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Case Report/Clinical Techniques

Management of 2 Teeth Diagnosed with Dens Invaginatus


with Regenerative Endodontics and Apexification
in the Same Patient: A Case Report and Review
Harleen Kumar, BDSc, DCD, Muna Al-Ali, BDSc, MFDS, DCD,
Peter Parashos, BDSc, LDS, MDSc, FRACDS, PhD, FICD, FACD,
and David J. Manton, BDSc, MDSc, PhD, FRACDS, FICD, FADI
Abstract
Introduction: This review and case report present the
treatment of a 10-year-old boy with both permanent
maxillary lateral incisors demonstrating Oehlers type II
dens invaginatus and pulpal involvement. Treatment
was complicated by dental anxiety, supraventricular
tachycardia, immature tooth development, and facial
cellulitis. Methods: An infected necrotic pulp of the
permanent maxillary left lateral incisor was treated by
apexification and endodontic treatment with mineral
trioxide aggregate. The necrotic pulp of the permanent
maxillary right lateral incisor was treated with canal
debridement and dressing under general anesthesia.
Results: Periapical healing of both teeth occurred, with
the right lateral incisor showing continued root growth,
thickening of the dentinal root walls, and completed
apex formation. This tooth responded normally to pulp
testing. Twenty-eight months after initial treatment, the
right lateral incisor displayed progressive sclerosis of the
canal. Conclusions: This case demonstrates possible
pulpal regeneration of an infected maxillary right lateral
incisor with dens invaginatus and an immature apex after
minimal canal debridement. (J Endod 2014;40:725731)

Key Words
Dens in dente, dens invaginatus, mineral trioxide aggregate, revascularization, revitalization, supraventricular
tachycardia, tissue regeneration

From the Melbourne Dental School, University of Melbourne, Melbourne, Victoria, Australia.
Address requests for reprints to Dr Peter Parashos, Melbourne Dental School, University of Melbourne, 720 Swanston
Street, Melbourne, Victoria, Australia 3010. E-mail address:
parashos@unimelb.edu.au
0099-2399/$ - see front matter
Copyright 2014 American Association of Endodontists.
http://dx.doi.org/10.1016/j.joen.2013.10.030

JOE Volume 40, Number 5, May 2014

ndodontic treatment of immature permanent teeth with infected necrotic pulps


presents challenges with procedures such as chemomechanical preparation and
obturation of thin-walled roots with wide-open blunderbuss apices. These teeth are at
a higher risk of fracture because of structural inadequacies (1). Traditional and contemporary apexification methods allow for management of the apical periodontitis; however,
the major drawback is root fracture, subsequently leading to eventual loss of these teeth
because of non-restorability (2). Regenerative endodontic procedures have been advocated recently to address these concerns (3, 4). Current interest in regenerative
endodontic procedures has sparked many studies and reports in the endodontic
literature since 2 case reports in the early 2000s (5, 6). However, the concept itself
was introduced in the early 1960s in a study conducted by Nygaard-stby (7).
Regenerative endodontic procedures aim to restore or regenerate pulpal tissues to
resume their sensory, immunocompetency, root development, and formation roles.
Significantly higher tooth survival rates were reported when regenerative endodontic
procedures (100%) were performed as compared with mineral trioxide aggregate
(MTA) apexification (95%) or calcium hydroxide apexification (77%) (2). The percentage increase in root length and canal wall thickness was also significantly higher
in regenerative endodontic cases than in both apexification procedures (2, 8).
Pulpal regeneration can be achieved by following procedures that make use of
basic tissue engineering concepts (913). These concepts include provision of stem
cells, a scaffold, and signaling molecules or cues to guide stem cell differentiation
into the desired cell type (12, 13). Clinical application of pulp regeneration
procedures involves disinfection of the canal(s), allowing for a bacteria-free environment for stem cell differentiation (14), conditioning of the dentin surface for stem
cell attachment (15), and releasing dentin matrix growth factors (15). Disinfection
of the canal is typically, but not exclusively, achieved by minimal instrumentation,
together with use of low concentration sodium hypochlorite irrigation solution, triple
antibiotic paste, or calcium hydroxide paste (6, 810). As a result, treatment is
usually completed during 2 to 3 visits and demands patient compliance with
appointment times. Alternatively, treatment can be performed in 1 visit (16). In addition, EDTA is recommended during final irrigation to condition the dentin for stem
cell attachment and allow for further release of growth factors (15).
After canal disinfection, stem cells are introduced into the canal through induced
bleeding from the periapical tissues that are known to be stem cellrich tissues (1719).
However, stem cell origin is debatable, but it is speculated to be derived from the apical
papilla, periodontal ligament (PDL), Hertwigs root sheath, or mesenchymal cells from
the surrounding periapical bone marrow (12, 18, 19). Blood-derived stem cells are an
unlikely source of stem cells, as reported recently (17). The resulting intracanal blood
clot acts as a scaffold, supporting stem cell migration and differentiation, and provides a
multitude of growth factors that encourage stem cell differentiation (6, 2023). Use of
blood products like platelet-rich plasma as a scaffold in regenerative endodontic procedures has also been reported with some success (24, 25). Furthermore, gelatin
microspheres and collagen suspensions were successfully used to induce pulp
regeneration in a recent animal study (20). This study also elegantly demonstrated

