Aust Endod J 2019

CASE REPORT

Atypically grown large periradicular cyst affecting adjacent teeth

and leading to confounding diagnosis of non-endodontic
pathology
Domenico Ricucci, MD, DDS1 ; Massimiliano Amantea, MD, MS2; Christian Girone, DDS2; and

F. Siqueira, Jr, DDS, MSc, PhD3
Jose
1 Private practice, Cetraro, Italy
2 Private practice, Montalto Uffugo, Italy
3 Department of Endodontics, Grande Rio University, Duque de Caxias, RJ, Brazil

Keywords
differential diagnosis, non-endodontic lesion,
periradicular cyst, radiolucent mandibular
lesions.
Correspondence
Domenico Ricucci, Private practice, Cetraro,
Italy, Piazza Calvario, 7, 87022 Cetraro (CS) –
Italy. Email: dricucci@libero.it
doi: 10.1111/aej.12381
(Accepted for publication 22 September 2019.)
Abstract
This article reports a case of a large osteolytic lesion in the mandible, mostly
associated with the apices of the premolars, and suspected as having a non-en-
dodontic origin because the 2 premolars responded positively to the cold sensi-
bility test. The distal border of the lesion reached the mesial root of the first
molar, which also had a small lesion in its distal aspect. Cone-beam computed
tomography revealed that the large lesion communicated with the small molar
lesion. Because the large lesion was suspected as having a non-endodontic ori-
gin, surgery was scheduled for enucleation and biopsy. The molar was root
canal-retreated, and the 2 premolars treated. Histologic analysis of the premo-
lar pulps showed vitality but advanced degenerative changes. The lesion was
histologically diagnosed as an inflammatory periradicular cyst, which origi-
nated in the first molar and had an atypical growth to the premolar area. Fol-
low-up revealed that the affected area healed uneventfully.

associated with the roots of teeth with vital pulps are

Introduction
Radiolucent lesions in the mandible are not uncommon
and may have an odontogenic or non-odontogenic origin
(1). The large majority of these lesions are inflammatory
in nature, while a minor fraction is represented by lesions
of non-inflammatory or neoplastic origin, with malignant
or metastatic lesions being less frequent (2). Inflamma-
tory lesions of endodontic origin, also known as apical
periodontitis, manifest themselves histologically as gran-
uloma, abscesses and cysts (3) and are caused by bacterial
infection of the necrotic pulp tissue, usually organised in
the form of biofilms (4).
The diagnosis of large radiolucencies that are contigu-
ous to root apices may sometimes pose a great challenge
for the clinician, as the radiographic appearance of
inflammatory and non-inflammatory (sometimes life-
threatening) disease processes of the jaws may be similar.
The literature is replete with reports of non-endodontic
lesions misdiagnosed as apical periodontitis (5–9). One of
the most important factors generally used for differential
diagnosis is the results of pulp sensibility tests; lesions
regarded as of non-endodontic origin (9). Diagnosis
becomes difficult when the pulp became necrotic because
of an unrelated process, the root canal is treated or the
results of pulp sensibility tests are inconclusive.
There are numerous cases reported in which non-en-
dodontic lesions, as for instance calcifying odontogenic
cysts (10), central giant cell lesions causing tooth dis-
placement (8) and unicystic ameloblastoma (7), mim-
icked apical periodontitis in teeth with vital pulps. There
are also less frequent reports of apparently intact teeth or
teeth with only shallow caries or restorations that
showed loss of pulp vitality and were associated with
non-endodontic radiolucencies (9,11), including multiple
myeloma (12), Ewing’s sarcoma (13) and ameloblas-
tomas (6,7).
Although it is plausible that any expansive bone
destructive process taking place in the periapical region
of a vital tooth may exert pressure on the apical circula-
tion, in the literature there are only a few reports of teeth
that became devitalised as a consequence of an expand-
ing inflammatory periapical lesion from an adjacent

