported that treatment of root canals with
IKI prior to calcium hydroxide dressing

46
did not significantly reduce the amount of
bacteria but that it might reduce the
frequency of persisting strains of E
faecalis. The ability of calcium hydroxide
to kill E faecalis have been shown to be
improved by combining it with IKI or
chlorhexidine (16)
The impact of mechanical agitation of the
hypochlorite solutions on tissue disso-
lution was found to be very important by
Moorer and Wesselink (17) who
emphasized the great impact of violent
fluid flow and shearing forces caused by
ultrasound on the ability of hypochlorite to
dissolve tissue. However, the mechanisms
involved are not completely understood
(18). Optimizing the concentration,
temperature, flow, and surface tension can
improve the tissue-dissolving effectiveness
of hypochlorite even 50-fold (19).
The patient in the present case had a tooth
with acute apical periodontitis.
In an early study by Haapasalo et al., (20)
black-pigmented Bacteroides spp. were
identified in acute and clinically
asymptomatic symptomatic cases of apical
periodontitis. They suggested that the
presence of B. gingivalis and B.
endodontalis in necrotic root canal is
closely related to an acute infection and
that fermentative BP Bacteroides species,
including B. intermedius, are frequently
present both in symptomatic and
asymptomatic infections. It is also possible
that the risk for persisting symptoms may
be greater when BP Bacteroides species
are part of the infective flora.
It has been demonstrated that many
bacterial species are virulent or more
virulent when in association with other
species (21–24).
In a recent study using molecular
techniques (25), samples were taken from
necrotic root canals of teeth with
symptomatic or asymptomat apical
periodontitis in addition to teeth with
chronic apical abscesses. They found that
basically the same species were highly
prevalent in the different clinical
conditions evaluated, and none of these
most prevalent taxa were positively
associated with symptoms. However, the
results revealed that the taxa identified
formed different partnerships and
associations in samples from cases with or
without pain. They speculated in that some
bacterial associations can result in a more
virulent multispecies community.
The composition of the microflora might
vary according to the geographic location
of the study (26,27) .
Nine months follow-up in the present case
shows healing of the periapical lesion, and
no clinical symptoms. The intracanal
infection appears to be controlled, most
likely because of additional chemical
(chlorhexidine-di-gluconate 2%) and
mechanical cleaning of the root-canal , and
a tight coronal restauration.
References
1.Engström, B.The significance of enterococci in
root canal treatment. Odontol Revy 1964; 15: 87–
106.
2. Molander, A., Reit, C., Dahle ́n, G. and Kvist, T.
Micro- biological status of root-filled teeth with
apical periodontitis. Int Endod J 1998; 31: 1–7.
3. Sundqvist, G., Figdor, D., Persson, S. and
Sjo ̈gren, U. Microbiologic analysis of teeth with
failed endodontic treatment and the outcome of
conservative re-treatment. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 1998; 85: 86–93.
4. Peciuliene, V., Balciuniene, I., Eriksen, H.M. and
Haapasalo, M. (2000) Isolation of Enterococcus
faecalis in previously root-filled canals in a
Lithuanian population. J Endod 26, 593–595.
5. Peciuliene, V., Reynaud, A.H., Balciuniene, I.
and Haapasalo, M. (2001) Isolation of yeasts and
enteric bacteria in root- filled teeth with chronic
apical periodontitis. Int Endod J 34, 429–434.
6. Zoletti, G.O., Siqueira, J.F. Jr and Santos, K.R. (
Identifi- cation of Enterococcus faecalis in root-
filled teeth with or without periradicular lesions by
culturedependent and – independent approaches. J
Endod 2006; 32: 722–726.
7. Tendolkar, P.M., Baghdayan, A.S. and Shankar,

47
N. Pathogenic Enterococci: new developments in
the 21st cen- tury. Cell Mol Life Sci 2003; 60:
2622–2636.
8. Vidana R, Sullivan A, Billstro ̈ m H, Ahlquist M,
Lund B. Enterococcus faecalis infection in root
canals – host-derived or exogenous source? Letters
in Applied Microbiology 2010; 52: 109–15.
9. Safavi KE, Spangberg LS, Langeland K. Root
canal dentinal tubule disinfection. J Endod
1990;16:207-10.
10. Heling I, Steinberg D, Kenig S, Gavrilovich I,
Sela MN, Fried- man M. Efficacy of a sustained-
release device containing chlorhexidine and
Ca(OH)2 in preventing secondary infection of
dentinal tubules. Int Endod J 1992;25:20-4.
11. Haapasalo M, Ørstavik D. In vitro infection and
disinfection of dentinal tubules. Journal of Dental
Research 1987; 66: 1375-9.
12. Saleh IM, Ruyter IE, Haapasalo M, Ørstavik D.
Survival of Enterococcus faecalis in infected
dentinal tubules after root canal filling with
different root canal sealers in vitro. International
Endodontic Journal 2004; 37, 193–8.
13. Siqueira JF Jr, de Uzeda M. Disinfection by
calcium hydroxide pastes of dentinal tubules
infected with two obligate and one facultative
anaerobic bacteria. J Endod 1996;22:674-6.
14. Stuart CH, Schwartz SA, Beeson TJ, Owatz
CB. Enterococcus faecalis: its role in root canal
treatment failure and current concepts in
retreatment. J Endod 2006;32:93-8.
15. Kuruvilla JR, Kamath MP. Antimicrobial
activity of 2.5% so-dium hypochlorite and 0.2%
chlorhexidine gluconate separatelyand combined,
as endodontic irrigants. J Endod 1998;24:472-6.
16. Siren EK, Haapasalo MP, Waltimo TM,
Orstavik D. In vitro antibacterial effect of calcium
hydroxide combined with chlorhexidine or iodine
potassium iodide on Enterococcus faecalis. Eur J
Oral Sci 2004;112:326-31.
17. Moorer WR, Wesselink PR. Factors promoting
the tissue dissolving capability of
sodium hypochlorite. Int Endod J 1982;15:187–96.
18. Zehnder M. Root canal irrigants. J Endod
2006;32:389–98.
19. Stojicic S, Zivkovic S, Wei Qian Z, Zhang H,
Haapasalo M.Tissue Dissolution by Sodium
Hypochlorite: Effect of Concentration,
Temperature, Agitation, and Surfactant. J Endod
2010;36:1558–62.
20. Haapasalo M, Ranta H, Ranta K, H, Shah H.
Black-Pigmented Bacteroides spp. In Human
Apical Periodontitis. Infection and Immunity
1986; 53: 149-153
21. Sundqvist GK, Eckerbom MI, Larsson AP,
Sjogren UT. Capacity of anaerobic bacteria from
necrotic dental pulps to induce purulent infections.
Infect Immun 1979;25:685–93.
22.. Baumgartner JC, Falkler WA Jr, Beckerman T.
Experimentally induced infection by oral anaerobic
microorganisms in a mouse model. Oral Microbiol
Immunol 1992; 7:253–6.
23. Siqueira JF Jr, Magalhaes FA, Lima KC, de
Uzeda M. Pathogenicity of facultative and obligate
anaerobic bacteria in monoculture and combined
with either Prevotella intermedia or Prevotella
nigrescens. Oral Microbiol Immunol 1998;13:368–
72.
24. Kesavalu L, Holt SC, Ebersole JL. Virulence of
a polymicrobic complex, Treponema denticola and
Porphyromonas gingivalis, in a murine model. Oral
Microbiol Immunol 1998;13:373–7.
25. Rocas IN, PhD, Siqueira JF, Debelian GJ.
Analysis of Symptomatic and Asymptomatic
Primary Root Canal Infections in Adult Norwegian
Patients. J Endod 2011;37:1206–1212
26. Machado de Oliveira JC, Siqueira JF Jr, Rocas
IN, et al. Bacterial community profiles of
endodontic abscesses from Brazilian and USA
subjects as compared by denaturing gradient gel
electrophoresis analysis. Oral Microbiol Immunol
2007; 22:14–8.
27. Siqueira JF Jr, R^oc ̧as IN, Debelian GJ, et al.
Profiling of root canal bacterial commu- nities
associated with chronic apical periodontitis from
Brazilian and Norwegian subjects. J Endod
2008;34:1457–61.

48
Case 9
Retreatment of a mandibular left first molar with post and two separated
instruments
Fig. 1 Frontal view
Patient: 53-year-old Caucasian female
Chief complaint
Episodes of pain and discomfort.
Periodically tender when chewing and
biting. No symptoms at the moment.
Medical record: Elevated cholesterol
blood level, depressive.
Medication: Symvastetin (hart) and
Sypralex (antidepressant).
Dental history: referred to the post-
graduate endodontic clinic from the
graduate clinic for retreatmet of tooth 36.
of October 2011
Dental: Tooth 36 has a composite
restauration and secondary caries. Several
teeth have erosions, lost fillings and
discolorations.
Fig. 2 Lingual view
Fig. 3 Buccal view
of October 2011
33 34 36
EPT (0-80) 34 26 -
Cold + + -
Percussion
Vertical/horizontal
- - -
palpation - - -
PPD 3 3 3
Mobility - - I
of October
2011
Dental: Tooth 36 has an inadequate root
filling. Separated instruments in mb and ml
canals, post in distal root, radiopaque
restauration
Apical: Diffuse apical and lateral
radiolucency mesial root tooth 34 (PAI 4)
and widened PDL (PAI 3) distal root

49
Diagnosis 25 th
of October 2011
Root filled tooth (K4.19)
(K04.50) (PAI 5)
Treatment plan
Retreatment, removal/bypassing separated
instruments and removal of post
Problem list
Removal/bypassing separated struments
and removal of post
Treatment 25 th
of October 2011
Composite and caries were removed.
Removal of post in distal canalwith
ultrasound (Fig. 5 ). Bypassed intrsument
in ml canal. Not possible to negociate
distal canal due to calsification
Fig. 5 Post in distal canal, old guttapercha in ml and
mb canals
Fig. 6 Removed post
Fig. 7 Removed separeted instrument (arrow),
paperpoint and cotton pellet in ml and d canals
respectively
Mechanical: Bur, Irrisafe®, Ultrasound in
distal canal. Prebent stainless steel in ml
canal because of step -ML 14/35#
Chemical:
1% NaOCl
16% EDTA
clorhexidine-di-gluconate 2%
Intracanal medicament:
Ca(OH)2
Fig 8. Working length radiograph ml canal

50
Treatment 22 th
of November 2011
Since last vistit, the patient had an espisode
of exacerbation while she was in Denmark.
She got Apocillin 660 mg prescription for
one week.
Access preparation and removal of
separated instrument in mb canal was
performed with modified Gates glidden
and ultrasound.
During ultrasound removal of instruments,
the separated instrument in the ml canal
moved more apically in the canal. Mesial
root had one apical foramen.
Prebent stainless steel because of
Step in mb canal -MB 13/35#
Chemical:1% NaOCl, 16% EDTA,
clorhexidine-di-gluconate 2%
Ca(OH)2
Fig. 9 Working length radiograph mesial canals
Treatment 10 th
of January 2012
warm guttapercha in distal canal. Sealed
with IRM
Prognosis
good
Tooth: The prognosis seemed too be
uncertain
Follow up examination 13 March 2012 (2
months)
Radiograph was taken by graduate student
before placement of dental crown. No
clinical tests were done.
3)

51
Fig 12.Follow up radiograph 13.03.2012
Discussion
The use of vibrating mechanical energy
has been embraced by endodontists as a
highly efficient method of dislodging and
removing metallic posts from the cemented
or bonded interface of the root canal wall
(1–4).
It is generally accepted that external root
temperature increases that exceed 10 0
C
produce irreversible bone and attachment
damage as well as dehydration effects on
dentin, often resulting in resorption and
necrosis (5, 6).
As evidence accumulates in the literature
for the considerable heat buildup and
transfer that occur during ultrasonic
vibration in the removal of posts, a number
of studies during the past few years have
cautioned the practitioner regarding the
need for adequate coolant to counter heat
buildup (7-9).
Ruddle (10) proposed a technique for the
removal of broken instruments using Gates
Glidden drills (size 3 or 4) to prepare a
circumferential “staging platform” at the
coronal aspect of the ob- struction.
Attention must be paid during preparation
of a staging platform, because a size 3 or 4
Gates Glidden may perforate or weaken a
root, for instance the mesial (11, 12) and
distal root (13) of mandibular molars,
References
1. Machtou P, Sarfati P, Cohen AG. Post removal
prior to retreatment. J Endod 1989; 15:552–4.
2. Goon WWY. Managing the obstructed root canal
space: ensuring the soundness of the remaining
tooth structure. J Calif Dent Assoc 1991;19:51–60.
3. Ruddle CJ. Nonsurgical endodontic retreatment.
In: Cohen S, Burns RC, eds. Path- ways of the pulp.
8th ed. St Louis: Mosby; 2002:875–929.
4. Plotino G, Pameijer CH, Grande NM, Somma F.
Ultrasonics in endodontics: a review of the
literature. J Endod 2007;33:81–95.
5. Atrizadeh F, Kennedy J, Zander H. Ankylosis of
teeth following thermal injury. J Perio Res
1971;6:159–67.
6. Eriksson AR, Albrektsson T. Temperature
threshold levels for heat-microscope study in the
rabbit. J Prosthet Dent 1983;50: 101–7.
6. Dominici JT, Clark S, Scheetz J, Eleazer PD.
Analysis of heat generation using ultrasonic
vibration for post removal. J Endod 2005;31:301–3.
7. Budd JC, Gekelman D, White JM. Temperature
rise of the post and on the root surface during
ultrasonic post removal. Int Endod J 2005;38:705–
11.
8a. Gluskin AH, Ruddle CJ, Zinman EJ. Thermal
injury through intraradicular heat transfer using
ultrasonic devices: precautions and practical
preventive strategies. J Am Dent Assoc
2005;136:1286–93.
8b.Davis S, Gluskin AH, Livingood PM, Chambers
DW. Analysis of Temperature Rise and the Use of
Coolants in the Dissipation of Ultrasonic Heat
Buildup During Post RemovalJ Endod
2010;36:1892–1896)
9.HuttulaA,Tordik P,Imamura G, EichmillerF,Mc
Clanahan S.The effect of ultrasonic post
instrumentation on root surface temperature. J
Endod 2006;32:1085–7.
10. Ruddle CJ. Micro-endodontic non-surgical
retreatment. Dent Clin North Am 1997;41:429 –54.
11. Wu MK, van der Sluis LW, Wesselink PR. The
risk of furcal perforation in mandib-
ular molars using Gates-Glidden drills with
anticurvature pressure. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 2005;99:378 –
82.
12. Zuckerman O, Katz A, Pilo R, Tamse A, Fuss
Z. Residual dentin thickness in mesial roots of
mandibular molars prepared with Lightspeed rotary
instruments and Gates- Glidden reamers. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 2003;

52
96:351–5.
13. Kuttler S, McLean A, Dorn S, Fischzang A. The
impact of post space preparation with Gates-
Glidden drills on residual dentin thickness in distal
roots of mandibular molars. J Am Dent Assoc
2004;135:903–9.