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the importance of direct proximity to vascularity in survival of stem cells
and subsequent pulp regeneration (20).
Stem cells under a controlled environment can differentiate into
odontoblast-like cells and form new pulp tissue capable of performing
normal functions (26, 27). A bacteria-tight seal coronally allows for
maintenance of an ideal environment for stem cell differentiation. MTA
reportedly facilitates stem cell differentiation and migration (28, 29),
but other materials (calcium hydroxide, calcium enriched matrix,
glass ionomer cement, gutta-percha, amalgam, composite resin, and
Cavit) have been successfully used in clinical settings (5, 3032).
Histologic animal studies of cases treated under conditions similar
to clinical scenarios have demonstrated that the tissue formed is mainly
PDL, and the hard tissue deposited on dentinal walls is cementum
or bone-like tissue (21, 33). The histologic nature of the tissues
occupying canals in human teeth is unclear. Three case reports have
presented different results. Torabinejad and Turman (24) found a loose
pulp-like tissue in a tooth that displayed signs of reversible pulpitis after
14 months of a regenerative endodontic procedure that used plateletrich plasma. Another report described a similar result after only 34
weeks postoperatively, with an indication of vital tissue remaining in
the canal before the procedure (34). However, both reports could
not demonstrate the presence of odontoblasts with their typical polarized and organized pattern along the canal wall. Another recent report
described calcified bone or cementum-like tissue in canals that were
instrumented extensively (25).
Expected clinical and radiographic results of regenerative endodontic procedures would be restoration of response to pulp testing, increased
length and thickness of the root, along with resolution of all signs and
symptoms of the associated apical periodontitis (46, 9, 10, 13).
However, clinical reality has shown that restoration of response to
pulp testing is unpredictable. For example, the response to pulp testing
was restored in 2 of 6 cases in 1 report (35). Furthermore, there are
a number of radiographic results after regenerative procedures. These
include the following (36):
1. Increased thickness of the canal walls and continued root maturation
2. No significant continuation of root development with the root apex
becoming blunt and closed
3. Continued root development with the apical foramen remaining
open
4. Severe calcification (obliteration) of the canal space
5. A hard-tissue barrier formed in the canal between the coronal restoration and the root apex
As a result of such variable histologic and clinical results after the
aforementioned procedures, controversies emerged as to the terms to be
allocated to describe these procedures. The term revascularization was
borrowed from dental trauma literature whereby vascularity of an existing partially or completely ischemic pulp is reestablished, facilitating
continued root development. However, revascularization under such
conditions does not strictly incorporate tissue engineering concepts
and trivializes the importance of incorporating scaffolds and growth
factors in the process of regeneration of intracanal tissues (13). The
term revitalization is described as ingrowth of tissues into the canals
regardless of its nature (9, 33). On the other hand, the term
maturogenesis was suggested as a focus on inducing continued root
development and maturation. However, this term does not distinguish
these procedures from normal physiological root development or
apexogenesis procedures where a vital functional pulp is preserved
and protected from further injury, allowing for root development
and maturation. The term regenerative endodontic procedure
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Kumar et al.

encompasses revascularization, revitalization, and maturogenesis. It


specifies the use of tissue engineering concepts and best describes the
main purpose of such procedures, ie, regeneration of damaged dental
structure, regardless of the nature of the tissue, and allows for the
range of clinical, radiographic, and histologic results obtained (9, 13).
It has been suggested that regardless of the nature of the tissues in
the root canal system and even if continued root development was not
achieved, treatment should be considered successful if the tooth is
maintained in function, with resolution of the signs and symptoms of
apical periodontitis (3).
Dens invaginatus (DI) is a developmental anomaly with an invagination of an accessory enamel organ into the dental papilla, producing
a small tooth-like structure within the future pulp chamber, before
calcification of the dental tissues (37). In severe types of DI, there is
an infolding of Hertwigs epithelial root sheath into the developing
root, producing enamel and dentin within the root (38, 39). This
malformation is also known as dens in dente, invaginated odontoma,
dilated gestant odontoma, dilated composite odontoma, tooth
inclusion, and dentoid in dente (37, 4042). Of the various terms,
dens invaginatus appears to be the most appropriate, representing
the range of presentations (43).
The wide-ranging prevalence of DI (0.04%10%) may be explained by the different cohorts studied, identification criteria used,
and diagnostic difficulties (4446). The maxillary lateral incisor
is most commonly involved, followed in decreasing frequency by the
permanent central incisors, premolars, canines, and molars (47, 48).
Dens invaginatus can occur bilaterally and less commonly in
mandibular, supernumerary, and primary teeth (37, 45, 48). Gender
predilection is disputed (48, 49). The most commonly used
classification is that of Oehlers (43), which describes 3 categories
according to the depth of penetration and the extent of communication
with periapical tissue or PDL. In the predominant type I DI, the invagination is confined inside the crown, not extending beyond the cementoenamel junction (CEJ); types II and III are less frequently observed
(50). In type II DI cases, the invagination extends beyond the CEJ
into the pulp chamber but remains within the root canal with no
communication with the PDL; it may communicate with the pulp. In
type IIIA DI, the invagination extends through the root and communicates laterally with the PDL space through a pseudo-foramen; there is
usually no communication with the pulp. In type IIIB DI, the invagination extends through the root and communicates with the PDL at the
apical foramen; there is usually no communication with the pulp (43).
This article reports the management of type II DI in a child with
dental anxiety and supraventricular tachycardia (SVT) who presented
with an infected necrotic pulp of the permanent maxillary left lateral
incisor and later, facial cellulitis associated with a necrotic pulp of
the permanent maxillary right lateral incisor.