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Large Apical cyst Mimicking a Non-Endodontic Lesion
tooth (14–16). Moreover, information is limited to the
histopathologic conditions of the pulp tissue of teeth
associated with non-endodontic lesions. Todd and Lange-
land (12) reported that the pulp of a mandibular premo-
lar associated with a multiple myeloma showed
‘progressive degeneration compatible with ischaemic
conditions’.
The purpose of this communication is to report a case
of a large osteolytic lesion in the mandible, mostly associ-
ated with the apices of the premolars, which was sus-
pected as having a non-endodontic origin. Histologic
analysis of the excised lesion and the pulps of the premo-
lars revealed it was an atypically grown inflammatory
periradicular cyst, originated in the first molar, which
was also the most likely cause of the degenerative
changes observed in the premolars pulps.
Case report
A 36-year-old man was referred to an endodontist by a
general clinician for evaluation of a large osteolytic lesion
occurring in the right side of the mandible, which was
disclosed in a panoramic radiograph taken for routine
dental treatment (Fig. 1a). Radiographically, the lesion
showed round and regular margins and had close rela-
tionship with the apices of the mandibular right premo-
lars, which exhibited shallow composite coronal
restorations (Fig. 1a,b). The general clinician reported
that both mandibular right premolars did not respond to
thermal tests, for which reason they were deemed as
having necrotic pulps. The margins of the lesion also
appeared to be proximal to the mesial root of the
mandibular first molar (#30), which exhibited substan-
dard root canal treatment, with some filling material in
the distal canal and apparently empty mesial canals. The
molar crown had an extensive amalgam restoration
(Fig. 1a,b). The mesial root showed a second periradicular
radiolucency on its distal aspect, apparently separated or
at least only slightly communicating with the larger
lesion (Fig. 1a,b). The profile of the mandibular canal
could not be appreciated within the radiolucency, which
seemed to almost reach the mandible border (Fig. 1a).
The patient had no more information about the dental
treatments of the right mandibular teeth and did not
report any pain episodes in the past. He declared that
only recently had experienced a slight discomfort when
applying pressure on the right side of the mandible. Med-
ical history was non-contributory.
Teeth #28, #29 and #30 responded normally to vertical
and lateral percussion tests. Palpation on the vestibule
revealed that the buccal cortical profile was swollen, with
hard consistency, and there was some discomfort to pres-
sure. Cold pulp test gave a weak positive response for
2 © 2019 Australian Society of Endodontology Inc
D. Ricucci et al.
teeth #28 and #29, only after application of the stimulus
on the cervical region (Pulpofluorane, Septodont, Saint-
Maur-des-Foss
es, Cedex, France). These teeth gave no
responses to hot and electric tests. Periodontal probing
depth did not exceed 2 mm.
The diagnosis of lesion with possible non-endodontic
origin was suspected, and surgical enucleation was
scheduled. Treatment plan included pulpectomy of teeth
#28 and #29, in order to avoid their devitalisation during
surgery and retreatment of tooth #30.
After anaesthesia, rubber dam isolation and field disin-
fection, restorative materials were removed. Some cari-
ous tissue was found underneath the restoration of tooth
#28, which was removed until hard dentin was observed
on the cavity floor (Fig. 1c). Access cavities were pre-
pared, and efforts were made to remove the pulps in their
entirety (Fig. 1d,f) with the help of a Hedstr€ om file of
adequate size placed in the proximity of the apical con-
striction to cut the pulp. Working length was established
for both teeth at 0.5 mm short of the foramen based on
the EAL readings (Root ZX, Morita corp, Tokyo, Japan).
Canals were instrumented with Gates-Glidden burs in
the coronal two-thirds and hand Hedstr€ om files in the
apical third, under copious irrigation with 1% NaOCl.
Root canal obturation was accomplished in the same visit
using cold lateral compaction of gutta-percha and a sea-
ler. Tooth #30 was treated using the same protocol,
except that the canals received an interappointment
medication with a calcium hydroxide paste for one week
and then filled. The teeth were adequately restored, and
a postoperative radiograph taken (Fig. 1g). The patient
gave consent for histologic analysis of the premolar pulps,
which were immediately immersed in fixative. Surgery
was scheduled 2 months after placing the root canal fill-
ing according to the patient’s convenience. For this rea-
son, it was decided to proceed with histologic processing
of the pulps with the aim of gaining some more informa-
tion about the nature of the pathologic process.
The pulps were fixed in formalin, embedded in paraffin
and 5 lm thick longitudinal serial sections were cut.
Details of histologic processing are given below. Haema-
toxylin and eosin staining confirmed that both pulps
were vital, although hypocellular and fibrosed, with
extensive deposits of haematoxyphilic round bodies con-
sistent with dystrophic calcification (Figs. 1h–j, Fig. 2a–
d), a condition also known as calcific metamorphosis. A
reduced number of vessels could be observed, and their
lumen often appeared filled with degraded erythrocytes,
indicating circulatory disturbances (stasis) (Fig. 2c–d).
Bacterial staining did not reveal stainable bacterial cells
in any of the serial sections. These histologic findings
allowed to exclude that the 2 premolars had any implica-
tion in the aetiology of the large lesion. Rather, they
D. Ricucci et al. Large Apical cyst Mimicking a Non-Endodontic Lesion