53
Case 10
Non surgical - and surgical endodontic treatment of a maxillary right central incisor
with radicular cyst
Fig. 1 Frontal view
Patient: 23 year old African male
Chief complaint:
Tender when chewing and biting
Sensation of slight mobility
Dental history: Referred to the post-
graduate endodontic clinic from his private
practitioner.
Endodontic treatment was started earlier
by another postgraduate student when I
saw the patient for the first time. Calsium -
hydroxide inlay in the canal.
The patient thought that he might have had
a trauma 15 years ago, but was not sure.
of May 2009:
Dental: Tooth 21 has a yellowish
discoloration and a palatal temporary
filling. All other teeth are sound except for
tooth 15, which are root filled and
fractured to the gingival level.
Fig 2. Occlusal view
Fig. 3 Frontal view
Fig. 4 Palatal view

54
of May 2009
11 21 22
EPT (0-80) 24 - 22
Cold + + +
Percussion
Vertical/horizontal
- v -
palpation - + -
PPD 3 5 4
Mobility - I -
of May 2009:
Dental: Tooth is 11 sound, tooth 21has a
radiopaque filling material coronally and
1/3 into the canalspace.
Pulpal: Tooth 21 has a wide canal, open
apex?
Periodontal: Attachment 2/3
Apical: Tooth 11 has a continuous PDL
while 21 has apical circumferencial
radiolucency (PAI 5 )
Fig 5. Periapical radiograph 19.05.2009
Diagnosis 19 th
of May 2009:
(K04.50)
Periodontal: Normal
Treatment plan:
periodontitis and most likely apical surgery
Problem lis:t
Open apex?
Large lesion and the tooth has already had
an intracal inlay with CaOH2 for one
month; compromised healing?
Treatment 19 th
of May 2009:
Access opening and location of a wide
canal. Liquid in the canal (cystic?).
Mechanical: Irrisafe®, NiTi
handinstruments/Haedstrøm
One canal: #70/23 mm,
Treatment 18 th
of June 2009:
Less symtoms, less liquid in the canal,
but too much liquid that final treatment
could be done
Mechanical:Irrisafe®
Chemical1% NaOCl, 16% EDTA
longterm Ca(OH)2
Treatment 03rd
November 2009:
Less symptoms, but still tender to
percussion. To make surgery easier, it was
decided to put an apical plug with MTA
angulus. Moist cotton pellet. IRM.

55
Fig 7. MTA apically
Treatment 10 th
of November 2009
Still tender to percussion, not tender to
palpation. Filled with warm gutta-percha
and AH plus, sealed with composite
restauration. It was decided to perform
surgery
Fig. 8 MTA apically and
warm gutta-percha above
Prognosis
poor
Tooth: the prognosis seemed too be
uncertain due too thin root canal walls
of September
2010 (9 months)
Due to studies abroad, he was not able to
come for surgical treatment before the date
above. Radiograph showed no healing of
the periapical lesion. The patient
The radiographs showed no sign of
healing. (PAI 4.) A lamina dura was
evident around the lesion
Fig. 6 Panoramic view 07.09.2010 shows distinct
radiolucent area from 11 distally to 23 mesially
extending to the nasal cavity
Fig. 8 Follow up radiograph
07.09.2010

56
Surgical treatment 11 th
of November
2010:
1. Anaesthesia 2. Sulcular flap from 13M-
24D, with a buccal releasing incision 13D
3. Osteotomy 4. Biopsy and
microbiological sample 5. Apical root
resection without retrograde filing 6.
Haemostasis 7. Sutures 8. Prescription of
analgesics and post-op information.
Fig. 9 Elevation of flap reveals destruction of
buccal bone and bluish cystic cavity wall
Fig. 10 Elevation of flap reveals fenestration of
buccal bone and a bluish cystic cavity wall
Fig. 11 Enucleaton of cyst
Fig. 12 Enucletion of cyst reveals several sulfur
granules (arrows)
Fig. 13 Cavity after cleaning
Fig. 14 Cystic lesion

57
Fig. 15 Lesion on formalin. Sulfur granules
can be seen
Fig. 16 After suturing
Fig. 17 Treatment result11.11.2010
Prognosis
Endodontic: seemed to be good
Tooth: seemed to be uncertain
Treatment 16 th
of November 2010:
The patient returned after one week for
suture removal. He could tell about
extraoral swelling and colorchange of the
skin (blue). He was symptom-free at suture
removal,
Fig. 18 Removal of sutures after one week
Histological findings (Hanna Strømme
Koppang)
Epithelized lumen (15 mm in diameter),
with fibrous capsula. Inflammatory cells.
Foreign body material. Histological
findings show most likely a radicular cyst
Bacteriological findings (with DNA-DNA
hybridization): Diagnostic service,
Institute of Oral Biology
• Streptococcus intermedius
• Actinomyces israelii
• Actinomyces viscosus
• Treponema denticola
• Prevotella intermedius
• Eubacterium sabbureum
Result SEM (scanning electron
microscopy). Institute of Oral Biology-
Steinar Stølen
Fig. 19 SEM photo shows microorganisms, mostly
long rods, and extracellular material

58
Fig. 20 SEM photo shows microorganisms
embedded in extracellular material
Fig. 21 SEM photo shows microorganisms; cocci
and rods embedded in an extracellular material
Prognosis:
Endodontic: The prognosis seemed to bee
uncertain
Dental: the prognosis seemed to be
uncertain due to thin root canals walls
Follow-up examination 17 th
of February
and 11th
of October 2011 and 12th
of April
2012 (3 , 11 and 16 months)
The radiographs showed healing of the
periapical lesion. The patient was
asymptomatic and experienced no
sensitivity to percussion or palpation tests.
(3 months)
(11 months)
(16 months)
Discussion
Occasionally, strands of epithelial cells are
present within the periapical lesion. These
cells are thought to originate from strands
of Malassez in the periodontal ligament. In
the inflammatory process, cytocines and
growth factors are released that bring the
epithelial cells to proliferate. It is estimated
that about 50% of longstanding lesions
contain epithelium (1, 2). However, serial

59
sections revealed that only 15% of these
lesions were actually periapical cysts (2).
Radicular cysts develop as a sequel to
apical periodontitis. A cyst is a cavity with
epithelial lining filled by fluid or semisolid
material surrounded by a dense connective
tissue.
Radicular cysts are devided into true cysts
and pocket cysts (2). In a pocket cyst there
is direct continuity between the cyst cavity
and the root canal space, whereas no such
direct communication is present with the
true cyst.
Apical periodontitis cannot be
differentially diagnosed into cystic and non
cystic lesions based on radiographs alone
(3, 4).
The radiologic appearance of the periapical
tissues after surgical therapy has some
unique features (5).
Surgical treatment of periapical lesions
may sometimes result in the formation of
scar tissue, leaving a permanent defect in
the bone that is visible on the radiograph
(Fig 23,24 in the present case).
Typical findings indicative of scar tissue
are - according to Molven et al (6): the
reduction of the bone defect but
persistence of a widened periodontal
membrane. A pattern of irradiating fine
bone trabeculae in contact with the root
end. A solitary defect surrounded by
compact bone but without root contact.
In the present case, several sulfur granules
were seen in the periapical lesion (Fig. 12,
15). Bacteria in the sulfur granules seem to
live in biofilm, and in the SEM pictures
microorganisms are seen embedded in-
and interspersed between an extracellular
matrix. (Fig. 10-21 present case).
The biofilm community lifestyle provides
microorganisms with a series of
advantagesand skills that are not observed
for individual cells living in a free-floating
(planktonic) state including establishment
of a broader habitat range for growth;
increased meta- bolic diversity and
efficiency; protection against competing
microorganisms, host defenses,
antimicrobial agents, and environmental
stress; and enhanced pathogenicity (7, 8).
Apical periodontitis is a biofilm-induced
disease (9). In situ investigations using
optical and/or electron microscopy have
allowed observations of bacteria
colonizing the root canal system in primary
or persistent/secondary infections as sessile
biofilms covering the dentinal walls (11–
16 ). Extraradicular bacteria have been
found in biofilms adhered to the apical root
surface (17, 18, 19) or located within the
body of the inflammatory lesion, usually
forming cohesive actinomycotic colonies
(20).So far, it has been suggested that the
main bacterial species implicated in
independent extraradicular infections are
Actinomyces species and
Propionibacterium propionicum in a
pathologic entity named apical
actinomycosis (20-23). However, tudies
have reported the extraradicular occurrence
of a complex microbiota (24, 26).
References
1. Nair PNR. Apical periodontitis: a dynamic
encounter between root canal infection and host
response. Periodontology 2000 1997; 13: 121-48.
2. Nair PNR, Pajarola G, Schroeder HE.Types and
incidens eof human periapical lesions obtained with
extracted teeth. Oral surg. 1996; 81: 93-102.
3. Mortensen H, winther JE, Birn H. Periapical
granulomas and cysts. Scand J Dent Res 1970; 78:
241-50.
4. Ricucci D, Manocci F, Pitt Ford TR. A study of
periapical lesions correlating the presence of a
radiopaque lamina with histological findings. Oral
Surg Oral Med Oral Pathol Oral Radiolog Oral
Endod. 2006; 101: 389-94.
5. Andreasen JO, Rud J. correlation between
histology and radiography in the assessment of
healing after endodontic surgery. Int Dent Oral
Surg 1972; 1: 161-73.
6. Molven O, Halse A, Grung B. Incomplete
healing (scar tissue) after periapical surgery-
radiographic findongs 8 to 12 years after treatment.
J Endod 1996; 22: 264-8.

60
7. Costerton JW, Lewandowski Z, Caldwell DE, et
al. Microbial biofilms. Annu Rev Mi- crobiol
1995;49:711–45.
8. Costerton JW, Stewart PS, Greenberg EP.
Bacterial biofilms: a common cause of persistent
infections. Science 1999;284:1318–22.
9. Svensàter G, Bergenholtz G. Biofilms in
endodontic infections. Endod Top 2004;9: 27–36.
11. Nair PNR. Light and electron microscopic
studies of root canal flora and periapical
lesions. J Endod 1987;13:29–39.
12. Siqueira JF Jr, Roˆc ̧as IN, Lopes HP. Patterns
of microbial colonization in primary root canal
infections. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 2002; 93:174–8.
13.Molven O,Olsen I,Kerekes K.Scanning electron
microscopy of bacteria in the apical part of root
canals in permanent teeth with periapical lesions.
Endod Dent Traumatol 1991;7:226–9.
14.Ricucci D,Siqueira JF Jr, Bate AL,etal.
Histologic investigation of root canal-treated teeth
with apical periodontitis: a retrospective study from
twenty-four patients. J Endod 2009;35:493–502.
15.Carr GB, Schwartz RS, Schaudinn C, etal.
Ultrastructural examination of failed molar
retreatment with secondary apical periodontitis: an
examination of endodontic biofilms in an
endodontic retreatment failure. J Endod 2009; 35:
1303–9.
16. Schaudinn C, Carr G, Gorur A, et al. Imaging of
endodontic biofilms by combined microscopy
(FISH/cLSM - SEM). J Microsc 2009;235:124–7.
17. Tronstad L, Barnett F, Cervone F. Periapical
bacterial plaque in teeth refractory to endodontic
treatment. Endod Dent Traumatol 1990;6:73–7.
18. Ferreira FB, Ferreira AL, Gomes BP, et al.
Resolution of persistent periapical infection by
endodontic surgery. Int Endod J 2004;37:61–9.
19. Ricucci D, Martorano M, Bate AL, Pascon EA.
Calculus-like deposit on the apical external root
surface of teeth with post-treatment apical
periodontitis: report of two cases. Int Endod J
2005;38:262–71.
20. Happonen RP. Periapical actinomycosis: a
follow-up study of 16 surgically treated cases.
Endod Dent Traumatol 1986;2:205–9.
21. Sjögren U, Happonen RP, Kahnberg KE,
Sundqvist G. Survival of Arachnia propionica in
periapical tissue. Int Endod J 1988;21:277– 82. 8.
22.Sundqvist G, Reuterving CO. Isolation of
Actinomyces israelii from periapical lesion.J Endod
1980;6:602– 6. 9.
23. Byström A, Happonen RP, Sjogren U,
Sundqvist G. Healing of periapical lesions of
pulpless teeth after endodontic treatment with
controlled asepsis. Endod Dent Trau-
matol 1987;3:58 – 63.
24. Sunde PT, Olsen I, Debelian GJ, Tronstad L.
Microbiota of periapical lesions refractory to
endodontic therapy. J Endod 2002;28:304 –10.
25. Sunde PT, Olsen I, Göbel UB, Theegarten D,
Winter S, Debelian GJ, Tronstad L, Moter A.
Fluorescence in situ hybridization (FISH) for direct
visualization of bacteria in periapical lesions of
asymptomatic root-filled teeth. Microbiology. 2003;
149:1095-102.
26. Su L, Gao Y, Yu C, Wang H, Yu Q. Surgical
endodontic treatment of refractory periapical
periodontitis with extraradicular biofilm. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2010
Jul;110(1):e40-4.

61
Case 11
Surgical endodontic treatment of the right maxillary first incisor with sinus tract
Fig. 1 Frontal view
Patient: 64-year-old Caucasian female
Chief complaint:
Tender when chewing and biting.
Sporadically swollen with pus
Medical record: Rheumatisms (Lupus)
High blood pressure
Prednisolon 2,5 mg/week
Aprovel 150 mg (for hypertension)
Carredilol 25 mg (α og β bloccant)
Efexor Depot 75 mg (for depression)
Dental history: endodontically treated by
specialist in endodontics. Referred to the
postgraduate clinic for surgical treatment
because of persisting suppurative sinus
tract
of February 2011
Soft tissue: Sinus tract buccaly 11
Dental: dental crowns
Fig. 3 Occlusal view. Guttapercha in sinus tract
of February 2011
12 11 21
EPT (0-80) 65 - -
Cold + - -
Percussion
Vertical/horizontal
- v and h -
palpation - + -
PPD 4 4 4
Mobility - I -
of February
2011
Dental: Teeth 21,11 are root filled and
have dental crowns
Periodontal: Attachment 2/3
Apical: Tooth 11 apical radiolucency (PAI
3).
Fig. 4 Periapical fistulogram

62
Diagnosis 08 th
of February 2011:
Periapical: Apical periodontitis with sinus
tract (K04.62)
Periodontal: normal
Treatment plan:
Apical surgery 11 with retrograde filling
Problem list:
Esthetic wound healing
Surgical treatment 09 th
of March 2011:
1. Anaesthesia 2. Sulcular flap from 13D-
microbiological sampling 5. Apical root
resection 6. Retro-preparation 7.
Haemostasis 8. Retrograde filling with M
T A 9. Sutures 10. Prescription of
Inspection of the root apex before root
resection revealed extrusion of gutta-
percha, most likely because of resorptions.
It was also evident that here was a crack in
the root surface starting apically with
extension coronally but which ended at the
distal aspect some mm from the apex.
Fig. 5 After ostetomy
Fig. 6 removal of granulation tissue
Fig. 7 Root apex with extrusion of gutta-percha,
Arrow shows crack line apically.
Fig. 8 After root resection
Fig. 9 Root end filling with MTA

63
Fig. 11 Treatment result 12.03.2011
Treatment 17 th
of March 2011
suture removal. She had not experienced
any post-op problems. The sinus tract was
closed, but there was irritation in the
papillas and retraction of the periodontium
(Fig.12).
Fig. 12 Removal of suteures after one week
Histological findings (Hanna Strømme
Koppang)
Granulation tissue with intense chronic
inflammation. Connective tissue with
moderate chronic inflammation and
foreign body material
Bacteriological findings (with DNA-DNA
hybridization): Diagnostic service,
Treponema denticola
Prevotella nigrescens
Campylobacter rectus
Treponema socranskii spp. socranskii
Fusobacterium nucleatum spp. vincentii
Porphyromonas gingivalis
Steinar Stølen
Fig. 13 SEM photo shows branching filamentous
rods and extracellular material
Fig. 14 SEM photo shows rods and extracellular
material