Case Report
A 10-year-old boy was referred by a private general dental practitioner to the endodontic unit of the Royal Dental Hospital of Melbourne,
Australia for evaluation and management of persistent infection arising
from the permanent maxillary left lateral incisor with a history of recurrent pain and parulis formation. Three courses of amoxicillin (Amoxil;
GlaxoSmithKline, Victoria, Australia) were prescribed during a 2-month
period by the local general medical practitioner, with no resolution of
the parulis. At the dental examination, a systems review revealed the
patient had SVT, was not taking any medications, and was otherwise
healthy. The patient was able to control his frequent cardiac palpitations
with the Valsalva maneuver (51).
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Case Report/Clinical Techniques

Figure 1. Clinical photograph at initial presentation of a 10-year-old boy with


a parulis labial to the permanent maxillary left lateral incisor.

Clinical examination of the permanent left lateral incisor revealed


the presence of a parulis labial to the tooth, very delayed and realistically
negative response to carbon dioxide snow (CO2) pulp testing as
compared with neighboring teeth, a 5-mm periodontal pocket on the
distobuccal aspect, and tenderness to percussion and palpation
(Fig. 1). Radiographically, an associated periapical radiolucency
partially involving the distal radicular area, an immature apex, and an
invagination extending beyond the CEJ were noted (Fig. 2A). The tooth
was diagnosed with an infected necrotic pulp and chronic apical
abscess associated with a type II Oehlers DI.
Clinical and radiographic examination of the permanent maxillary
right lateral incisor revealed a positive and normal pulpal response to
CO2 testing, a type II Oehlers DI, an immature apex, and normal periapical appearance (Fig. 2B). The crowns of the affected teeth showed no
morphologic signs of malformation, although small cingulum pits of the
permanent maxillary left and right central incisors were noted clinically
and radiographically (Fig. 2A and B).
A 3-dimensional cone-beam microcomputed tomography scan
(3D Accuitomo; J. Morita, Kyoto, Japan) was taken of both maxillary
lateral incisors at 0.125-mm-slice intervals to further elucidate tooth
anatomy (Fig. 3). This revealed a DI extending beyond the CEJ and
communicating with the cingulum coronally in both teeth. Apically,
the invagination was enamel-lined and apparently unconnected to the
remainder of the pulp chamber.
The proposed treatment plan was to remove the DI and attempt a
regenerative endodontic procedure of the left lateral incisor. For the

Figure 3. Preoperative cone-beam micro-CT demonstrating the anatomy of


type II Oehlers dens invaginatus (A) of the permanent maxillary left lateral
incisor and (B) of the permanent maxillary right lateral incisor. Note the
communication of the dens coronally with the cingulum of the teeth.

right lateral incisor, prophylactic removal of the DI only (avoiding


access to the remainder of the pulp tissue), followed by an MTA filling,
was planned. The patient was not cooperative for treatment in the dental
chair and was referred for treatment under general anesthesia (GA).
Before his scheduled examination appointment, the patient
presented to the Royal Childrens Hospital, Melbourne, Australia with
acute pain and facial swelling from the previously asymptomatic permanent right lateral incisor. Extraoral examination revealed a fluctuant,
tender, warm to touch, erythematous area with mild edema on the right
cheek and the infraorbital space. Intraorally, swelling and tenderness in
the labial sulcus adjacent to the right lateral incisor were noted in
addition to gingival erythema, purulent discharge, and swelling around
the cingulum area. The tooth was tender to percussion with grade II
mobility. Electric and CO2 pulp-testing revealed all 4 permanent
maxillary incisors were deemed unreliable because of extreme patient
anxiety during testing.
The on-call cardiologist was contacted concerning the patients
SVT and advice on any precautions with providing GA, future nitrous
oxide sedation, and epinephrine-containing local anesthetics. Approval
was provided for the use of these substances for this patient, and a GA
was organized. The treatment plan involved debridement of the canal of

Figure 2. (A) Preoperative radiograph of the permanent maxillary left lateral incisor demonstrating type II Oehlers dens invaginatus with an associated periapical
radiolucency. (B) Preoperative radiograph of the permanent maxillary right lateral incisor demonstrating type II Oehlers dens invaginatus. (C) Preoperative radiograph of the permanent maxillary right lateral incisor 7 weeks later with associated periapical radiolucency.