(a) (b)

(c) (d) (e) (f)

(g) (h) (i) (j)

Figure 1 (a) Panoramic radiograph showing a large round radiolucency in the mandible, adjacent to the roots of the right premolars, and a minor radi-
olucency on the distal aspect of the mesial root of the right mandibular molar. (b) Periapical radiograph. Note the reduction of volume of the pulp
chamber and of the root canal of tooth #29. (c) Cavity in the crown of the first premolar after removal of composite restoration and of the residual cari-
ous tissue. (d) Pulp tissue removed in one piece. (e) Shallow occlusal cavity in the second premolar after removal of the existing composite restoration.
(f) Pulp tissue extracted from the canal of the second premolar. (g) Postoperatory radiograph. (h) Apical half of the first premolar’s pulp in (d) (haema-
toxylin and eosin, original magnification 925). (i, j) Apical and coronal portion of the second premolar’s pulp in (f) (original magnification 916).

suggested that the pulp changes in premolars may have
been resultant of the expanding lesion affecting their
periapical region, whose nature was to be determined fol-
lowing the upcoming surgery.
The patient did not report postoperative symptoms.
Two months later, he declared that there was no
spontaneous pain, but palpation of the mucosa over the
apices still caused some discomfort. Before surgery, a
cone-beam computed tomography (CBCT) examination
was performed to ascertain the relationship of the lesion
with the neighbouring structures. Axial scans confirmed
that the buccal mandibular profile was swollen and the

© 2019 Australian Society of Endodontology Inc 3

Large Apical cyst Mimicking a Non-Endodontic Lesion D. Ricucci et al.

(a) (b)

(c) (d)

