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doi:10.1111/iej.

12417

CASE REPORT

Periapical cemento-osseous dysplasia:


a case report with twelve-year
follow-up and review of literature
E. S. Senia1 & M. S. Sarao2
1
Department of Endodontics, Wilford Hall Medical Center, Lackland Air Force Base, San
Antonio, TX; and 2Department of Surgical Dentistry, Division of Endodontics, School of Dental
Medicine, University of Colorado, Aurora, CO, USA

Abstract
Senia ES, Sarao MS. Periapical cemento-osseous dysplasia: a case report with twelve-year follow-up
and review of literature. International Endodontic Journal.

Aim To present a case report describing the long-term behaviour of periapical cemento-osseous dysplasia by observing the radiographic changes that took place over a period of 12 years. A review of the pertinent literature is also presented.
Summary A healthy 26-year-old white female was referred to the Wilford Hall USAF
Medical Center Endodontic Department for evaluation of an asymptomatic radiolucency at
the apex of the right mandibular lateral incisor. Following a clinical evaluation that included
pulp testing, a diagnosis of periapical cemento-osseous dysplasia (PCOD) was made. No
treatment was rendered but follow-up visits were recommended. The patient was subsequently re-evaluated 8 times over a period of 12 years. During that time the lesion changed
in appearance, displaying the various phases of PCOD. At the same time, lesions affecting
the three adjoining incisors appeared and behaved in a similar manner. At the 12-year recall,
the right lateral and both central incisors revealed no evidence of PCOD and an almost normal trabecular pattern of bone could be seen. Misdiagnosis and unnecessary treatment of
PCOD may be avoided with careful pulp testing and knowledge of its most common locations of occurrence, radiographic appearances (phases) and benign behaviour.
Key learning points
The aetiology of periapical cemento-osseous dysplasia is unknown.
Periapical cemento-osseous dysplasia is asymptomatic, detected radiographically and
usually requires no treatment.
Pulp testing is an important tool in diagnosing periapical cemento-osseous dysplasia,
and limited-field CBCT may also be useful when available.
A correct diagnosis of periapical cemento-osseous dysplasia can be validated with
follow-up radiographs.
Long-term evaluation of periapical cemento-osseous dysplasia lesions is proposed.

Correspondence: Manpreet Singh Sarao, Department of Surgical Dentistry, Division of Endodontics, School of Dental Medicine, University of Colorado, 13065 E. 17th Ave., Room 104E,
Aurora, Colorado 80045, USA, (Tel.: 303-724-6423; Fax: 303-724-6986;
e-mail: saraok2002@yahoo.com).

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CASE REPORT

Keywords: benign fibro-osseous lesions, cementoma, periapical cemental dysplasia, periapical cemento-osseous dysplasia, periradicular cemental dysplasia,
periradicular osteofibrosis.
Received 25 January 2013; accepted 20 November 2014

Introduction
Fibro-osseous lesions of the jaws (FOLs) represent a diverse group of processes that
are characterized by the replacement of normal bone with a fibrous tissue containing
varying amounts of a mineralized substance which may be bony or cementum-like in
appearance. There is considerable inconsistency in the literature regarding the classification and nomenclature of FOLs. Many authors attempted to classify FOLs but Waldrons classification has been widely accepted and referenced. Waldron classified FOLs
into three groups: (i) fibrous dysplasia, (ii) reactive (dysplastic) lesions and (iii) fibro-osseous neoplasms (Waldron 1993).
Periapical cemento-osseous dysplasia (PCOD) has been described as a reactive or dysplastic FOL in the tooth-bearing area, presumably of periodontal ligament origin (Waldron
1993) or unknown aetiology. The World Health Organization (WHO) in their Histological
Typing of Odontogenic Tumours (1992) referred to PCOD as periapical cemental dysplasia (PCD) (Kramer et al. 1992) and classified PCD as a type of cement-osseous dysplasia
under nonneoplastic bone lesions. Other names for PCOD found in the literature are:
cementoma, periradicular cemental dysplasia, periradicular fibrous dysplasia, periradicular
osteofibrosis (Eleazer et al. 2012), periapical fibrous dysplasia (Kramer et al. 1992) and
periapical osteofibrosis (Falace & Cunningham 1984). In 1956, Hamilton B.G. Robinson
described similar lesions as periapical osseous dysplasia (Robinson 1956).
The terms PCOD and PCD have been interchangeably used in the literature and oral
pathology textbooks. Even the WHO Classification of Odontogenic Tumours (1992) has
grouped PCD under the subheading of cemento-osseous dysplasias (Kramer et al.
1992). During the literature search, the authors found that in recent years the term
PCOD was being used more commonly than the term PCD. Also, some of the recently
published oral pathology textbooks have used the term PCOD rather than PCD (Regezi
et al. 2008, Angela 2009). The authors will use the term PCOD in this article.
Forget in 1860 was most likely the first one to report a lesion closely resembling the
clinico-pathological features of PCOD (Forget 1860). He described an osseous tumour
encysted in the upper jaw of a horse. In 1915, Brophy described a lesion resembling
PCOD in human beings (Brophy 1915). In 1926, Siegmund & Weber proposed that a
central fibroma has the potential to differentiate into a cementoma (Siegmund & Weber
1926). In 1933, Stafne presented the first detailed clinical report of thirty-five cases of
cementomas (Stafne 1933). In 1964, Zegarelli and coworkers reported an incidence of
PCOD in the general population to be 2-3/1000 in their extensive case series of over
435 cementomas in 230 patients (Zegarelli et al. 1964). Recently, Alsufyani & Lam
(2011) reported a retrospective chart analysis of clinical and radiographic findings of
cement-osseous dysplasia (COD) of jaws in 118 patients. They reported an incidence of
82.9% in females with an age range of 1373 years; 72.2% of the patients were
asymptomatic; 78.8% of the lesions were classified as PCOD; and the remaining
21.2% were classified as florid cemento-osseous dysplasia. Radiographically, 81.4% of
the lesions were located in the mandible (91.5% were well defined), 72% were mixed
radiolucentradiopaque lesions, 61.4% were dense, cementum-like radiopacities; and
92.1% had normal periodontal ligament space with 77.6% having intact lamina dura.