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Figure 4. Five months after initial canal debridement, periapical healing of both (A) permanent maxillary right and (B) left lateral incisors is evident radiographically. (C) Twenty-six months postoperative radiograph of the permanent maxillary left lateral incisor. Radiographs of the permanent maxillary right lateral incisor
displaying apexogenesis and progressive canal sclerosis taken (D) 8 months, (E) 18 months, and (F) 28 months postoperatively.

the right lateral incisor. The left lateral incisor was not to be treated at
this time because of after-hours emergency time constraints.
A radiograph taken under GA of the right lateral incisor revealed a
periapical radiolucency (which was not present in the radiograph taken
7 weeks earlier), consistent with the clinical presentation. The diagnosis
of an infected necrotic pulp with an acute apical abscess and facial
cellulitis associated with a type II Oehlers DI was made (Fig. 2C). Under
rubber dam isolation, an access cavity was prepared where a highspeed diamond fissure bur was used to remove the DI and create
straight-line access to the canal. Purulent discharge from the canal
along with bleeding was noted. The canal was irrigated copiously
with 1% sodium hypochlorite (Endosure hypochlor 1%; Dentalife,
Croydon, Victoria, Australia). Bleeding tissue was encountered in the
apical 4 mm of the canal, and thus the canal walls were lightly hand
instrumented with an ISO 25 K file to the level of the bleeding tissue.
Once bleeding was deemed to have been sufficiently controlled,
Odontopaste (5% clindamycin hydrochloride and 1% triamcinolone
acetonide; ADM, Brisbane, Queensland, Australia) was placed with an
ISO 25 K-file as the canal dressing. This was followed by a 3-mm-thick
zinc oxide-eugenolfree temporary primary access seal (Coltosol F;
Coltene/Whaledent Inc, Cuyahoga Falls, OH) placed in the pulp
chamber and a light-cured resin reinforced glass ionomer cement
secondary filling (Fuji II LC; GC Corp, Sydney, Australia). This
double-seal temporary filling was limited to the pulp chamber of the
tooth and did not extend into the canal (Fig. 4).
A postoperative review at 8 days revealed complete resolution of
the swelling. Both lateral incisors were asymptomatic, but the parulis
of the left lateral incisor was still present. Behavioral desensitization
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Kumar et al.

was instituted, and the patient was introduced to dental materials


and the nosepiece of the nitrous oxide apparatus. At the following
appointment 2 weeks later, another desensitization session was
conducted with the use of nitrous oxide sedation. The patient was
compliant, allowing fissure sealants and restorative treatment by using
rubber dam isolation. Subsequently, canal debridement of the left
lateral incisor was conducted under local anesthesia with nitrous oxide
sedation. A similar endodontic procedure to the one described
previously was conducted, except the canal was dressed with calcium
hydroxide paste (Pulpdent; Pulpdent Corp, Watertown, MA). The
decision to promote apexification in this tooth rather than attempt
a regenerative endodontic procedure was based on the patients
unreliable compliance and the significant dental anxiety.
Five months after initial treatment, substantial periapical healing of
both teeth was evident radiographically (Fig. 4A and B). The right lateral
incisor showed continuing root growth with thickening of the dentinal
root walls; a decision was made to defer any intervention and monitor
the tooth long-term. The sinus tract of the left lateral incisor had
resolved completely. After removal of the temporary restoration, by
using the dental operating microscope, the left lateral incisor displayed
an apical barrier with a soap-bubble appearance that was firm to
probing with hand files.
The left lateral incisor canal was instrumented lightly with a large
hand file (Hedstrom file ISO #100), along with ultrasonically activated
1% sodium hypochlorite irrigation. White MTA (ProRoot MTA; Dentsply
Tulsa Dental, Tulsa, OK) was compacted with an endodontic plugger
(#5/7 DE Plugger; Hu Friedy, Chicago, IL) to create an apical plug of
approximately 4-mm thickness. The canal was then back-filled with
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Case Report/Clinical Techniques


thermoplasticized gutta-percha (Beefill; VDW, Munich, Germany) with
AH26 sealer (DeTrey Dentsply, Konstanz, Germany). A polycarboxylate
cement base (Durelon; 3M ESPE, Seefeld, Germany) was placed,
followed by glass ionomer cement (Fuji IX; GC Corp, Tokyo, Japan)
and resin composite restoration (Filtek Supreme XT; 3M ESPE, St
Paul, MN).
The patient was reviewed every 3 months. At all subsequent recall
visits, the right lateral incisor was asymptomatic and responded
normally to CO2 pulp testing until 9 months after initial treatment, after
which there was a delayed response to CO2 pulp testing but with a
normal response to electric pulp testing. Radiographically, the root
exhibited continuing development with completed apex formation
and hard-tissue deposition on the canal walls (Fig. 4D and E).
Twenty-eight months after initial treatment, the right lateral incisor
displayed progressive sclerosis of the canal, which was not as advanced
in the coronal third (Fig. 4F). The left lateral incisor was also asymptomatic and radiographically demonstrated evidence of apical bone healing
(Fig. 4C). The findings of the periodontal examination were within
normal limits for both maxillary lateral incisors.