4 © 2019 Australian Society of Endodontology Inc

D. Ricucci et al.
Figure 2 (a, b) Progressive magnifications of the area of the first premolar’s pulp indicated by the arrow in Fig. 1h. The pulp is hypocellular with large
mineralised masses in its context (haematoxylin and eosin, original magnification 9100 and 9400). (c, d) Progressive magnifications of the apical por-
tion of the second premolar’s pulp indicated by the arrow in Fig. 1i. The pulp architecture is obscured by the presence of a large number of mineralised
masses. A vessel is present with degraded erythrocytes in its lumen (haematoxylin and eosin, original magnification 9100 and 9400).
cortical bone consistently thinned (Fig. 3a). Sagittal scans
were studied with special care, to clarify the relationship
of the lesion with the apices of the involved teeth. In the
majority of the scans, the apices of both premolars
appeared to project into the lesion (Fig. 3b,c), while the
mesial root of the molar was somewhat distant from the
lesion margins; the minor radiolucency on the distal
aspect of the mesial root was apparently not communi-
cating with the main lesion (Fig. 3b,c). However, some
CBCT slices revealed a quite different picture, with the
apex of the first molar mesial root centering the large
radiolucency, and an apparent continuity between the
large osteolytic lesion and the small radiolucency on the
distal aspect of the mesial root (Fig. 3d). This condition
was confirmed by coronal scans and 3-D reconstructions,
which showed 2 split apices in the mesial root in close
contact with the main lesion (Fig. 3e,f).
Surgery was performed under deep intravenous seda-
tion with Diprivan 1%, Fentanest 0.1 mg and Midazolam
3 mg. Before surgery, platelet-rich fibrin (PRF) was pre-
pared according to the following procedure: 4 samples of
venous blood were collected in sterile 10-mL vacutainers
without anticoagulant. The vacutainers were immedi-
ately centrifuged at 408 g for 12 min (17). A fibrin clot
was obtained in the middle of tubes, just between the red
corpuscles at the bottom and acellular plasma at the top.
Resistant autologous fibrin membranes were easily
obtained by driving out the serum from the clot.
After mucoperiosteal incision and flap reflection, it was
evident that the lesion had caused erosion of the cortical
bone in some areas (Fig. 4a). A window was created in
the buccal bone by using an ultrasonic instrument
(Piezosurgery 3, Mectron spa, Carasco, Italy) to expose
the pathologic tissue (Fig. 4b,c). The lesion was easily
detached from the bone crypt and adjacent root apices
(Fig. 4d), and the mandibular nerve could be inspected,
dislodged at the lower margin of the cavity and deprived
of the mandibular canal’s roof. Root-end resection was
performed on the molar mesial root, approximately
3 mm short of the apex by using a fissure bur, and the
exposed gutta-percha was burnished with a hot instru-
ment. Two separate apical fragments were obtained,
together with the pathologic tissue located distally to the
mesial root. The surgical cavity was flushed with saline
and an antibiotic solution and, after control of haemosta-
sis, filled with PRF membranes (Fig. 4e). The flap was
repositioned without stress and sutured with 5/0 Coated
© 2019 Australian Society of Endodontology Inc
Large Apical cyst Mimicking a Non-Endodontic Lesion
Vicryl synthetic absorbable sutures (Fig. 4f). Amoxicillin
plus clavulanate (2 g day 1) and diclofenac
1
(100 mg day ) was prescribed for 5 days. Oral rinses
with 0.12% chlorhexidine gluconate were recommended
for 14 days. The postoperative period was uneventful,
and suture was removed after 10 days. A CBCT examina-
tion performed 1 year and 2 months after surgery
revealed that healing was almost complete, with new
bone filling the cavity and relocation of the previously
swollen cortical plate (Fig. 3g–i).
Histologic processing
All the excised tissues, including the premolars pulps,
(Fig. 1d,f) the large lesion (Fig. 4g), the 2 molar mesial
apical fragments, the minor soft tissue lesion (associated
with the molar mesial root) and the fragment of cortical
bone (Fig. 4h) were immediately immersed in fixative for
histologic analysis. Biopsies were fixed in a 10% neutral
buffered formalin solution for 48 h. The large and the
small soft tissue lesions were dehydrated in ascending
grades of ethanol and cleared in xylene. Before paraffin
infiltration, the major lesion was cut with a sharp razor
blade in 3 segments, perpendicularly to the mesiodistal
axis and then embedded separately. The two apices and
the cortical bone fragments were demineralised in a solu-
tion consisting of 22.5% (vol/vol) formic acid and 10%
(wt/vol) sodium citrate for 4 weeks. The end point was
determined radiographically. At the end of the deminer-
alization process, specimens were washed in running
water for 24 h and dehydrated in ascending grades of
ethanol. After clearing in xylene, they were infiltrated
and embedded in paraffin. The two apices were oriented
parallel to the long axis of the main root canal in order to
obtain longitudinal sections through the apical canal.
Serial sections were taken with the microtome set at 4 to
5 lm until the apical canal was exhausted. The buccal
cortical bone was separated in two portions, and approxi-
mately 100 sections were taken from both segments per-
pendicularly to the bone plate. Approximately 200
sections were taken for each of the 3 segments of the
major lesion and for the minor soft tissue fragments.
Sections were stained with haematoxylin and eosin
and with the Taylor’s modified Brown and Brenn tech-
nique for bacteria. Selected slides from the major lesion
were stained with the Masson’s trichrome and with the
Periodic acid-Schiff (PAS) for polysaccharides.
5
Large Apical cyst Mimicking a Non-Endodontic Lesion D. Ricucci et al.