64
Fig 15 SEM photo shows filamentous organisms,
blood cells
Prognosis
good
Dental: The prognosis seemed to be good
Follow-up examination 6 th
of September
2011 and 13 th
of March 2012, (6 and 12
months)
The tooth was asymptomatic, but in
September 2011 clinical gingival
conditions were not satisfactory because of
gingival retractions. In March 2012, twelve
months after surgery, the clinical
conditions were satisfactory, and the
patient was pleased. Radiographic signs of
healing with a continuous PDL
surrounding the apex. No sinus tract is
evident.
Fig. 16 Healing; 6 months
Fig. 17 Healing; 12 months
Fig. 18 Follow up radiograph 6 months
Fig. 19 Follow up radiograph 12 months
Dicussion
In the present case, a crack line was seen in
the apical 1/3 of the root starting apically
and extendet only about 5 mm coronally.
Vertical root fracture (VRF) originate from
the apical end of the root and propagate
coronally and is one of the frustrating
complications of root canal treatment,
which often results in tooth extraction (1).
The root fracture might occur as result of a
microcrack or craze line that propagates

65
with repeated stress application by occlusal
forces. Bier et al (2) showed dentinal
damage (microcracks) in teeth that were
prepared with several nickel-titanium
(NiTi) rotary instruments with the
exception of S-Apex rotary files. They
found the highest defect ratio when
ProTaper was used, whereas no defect was
observed with hand files. In another study
by Yoldas et al (3) they found that all
rotary files created microcracks in the root
dentin of extracted teeth, whereas the SAF
file and hand instrumentation presented
with satisfactory results with no dentinal
microcracks.
It has been shown that root canal filling
procedures could also create cracks (4).
Shemesh et al (5) observed significantly
more dentinal defects (microcracks) in
teeth that were obturated with spreader
than when no spreader was used.
The size of the initial spreader may be
important to prevent extra loading. In the
study by Piskin et al., (6) they revealed that
spreader size equal to the master apical file
decreased the fracture resistance of
maxillary incisor roots. A size 25 spreader
on the other hand, which reached to within
1–2 mm of the working length, did not
influence the fracture resistance of
maxillary roots.
Kim et al (7) have found a potential
relationship between the design of NiTi
instruments and the incidence of vertical
root fractures. They concluded that file
design affected apical stress and strain
concentrations during root canal
instrumentation.
The flap design is important for the healing
of the wound after apical surgery and
many factors play an important role when
the choice of design is considered.
Amongst them are marginal gingival
recession, necrosis of the gingival papilla,
ease of access, maintenance of an adequate
blood supply, trauma to the wound
margins, and scarring (8).
It is crucial that the submarginal incision is
used only when there is a broad zone of
attached gingiva with a minimum of 2mm
In addition; the underlying apical lesion or
surgical bony access must not extend to the
flap margins. (9). This is because a
sufficient amount of marginal attached
gingiva in place is important to avoid
deprivation of blood supply to this
unreflected tissue and risk its necrosis.
Such tissue breakdown will lead to a major
recession with a compromised aesthetic
result
Kamper et al. (8) looked at three different
flap designs used in apical surgery where
the purpose was to evaluate the clinical
and histological features of healing of three
types;
They found that the intrasulcular incision
showed some level of alveolar bone loss
and gingival recession, which could be
avoided using the submarginal incision.
Scar formation was the biggest problem
with the submarginal flap.
It might be that a papilla preserving
incision could have been the
incisiontechniqu to shoose in the present
case. The evaluation of healing patterns of
the papilla base incisions after 3 months
revealed mainly completely undetectable
or only partially detectable incision lines
and generally demonstrated ex- cellent
healing. None of the operated sites
displayed any measur- able loss of papilla
height, or other complications (10).
Another study analyzed degrees of papilla
shrinkage, when papilla base flaps and
sulcular full-thickness flaps were raised
(11). The comparison revealed significant
loss of papilla height, when the papilla was
mobilized during the surgical procedure. In
contrary, the papilla base incision resulted
in rapid and predictable recession-free
healing. To avoid opening of the
interproximal space in esthetically relevant
areas, the use of the PBI was recom-
mended for periradicular surgical
procedures. A further study (12)
investigated surgical outcomes concerning
main vertical loss of height during 12
months.. In cases of full thickness flap
elevation, mean papilla loss of height after
1 yr was 0.98 mm. In contrast to full

66
mobilization of the papilla, the PBI
resulted in significantly lower recession
depths of only 0.21 mm after one year.
References
1.TsesisI, RosenE, TamseA, TaschieriS,KfirA.
Diagnosis of vertical root fractures in
endodontically treated teeth based on clinical and
radiographic indices: a systematic review. J Endod
2010;36:1455–8.
2. Bier CA, Shemesh H, Tanomaru-Filho M,
Wesselink PR, Wu MK. The ability of different
nickel-titanium rotary instruments to induce
dentinal damage during canal preparation. J Endod
2009;35:236–8.
3.Yoldas O, Yilmaz S, Atakan G, Kuden C, Kasan
Z. Dentinal Microcrack Formation during Root
Canal Preparations by Different NiTi Rotary
Instruments and the Self-Adjusting File. J Endod
2012;38:232–235.
4. Shemesh H, Roeleveld AC, Wesselink PR, Wu
MK. Damage to root dentin during retreatment
procedures. J Endod 2011;37:63–6.
5. Shemesh H,Bier CA,Wu MK,Tanomaru-Filho
M,Wesselink PR.The effects of canal preparation
and filling on the incidence of dentinal defects. Int
Endod J 2009;42: 208–13.
6.Piskin B, Aydin B, Sarıkanat M. The effect of
spreader size on fracture resistance of maxillary
incisor roots. Int End J 2008; 41; 54–59.
7. Kim HC, Lee MH, Yum J, Versluis A, Lee CJ,
Kim BM. Potential relationship between design of
nickel-titanium rotary instruments and vertical root
fracture. J Endod 2010;36:1195–9.
8 Kamper BJ, Kaminski EJ, Osetek EM, Heuer
MA. A comparative study of the wound healing of
three types of flap design used in periapical
surgery. J Endod 1984;10:17-25
9. Lang NP, Loe H. The relationship between the
width of keratinized gingiva and gingival health. J
Periodontol 1972;43:623–7.
10. Velvart P. Papilla base incision: a new approach
to recession-free healing of the interdental papilla
after endodontic surgery. Int Endod J 2002;
35:453– 60.
11. Velvart P, Ebner-Zimmermann U, Ebner JP.
Comparison of papilla healing following sulcular
full-thickness flap and papilla base flap in endodon-
tic surgery. Int Endod J 2003;36:653–9.
12. Velvart P, Ebner-Zimmermann U, Ebner JP.
Comparison of long term papilla healing following
sulcular full thickness flap and papilla base flap in
endodontic surgery. Int Endod J 2004; 37:687-93.

67
Case 12
Surgical endodontic treatment of a maxillary left canine with sinus tract
Fig 1. Frontal view
Patient: 52-year-old African male
Chief complaint
Experience of dull pain before and after
endodontic treatment performed in
February 2010.
Dental history: Graduate student
endodontically treated tooth 23 in
December 2009. The sinus tract persisted
even after 3 months long-term inlay with
calsiumhydroxide. The tooth was then
obturated and the patient was referred to
the post-graduate clinic for apical surgery.
of April 2010
Soft tissue: sinus tract buccaly regio 23, 24
Dental: All teeth sound
Discoloration (dental fluorosis?)
Fig. 2 Buccal view. Guttapercha point in sinus
tract
Fig 3. Palatal view
of April 2010
22 23 24
EPT (0-80) 14 - -
Cold + - +
Percussion
Vertical/horizontal
- v and h -
palpation - + -
PPD 3 6 4
Mobility - - -
of April 2010
Dental: Tooth 23 has an homogenous root
flling, 1 mm from radiological apex
Periodontal: attachment ½-2/3
Apical: tooth 23 apical radiolucency (PAI
4).
Fig. 4 Before endodontic treatment 01.12.2009

68
Fig 5. Periapical radiograph 28.04. 2010
Diagnosis 28th
of April 2010
Periapical : Apical periodontitis with
sinus tract (K04.62)
Treatment plan
The root-filling appeared dense and good,
and it was decided to do apical surgery 23
with retrograde filling without re-treatment
Treatment 12th
of May 2010
microbiological sampling 5. Apical root
Haemostasis 8. Retrograde filling with
MTA 9. Sutures 10. Prescription of
Fig. 6 Fenestration of buccal bone. Enucleation of
lesion
Fig. 7 Apex is visible after ostetomy
Fig. 8 After rootresection and retropreparation
Fig. 9. Rerograde filling MTA

69
Fig. 11Treatment result 01.05.2011
Treatment 5th
of May 2010:
suture removal. He had not experienced
any post-op problems. The sinus tract was
closed (Fig. 11).
Fig 12. Healing one week after surgery
Fig. 13 Healing one week after surgery
Bacteriological findings with DNA-DNA
hybridization): diagnostic service,
Actinomyces israelii
Treponema denticola
Prevotella nigrescens
Fusobacterium nucleatum
Porphyromonas endodontalis
Eicenella corrodens
Steinar Stølen
Fig. 14 Branching filamenteous rods
Fig. 15 Rods and extracellular material
Prognosis:
good
Dental: the prognosis seemed to be
uncertain
Follow-up examination 24th
of January
2012 (22 mnd):
The tooth is asymptomatic and the clinical
conditions ae satisfactory with no sinus
tract (Fig. 16, 17). Radiographic signs of
healing with a continuous PDL
surrounding the apex (PAI 2) (Fig. 18).

70
Fig. 16 Buccal view. Healing; 22 months
Fig. 17 Buccal view. Healing; 22 months
Discussion
Microbiological sampling detected
Actinomycs israelii in the periapical tissue
in the present case. It is well known that A.
israelii can be established in periapical
tissues (1). In addition, SEM photos (Fig
14,15) showed microorganisms
interspersed between an extracellular
matrix. These extraradicular findings
confirmed that apical surgery was the right
treatment choice. A retreatment procedure
would most likely not have eradiated the
infection.
The patient in the present case had a
persistent sinus tract. A sinus tract is
defined as a passage of pus from an
abscess cavity to and external environment
through a tissue membrane such as the oral
mucosa or the skin. The reason that a sinus
tract develops is not fully understood.
Mortensen et al. (2) investigated 1600
teeth with periapical lesions; 136 (9.0%)
teeth had sinus tracts. They found that the
size of the radiolucency seemed to matter,
because teeth with periapical lesions
smaller than 5 mm had sinus tracts in 5%
of cases, whereas teeth with periapical
lesions greater than or equal to 5 mm had
sinus tracts in 19%.
Some studies have suggested that the
odontogenic sinus tract is lined with
epithelium (3, 4). Valderhaug (5) studied
experimentally induced sinus tracts in
monkeys. He found that most of the sinus
tracts were completely or partly lined with
epithelium. However, studies by Grossman
(6) and Bender and Seltzer (7) state that
the sinus tract is not lined with epithelium,
but lined with granulation tissue.
According to Grossman (6) sinus tracts can
heal and closure occurs after root-canal
treatment. In this case the sinus tract
persisted after treatment of the tooth. It
was an indication of treatment failure and a
surgical approach had to be done.
For non surgical endodontic treatment, it
has been shown that the presence of a sinus
tract will not influence the long-term
outcome of endodontic treatment (8-12).
However, another study fond that the
presence of sinus was found to be a
significant prognostic indicator (13).
In surgical endodontic, studies have
reported a comparable treatment otcome
(14,15).

71
References
1. Happonen RP. Periapical actinomycosis: a
follow-up study of 16 surgically treated cases.
Endod Dent Traumatol 1986; 2: 205-9.
2. Mortensen H, Winther JE, Birn H. Periapical
granulomas and cysts. Scand J Dent Res
1970;78:241–50.
3. Harrison JW, Larson WJ. The epithelized oral
sinus tract. Oral Surg 1976;42:511–7.
4. Baumgartner JC,PickettAB, Muller JT.
Microscopic examination of oral sinus tracts and
their associated periapical lesions. J Endod
1984;10:146-152
5. Valderhaug J. A histologic study of
experimentally produced intra-oral odontogenic
fistulae in monkeys. Int J Oral Surg 1973;2:54–61.
6. Grossman LI. Endodontic practice. Philadelphia:
Lea & Febiger, 1965: 78 –92.
7. Bender IB, Seltzer S. The oral fistula: its
diagnosis and treatment. Oral Surg 1961;14:1367–
76.
8. Strindberg LZ. The dependence of the results of
pulp therapy on certain factors. Acta Odont Scand
1956;14(Suppl 21):1–175.
9. Sjögren U, Hagglund B, Sundqvist G, Wing K.
factors affecting the long-term result of endodontic
treatment. J Endod 1990; 16: 498-82.
10. Chugal NM, Clive JM, Spångberg LSW. A
prognostic model for assessment of the outcome
of endodontic treatment: effect of biologic and
diagnostic variables. Oral Surg Oral Med Oral Path
Oral Radiol Endod. 2001; 91. 342-52
11. Farzaneh M, Abitol S, Friedman S. treatment
outcome in endodontics: the Toronto study. Phases
I and II: Orthograde retreatment. J Endod 2004; 30:
627-33
12. Ricucci D,Russo J, Rutberg M, DMD,c
Burleson JA, Spångberg LSW,.A prospective
cohort study of endodontic treatments of 1,369 root
canals: results after 5 years Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 2011;112:825-42.
13. Ng YL, Mann V, gulabivala K. A prospective
study of the factors effecting outcomes of
nonsurgical root canal treatment: part 1: periapical
health. Int Endod J 2011; 344: 583-609.
14. Treatment outcome in endodontics-The Toronto
Study. Phases I and II: apical surgery.Wang N,
Knight K, Dao T, Friedman S. J Endod. 2004;
30:751-61.
15. Rahbaran S, Gilthorpe MS, Harrison SD,
Gulabivala K. Comparison of clinical outcome of
periapical surgery in endodontic and oral surgery
units of a teaching dental hospital: a retrospective
study. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2001; 91:700-9.

72
Case 13
Surgical endodontic treatment of a maxillary right first premolar
Fig. 1 Frontal view
Chief complaint
Experience of dull pain after-treatment of
tooth 14 done by post graduate student in
2008
Medical record:
High blood pressure
Fibromyalgia
Marevan 3,5 mg, 2 tablets daily
Cozaar (blood pressure)
Sarotex 10 mg (antidepressive)
Zoloft 100 mg (antidepressive)
Dental record: Tooth 14 was
endodontically treated by graduate student
in 2006 and retreated by post graduate
student in 2008
Clinical findings 17th
of February 2010
Dental: Tooth 13 sound, tooth 14 has a
dental crown, tooth 16 MOD amalgam
filling while tooth 17 has caries and tooth
fracture
Fig. 2 Buccal view
Clinical tests 17th
of February 2010
14 16 17
EPT (0-80) - 45 40
Cold - + +
Percussion
Vertical/horizontal
- v and h -
palpation - + -
PPD 2 2 2
Mobility - - -
of February
2010
Dental: Tooth 17 has loss of tooth
substance, no filling. Tooth 16 MOD
amalgam filling, tooth 15 has a dental
crown and is root filled
Periodontal: normal
Apical: Tooth 16 has a continuous PDL
and tooth 15 has apical radioluceny (PAI
4).