Discussion
The described case demonstrated possible pulpal regeneration of
an infected maxillary right lateral incisor with DI and an immature apex
after minimal canal debridement and dressing with an antibiotic/corticosteroid paste (Odontopaste). To the authors knowledge, there are no
similar reports. The possibility of Hertwigs root sheath and pulpal and
apical papilla stem cells surviving the destructive effect of the acute
infection has been proposed (19). Their survival would have allowed
for regeneration of the pulp and continued root maturation endowed
by a favorable environment after controlling the infection in the root
canal system (14). The response of this lateral incisor could imply
some remaining vital tissue in the apical portion of the canal, which
may then represent partial pulp regeneration as opposed to de novo
regeneration as defined by Huang (52). Geisler (10) proposed that
the degree of success of regenerative endodontic procedures can be
measured by the attainment of primary (control of symptoms and
healing of apical periodontitis), secondary (increased root wall
thickness and/or increased root length), and tertiary (positive response
to pulp testing) goals. Accordingly, the upper right incisor in this report
demonstrates a high degree of success despite minimal disinfection.
Dentin matrix contains growth factors that have been found to
induce odontoblast-like cell differentiation as well as angiogenesis
(15, 26, 5355). These growth factors (eg, transforming growth
factor-b1, dentin matrix protein-1) are released in varying concentrations by endodontic irrigants such as sodium hypochlorite, citric acid,
and EDTA, with the latter releasing the highest concentrations of
transforming growth factor-b1 (53). In addition to the well-known
cytotoxicity, high concentration of sodium hypochlorite (5.25%)
conditioning of dentin may cause clastic activity on the dentin surface
(15, 56). This clastic activity is assumed to be due to masking of the
dentin surface with a heavy smear layer (15). On the other hand,
conditioning of the dentin surface with EDTA and removal of the smear
layer may facilitate binding sites for stem cells and encourage differentiation of odontoblast-like cells (15). In this report, EDTA was not used
in the upper right lateral incisor because the treatment provided was
only intended to be emergency GA management under tight time constraints rather than definitive treatment. In this case, light instrumentation of the canal of the maxillary right lateral incisor may have served to
release growth factors and avoid large areas of smear layer formation,
whereas the low concentration of sodium hypochlorite (1%) allowed
for microbial control and avoided destruction of potential stem cells.
JOE Volume 40, Number 5, May 2014

Dressing with the Odontopaste may potentially have encouraged


cell differentiation and dentinogenesis. Corticosteroids (dexamethasone) encourage the differentiation of odontoblast-like cells and
dentinogenesis (5759), but whether triamcinolone in Odontopaste
can induce the same effects as dexamethasone on stem cells is
unknown and merits further investigation.
There is a possibility that the tissue inside the canal has a pulp-like
nature, and the hard tissue deposited is dentin or dentin-like (34).
However, the new tissue may be cementum-like or bone-like tissue, along
with PDL tissue occupying the canal space, as has been reported in
animal studies (21, 33). This scenario would imply that no pulpal
stem cells survived the acute infection, and the hard tissuedepositing
cells were of bone marrow stem cell or PDL stem cell origin (21, 33).
Circulating stem cells (in the blood) are not implicated as a source of
differentiating cells in the canal system in regenerative endodontic
procedures as reported recently (17).
One of the prerequisites for pulp regeneration is the presence of a
scaffold (12). Bleeding into the canal may have taken place, despite the
Odontopaste in the canal, as a result of the hyperemia associated with
the acute infection that was difficult to control and may have washed out
the medicament. The blood clot would provide the necessary scaffold
and some growth factors for stem cells, regardless of their origin, to
reach into the canal and differentiate into hard tissuedepositing cells.
Calcium hydroxide at clinically used concentrations denies stem
cells access into the canal and thus does not allow for thickening of
the canal walls (1, 6, 8, 30). In addition, formation of a calcific
barrier at the interface with vital tissues acts as a dam against cell
access at later stages of treatment. Odontopaste use has not been
reported previously in such pulp regeneration procedures. It is
postulated that because its main component (clindamycin hydroxide)
is minimally cytotoxic, the stem cells ability to survive and
differentiate was minimally influenced; however, further research is
indicated (60).
Apexification was the treatment adopted for the upper left lateral
incisors because of demonstrated behavioral problems. The apical
barrier subsequent to apexification has been shown to be porous
and often incomplete with many connective tissue inclusions, which
might render sealing the canal difficult when using gutta-percha alone
(61, 62). Taking into consideration the superior biocompatibility,
bioactivity, antibacterial effect, and better sealing ability of MTA, an
apical plug of MTA was preferred in this case rather than compacting
gutta-percha against a porous apical hard-tissue barrier (6365).
Management of the current case was complicated further by the
patients SVT and dental anxiety. Consultation with the patients cardiologist was required because procedures under local anesthesia or GA
can have adverse effects on the patients health. Dental anxiety and
pain can elevate stress levels, which in turn increases the epinephrine
levels in the body and can trigger an SVT episode (66). These triggers
can initiate release of endogenous catecholamines, which can cause
hemodynamic disturbances, including increases in blood pressure,
heart rate, and the frequency of arrhythmias (67). Thus, adequate
analgesia is essential during dental procedures to aid in preventing
stress and pain (66).
Clinicians should consult with the patients cardiologist before
administering any type of anesthesia to patients with SVT. Epinephrine
injected into a blood vessel may initiate tachycardia, chest pain,
shortness of breath, hyperventilation, hypotension/hypertension, syncope, or cardiovascular collapse (6872). Local anesthesia should
be administered slowly, with preliminary aspiration to reduce the
chance of intravascular introduction of epinephrine (73). Intraosseous
and PDL injections are not recommended for any patient with a history
of cardiovascular disease (74, 75). Pharyngeal stimulation by dental