(a) (b) (c)

(d) (e) (f)

(g) (h) (i)

14 mo 14 mo 14 mo

Figure 3 (a) CBCT axial scan. Buccal cortical bone is consistently swollen. (b, c) Sagittal scans showing close relationship of the lesion with the apices
of the two premolars. (d) Sagittal scan showing that the large lesion apparently extends to the distal aspect of the mesial root. (e) Coronal scan. The
two split apices of the mesial root appear contiguous to the radiolucency. (f) 3-D reconstruction showing the anatomy of the molar mesial root with
two split apices (arrows). (g–i) CBCT axial, sagittal and coronal scans taken 14 months after surgery. Healing is almost complete.

debris (Fig. 4j–k) and clusters of cells in various stages of

Results
degradation. Void spaces with a typical pointed appear-
Histologic analysis revealed that the major lesion was a ance suggestive of cholesterol crystals could be discerned
periradicular cyst, with a large lumen filled with necrotic within the cyst content. The lumen was lined by a non-

6 © 2019 Australian Society of Endodontology Inc

D. Ricucci et al. Large Apical cyst Mimicking a Non-Endodontic Lesion

(a) (b) (c)

(d) (e) (f)

(g) (h) (i)

(j) (k)

Figure 4 (a) After reflection of the flap, the cortical bone appears swollen and eroded in one point. (b) Osteotomy. (c) Exposure of the pathologic tis-
sue. (d) Bone crypt after removal of the lesion. (e) Bone cavity filled with PRF. (f) Suture of the flap. (g) Pathologic tissue removed from the large cavity.
(h) Top (from left to right): apices of the mesial root and soft tissue mass from its distal profile. Bottom: cortical bone fragment. (i) Buccal apex after
clearing in xylene. (j) Section of the main lesion at the level of the line in (g) (haematoxylin and eosin, original magnification 92). (k) Left portion of the
lesion in (J). The lumen contains necrotic debris and cholesterol clefts and is lined by epithelium (original magnification 916). Left inset: high power
view of the area of the epithelial wall indicated by the arrow in (K). Some large cells with dark cytoplasms (original magnification 9400). Right inset:
other section. The material in the cytoplasm is proven to be mucopolysaccharides (PAS, original magnification 9 400).

© 2019 Australian Society of Endodontology Inc 7

Large Apical cyst Mimicking a Non-Endodontic Lesion D. Ricucci et al.