73
Radiographic findings; history
Root filled in 2006 by graduate student and
in 2008 by postgraduate student.
Radiograph 2009 showed no radiographic
healing of the lesion
Fig. 5 September 2006
Diagnosis 17th
of February 2010
Pulpal: Root filled tooth (K 04.19)
Periapical : Chronic apical periodontitis
(K04.50)
Periodontal: normal
Treatment plan
Apical surgery 14 with retrograde filling
Treatment 14th
of April 2010
17D, with a buccal releasing incision 13M
3. Osteotomy 4. Biopsy 5. Apical root
analgesics and post-op information
Fig. 8 Enucleation of lesion
Fig. 9 Buccal and palatinal roots after root resection
(arrows)

74
Fig. 11 Before retrograde filling in palatinal canal
Fig. 12 Retrograde fillings in buccal and palatinal
canals
Treatment 21th
of April 2010
suture removal. She had not
experiencedany post-operative problems.
Fig. 13 Before suture removal
Fig 14. Removal of sutures
Prognosis
good
Dental: the prognosis seemed to be good
Follow-up examination 30th
of January
2012 (21 months)
The radiograph was taken by graduate
student. Radiographic healing was evident
with a continuous PDL surrounding the
apex. Tooth 17 had been extracted since
last visit.
Fig. 15 Follow up radiograph 30.01
.
Dicussion
In a review by Friedman (1), where
selected studies on apical surgery were
included, the succees rate was reported to
be 37-91% while up to 33% can still be
healing several years after surgery. This
unsually high and low rates (2, 3 ) were
found to fall considerably outside the range
of rate reported in the remaining studies,
and the change for complete healing after
surgical endodontics is 60-78%(4-7).
Lesions >10 mm do show a lower rate of
complete healing and a greater incidence
of incomplete healing by scar tissue
formation (8, 9).
The root anatomy of the maxillary first
molar can vary depending on whether one,
two, or three roots are present. Prominent
root concavities are present on both the
mesial and distal surfaces of the root. The
mesial root concavity is more prominent
and extends onto the cervical third of the
crown (10) The palatinal aspect of the

75
buccal root tip of the two-rooted maxillary
first premolars usually has a deep
longitudinal depression along its
length.(11). Joseph et al.(12) found an
incidence of buccal furcation groove in
62% of teeth with bifurcated roots.
The majority of anatomical studies have
reported that the most common form of the
maxillary first is the two-rooted form in a
Caucasian material (13), whereas in
studies of the Asian population, single-
rooted maxillary premolars are the
dominant form (14).
1. Friedman S. The prognosis after apical surgery.
Endod Topics 2005; 11: 219-262.
2. Rahbaran S, Gilthorpe MS, Harrison SD,
Gulabivala K. Comparison of clinical outcome
of periapical surgery in endodontic and oral surgery
units of a teaching dental hospital: a retrospective
study. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 2001: 91: 700– 709.
3..Zuolo ML, Ferreira MOF, Gutmann JL.
Prognosis in periradicular surgery: a clinical
prospective study. Int Endod J 2000: 33: 91–98.
4. Wang N, Knight K, Dao T, Friedman S.
Treatment outcome in endodontics – the Toronto
study. Phase I and II: apical surgery. J Endod 2004:
30: 751–761.
5. Gagliani MM, Gorni FG, Strohmenger L.
periapical resurgery versus periapical surgey: a 5
year longitudinal comparison. Int Endod J 2005; 38:
320-7.
6. Jensen SS, Nattestad A, Egdø P, Sewerin I,
Munksgaard EC, Schou S. A prospective,
randomized , comparative clinical study of resin
composite and glass ionomer cement for retrograde
rootfilling. Clin Oral Investig 2002; 6: 236-43.
7. Kvist T, Reit C. Result of endodontic
retreatment: a randomized clinical study comparing
surgical surgical and non-surgical precedures. J
Endod 1999; 25: 814-17.
8. Molven O, Halse A, Grung B. Surgical
management of endodontic failures: indications and
treatment results. Int Endod J 1991: 41: 33–42.
9. Grung B, Molven O, Halse A. Periapical surgery
in a Norwegian county hospital: follow- up findings
of 477 teeth. J Endod 1990; 16: 411-17-
10. Booker BW, 3rd Loughlin DM. A morphologic
study of the mesial root surface of the adolescent
maxillary bicuspid. J Periodontol 1985;556:66-670.
11. Gher Me, Vernion AR. Root morphology –
clinical significance in pathogenesis and treatment
of periodontal disease. J Am Dent Assoc
1980;101:627-33.
12. Joseph I, Varma BR, Bhat KM. Clinical
significance of furcation anatomy of the maxillary
first premolar: a biometric study of extracted teeth.
J Periodontol 1996;67:386-89.
13. Vertucci FJ. Root canal anatomy of the human
permanent teeth. Oral Surg Oral Med Oral Pathol.
1984; 58:589-99.
14.Walker RT. Root form and canal anatomy of
maxillary first premolars in a southern Chinese
population. Endod Dent Traumatol 1987;3:130-4.

76
Case 14
Non surgical retreatment and later surgical retreatment of a mandibular right first
molar with carbon post and separated instrument
Fig. 1 Frontal view
Chief complaint:No complains, but he
wants restaurations maxilla right side for
esthetical reasons. He has never
experienced pain from tooth 46
Medical record: He has high blood
pressure but he takes no medication.
Dental history: Tooth 46 was previously
endodontically treated but the date is
unknown.
The patient was referred from the graduate
clinic for retreatment of tooth 46 before
dental crown therapy
Clinical findings 02nd
of September 2009
Dental: He has a well conserved dentition.
Tooth 46 has a composite filling, caries
mesially and carbon post in distal root
Tooth 45 has an unsatisfactory composite
filling
Clinical tests 02th
of September 2009
43 44 46
EPT (0-80) 35 21 -
Cold + + -
Percussion
Vertical/horizontal
- - v
palpation - - -
PPD 3 3 3
Mobility - - -
of September
2009
Dental: Tooth 44 has a radiopaque filling
material. Tooth 45 has an incomplete root
filling and post. Tooth 46 has an
incomplete root filling, caries mesially,
post in the distal canal and separated
instrument in the mesial canal
Periodontal: attachment >⅔
Apical: Tooth 46: apical radiolucency (PAI
4)
Tooth 45: continuous PDL space

77
Fig 3. Periapical radiograph 02.09.2009
Diagnosis 02th
of September 2009
Pulpal: Endodontically treated tooth
(K04.19)
Periapical : Chronic apical periodontitis
(K04.50)
Periodontal: normal
Treatment plan
Retreatment of endodontically treated
tooth
Problem list
Removal of post, and removal of separated
instrument?
Treatment 16th
of September 2009
Carbonpost in distal canal was removed
with LN bur and long burs.
Separated instrument in ml canal was
removed with modified Gates Glidden to
make a shelf, and ultrasound in a
counterclockwise direction around the
instrument
NiTi handinstruments, BioRace
MB: 17mm/40#
ML: : 17mm/40#
D: : 16mm/50#
Chemical
1% NaOCl, 17% EDTA, 2% chlorhexidine
digluconate
Intracanal medicament
Ca(OH)2
Fig. 4 Separated instrument in cavity after removal
Fig. 5 Separated instrument in ml canal
Fig. 6 Working lenght in ml canal achieved after
removal of separated instrument
Progress notes 10th
of October 2009
sealed with IRM

78
Prognosis
good
uncertain
of October
2010 (12 months)
Radiograph showed no healing of the
apical radiolucency (PAI 4). The Patient
sitivity to percussion or palpation tests. He
was under treatment at the student clinic,
but had still an IRM filling (although
written instructions in the journal about the
importance of permanent filling or at least
an semipermanent solution like
composite). The reason for IRM was that
they would not make any permanent
restauration unless healing occurred. The
patiens graduate student was contacted and
asked to make at least a composite
restauration, which was done.
Tooth 45 had a new dental crown without
endodontic retreatment of unsatisfactory
rootfilling and widened periodontal
ligament apically. The patient was
informed that apical surgery on tooth 46
was advisable. He wanted to wait for some
months because of vacation, and then
contact the clinic.
Follow up examination September 2011
(23months)
No apical healing. Composite filling. The
patient wants surgical endodontic
treatment to be done.
Fig. 11 Follow up radiograph 09.2011
Progress notes 19th
of October 2011
regio 47D, with a buccal releasing incision
43M 3. Osteotomy 4. Biopsy 5. Apical root
analgesics andpost-op information.
Fig. 12 Reflection of mucoperiosteal fla

79
Fig. 13 After ostetomy
Fig. 14 Root resection of mesial root
Fig. 15 Close up of root resected roots, an isthmus
can be observed in the mesial root (arrow)
Fig. 16 MTA in distal, ml and mb canals and in the
isthmus between ml and mb canals
Fig. 18 Treatment result
Treatment 25th
October 2011: Removal of
sutures. Soft tissue healing and the patient
had no symptoms

80
Fig. 19 Before removal of sutures; one week after
surgery
Microbiological findings (diagnostic
service, Institute of Oral Biology)
• Porphyromonas gingivalis
• Prevotella nigrescens
• Treponema socranskii spp. Socranskii
• Eubacterium saburreum
• Streptococcus intermedius
• Treponema denticola
• Prevotella melaninogenica
• Porphyromonas gingivalis
• MCK plate: Sphmon. paucimobilis
Steinar Stølen
Fig. 20 Microorganisms embedded in an
extracelluar material
Fig. 21 Microorganisms embedded in extracellular
matrix
of March 2012
(6 months after surgery)
No symptoms on palpation and percussion.
No pathological pocket depths. Signs of
apical healing
Fig. 23 Buccal view; 6 months after surgery

81
Discussion
The patient in the present case had not got
a permanent filling at the one year recall.
Multiple in vitro studies have shown that
even the best root canal treatment can
allow leakage of bacteria and their
byproducts through an apparently well-
filled canal system (1). The work of Ray
and Trope (2) was a paradigm shift in
endodontic treatment philosophy when
they found that the coronal restoration had
a greater impact on success than the
quality of root canal treatment.
Yet, other studies have shown that even in
the presence of obvious contamination,
periapical disease does not necessarily
develop in all patients (3,4,5). Whilst most
laboratory studies found microbial leakage
through filled root canals to occur within
weeks (1), histological observations on
unrestored, adequately root filled teeth that
were extracted from patients have
indicated otherwise (4,6,). In a recent study
by Rechenberg et al., (7) they assess the
routes of bacterial leakage in a commonly
used two-chamber model designed to eval-
uate root fillings. Under the current
conditions, bacterial leakage occurred
through the sticky wax seal separating the
two chambers of a standard laboratory set-
up and through the root canal filled with
gutta-percha and an epoxy resin sealer.
Bacteria permeated tubular aspects of
dentine in root filled teeth, whilst sclerotic
or atubular dentine and the interface
between sealer and dentine devoid of
patent tubules remained bacteria-tight.
Bacterial leakage through secondary
dentinal tubules (i.e. lateral branches
connecting the main tubules) was
observed. This suggests that bacteria do
not necessarily penetrate filled roots at the
immediate interface between root filling
material and the canal wall, but also deeper
in the (tubular) dentine. They concluded
that the current experimental method
proved to be unsuitable to compare root
fillings.
In a recent systematic review and
metaanalysis (8) on the impact of the
quality of coronal restaurations versus the
quality of root canal filing on periapical
healing, they concluded that odds for
healing of apical periodontitis increase
with both adequate root canal treatment
and adequate restorative treatment.
Although poorer clinical outcomes may be
expected with adequate root filling–
inadequate coronal restoration and
inadequate root filling–adequate coronal
restoration, there is nosignificant
difference in the odds of healing between
these 2 combinations.
The prevalence of root canal isthmuses in
the apical 5 mm of the mesial root of
mandibular molars were investigated by
means of micro-computed tomography
(MCT) (9). They found that isthmuses
were present in the vast majority of roots
observed. The third millimetre from the
apex showed more isthmuses than
expected. The results of clinical and
surgical endodontic procedures performed
in the mesial root of mandibular molars
may be affected by this aspect of the root
canal anatomy.
In a recent study a three-dimensional
analysis of the isthmus area of the
mesiobuccal root canal system in
mandibular molars were obtained using
high-resolution micro–computed
tomography (m-CT) scanning (10). They
measured the amount of debris and root
filling material in the isthmus after
instrumenta-tion/irrigation and root filling.
A considerable amount of dentin debris is
produced and packed into the isthmus area
during rotary instrumentation of mesial
canals of lower molars despite continuous
irrigation during and after instrumentation.
The average percentage of volume of
filling material in the isthmus areas was
significantly lower (57.5%) than in the
main root canals (98.5%, p < 0.001).
Sphingomonas paucimobilis was in he
present case identified with DNA-DNA
hybridization in the periapical lesion.

82
Sphingomonas paucimobilis, formerly
known as Pseudomonas paucimobilis, is a,
strictly aerobic, Gram-negative bacillus
with a single polar flagellum. It was
initially reported to be a human pathogen
in 1979. The natural habitat of this
organism has not been fully defined but it
is known to be widely distributed in the
natural environment, particularly in water
and soil, and has also been isolated from
hospital settings, including hospital water
systems, distilled water, dialysis fluid,
nebulizers, and other respiratory
therapy equipment. S. paucimobilis has
been associated with a variety of infections
in humans, including bacteremia,
pneumonia, catheter- related infections,
meningitis, peritonitis, osteomyelitis,
septic arthritis, postoperative
endophthalmitis, lung em- pyema, splenic
abscesses, urinary tract infections, and bil-
iary tract infections (12).
1. Rechenberg DK, De-Deus G, Zehnder M (2011)
Potential systematic error in laboratory experiments
on microbial leakage through filled root canals:
review of published articles. International
Endodontic Journal 44, 183–94.
2.RayHA,TropeM.Periapicalstatusofendodontically
treatedteethinrelationtothetech-
nical quality of the root filling and coronal
restoration. Int Endod J 1995;28:12–8.
3. Ricucci D, Grondahl K, Bergenholtz G.
Periapical status of root-filled teeth exposed
to the oral environment by loss of restoration or
caries. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 2000;90:354–9.
4. Ricucci D, Lin LM, Spangberg LS. Wound
healing of apical tissues after root canal therapy: a
long-term clinical, radiographic, and
histopathologic observation study. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 2009;108:609–
21.
5. Ricucci D, Siqueira JF Jr. Biofilms and apical
periodontitis: study of prevalence and association
with clinical and histopathologic findings. J Endod
2010;36 2010; 1277–88.
6. Ricucci D, Bergenholtz G Bacterial status in
root-filled teeth exposed to the oral environment by
loss of restoration and fracture or caries – a
histobacteriological study of treated cases. Int
Endod J 2003; 36, 787–802.
7.Rechenberg D-K, Thurnheer T& Zehnder M.
Potential systematic error in laboratory experiments
on microbial leakage through filled root canals: an
experimental study. Int Endod J 2011; 44: 827-835.
8. Gillen BM, Looney SW, Loushine BA, Weller
RN, Loushine RJ, Pashley DH, Tay FR. Impact of
the Quality of Coronal Restoration versus the
Quality of Root Canal Fillings on Success of Root
Canal Treatment: A Systematic Review and Meta-
analysisJ Endod 2011;37:895–902).
9. Mannocci F, Peru M, Sherriff M, Cook R, Pitt
Ford TR.The isthmuses of the mesial root of
mandibular molars: a micro-computed tomographic
study. International Endodontic Journal, 38, 558–
563, 2005.
10. Endal U, sjen Y, Årving K, gao Y, Haapasalo
M. A High-resolution Computed Tomographic
Study of Changes in Root Canal Isthmus Area by
Instrumentation and Root FillingJ Endod
2011;37:223–227
11. Lina JN, Laia CH, Chenb YH, et al..
Sphingomonas paucimobilis Bacteremia in
Humans: 16 Case Reports and a Literature Review
.J Microbiol Immunol Infect 2010;:35–42.