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729

Case Report/Clinical Techniques


procedures can also stimulate SVT. This can be avoided by the use of a
rubber dam when providing dental treatment.
Treatment under local anesthesia has an advantage over GA
because it avoids administration of multiple drugs, noxious pharyngeal
stimuli such as during laryngoscopy, and pain in the lighter plane of
anesthesia, all of which may increase the chance of cardiac arrhythmias
(76). Many anesthetic drugs change the physiology of the atrioventricular and other preexisting anomalous pathways and alter their
conduction, thereby affecting the patients behavior under anesthesia.
They can precipitate arrhythmias, dyspnea, anxiety, or fatigue (77).

Conclusion
Pulpal regeneration techniques are an emerging approach to management of infected necrotic immature teeth. This article has reported 2
different treatment outcomes of permanent lateral incisors with type II
Oehlers DI and apical abscesses. This report introduces the possibility
of the use of Odontopaste in endodontic regeneration procedures and
highlights the need for regular reviews of teeth with open apices and
caution when treating a patient with SVT under local anesthesia or GA.

Acknowledgments
The authors acknowledge Emeritus Professors Louise BrearleyMesser and Harold Messer, both at Melbourne Dental School,
University of Melbourne, Australia; Clinical Associate Professor
Kerrod Hallett, director of dentistry at The Royal Childrens
Hospital, Melbourne, Australia; and Dr Justin Wong, pediatric
dentist, for their contributions to this case report.
The authors deny any conflicts of interest related to this study.

References
1. Cvek M. Prognosis of luxated non-vital maxillary incisors treated with calcium
hydroxide and filled with gutta-percha: a retrospective clinical study. Dent Traumatol 1992;8:4555.
2. Jeeruphan T, Jantarat J, Yanpiset K, et al. Mahidol study 1: comparison of radiographic and survival outcomes of immature teeth treated with either regenerative
endodontic or apexification methodsa retrospective study. J Endod 2012;38:
13306.
3. Huang GT. Pulp and dentin tissue engineering and regeneration: current progress.
Regen Med 2009;4:697707.
4. Trope M. Treatment of the immature tooth with a non-vital pulp and apical periodontitis. Dent Clin North Am 2010;54:31324.
5. Iwaya SI, Ikawa M, Kubota M. Revascularization of an immature permanent tooth
with apical periodontitis and sinus tract. Dent Traumatol 2001;17:1857.
6. Banchs F, Trope M. Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? J Endod 2004;30:196200.
7. Nygaard-stby B. The role of the blood clot in endodontic therapy: an experimental
histologic study. Acta Odontol Scand 1961;19:32453.
8. Bose R, Nummikoski P, Hargreaves K. A retrospective evaluation of radiographic
outcomes in immature teeth with necrotic root canal systems treated with regenerative endodontic procedures. J Endod 2009;35:13439.
9. Law AS. Considerations for regeneration procedures. J Endod 2013;39:S4456.
10. Geisler TM. Clinical considerations for regenerative endodontic procedures. Dent
Clin North Am 2012;56:60326.
11. Wigler R, Kaufman AY, Lin S, et al. Revascularization: a treatment for permanent
teeth with necrotic pulp and incomplete root development. J Endod 2013;39:
31926.
12. Hargreaves KM, Giesler T, Henry M, Wang Y. Regeneration potential of the young
permanent tooth: what does the future hold? J Endod 2008;34:S516.
13. Hargreaves KM, Diogenes A, Teixeira FB. Treatment options: biological basis of
regenerative endodontic procedures. J Endod 2013;39:S3043.
14. Cvek M, Cleaton-Jones P, Austin J, et al. Effect of topical application of doxycycline
on pulp revascularization and periodontal healing in reimplanted monkey incisors.
Endod Dent Traumatol 1990;6:1706.
15. Galler KM, DSouza RN, Federlin M, et al. Dentin conditioning codetermines cell fate
in regenerative endodontics. J Endod 2011;37:153641.

730

Kumar et al.