keratinised epithelium showing varying thickness. The
epithelial lining showed signs of exfoliation towards the
lumen, with cells that tended to assume indistinct nuclei.
Some epithelial cells exhibited a very large size with the
cytoplasm engulfed by a haematoxyphilic matter (inset
in Fig. 4j). PAS staining revealed this material to be
mucopolysaccharides (inset in Fig. 4k), for which reason
these large cells where recognised as mucous type cells,
and not foamy histiocytes or macrophages. The cystic
walls were surrounded by thick bundles of collagen fibres
(Fig. 4j–k) with scattered chronic inflammatory cells.
While in most sections the epithelial lining appeared to
be continuous, sections from the distal region of the
lesion showed that the epithelium crossed the connective
wall, giving rise to a channel that likely connected the
cyst lumen with the apices of the molar mesial root
(Fig. 5a,b). Along the course of this communication,
numerous rounded or polycyclic bodies could be distin-
guished, surrounded by inflammatory cells, suggestive of
Rushton bodies (Fig. 5b,c). Bacterial staining showed no
residual bacterial infection in both molar mesial apices or
in the cyst lumen. Sections cut through the mesiobuccal
canal and foramen revealed elongated bodies both in the
apical foramen and on the external apical surface with a
close similarity to the Rushton bodies present in the cyst
lesion (Fig. 5d,e).
Sections from the minor soft tissue mass present on the
distal aspect of the mesial root of the mandibular molar
revealed a granulomatous tissue with severe concentra-
tion of chronic inflammatory cells. Strands of epithelium
could be observed throughout this mass.
Histologic analysis of the fragment of cortical bone did
not show pathologic changes, except signs of resorption
in the areas adjacent to the lesion.
Discussion
This case presented with some atypical and interesting
conditions that are worth highlighting. The apical peri-
odontitis lesion originated in the mandibular first molar

(a) (b) (c)

(d) (e)

Figure 5 (a) Section from the distal portion of the lesion (Taylor modified Brown & Brenn, original magnification 92). (b) Area demarcated by the rect-
angle in (a). The cyst wall is crossed by epithelium (original magnification 9 16). (c) Middle magnification of the area indicated by the arrow in (b).
Round polycyclic bodies stained with fuchsin (original magnification 9100. Inset 9400). (d) Section through the mesiobuccal canal and foramen in
Fig. 4i (original magnification 9100). (e) High power view of the area of the external apical surface indicated by the arrow in (d). Bodies showing similar
morphology to those present in the cyst walls (original magnification 9400).