83
Case 15
Treatment of maxillary central incisors with external inflammatory resorptions
Fig. 1 Frontal view
Chief complaint: The patient had vague
symptoms from the upper front teeth. She
was referred from her GP for endodontic
treatment 11 and 21
Medical record: non-contributory
Dental history:
She had a bicycle accident and dental
trauma in june 2008 and was treated at
Ullevål hospital: teeth 11 and 21 had
complicated crown fractures and were
mobile, no splinting, soft food for 2 weeks,
there was no information about the type of
injury of the tooth in the journal from
Ullevål hospital. Teeth 11 and 21 got
composite restaurations at her private
dentist and the teeth were after that
observed. Root resorptions were
discovered in November 2011 and the
patient was referred to the post -graduate
endodontic clinic for endodontic treatment.
of January 2009
Dental
Tooth 11 has a composite filling mesially,
sign of complicated crown fractur
Tooth 21 has a composite filling distally,
and sign of complicated crown fracture.
Tooth 22 has a small enamel fracture while
tooth 12 is normal
The patient is caries free with few
restaurations
Fig. 2 Palatal view
Fig. 3 Buccal view
Clinical tests 07th
of January 2009
12 11 21 22
EPT (0-80)
Cold
65
+
-
-
-
-
15
+
Percussion
Vertical/horizontal
- v +h v + h -
palpation - + + -
PPD 3 4 4 3
mobility - - - -
of January
2009
Dental: Tooth 12 is normal
Tooth 11 has a composite filling mesially
and a pulpstone can be observed in the
pulpchamber.
Tooth 21 has a composite filling distally,

84
Tooth 22 is normal
Periodontal:
3 mm bone destruction between 11
and 21
Apical:Tooth has an expanded PDL space
and diffuse radiolucent area, external root
resorption in middle and apical 1/3 of the
root , (PAI 3)
Tooth 21 has widened PDL space and
diffuse radiolucent area, external root
resorption in apical 1/3 (PAI 3).
Teeth 12 and 22 have continuous PDL
Diagnosis 07th
of January 2009
Teeth 11 and 21:
Pulpal : Infected necrosis (K04.11)
(K04.50)
Pathologic resorption: External
inflammatory resorption (K03.30)
Treatment plan
periodontitis teeth 11 and 21
Follow up
Problem list:
External inflammatory resorption –
perforation during instrumentation ?
Treatment 07 th
of January 2009
Access cavity preparation and location of
one canal, pulpstone in canal removed with
ultrasound
Mechanical:Bur, IrriSafe, ultrasound
NiTi haninstrumentation
#70/23mm adjusted to 22 mm
Chemical:1% NaOCl, 16% EDTA,
2% chlorhexidine digluconate
Fig 5. Working length radiograph tooth 11
Treatment 08th
of January 2009
Mechanical:Bur, IrriSafe
NiTi haninstrumentation #70/22mm
Ca(OH)2
Treatment 22th
of January 2009
Tooth11: Slightly tender to palpation
buccaly

85
Tooth 21: Tender to palpation buccaly,
tenderness to percussion
Chemical:Bur, IrriSafe
1% NaOCl, 16% EDTA,
Intracanal medicament
Ca(OH)2
Treatment 11th
of February 2009
No symptoms, not tender to palpation
/percussion.
Kofferdam and instruments changed after
final treatment of tooth 21.
MTA plug apically both teeth,
Filled with gutta-percha varm technique,
AH plus, sealed with IRM and composite
Fig. 7 Apical plug with MTA tooth 21
Fig. 8 Apical plug with MTA tooth 11
Fig. 9 After treatment11.03.2009
MTA, warm guttapercha, IRM and composite
of September
2010 and 06th
of December 2011(18 and
32 months)
Radiograph showed evidence of healing of
the periapical radiolucency, but the lamina
dura is widened (PAI 2) Cement repair in
resorptions is evident (Fig. 10, 11.1 and
11.2) . She has new porcelain laminates on
teeth 11 and 21 (Fig. 12). The patient was
asymptomatic and experienced no
sensitivity to percussion or palpation tests.
12 and 22 were sensitive to ice and EPT
(18 months)

86
Fig. 11.1 Follow up radiograph 06.12.2011
(32 months)
Fig. 11.2 Follow up radiograph 06.12.2011
(32 months)
Fig. 12 Frontal view (32 months aftre treatment)
Discussion
Inflammatory root resorption (external
infection related resorption) is a
combination of disruption to the outer
cementum layer of the root surface and an
intracanal infection that triggers
osteoclastic activity. This type of resortion
can affect all parts of the root and is a
rapidly progressing progress that may
result in total resorption of the root within
a few months. It is usually a sequelae to
acute trauma and is especially common
after intrusion and replantation of avulsed
teeth (1, 2).
When the resorption has penetrated the
cementum and exposed dentinal tubules,
toxins from bacteria in the root canal and
dentinal tubules can diffuse to the PDL.
This results in continuation of the
osteoclastic process and an associated
inflammation in the PDL, leading to
resorption of alveolar bone. If bacteria are
eliminated from the root canal by
endodontic therapy, the resorptive process
will be arrested (3, 4). The resorption
cavity will then be filled with cementum or
bone.
The patient in the present case had most
likely a subluxation injury combined with
a complicated crown fracture in both of
central incisors
The reported risk of pulp necrosis (PN) is
generally low in teeth with subluxation
injuries. In a recent article by Lauridsen et
al. (5) they report that a concomitant crown
fracture may increase the risk of PN in
subluxated injured teeth, also in teeth with
mature root development. They concluded
that a concomitant crown fracture and no
response to EPT at the initial examination
may be used to identify teeth at increased
risk of PN following subluxation injury.
The goal in treatment of a severely luxated,
intruded, or avulsed tooth is to
endodontically treat the tooth before it
becomes infected and to halt osteoclastic
activity on the outer root surface (6).
Long-term CH placement is recommended
for teeth in which external resorption is
already radiographically visible (7).
However; root fracture could be a
consequence of long-term treatment of CH
(8, 9)
MTA, as with with CH, shares a similar
highly alkaline pH when freshly mixed
(10) and demonstrates some antimicrobial
activity (11).
Beyond showing that CH can maintain a
high pH over time in the root canal, several

87
studies have also confirmed hydroxyl ion
diffusion through dentin by detecting
elevated pH levels on the external root
surface (12-14). Similarly, calcium ions
from intracanal MTA have been shown to
diffuse from the root canal through
radicular dentin into simulated external
root surface cavities (15).
The reason for an MTA plug in the present
study was primarly to get practice.
However, the alkaline pH of MTA found
in simulated resorptive lesions combined
with its good sealing ability warrant further
studies as a treatment option in cases with
external inflammatory root resorp tion,
particularly in cases in which root fracture
could be a consequence of long-term and
short-term treatment with CH (16).This is
a problem in immature teeth, but the
problem apparently does not exist in
mature teeth. (4).
References
1Andreasen JO. Relationship between surface and
inflammatory resorption and changes in the pulp
after replantation of permanent incisors in
monkeys. J Endod 1981;7:294–301.
2.Andreasen JO, Andreasen FM. Root resorption
following traumatic dental injuries. Proc Finn Dent
Soc 1991; 88:95-114.
6.
3. Andreasen JO. The effect of pulp extirpation or
root canal treatment on periodontal healing after
replantation of permanent incisors in monkeys. J
Endod 1981; 7: 245-52.
4. Cvek M. Prognosis of luxated non-vital
maxillary incisors treated with calcium hydroxide
and filled with gutta –percha. Endod Dent
Traumatol. 1992; 8: 45-55.
5. Lauridsen E, Hermann NV, Gerds TA,
Ahrensburg SS, Kreiborg S, Andreasen JO.
Combination injuries 1. The risk of pulp necrosis in
permanent teeth with concussion injuries and
concomitant crown fractures. Dent Traumatol 2012
6.Cvek M. Treatment of non-vital permanent
incisors with calcium hydroxide: II— effect on
external root resorption in luxated teeth compared
with effect of root filling with gutta percha: a
follow-up. Odontol Revy 1973;24:343–54.
7. AAE. Guidelines for treatment of traumatic
dental injuries. Chicago: American Association of
Endodontists; 2004.
8. Andreasen JO, Farik B, Munksgaard EC. Long-
term calcium hydroxide as a root canal dressing
may increase risk of root fracture. Dent Traumatol
2002;18:
134–7.
9. Sahebi S, Moazami F, Abbott P. The effects of
short-term calcium hydroxide application on the
strength of dentine. Dent Traumatol 2010;26:43–6.
10. Torabinejad M, Hong CU, McDonald F, Pitt
Ford TR. Physical and chemical properties of a new
root-end filling material. J Endod 1995;21:349–53.
11. Zhang H, Shen Y, Ruse ND, Haapasalo M.
Antibacterial activity of endodontic sealers by
modified direct contact test against Enterococcus
faecalis. J Endod 2009;35:1051–5.
12. Chamberlain TM, Kirkpatrick TC, Rutledge
RE. pH changes in external root surface cavities
after calcium hydroxide is placed at 1, 3 and 5 mm
short of the radiographic apex. Dent Traumatol
2009;25:470–4.
13. Nerwich A, Figdor D, Messer HH. pH changes
in root dentin over a 4-week period following root
canal dressing with calcium hydroxide. J Endod
1993;19:302–6.
14. Tronstad L, Andreasen JO, Hasselgren G,
Kristerson L, Riis I. pH changes in dental tissues
after root canal filling with calcium hydroxide. J
Endod 1981;7:17–21.
15. George GK, Rajkumar K, Sanjeev K,
Mahalaxmi S. Calcium ion diffusion levels from
MTA and ApexCal in simulated external root
resorption at middle third of the root. Dent
Traumatol 2009;25:480–3.
16. Heward S and Sedgley CM. Effects of
Intracanal Mineral Trioxide Aggregate and Calcium
Hydroxide During Four Weeks on pH Changes in
Simulated Root Surface Resorption Defects: An In
Vitro Study Using Matched Pairs of Human Teeth J
Endod 2011;37:40–44.

88
Case16
Endodontic treatment in conjunction with surgical treatment of maxillary right first
central, mandibular left second premolar and first molar in patient with multiple
inflammatory cervical resorptions
Fig. 1 Frontal view
Chief complaint
She complains about lots of problems with
her teeth. She is afraid of not to be taken
seriously. For example about her muscular
problems and allergies she thinks she has
to metals.
Medical record: Muscular problems not
diagnosed. Low blood pressure.
the student clinic because of discovery of a
resorption on tooth 36 below a crown
made 1 year earlier. It was observed on a
routine x ray.
The student came to the postgraduate
endodontic clinic for discussion, and CT
were ordered from the Department of
Maxillofacial Radiology
of February 2011
Dental:
Tooth 35 has a composite filling
Teeth 36 and 37 have dental crowns
Fig. 3 Lingual view
Fig. 4 Buccal view

89
Fig. 5 Frontal view
Clinical tests 15th
of February 2011
12 11 21 35 36 37
EPT (0-80) 17 7 12 25 - 44
Cold + + + + + +
Percussion
Vertical/horizontal
- - - - v -
palpation - - - - - -
PPD 4 7 4 4 5 4
Mobility - I - - - -
Radiographic findings: history
(radiographs taken at the graduate clinic)
Fig. 7 Bite wing taken after placement of dental
crown 11.02.2010
Fig. 8 Periapical radiograph taken 03.02.2011 by
student
of February
2011
After examination of the radiographs that
followed the referral 03.02.2011, it was
decided to order a CT- scan of both jaws.
That would provide valuable information
about the extension of the defect s, and
also give information about resorptions
elsewhere.
In addition to cervical resorptions on teeth
35 and 36, a cervical resorption on tooth
11 was identified on CT scan.
Dental: Tooth 36 has a dental crown,
radiolucent area in furcation
Tooth 35 MOD radiopaque filling material
and radiolucent area mesially in the
cervical area
Tooth 11 has a radiolucent area mesially in
the middle 1/3 of the root, located at the
bone level.
Periodontal: attachment ½-2/3
Apical : normal PDL teeth 35, 36 and 11

90
Radiologic description (in Norwegian) from the Department of Maxillofacial Radiology
Fig. 10 CT scan axial view of left lower first molar
with cervical resorptions. The resorption can be
seen in the lingual furcal area at the level of
marginal bone. The perforation seemed to perforate
into the pulp
Fig. 11 CT scan axial view of vital left lower
second premolar with cervical resorption. The
resorption can be seen mesiobuccal to the pulp
chamber at the level of marginal bone. The
resorption has not perforated into the pulp.