16. Shin SY, Albert JS, Mortman RE. One step pulp revascularization treatment of an
immature permanent tooth with chronic apical abscess: a case report. Int Endod
J 2009;42:111826.
17. Lovelace TW, Henry MA, Hargreaves KM, Diogenes A. Evaluation of the delivery of mesenchymal stem cells into the root canal space of necrotic
immature teeth after clinical regenerative endodontic procedure. J Endod
2011;37:1338.
18. Huang GT. A paradigm shift in endodontic management of immature teeth: conservation of stem cells for regeneration. J Dent 2008;36:37986.
19. Huang GT, Sonoyama W, Liu Y, et al. The hidden treasure in apical papilla: the potential role in pulp/dentin regeneration and bioroot engineering. J Endod 2008;34:
64551.
20. Srisuwan T, Tilkorn DJ, Al-Benna S, et al. Revascularization and tissue regeneration
of an empty root canal space is enhanced by a direct blood supply and stem cells.
Dent Traumatol 2013;29:8491.
21. Thibodeau B, Teixeira F, Yamauchi M, et al. Pulp revascularization of immature dog
teeth with apical periodontitis. J Endod 2007;33:6809.
22. Vogel JP, Szalay K, Geiger F, et al. Platelet-rich plasma improves expansion of human
mesenchymal stem cells and retains differentiation capacity and in vivo bone formation in calcium phosphate ceramics. Platelets 2006;17:4629.
23. Marx RE. Platelet-rich plasma: evidence to support its use. J Oral Maxillofac Surg
2004;62:48996.
24. Torabinejad M, Turman M. Revitalization of tooth with necrotic pulp and open apex
by using platelet-rich plasma: a case report. J Endod 2011;37:2658.
25. Martin G, Ricucci D, Gibbs JL, Lin LM. Histological findings of revascularized/revitalized immature permanent molar with apical periodontitis using platelet-rich
plasma. J Endod 2013;39:13844.
26. Prescott RS, Alsanea R, Fayad MI, et al. In vivo generation of dental pulp-like tissue
by using dental pulp stem cells, a collagen scaffold, and dentin matrix protein 1 after
subcutaneous transplantation in mice. J Endod 2008;34:4216.
27. Yu J, Deng Z, Shi J, et al. Differentiation of dental pulp stem cells into regular-shaped
dentin-pulp complex induced by tooth germ cell conditioned medium. Tissue Eng
2006;12:3097105.
28. DAnto V, Di Caprio MP, Ametrano G, et al. Effect of mineral trioxide aggregate on
mesenchymal stem cells. J Endod 2010;36:183943.
29. Moghaddame-Jafari S, Mantellini MG, Botero TM, et al. Effect of proroot mta on pulp
cell apoptosis and proliferation in vitro. J Endod 2005;31:38791.
30. Chueh LH, Huang GT. Immature teeth with periradicular periodontitis or abscess
undergoing apexogenesis: a paradigm shift. J Endod 2006;32:120513.
31. Shah N, Logani A, Bhaskar U, Aggarwal V. Efficacy of revascularization to induce
apexification/apexogensis in infected, nonvital, immature teeth: a pilot clinical study.
J Endod 2008;34:91925.
32. Nosrat A, Seifi A, Asgary S. Regenerative endodontic treatment (revascularization)
for necrotic immature permanent molars: a review and report of two cases with
a new biomaterial. J Endod 2011;37:5627.
33. Wang X, Thibodeau B, Trope M, et al. Histologic characterization of regenerated tissues in canal space after the revitalization/revascularization procedure of immature
dog teeth with apical periodontitis. J Endod 2010;36:5663.
34. Shimizu E, Jong G, Partridge N, et al. Histologic observation of a human immature
permanent tooth with irreversible pulpitis after revascularization/regeneration procedure. J Endod 2012;38:12937.
35. Petrino JA, Boda KK, Shambarger S, et al. Challenges in regenerative endodontics: a
case series. J Endod 2010;36:53641.
36. Chen MYH, Chen KL, Chen CA, et al. Responses of immature permanent teeth with
infected necrotic pulp tissue and apical periodontitis/abscess to revascularization
procedures. Int Endod J 2012;45:294305.
37. Hulsmann M. Dens invaginatus: aetiology, classification, prevalence, diagnosis, and
treatment considerations. Int Endod J 1997;30:7990.
38. Bhaskar S. Synopsis of Oral Pathology, 7th ed. St Louis: C.V. Mosby; 1986.
39. Sathorn C, Parashos P. Contemporary treatment of class II dens invaginatus. Int Endod J 2007;40:30816.
40. Hunter HA. Dilated composite odontome: reports of two cases, one bilateral and one
radicular. Oral Surg Oral Med Oral Pathol 1951;4:66873.
41. Oehlers FA. The radicular variety of dens invaginatus. Oral Surg Oral Med Oral
Pathol 1958;11:125160.
42. Sutalo JKA, Negotevic-Mandic V. Endodontic treatment of dens invaginatus: case
report. Acta Stomatol Croat 2004;38:2158.
43. Oehlers FA. Dens invaginatus (dilated composite odontome): Ivariations of the
invagination process and associated anterior crown forms. Oral Surg Oral Med
Oral Pathol 1957;10:120418.
44. Hovland EJ, Block RM. Nonrecognition and subsequent endodontic treatment of
dens invaginatus. J Endod 1977;3:3602.
45. Alani A, Bishop K. Dens invaginatus: part 1classification, prevalence and aetiology. Int Endod J 2008;41:112336.