8 © 2019 Australian Society of Endodontology Inc

D. Ricucci et al.
with a substandard root canal treatment had an abnormal
growth, prominently advancing to the premolar area and
forming what appeared radiographically as 2 separate
lesions but with a small communication between them
only revealed by some CBCT slices. Given the 2 separate
molar mesial apices with distinct apical foramina, it is
likely that the lesions may have initiated as separate enti-
ties and in a given moment became connected. The large
lesion size associated with 2 premolars that responded
positively to cold suggested that it might be a lesion of
non-endodontic origin and prompted the endodontist to
indicate surgery.
The reason why one of the lesions was much larger
than the other is not clear, especially because it was asso-
ciated with the same root. The possibility exists that there
were 2 independent mesial canals (Vertucci’s class IV),
each one harbouring a bacterial community with differ-
ent composition and virulence. It is even more difficult to
explain the aberrant expansion of the lesion. Possibly, it
may be related to the position of the apical foramen, pres-
ence of undetected lateral foramina or iatrogenic perfora-
tion in the mesial root aspect and/or defects in bone
anatomy that predisposed lesion growth to an area of less
resistance.
Information on the histologic changes taking place in
the pulp tissue because of a disease process advancing to
its periapical area is scarce in the literature. It seems that
some malignant lesions may directly invade the apical
connective tissue and/or mechanically strangulate the
pulp circulation. Todd and Langeland (12) examined his-
tologically the pulp extirpated from a premolar associated
with a large periapical radiolucency diagnosed as multiple
myeloma. They observed that the pulp had degenerated
because of ischaemia and not neoplastic changes taking
place in it. Dated histologic reports, based on autopsy
material, described invasion of or metastasis to the dental
pulp (18). Snyder and Cawson (19) showed nests of
tumour cells of adrenal neuroblastoma within the pulpal
blood vessels of a mandibular deciduous molar. Despite
the different nature of the disease, it is similarly possible
that actively growing cysts may cause damage to the pulp
circulation of adjacent teeth by mechanically compressing
vessels that enter the pulp space.
Reports of teeth that became devitalised because of an
inflammatory apical periodontitis lesion from an adjacent
tooth are also scarce in the literature (14–16). Like the
present one, the cases previously reported were diag-
nosed as periradicular cysts (15,16). The previous reports
also showed clinical conditions suggestive of exacerba-
tion with abscess formation (14–16), which was not
observed in the present case.
The pulps of the 2 premolars affected by the large
lesion showed degenerative changes typical of
© 2019 Australian Society of Endodontology Inc
Large Apical cyst Mimicking a Non-Endodontic Lesion
exacerbated ageing process, including decreased cellular-
ity, fibrosis and foci of dystrophic calcification. The possi-
bility exists that the pressure exerted by the growing cyst
compressed blood vessels that penetrate through the api-
cal foramen of adjacent teeth, causing reduction of oxy-
gen and nutrient supply to the pulp and consequent
hypoxia and ischaemia, with damage to the cells. Dys-
trophic calcification usually results from calcium deposi-
tion in areas of damaged or necrotic cells. It usually
initiates by extracellular deposition of calcium phosphate
crystals in membrane-bound vesicles from damaged cells
or intracellular accumulation in the mitochondria of
dying cells (20). The crystals propagate to give rise to lar-
ger calcific deposits (20). Because the pulps were not
necrotic, the cyst-induced pressure is not expected to
have caused total strangulation of vessels and collapse of
circulation, but was apparently sufficient to cause degen-
erative changes in the pulp tissue, possibly affecting the
neural content and/or response to stimuli (21), as evi-
denced by the faint response to cold pulp test and lack of
response to the other tests. Degenerative changes typical
of ageing process may also be exacerbated by the effects
of prolonged chronic inflammation on cells and adjacent
vessels (20). To summarise, the chronic inflammatory
process and the pressure associated with cysts may have
led to changes in the blood supply to the pulps of adja-
cent teeth, not drastic enough to cause total tissue necro-
sis but sufficiently deleterious to exacerbate degenerative
ageing processes with dystrophic calcification.
Both premolars had previous restorations and radio-
graphs revealed that the pulp of tooth #29 had receded.
Because there are no control pulps from other vital teeth
for comparisons, one cannot discard the possibility that
the pulps of the 2 premolars showed degenerative fea-
tures in response to long-standing caries process and/or
restorative procedures.
Had the clinician been sure that the lesion was inflam-
matory and caused exclusively by the molar, the decision
to be made would be retreatment of the molar and fol-
low-up examination. However, given its atypical pattern
of expansion, clinical and radiographic diagnosis of the
large lesion was misleading. Surgery was the treatment of
choice because the 2 premolars were proven not to be
the cause of the lesion, and it was not possible to ascer-
tain whether or not the lesion was inflammatory in nat-
ure. This doubt alone would suffice to indicate surgery,
but the fact that symptoms (discomfort to palpation) had
not subsided after retreatment of the molar reinforced
the need for a surgical solution. Premolars had to be root
canal-treated because they would be inevitably devi-
talised during the lesion enucleation procedure.
In conclusion, this article reports a case of large lesion
originated in a mandibular first molar that exhibited an
9
Large Apical cyst Mimicking a Non-Endodontic Lesion
abnormal pattern of expansion that roused a suspicion of
non-endodontic origin, especially because it was initially
judged to be associated with the adjacent premolars,
which showed positive, yet faint, results in the cold pulp
test. Histopathology demonstrated it was an inflamma-
tory periradicular cyst, which may also have caused
advanced degenerative changes in the pulps of the adja-
cent premolars.
Acknowledgement
The authors received no grants or other funding.
Disclosure
The authors have no interest to disclose.
Author contribution
All authors have contributed significantly. All authors
are in agreement with the manuscript.
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