91
Fig 12 CT scan-axial view-of upper right first
central with cervical resorption. The resorption can
be seen mesiobuccal to the pulp chamber at the
level of marginal bone with eextension to about half
the root lenght .The resorption has perforated into
the pulp.
Fig. 13 CT scan saggital view of upper right first
central with cervical resorption. The resorption has
extended below the marginal bone to about half the
root length.
Diagnosis 15th
of February 2011
Pulpal: Chronic irreversible pulpitis 11, 35
and 36 (K04.03)
Periapical: Normal
Periodontal: Chronic marginal priodontitis
Resorption: Cervical resorption (K03.38)
Multiple cervical resorptions (MIR)
Treatment plan
The patient was told about the poor
prognosis for tooth 11 (see discussion),
and treatment alternatives were discussed.
She wanted under no circumstances to
extract the tooth before treatment was
tried. She did not want implant treatment
because of her fear of metals.
-Pulpectomy teeth 11, 35 and distal root
tooth36.
-Flap-elevation to fill the defects in teeth
11, 35 and 36 externally with composite.
-Hemisection tooth 36: the patient wanted
to keep tooth 36 despite the uncertain
prognosis, and tooth 36 was discussed with
a prosthodontist who meant it was possible
to preserve the distal root to be
incorporated into a bridge later on.
Problem list
The extension of the lesions were large
according to CT findings (grade IV on
tooth 11 according to Haithersays
classification) and it seemed difficult to get
an acceptable outcome of the treatment
according to the radiographic findings on
36 and 11
Progress notes 15th
of February 2011
Tooth 36: Access opening and location of
two distal canals.
Short of time. Cavit was placed below
resorption communication with PDL in the
furcation area (that could be observed in
the miscroscope). Patient went on vacation
for 3 weeks.
Mechanical: Bur and ultrasound
NiTi rotary intrsumentation BioRace
-DB 19,5/50#
-DL 19/50#

92
Fig. 14.Working length radiographs
Treatment 31st
of March 2011
sealed with IRM
Fig 16. Final radiograph
Treatment 05th
of April 2011
one canal.
Mechanical: NiTi rotary instrumentation
- 20,5/40#
Sealed with IRM
Fig. 18 Removal of gutta-percha in
root canal to below the resorption process
Fig. 19 final radiograph 05.04.2011
Prognosis
uncertain
Tooth: The prognosis seemed too be
uncertain
Treatment 6th
of April 2011
one canal.
Mechanical: NiTi rotary instrumentation
-one canal 20,5/60#

93
Chemical
1% NaOCl, 16% EDTA
Sealed with IRM
Fig. 20 Upper row shows working length and
masterpoint radiographs. Removed guttaparcha in
root canal to half the root length,and final
radiograph below
Treatment 11th
of May 2011
Surgery: Hemisection tooth 36
Marginal incision from 33d-37 d.
Cleaning of resorption lacunae and
placement of composite restaurations
Lot of bleeding for unknown reason
Fig. 21 Elevation of flap
Fig. 22 Tooth 36 hemisectioned placement of
composite in cavity tooth 35
Fig. 23 After sutures
Fig. 24 Radiograph after surgery
Treatment 18th
of May 2011
Surgery: Treatment : Tooth 11
Marginal incision from 12d-21 d.
Removal of bone 11 buccaly 4 mm (Fig.
25). Cleaning of resorption lacunae and
placement of composite restoration

94
Fig. 25 Buccal bone removed, placement of
composite in cavity after cleaning of resorption
lacunae
Fig. 26 Radiograph after surgery
Removal of sutures. Healing. Discoloration
of all teeth. No symptoms
Removal of sutures maxilla was done by
graduate student
Fig. 27 Removal of sutures after one week.
of October
2011 and 1st
months after surgery)
Radiograph showed no recurrence of
resorption lesions. The patient
Dicoloration of all teeth, possibly due to
tea drinking. Estethic conditions in front
had improved from October 2011 to March
2012. The composite filling had a
discoloration that might be a result from
blood contamination in the surgical
procedure It did not bother the patient.
She had a new prosthetic bridge 44-47
.Fig. 28 Follow up radiograph 19.10.2011 (5
months)
months)
months)

95
months)
Fig. 31 Healing (5 months)
Discussion
Pathologic root resorption can be classified
based on the site, nature, and pattern of the
process (1). Invasive cervical resorption is
a form of external root resorption,
characterized by its cervical location and
invasive destructive nature (2). It runs an
insidious and often aggressively
destructive course that is characterized by
invasion of the cervical region of the root
by fibro vascular tissue derived from the
periodontal ligament (3).
This pathological process appears to
follow an injury to the cervical attachment
apparatus, most importantly to an area of
the cervical root surface (precementum),
below the epithelial attachment.
Progressively, the resorption process will
involve cementum, enamel and dentin, to
eventually involve the pulp space late in
the process (3,4).
The aetiology of invasive cervical
resorption is poorly understood, but several
potential predisposing factors have been
identified. Trauma, orthodontics,
orthognathic and other dentoalveolar
surgery and periodontal treatment has also
been cited (4). A group of 222 patients
with a total of 257 teeth that displayed
varying degrees of invasive cervical
resorptions have been analyzed (3),
regarding a sole predisposing or a
combination of factors. Of the potential
predisposing factors identified,
orthodontics was the most common sole
factor identified in 47 patients (21,2%)
with 62 affected teeth. Trauma was the
second most frequent sole factor with 31
patients (14%) with 39 affected teeth
(15,1%). Thirty-three (14,9%) of the
patients who had a history of intra-coronal
bleaching, 10 (4,5%) had bleaching as a
sole factor, 17 (7,7%) a history of
bleaching and trauma, 2 (0,9%) bleaching
and orthodontics and 4 (1,8%) a
combination of bleaching, trauma and
orthodontics. Surgery, particularly
involving the cemento-enamel junction
area was identified in 13 patients (5,9%) as

96
a sole factor. The presence of an
intracoronal restoration was the only
identifiable factor in 15,3% of the patients
and 14,4% of the teeth, while 15% of the
patients and 16,4% of teeth showed no
identifiable predisposing factors.
Intracoronal bleaching in root-filled teeth
has been the most widely documented
factor and a direct cause-effect relationship
is evident (5,6).
The clinical presentation of invasive
cervical resorption varies considerably
depending on the extent of the resorptive
process. The condition is usually painless;
a pink discolouration of the crown
indicates the resorptive process and
probing may result in profuse bleeding.
Other teeth give no visual signs and
diagnosis is usually the result of a routine
radiologic examination. At advanced
stages when the lesion involves the pulp,
symptoms normally associated with
pulpitis will be manifested, and periodontal
infection adjacent to the infiltrating
resorptive tissue can result in pain and
swelling from an intrabony defect and a
periodontal pocket formation (2).
A clinical classification has been
developed by Heithesary for research
purposes and also to provide a clinical
guide in the assessment of cases of
invasive cervical resorption (3):
Class 1- Denotes a small invasive
resorptive lesion near the cervical area
with a shallow penetration into dentine
Class 2- Denotes a well-defined resorptive
lesion that has penetrated close to the
coronal pulp chamber but shows little or
no extensions into the radicular dentine
Class 3- Denotes a deeper invasion of
dentine by resorbing tissue, not only
involving the coronal dentine but also
extending into the coronal third of the root
Class 4- Denotes a large invasive
resorptive process that has extended
beyond the coronal third of the root
Fig Classes and extent of cervical root resorption
according to Heithersay (3).
Regarding which teeth that are most
commonly affected, Heithesary (3) showed
that the maxillary central incisors came
first, followed by maxillary canines,
maxillary lateral incisors, mandibular first
molars, maxillary first molars, mandibular
second molars and mandibular incisors.
Histological, the defect appears similar to
any external inflammatory root resorptive
defect. There is usually a small opening to
the root, with large amounts of
fibrovascular, granulomatous tissue inside
the defect and multinucleated giant cells
resorbing the dentinal structure. In
extensive defects, osseous tissue may be
seen inside the granulomatous tissue.
Resorption channels surrounding the root
canal can be seen as they burrow deep into
the dentin and interconnect more apically
with the periodontal ligament. The
predentin/ odontoblastic layer is unaffected
and protects the pulp (7,8). If pulpal
involvement occurs, the fibro- osseous
tissue can be found deposited within the
root canal system (2).
If the resorptive process occurs mesially or
distally on the root surface it is common
that the radiograph shows a small
radiolucent opening to the root. It usually
can be seen as radiolucency at the
attachment level and from there it can
spread further coronally or apically with a
mottled appearance. Because the pulp is

97
not involved, its outline can usually be
distinguished through the resorptive defect
(7). A computerized tomography
examination can give us valuable
additional information, especially when the
lesion is located buccally or lingually.
Treatment depends on the various classes
of invasive cervical resorption, as the
process becomes more complex, differing
between non-surgical or surgical treatment
will be required. The basic aims though is
the same, namely the inactivation of all
active resorbing tissue and the
reconstitution of the resorptive defect
either by the placement of a suitable filling
material or by the use of biological
systems such as membranes (9). A non-
surgical treatment regime were applied to
101 teeth from 94 patients displaying
varying degrees of invasive resorption and
followed up for a minimum of 3 years
(3b). It involved the topical application of
a 90% aqueous solution of trichloracetic
acid to the resorptive tissue, curettage,
endodontic treatment where necessary, and
restorations with glass-ionomer cement.
The result was complete success in Class 1
and Class 2 resorptions. Of the 63 teeth
classified with Class 3, 61 (96,8%) showed
resorption control. When all factors
(resorption control, angular bone loss,
periapical changes and extraction) were
included in the assessment, the overall
success rate of Class 3 treatment was
77,8%. In Class 4 resorptions 16 teeth
were treated and the results showed a
survival rate of 50% and a success rate as
judged above 12,5%. This represents an
unsatisfactory outcome for this treatment
regimen when applied to Class 4
resorptions, and alternative prosthodontic
replacement is generally suggested (9).
Using hemisection to preserve
multirooted teeth that have furcation
involvement has increased over the last
years. A reported failure rate of 13.1%
has been found over 5-10 years and
comparing the results with implants the
failure rates of the two treatments were
not so different (10). Fugazzotto (11)
reported success rates ranging from
95.2% to 100% for various root resected
molars in function. Only resection of the
distal root demonstrated a lower success
rate of 75%. Implants used in molar
position had a success rate ranging from
97% to 98.6%.
In a study by Blomhof et al., (12) they
compared tooth mortality of root-resected
molars with that of root-filled, single-
rooted teeth. Survival rates were 68% for
root-resected molars and 77% for root-
filled single-rooted teeth over a 10-year
period. This difference was not statistically
significant.
They concluded that the prognosis of root-
resection is not poorer than the prognosis
of single-rooted teeth with an equal
susceptibility to periodontitis, if
endodontic conditions and maintenance
care are optimal.
References
1.Benenati F. Root resorption: Types and treatment.
Gen Dent 1997; 45: 42-45.
2. Heithesary GS. Clinical, radiologic a2
histopatologic features of invasive
resorption.Quintessence Int 1999; 30: 27-37.
3a. Heithesary GS. Invasive cervical resorption. An
analysis of potential predisposing
factors. Quintessence Int 1999; 30: 83-95.
3b. Heithesary GS. Treatment of invasive cervical
resorption: An analysis of results using topical
application of trichloroacetic acid, curettage, and
restauration. QuintessenceInt 1999; 30: 96-110.
4. Tronstad L. Root resorptions- etiology,
terminology and clinical manifestations. Dent
Traumatol 1988; 4: 241-252
5. Harrington GW, Natkin E. External resorption
associated with the bleaching of
pulpless teeth. J Endod 1979; 5: 344-348.
6. Heithesary GS. Incidence of invasive cervical
resorption in bleached root-filled teeth. Aust Dent J
1994; 39: 82-87.
7. Trope M. Root resorptions due to dental trauma.

98
End Topics 2002; 1: 79-100 .
8. Wedenberg C. Evidence for a dentin-derived
inhibitor of macrophage spreading.
Scand J Dent Res 1987; 95: 381-388
9. Heithesary G. Invasive cervical resorptions. End
Topics 2004; 7: 73-92 .
10.BühlerH.Survivalrates of hemisected teeth:an
attempt to compare them with survival rates of
alloplastic implants. Int J Periodontics Restorative
Dent. 1994;14(6):536-43.
11.FugazzottoPA.A comparison of the success of
rootresected molars and molar position implants in
function in a private practice: Results of up to 15-
plus years. J Periodontol 2001;72:1113-1123.
12.Blomlof L, Jansson L, Appelgren R, Ehnevid H,
Lindskog S.Prognosis and mortality of root -
resected teeth molars. Int J Periodontics Restorative
Dent.1997 Apr;17(2):190-201.

99
Case 17
Non-surgical retreatment of the maxillary right lateral incisor with internal
resorption
Fig 1: Frontal view
Chief complaint
Tooth 12 has the last month been tender
when chewing and biting.
Dental history: Tooth 12 was
endodontically treated about 20 years ago.
No history of trauma that she can recall.
The patient was referred from the graduate
clinic for evaluation and treatment of the
right maxillary lateral
of June 2010
Dental:
Tooth 13 has a distal amalgam filling.
Tooth 12 has a distal and occlusal
composite filling and tooth
11 composite fillings mesially.
Fig 2: Buccal view
Fig 3: Palatal view
Clinical tests 17th
of June 2010
13 12 11
EPT (0-80) 14 - 25
Cold + - +
Percussion
Vertical/horizontal
- v -
palpation - - -
PPD 3 3 3
Mobility - - -
of June 2010
Dental: Tooth 12 has a radiolucent
restorative material
Pulpal: Resorption internal in apical 1/3

100
Intraradicular radiopaque material
Apical: Tooth 12 has a widened PDL (PAI
2)
Periodontal: Attachment ½- 2/3
Diagnosis 17th
of June 2010
Pulpal: Necrotic pulp K04.11
Endodontically treated K04.19:
Internal resorption K03.32:
Periapical: normal
periodontitis K05.03:
Treatment plan
Re-treatment 12 and filling of resorptive
process with MTA
Problem list
Extension of resorptive process is
unknown; communication externally?
Treatment 16th
of June 2010
Access opening. Difficulties in finding the
canal through the internal resorption (Fig.
5). Pus and bleeding in the canal;
resorptive process penetrating to the
periodontal ligament or it could be an
external resorption.
Mechanical: Bur, Irrisafe
NiTi handinstruments #60/17- corr. 16mm
Chemical: 1% NaOCl; 17% EDTA
Fig 5. Working lengths radiographs
Treatment 25th
of August 2010
Filled with MTA Angulus, warm gutta-
percha and AH plus, sealed with composite
restauration

101
Fig. 6 MTA in resortion and warm gutta-percha in
canal
Fig. 7 Final radiograph
Prognosis
uncertain
uncertain
of June 2011
and 13th
months)
Radiograph showed no recidive of
resorptionprocess
palpation tests.
Fig 8.1 and 8.2 Follow up radiographs 08.06.2011
and 13.03.2012 (10 and 19 months)
Discussion
Internal inflammatory root resorption
destroys dental hard tissue by odontoclast
activity (1, 2). Internal resorption starts
inside the root canal and requires at least
partially vital pulp tissue. If the resorption
is not detected and remains untreated, it
can potentially grow larger and eventually
perforate the root from inside. When
internal resorption is detected early
enough, the treatment is usually successful,
and the long-term prognosis of the affected
tooth is good. Only when a significant
amount of tooth structure has been
destroyed and/or the resorption is close to
the marginal bone (coronal third of the
root) will weakening of the tooth have a
negative impact on the prognosis of the
treatment.
Internal root resorption is regarded as rare,
but the frequency of internal resorption is
not well known. Many of the published
articles on internal resorption are case
reports (3, 4), with an emphasis on the
treatment of the resorption. In some
studies, the occurrence of internal
resorption has been estimated to be
between 0.01% and 1% (1). Thoma (5)
reported internal root resorption in 1 out of
1,000 teeth. However, Cabrini et al (6)
detected internal resorption by histological
examination in 8 out of 28 teeth (28%) 49
to 320 days after calcium hydroxide
pulpotomy. In another study of 33 au-
totransplanted maxillary canines, 17 (55%)
developed internal resorption during the