JOE Volume 40, Number 5, May 2014


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Case Report/Clinical Techniques


46. Tagger M. Nonsurgical endodontic therapy of tooth invagination: report of a case.
Oral Surg Oral Med Oral Pathol 1977;43:1249.
47. Thomas JG. A study of dens in dente. Oral Surg Oral Med Oral Pathol 1974;38:6535.
48. Hamasha AA, Alomari QD. Prevalence of dens invaginatus in jordanian adults. Int
Endod J 2004;37:30710.
49. Thongudomporn U, Freer TJ. Prevalence of dental anomalies in orthodontic patients. Aust Dent J 1998;43:3958.
50. Ridell K, Mejare I, Matsson L. Dens invaginatus: a retrospective study of prophylactic
invagination treatment. Int J Paediatr Dent 2001;11:927.
51. Derbes VJ, Kerr A Jr. Valsalvas maneuver and webers experiment. N Engl J Med
1955;253:8223.
52. Huang GT. Dental pulp and dentin tissue engineering and regeneration: advancement and challenge. Front Biosci 2011;E3:788800.
53. Zhao S, Sloan AJ, Murray PE, et al. Ultrastructural localisation of tgf-beta exposure in
dentine by chemical treatment. Histochem J 2000;32:48994.
54. Tziafas D, Alvanou A, Panagiotakopoulos N, et al. Induction of odontoblast-like cell
differentiation in dog dental pulps after in vivo implantation of dentine matrix components. Arch Oral Biol 1995;40:88393.
55. Roberts-Clark DJ, Smith AJ. Angiogenic growth factors in human dentine matrix.
Arch Oral Biol 2000;45:10136.
56. Heling I, Rotstein I, Dinur T, et al. Bactericidal and cytotoxic effects of sodium
hypochlorite and sodium dichloroisocyanurate solutions in vitro. J Endod 2001;27:
27880.
57. Wei X, Ling J, Wu L, et al. Expression of mineralization markers in dental pulp cells.
J Endod 2007;33:7038.
58. Huang GTJ, Shagramanova K, Chan SW. Formation of odontoblast-like cells from
cultured human dental pulp cells on dentin in vitro. J Endod 2006;32:106673.
59. Alliot-Licht B, Bluteau G, Magne D, et al. Dexamethasone stimulates differentiation of
odontoblast-like cells in human dental pulp cultures. Cell Tissue Res 2005;321:
391400.
60. Ferreira MB, Myiagi S, Nogales CG, et al. Time- and concentration-dependent
cytotoxicity of antibiotics used in endodontic therapy. J Appl Oral Sci 2010;18:
25963.
61. Binnie WH, Rowe AH. A histological study of the periapical tissues of incompletely
formed pulpless teeth filled with calcium hydroxide. J Dent Res 1973;52:11106.
62. Cvek M, Sundstrom B. Treatment of non-vital permanent incisors with calcium hydroxide: Vhistologic appearance of roentgenographically demonstrable apical
closure of immature roots. Odontol Revy 1974;25:37991.

JOE Volume 40, Number 5, May 2014

63. Parirokh M, Torabinejad M. Mineral trioxide aggregate: a comprehensive literature reviewpart I: chemical, physical, and antibacterial properties. J Endod 2010;36:1627.
64. Parirokh M, Torabinejad M. Mineral trioxide aggregate: a comprehensive literature
reviewpart III: clinical applications, drawbacks, and mechanism of action.
J Endod 2010;36:40013.
65. Torabinejad M, Parirokh M. Mineral trioxide aggregate: a comprehensive literature
reviewpart II: leakage and biocompatibility investigations. J Endod 2010;36:
190202.
66. Laragnoit AB, Neves RS, Neves IL, Vieira JE. Locoregional anesthesia for dental treatment in cardiac patients: a comparative study of 2% plain lidocaine and 2% lidocaine with epinephrine (1:100,000). Clinics (Sao Paulo) 2009;64:17782.
67. Davenport RE, Porcelli RJ, Iacono VJ, et al. Effects of anesthetics containing epinephrine on catecholamine levels during periodontal surgery. J Periodontol 1990;61:
5538.
68. Meechan JG, Parry G, Rattray DT, Thomason JM. Effects of dental local anaesthetics
in cardiac transplant recipients. Br Dent J 2002;192:1613.
69. Schechter E, Wilson MF, Kong YS. Physiologic responses to epinephrine infusion:
the basis for a new stress test for coronary artery disease. Am Heart J 1983;105:
55460.
70. Meechan JG. Supplementary routes to local anaesthesia. Int Endod J 2002;35:
88596.
71. Abraham-Inpijn L, Borgmeijer-Hoelen A, Gortzak RA. Changes in blood pressure,
heart rate, and electrocardiogram during dental treatment with use of local anesthesia. J Am Dent Assoc 1988;116:5316.
72. Groban L, Deal DD, Vernon JC, et al. Ventricular arrhythmias with or without programmed electrical stimulation after incremental overdosage with lidocaine, bupivacaine, levobupivacaine, and ropivacaine. Anesth Analg 2000;91:110311.
73. Muzyka BC. Atrial fibrillation and its relationship to dental care. J Am Dent Assoc
1999;130:10805.
74. Reisman D, Reader A, Nist R, et al. Anesthetic efficacy of the supplemental intraosseous injection of 3% mepivacaine in irreversible pulpitis. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 1997;84:67682.
75. Blanton PL, Jeske AH. Dental local anesthetics: alternative delivery methods. J Am
Dent Assoc 2003;134:22834.
76. Paris ST, Cafferkey M, Tarling M, et al. Comparison of sevoflurane and halothane for
outpatient dental anaesthesia in children. Br J Anaesth 1997;79:2804.
77. Ganzberg S. Local anesthetics and vasoconstrictors. Oral Maxillofac Surg Clin N Am
2001;13:6574.

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