102
follow-up time of 6 years (7). The results
of these studies point to inflammation as
an important factor in the etiology of
internal resorption. Inflammation was also
reported as the primary cause of internal
resorption in the classic animal studies by
Wedenberg and Lindskog (8–10), who
exposed pulps of monkey teeth to Freund’s
adjuvant (inflammation) or to Freund’s
adjuvant and oral bacteria (inflammation +
infection). A histological and scanning
electron microscopic study on resorption in
teeth with apical granulomas and cysts
showed that apical resorption was a
common finding and that intracanal
resorption was also often found (11). The
resorption zones of the external and
intracanal sides of the foramina seemed to
be interconnected. The study concluded
that intracanal resorption may be quite
common; however, exact numbers were
not given (11).
In a recent study by Haapasalo et al.(12),
they examined the occurrence of internal
resorption in teeth with healthy and
diseased pulps using a scanning electron
microscope with high magnification.
Four of the 8 teeth with pulpitis (50%) and
10 of the 13 teeth with necrotic pulps
(77%) had internal resorption (P < .01).
The average number of resorptive lesions
in the affected necrotic teeth was 2.4,
whereas in teeth with pulpitis and internal
resorption, the average number of lesions
was 1.25. The amount of resorption was
always <100-mm deep; the length of the
lesions varied from 200 mm to >1 mm.
Most lesions were detected in the middle
third of the root, followed by the apical
third. Only 1 internal resorptive lesion was
detected in the coronal third of the root
canal. They concluded that internal
resorption was a frequent finding in teeth
with pulp inflammation or necrosis.
In a systematic review and meta-analysis,
they evaluated clinical outcome differences
of root canal obturation by warm gutta-
percha (GP) or cold lateral condensation
(CLC) There were 10 clinical studies
evaluated. Postoperative pain, long-term
outcomes, obturation quality, and
overextension were the characteristics
investigated. The results suggest that the
two obturation techniques are not
significantly different except in
overextention. Overextension was more
likely to occur in the warm GP obturation
group in comparison with the CLC group.
Postoperative pain prevalence, long-term
outcomes, and obturation quality were
similar between the two groups
References:
1.HaapasaloM,EndalU.Internalinflammatoryrootres
orption:theunknownresorp- tion of the tooth. Endod
Topics 2006;14:60–79.
2.PatelS,RicucciD,DurakC,TayF.Internalrootresorpt
ion:areview.JEndod2010; 36:1107–21.
3. Altundasar E, Demir B. Management of a
perforating internal resorptive defect with mineral
trioxide aggregate: a case report. J Endod
2009;35:1441–4.
4.
BhuvaB,BarnesJJ,PatelS.Theuseoflimitedconebeam
computedtomographyin the diagnosis and
management of a case of perforating internal root
resorption. Int Endod J 2011;44:777–86.
5. Thoma K. Central osteoclastic resorption of
dentine and complete repair with osteo- dentine in
the permanent tooth of an adult. Dent Items Interest
1935;57:28.
6. Cabrini R, Maisto O, Manfredi E. Internal
resorption of dentine; histopathologic control of
eight cases after pulp amputation and capping with
calcium hydroxide. Oral Surg Oral Med Oral Pathol
1957;10:90–6.
7. Ahlberg K, Bystedt H, Eliasson S, Odenrick L.
Longterm evaluation of autotrans- planted
maxillary canines with completed root formation.
Acta Odontol Scand 1983;41:23–31.
8.WedenbergC,LindskogS.Experimentalinternalres
orptioninmonkeyteeth.Endod Dent Traumatol
1985;1:221–7.
9. Wedenberg C, Lindskog S. Evidence for a
resorption inhibitor in dentin. Scand J Dent Res
1987;95:205–11.
10. Wedenberg C. Evidence for a dentin-derived
inhibitor of macrophage spreading. Scand J Dent
Res 1987;95:381–8.
11. Delzangles B. Scanning electron microscopic
study of apical and intracanal resorption. J Endod
1989;15:281–5.

103
12. Gabor C, Tam E, Shen Y, Haapasalo M.
Prevalence of Internal Inflammatory Root
Resorption. J Endod 2012;38:24–27
13. Peng L, Ye L, Tan H, Zhou X. Outcome of
root canal obturation by warm gutta-percha versus
cold lateral condensation: a meta-analysis. J Endod
2007; 33(2):106-9.

104
Case 18
Patient with persistent pain maxilla left side
Fig. 1 Frontal view
Chief complaint
He had experienced pain from tooth 25 of
various intensity since 2007
Medical record:
By-pass surgery 1991
Albyl E; 160 mg
Dental history:
Referred from private practitioner because
of persisting pain 25 after endodontic
treatment April 2009.
He has had symptoms from tooth 25 since
2007. In October 2009 he got Apocillin
660 mg for14 days because of maxillary
sinusitis
Clinical examination 11th
of February
2010
Extraorally:
He had skin rubor, nasal secretion and
lacrimation on the left side
Intraorally:
No pathologica findings on mucosa
Dental:
Tooth 25 mod amalgam/composite filling,
26 missing (extracetd early childhood).
Fig. 4 Buccal view

105
Clinical tests 11th
of February 2010
24 25 27
EPT (0-80) 26 - 15
Cold + - +
Percussion
Vertical/horizontal
- both -
palpation - + -
PPD 3 3 3
Mobility - - -
of February
2010:
Dental: Tooth 24 has a dental crown, tooth
25 is root filled with radiopaque filling
material MOD. Tooth 27 has a MO
radiopaque filling material. Tooth 26 is
missing.
Periodontal: Attachment ⅔
Apical: 24, 25, 26 continuous PDL space
Diagnosis 11th
of February 2010
Pulpal: Endodontically treated (K04.19)
Periapical : normal
Treatment plan
Re-treatment
Problem list
Painmanagement was thought to be a
problem
Treatment 11th
of February 2010
The patient could tell about dull pain when
he wakes up in the morning. He does not
take any painkillers. The pain is of variable
intensity.
Tooth 25 was tender to percussion in each
blindtest, so a restinfection was suspected,
even though the pain was not easy to
interpret. The patient was informed that a
retreatment might not resolve his
painproblem. Access opening revealed
unsealed guttapercha in the pulpchamber.
The amalgam filling was removed and
staining of the tooh revealed a crackline
extending from the mesial to the distal
aspect (Fig.8). During the second visit, the
cusp became mobile and was removed
(Fig.9).
Mechanical:
Bur, Pre RaCe, Irrisafe®
NiTi handinstruments, BioRace
B: #40/19 mm,
P: #40/17,5
Chemical: 1% NaOCl 16% EDTA
Treatment 10th
of March 2010
Still symptoms, still tender to percussion,
but less symptoms since last vistit,
according to the patient.
He had still nasal secretion and
lacrimation.
Neuropatic pain and/or chronic maxillary
sinusitis were suspected.
The patients doctor was contaced. CT was
taken at the Department of Maxillofacial
Radiology, Institute of Clinical Dentistry,
UiO. MR caput was done at Ullevål
hospital.
The tooth was filled with gutta-percha and
AH plus, sealed with IRM

106
Fig. 7.1 and 7.2 Masterpoint and final radiographs
Fig. 8 Cracks stained with methylene blue (arrows)
Fig. 9 Removed fractured tooth substance at craze
lines
Prognosis
good
uncertain.
The patient did not want to come for
follow-up, but he could tell on the phone
that he had sinus surgery, which gave no
painrelief. He had still symptoms from the
tooth when he woke up every morning.
Radiologisvar ved spesialist Bjørn Bamse
Mork-Knutsen, avdeling for kjeve - og
ansiktsradiologi
”CT viser homogen sløring i hele venstre
maxillarsinus, og også betydelig sløring i
hele høyre maxillarsinus. Det er noe
slimhinnefortykkelse også i etmoidalceller
høyre side, men frontalsinus og
sphenoidalsinus er klare.”
”I høyre maxillarsinus sees fortykket bakre
benbegrensning, som uttrykk for (event.
tidligere) kronisk sinusitt”
”Med tynne snitt sees helt normale
periapikale bentegninger 1 og 2 kvadrant”
Fig. 10 Coronal CT scan shows homogenous
opacification of right and left maxillary sinuses
Discussion
The nerve fiber density within human teeth
is quite impressive. A number of
ultrastructural studies have evaluated the
type (as based on fiber diameter and

107
presence or lack of myelin) and number of
axons that innervate anterior and posterior
teeth. Comprehensive studies of nerve
fibers within posterior teeth are limited to
single-rooted premolars Nair (1) con-
cluded that human premolar teeth contain
2300 axons at the apex; 87% of these are
unmyelinated, and the remainder is
myelinated. The vast majority of the
myelinated fibers are thinly myelinated
and fall in the A-delta class, and the
remaining 7% represent the more thickly
myelinated A-beta nerve fibers. Even
though the ‘‘average’’ premolar tooth has a
significant nerve density, this can vary
depending on the developmental stage and
type of tooth [2] and can vary widely
among individual samples. Other axons
that enter the tooth pulp originate from
post- ganglionic sympathetic neurons
located in the superior cervical ganglion
whose role involves vasoconstriction [3],
Some of the peptides identified in tooth
pulp include the tachykinin SP
neuropeptide Y (NPY) CGRP. Peptides as
a group are important in nociception
because the expression of some change
considerably with injury or after
inflammatory insults. Sprouting of CGRP
fibers is seen in the rat tooth pulp after
inflammatory lesions [4], and similar
results involving increased fibers with
CGRP, NPY and SP have been described
in human teeth with carious lesions [,5].
These same neuropeptides is especially
implicated in inflammatory processes
because sensory nerve stim- ulation can
lead to their local release by way of an
axon-reflex [6], or they may be released
from nerves that innervate blood vessels,
leading to vasodi- lation and protein
extravasation, which results in a
neurogenic inflammation [7]. Neurogenic
inflammation and local tissue injury are
associated with the release or activation of
many different molecules that are involved
in the sensitization of peripheral
nociceptors, including their ability to
further enhance the release of CGRP and
SP. These substances include cytokines,
prostaglandins, histamine, bradykinin,
serotonin, lipids, nitric oxide, and
hydrogen ions. The local release of CGRP
and SP from peripheral terminals may bind
to CGRP and SP receptors on immune
cells, and this binding may be involved in
the regulation of the immune response in a
paracrine fashion. For example, SP
released from nerve terminals can bind to
mast cells, leading to degranulation and the
release of histamine (8).
The International Association for the Study
of Pain has introduced the concept of
neuropathic pain, defined as “a pain
initiated or caused by a primary lesion or
dysfunction in the nervous system” [9].
Recently, experts have defined neuropathic
pain as a direct consequence of a lesion or
disease regarding the somatosensory
system [10].
Proposed mechanisms for trigeminal
neuropathy include peripheral or central
sensitization, beta fibre reorganization and
sympathetically maintained pain due to
alpha receptor sprouting. (11)
Many patients with neuropathic pain
exhibit persistent or paroxysmal pain that
is independent of a stimulus. This
stimulus-independent pain can be shooting,
lancinating, or burning and may depend on
activity in the sympathetic nervous system.
Spontaneous activity in nociceptor C fibres
is thought to be responsible for persistent
burning pain and the sensitisation of dorsal
horn neurons. Similarly, spontaneous
activity in large myelinated A fibres
(which normally signal innocuous
sensations) is related to stimulus-
independent paraesthesias and, after central
sensitisation, to dysaesthesias and pain.
Stimulus-evoked pain is a common
component of peripheral nerve injury or
damage and has two key features:
hyperalgesia and allodynia. Hyperalgesia
is an increased pain response to a
suprathreshold noxious stimulus and is the
result of abnormal processing of
nociceptor input. Allodynia is the sensation
of pain elicited by a non-noxious stimulus

108
and can be produced in two ways: by the
action of low threshold myelinated A beta
fibres on an altered central nervous system;
and by a reduction in the threshold of
nociceptor terminals in the periphery.
Hyperalgesia is the consequence of an
increased central response to A beta fibre
input. Continual input to the dorsal horn as
a result of spontaneous firing in C fibre
sensory neurons causes sensitisation of
dorsal horn neurons, which increases their
excitability such that they respond to
normal inputs in an exaggerated and
extended way. Thus, stimuli that would
normally be innocuous are now painful.
(11) .
The patient in the present case had chronic
sinusitis, that was discovered on CT scans
after endodontic retreatment.
Maxillary sinusitis causes a constant
boring pain with zygomatic and dental
tenderness from the inflammation
of the maxillary sinus The character of the
pain of maxillary sinusitis is dull, aching,
boring and tender, of mild to moderate
severity. The pain is triggered by bending
forward, touching the area or biting on the
upper teeth (12).
Since the patient had persisting pain also
after sinus surgery, it was probably not
chronic sinusitis. It might have been
though, that having chronic sinusitis for
some time could give rise to neuropathic
pain due to nerve damage as discussed
above.
The patient in the present case had for a
long time an incompletely fractured tooth.
In a study by Brynjulfsen et al.,(13), thirty-
two patients with poorly localized
orofacial pain, were finally diagnosed with
46 incompletely fractured teeth. They
found that the longer the duration of pain
before the diagnosis of an incompletely
fractured tooth was established, the more
diffuse was the distribution of pain.
Endodontic or restorative treatment
relieved the symptoms in 90% of the
patients, whilst persisting symptoms in
10% were considered part of an orofacial
pain complex of obscure aetiology.
As discussed above, the patient in the
present case had most likely several
diagnosis; cracked tooth, infected tooth
and chronic maxillary sinusitis that could
explain his pain condition.
References
1.NairPN.Neural elements in dental pulp and
dentin.Oral Surg Oral Med Oral Pathol Ora l Radiol
Endod 1995;80:710–9.
2.RoddHD,Boissonade FM. Innervation of human
toothpulp in relation to caries and dentition type. J
Dent Res 2001;80:389–93.
3. Aars H, Brodin P, Andersen E. A study of
cholinergic and beta-adrenergic components in the
regulation of blood flow in the tooth pulp and
gingiva in man. Acta Physiol Scand 1993; 148:441–
7.
4. Byers MR. Dynamic plasticity of dental sensory
nerve structure and cytochemistry. Arch Oral Biol
1994;39(Suppl):13S–21S.
5. Rodd HD, Boissonade FM. Comparative
immunohistochemical analysis of the pepti- dergic
innervation of human primary and permanent tooth
pulp. Arch Oral Biol 2002; 47:375–85.
6. Lynn B. Neurogenic inflammation caused by
cutaneous polymodal receptors. Prog Brain Res
1996;113:361–8.
7. Jancso N, Jancso GaborA,Szolcsanyi J.Direc
tevidence for neurogenic inflammation and its
prevention by denervation and by pretreatment with
capsaicin. Br J Pharmacol Chemo- ther
1967;31:138–51.
8. Lorenz D, Wiesner B, Zipper J, et al. Mechanism
of peptide-induced mast cell degranulation:
translocation and patch-clamp studies. J Gen
Physiol 1998;112:577–91.
9. Mersey H, Bogduk N. Classification of chronic
pain. 2nd ed. Seattle: IASP Press; 1994. p. 209-14.
10. Treede RD, Jensen TS, Campbell JN, et al.
Neuropathic pain: redefinition and a
grading system for clinical and research purposes.
Neurology 2008;70:1630-5.
11. Woolf CJ, Mannion RJ.
Neuropathic pain: aetiology,
symptoms,mechanisms,and management
Lancet 1999; 353: 1959–64

109
12.Vickers ER, Zakrzewska JM. Dental causes of
orofacial pain. In: Orofacial Pain. Zakrzewska JM,
ed. Oxford: Oxford University Press, 2009: pp69–
81.
13. .Brynjulfsen A, Fristad I, Grevstad T, Hals-
Kvinnsland I. Incompletely fractured teeth
associated with diffuse longstanding orofacial pain:
diagnosis and treatment outcome. Int Endod J
2002;35:461–6.

110
Case 19
Endodontic treatment of a mandibular right first molar with C-shape anatomy
Fig. 1 Frontal view
Chief complaint:
Episodes of pain. Tender when chewing
and biting.
Medical record: Non-contributory
Dental histoy: The patient was referred to
the post-graduate endodontic clinic by his
general dental practitioner.
The patient had the diagnosis acute apical
periodontitis when he visited his dental
practitioner in November 2008. The
dentist had made an access cavity but he
found the pulp chamber to have an
“unusual” appearance and was not
successful in finding the root canal
orifices. Cavity was filled with eugenol
pellet and IRM
of January 2009
Dental:
Teeth 45 and 46 have dental crowns and
tooth 46 has an occlusal temporary filling
Teeth 57 and 48 have amalgam fillings
Clinical tests 20.01.2009
48 47 46
EPT (0-80) 15 20 -
Cold + +
Percussion
Vertical/horizontal
- - v
palpation - - -
PPD 3 3 3
Mobility - - -
of January
2009
Dental: Distal sweep of fused roots tooth
46. Fused root on tooth 47
Apical : Diffuse radiolucencies mesial and
distal roots tooth 46 (PAI 4)

111
Diagnosis 20th
of January 2009
(K04.50). PAI 3
Treatment plan
Treatment of infected pulp
Problem list:
Anatomical considerations 46
Treatment 29th
of January 2009
Access opening and location of first three,
then the forth canal located with ultrasound
Mechanical: Bur and ultrasound
NiTi handinstrumentation, BioRace
-MB 20/50#, -ML 22/40#
-DB 20/50#, -DL 20/40#
Fig 4. Working length radiograph 20.01.2009
Fig 5. Masterpoint radiograph 05.02.2009
Treatment 5th
of February 2009
sealed with IRM
Prognosis
good
Tooth: the prognosis seemed too be good
of April 2010
and 20th
of January 2012 (11 and 35
months)
1).The patient
Discussion
The first who reported c-shaped root canal
configurations were Cooke and Cox in
1979 (1).
Manning (2) speculated that the failure of
the Hertwig’s epithelial root sheath to fuse
on the lingual or buccal root surface was
the main cause of a C-shaped root, which
always contains a C-shaped canal. The
main feature of this variation is the
presence of a fin or web connecting the

112
individual root canals to form a letter ‘C’
shape at the root canal orifice. The C-
shaped slit may end in two or three canals
apically in the root, or the C-shaped may
be continuous throughout the length of the
root
This variation may occur in mandibular
first molars, maxillary molars , mandibular
first premolars , and even in maxillary
lateral incisors, but it is most commonly
found in mandibular second molars (3).
The C-shaped canal is most frequently
found in the mandibular second molar. It is
a significant ethnic variation that has a
high prevalence in Asians (4,5). Melton et
al. (6) first proposed the classification of
C-shaped canals based on their cross-
sectional shape. However, there was no
clear description of how to differentiate
between Category II and Category III. Fan
et al. (7) analysed the morphology of C-
shaped canals in mandibular second molars
using microcomputed tomography (micro-
CT) and modified Melton’s method (Fig.
1).
Category I (C1): the shape was an
uninterrupted “C” with no separation or
division
Category II (C2): the canal shape
resembled a semicolumn resulting from a
discontinuation of the “C”
Category III (C3): two or three separate
canals
Category IV (C4): only one round or oval
canal in that cross- section (Fig. 1E).
Category V (C5): no canal lumen could be
observed (which was usually seen near the
apex only)
Fig. Classification of C-shaped canal
configuration. Fan et al 2004. (a
modification of Melton’s method from
1991):
Irregular areas in a C-shaped root canal
system may house soft tissue remnants or
infected debris, so thorough cleaning,
shaping and a intracanal dressing with
Ca(OH)2 is recommended. These teeth
pose a considerable technical challenge but
by the use of microscopy, ultrasonic
instrumentation, and plasticized obturation
techniques have made treatment
successful1.
References
1. Cooke HG, Cox FL. C shaped canal
configurations in mandibular molars. J Am Dent
assoc 1979; 99: 836-9
2. Manning SA (1990) Root canal anatomy of
mandibular second molars. Part II. C-shaped canals.
International Endodontic Journal 23, 40–5.
3. Jafarzadeh H and Wu YN. The C-shaped Root
Canal Configuration: A Review J Endod
2007;33:517-23.
4.Yang ZP, Yang SF, Lin YC, Shay JC, Chi CY
(1988) C-shaped root canals in mandibular second
molars in a Chinese population. Dental
Traumatology 4, 160–3.
5. Seo MS, Park DS (2004) C-shaped root canals of
mandibular second molars in a Korean population:
clinical observation and in vitro analysis.
6. Melton DC, Krell KV, Fuller MW (1991)
Anatomical and histological features of C-shaped
canals in mandibular second molars. Journal of
Endodontics 17, 384–8.
7. Fan B, Cheung GS, Fan M, Gutmann JL, Bian Z
(2004) C-shaped canal system in mandibular
second molars: part I – anatomical features. Journal
of Endodontics 30, 899–903.

113
Case nr 20
Endodontic treatment of the immature maxillary left lateral incisor with dens
invaginatus
Chief complaint
Pain region 22.
Dental history
Referred to the post-graduate endodontic
clinic from the post-graduate clinic
pedodontics for treatment of tooth 22 with
dens invaginatus.
The patient had been treated at the dental
public clinic. Because of an abscess region
22, the dens invaginated tooth was
discovered. An incision of the abscess was
made and prescription of Apocillin 660
mg. The endodontic treatment was started,
but because of pulpanathomy difficulties,
the patient was referred to he post-graduate
clinic in pedodontics
The patient was teferred to the department
of Maxillofacial Radiology for cone beam
CT scan before endodontic treatment.
Clinical findings 01st
of February and
13 th
of March 2012
Soft tissue: When he came to the post-
graduate clinic in pedodontics, he had still
an abscess in region 22-63 and the incision
wound was still bleeding.
At the 13th
of March, at the post graduate
endodontic clinic, there is a hard palpable
tumor buccaly in the same region with
some fluctuation, no sinus tract.
Dental: Tooth 22 has a flat and wide
crown with a palatal temporary filling.
Mixed dentition
Fig. 1 Palatal view 01.02. 2012
Fig 2: buccal view 01.02.2012
Fig. 3 Buccal view 14.03.2012
of March
2012
Dental: Tooth 22 has a radiopaque
occlusal filling. Dens invagination, a

114
variant of Type II- Oeahlers classification
(see Fig. 1 in discussion). Axial and
saggital CBCT scans reveal that thers is a
separate invaginated apex that ends
apically. The pulp prober surrounds the
invagination, but the ct scans (Fig. 6, 7 and
8) reveal that there are some dential
bridges, especially at the palatal and mesial
aspect.
Apical: Diffuse apical radiolucency (PAI
5), 10 mm in diameter
Radiological description (in Norwegian) from the Department of Maxillofacial Radiology
Fig. 5 CT scan-Saggital view; invagination and
apical radiolucency can be seen

115
Fig. 6 CT scan- sagittal view shows invagination
and apical radioluvency
Fig 7: CT scan axial view shows an almost circular
pulp proper in tooth 22 wih a dentinal bridge
mesially.
Diagnosis 13 th
of March 2012
(K04.50) .
Other diagnosis: Dens invaginatus (K08.8)
Treatment plan
Treatment of infected invagination. In
addition, remove the whole invagination
with bur and ultrasound since the pulp
proper has been infected; most likely
because of perforation when previous
access opening.
Problem list
Cooperation problems; due to the time -
consuming work to be done and he patients
age.
Treatment 13 th
of March 2012
Access opening revealed previous pulpal
access at four places. Removal of tooth
substance with LN and round burs.
Instrumentation of invagination with
handinstruments and BioRace #90/18 mm
Fig 8. Working length
radiograph
Treatment 22 nd
of March 2012
No pain since last visit. There is still a
hard, palpable tumor buccaly, but with no
fluctuation.
Bur was used but the patient did not
tolerate the use of ultrasound because of
the sound and discomfort. It was therefore
not possible to remove all the invaginated
tooth substance, as seen in the radiograph
(Fig. 9).
Temporary filling: IRMIt was decided to
give the patient premedication next tme
(Flunizipam)

116
Fig.9 The invaginated tooth
substance is almost removed
Treatment 17 th
of April 2012
The patient got Flunizipam 45 minutes
before treatment. The sedative effect was
satisfactory, but the patient still did not
tolerate the use of ultrasound. The rest of
the ”invaginated toothsubstance” and the
pulp was anyway removed with ultrasound
and long burs. Irrigation with NaOCl and
EDTA.
It was an open apex (see CBCT scan
radiograph (Fig 5), and the MTA was
difficult to place properly. The apical
beeding was controlled with CaOH2
The tooth was filled with MTA, IRM and
composite.
Fig. 10 MTA apically
Prognosis
uncertain
uncertain
Discussion
Dens invaginatus is a well-recognized
phenomenon attributed to uncoordinated
growth of part of the epithelium of a tooth
germ in which the abnormal epithelium
invaginates (1). Various names have been
proposed to designate this phenomenon:
dens in dente, dilated composite odontome,
dents telescopes, gestant anomaly or dens
invaginatus. The term most commonly
used today is dens invaginatus, which was
first suggested by Hallett et al.,(2).
The aetiology of this anomaly remains
controversial (3,4), and although many
hypotheses have been proposed, none have
been proven or widely accepted (4). Thus,
controversy exists in the dental literature
regarding the terminology to be used for
this anatomical defect (5). Studies have
reported a high prevalence of variation for
this anomaly. The wide discrepancy in its
prevalence may be attributed to the
different criteria applied by various
investigators, (1,6) geographical
differences (6) or different investigation
methods (6,7).

117
Radiographically, this anomaly exhibits a
radiopaque invagination that is equal in
density to enamel and extends from the
cingulum into the root canal (8). Dens
invaginatus can be classified according to
severity, with the most commonly accepted
classification belonging to Oehlers (9),
who described three types: (Fig)
-Type I, an enamel invagination in the
crown only.
-Type II, an enamel-lined invagination that
invades the root but remains confined
within it as a blind sac and may
communicate with the dental pulp;
-and type III, an invagination that extends
from the crown to the apex and is
penetrated by a second foramen laterally or
apically on the root surface (c and d). In
this type, any infection within the
invagination can lead to an inflammatory
response within the periodontal tissues,
giving rise to a peri-invagination
periodontitis (10). ‘dens invaginatus’ the
clinical appearance of the crown may vary,
ranging from a normal form to more
unusual forms such as greater labio-lingual
or mesio-buccal diameter, peg-shaped,
barrel-shaped and conical. There may also
be an associated talon cusp or grooving of
the palatal enamel, coincident with the
entrance of the invagination (3, 5, 10b).
Because of its abnormal anatomical
configuration, an invaginated tooth
presents technical difficulties in its clinical
management. Depending on the degree of
malformation and the presence of clinical
symptoms, there are different treatment
modalities. Various techniques have been
reported to treat dens invaginatus,
including prophylactic treatment (11),
conservative restorative treatment (12,),
nonsurgical root canal treatment (15), ,
endodontic surgery (13,14) and extraction.
Bacterial contamination of the invagination
that occurred subsequent to the eruption of
the tooth resulted in infection of the
invagination, and this, in turn, led to the
development of periapical inflammation
(3). In this type of dens invaginatus, the
invagination penetrates the entire root,
usually without any communication with
the pulp (15). The presence of
communication between the invagination
and the pulp may have important
prognostic value; however, the tooth
reported in this case did not appear to have
any communication because the pulp
responded to sensibility tests both before
and after treatment. Clinical exploration
during treatment of the invaginated canal
corroborated this assumption.
If the invagination is necrotic or there is a
‘peri-invagination periodontitis’ and the
pulp remains healthy, only the invaginated
canal has to be treated (1, 3,15)
Dressing with Ca(OH)2 for extended
periods has been reported to be associated
with a higher risk of root fracture (16, 17).
Mineral trioxide aggregate (MTA) has been
proposed as a promising alternative to Ca(OH)2 in
the treatment of non-vital permanent teeth with open
apices (18,19).
Classification of invaginated teeth by
Oehlers 1957
References
1. Pitt Ford HE (1998) Peri-radicular inflammation
related to dens invaginatus treated without
damaging the dental pulp: a case report.
International Journal of Paediatric Dentistry 8, 283–
6.
2. Hallett GE (1953) The incidence, nature, and
clinical significance of palatal invaginations in the
maxillary incisor teeth. Proceedings of the Royal
Society of Medicine 46, 491–9.
3. Goncalves A, Goncalves M, Oliveira DP,
Goncalves N (2002) Dens invaginatus type III:
report of a case and 10-year radiographic follow-up.

118
4. Sathorn C, Parashos P (2007) Contemporary
treatment of class II dens invaginatus. International
Endodontic Journal 40, 308–16.
5. Rodekirchen H, Jung M, Ansari F (2006) Dens
invaginatus type II: case report with 2-year
radiographic follow-up. Oral Surgery, Oral
Medicine, Oral Pathology, Oral Radiology, and
Endodontics 102, e121– 5.
6. Ridell K, Mejare I, Matsson L (2001) Dens
invaginatus: a retrospective study of prophylactic
invagination treatment. International Journal of
Paediatric Dentistry 11, 92–7.
7. O’Sullivan EA (2000) Multiple dental anomalies
in a young patient: a case report. International
Journal of Paediatric Dentistry 10, 63–6.
8. Gotoh T, Kawahara K, Imai K, Kishi K, Fujiki Y
(1979) Clinical and radiographic study of dens
invaginatus. Oral Surgery, Oral Medicine, and Oral
Pathology 48, 88–91.
9. Oehlers FA (1957) Dens invaginatus (dilated
composite odontome). I. Variations of the
invagination process and associated anterior crown
forms. Oral Surgery, Oral Medicine, and Oral
Pathology 10, 1204–18.
10. Alani A, Bishop K (2008) Dens invaginatus.
Part 1: classification, prevalence and aetiology.
Bishop K, Alani A (2008) Dens invaginatus. Part 2:
clinical, radiographic features and management
options. International Endodontic Journal 41, 1137–
54.
11. Jung M (2004) Endodontic treatment of dens
invaginatus type III with three root canals and open
apical foramen. International Endodontic Journal
37, 205–13.
12. Hulsmann M (1997) Dens invaginatus:
aetiology, classification, prevalence, diagnosis, and
treatment
considerations. International Endodontic Journal
30, 79–90.
13. Nallapati S (2004) Clinical management of a
maxillary lateral incisor with vital pulp and type 3
dens invaginatus: a case report. Journal of
Endodontics 30, 726–31.
14. Soares J, Santos S, Silveira F, Nunes E (2007)
Calcium hydroxide barrier over the apical root-end
of a type III dens invaginatus after endodontic and
surgical treatment. International Endodontic Journal
40, 146–55.
15. Tsurumachi T (2004) Endodontic treatment of
an invaginated maxillary lateral incisor with a
periradicular lesion and a healthy pulp.
16. Andreasen JO, Munksgaard EC, Backland LK.
Comparison of fracture resistance in root canals of
immature sheep teeth after filling with calcium
hydroxide or MTA. Dent Traumatol 2006;22:154–
6.
17 .Andreasen JO, Farik B, Munksgaard EC. Long
term calcium hydroxide as a root canal dressing
may increase risk of root fracture. Dent Traumatol
2002;18:134–7.
18. Felippe WT, Felippe MC, Rocha MJ. The effect
of mineral trioxide aggregate on the apexification
and periapical healing of teeth with incomplete root
formation. Int Endod J 2006;39: 2–9.
19. Shabahang S, Torabinejad M, Boyne PP, Abedi
H, McMillan P. A comparative study of root-end
induction using osteogenic protein-1, calcium
hydroxide, and mineral trioxide aggregate in dogs. J
Endod 1999;25:1–5.

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