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CASE REPORT

The majority of lesions were not associated with root resorption, hypercementosis,
periosteal reaction or displacement of anatomic structures (Alsufyani & Lam 2011).
The typical clinical presentation of PCOD is a well-defined, radiolucent, mixed radiolucentradiopaque or radiopaque lesion associated with one or more vital and asymptomatic mandibular anterior teeth in a middle-aged African American female. The diagnosis
is usually made with a routine radiographic examination. PCOD has been described as
progressing through three radiographically and histologically distinct stages (Sapp et al.
2002): (i) osteolytic stage: this is the early stage of PCOD characterized by well-defined
radiolucencies at the apex of one or more teeth. The radiolucencies surrounding the
root apex are usually indistinguishable from inflammatory periapical lesions of pulpal origin. Histologically, the tissue consists primarily of cellular connective tissue replacing
normal trabecular bone with calcified structures of insufficient size to be evident radiographically. (ii) Cementoblastic stage follows the initial lytic phase and is characterized
by the presence of radiolucent areas containing nodular radiopaque deposits. Histologically, there is a mixture of spherical calcifications and irregularly shaped deposits of
osteoid and mineralized bone. (iii) Mature stage: this late stage of PCOD is characterized by well-defined, dense radiopacities usually surrounded by a radiolucent rim. The
periodontal ligament can be seen separating the lesion from the root. Histologically, the
tissue in the mature stage is composed mainly of coalesced spherical calcifications and
sclerotic mineralized bone with scant connective tissue.
Most of the PCOD cases reported in the literature demonstrate the disease process
over one or two of its stages. Rarely has a case of PCOD been presented with the
end-point of an almost normal architecture of bone trabeculae. The aim of this study
was to present a case report of PCOD with a follow-up of 12 years in which the final
radiographs show a close resemblance to normal bone architecture. A review of the
pertinent literature is also presented.

Case report
A 26-year-old white female presented to the Wilford Hall USAF Medical Center dental
clinic at Lackland AFB, San Antonio,Texas, USA, for her annual examination. A fullmouth radiographic survey revealed a radiolucency at the apex of the mandibular right
lateral incisor (tooth 42; Fig. 1). She was referred to the Endodontic Department for
evaluation. Her medical and dental histories were noncontributory; she reported no
pain, swelling, sensitivity, orthodontic treatment or trauma. An intra-oral examination of
the mandibular anterior area revealed no caries or restorations and the gingiva appeared
pink and healthy with 23 mm pocket depths. Palpation and percussion gave no evidence of swelling, bony expansion or pain. Tooth 42 responded to cold, heat and electric pulp testing. No other abnormal radiographic findings were noted. Based on the
evidence gathered, a working diagnosis of PCOD (osteolytic stage), tooth 42, was
made. The findings were explained to the patient who was advised to have follow-up
evaluations and was re-evaluated eight times over a period of 12 years. At all recall
appointments, the clinical examination included palpation, percussion, cold, heat and
electric pulp tests, and probing of the mandibular anterior teeth. The pulps of all teeth
responded normally during the entire 12-year period, and the results of clinical examination were within normal limits. The results of the radiographic findings (Figs. 29) during
the eight recall visits are presented.
The first recall, at 8 months, showed a significant reduction in the size of the lesion
at the apex of tooth 42 (Fig. 2). At 1 year 3 months, the lesion was slightly smaller and
radiopaque (Fig. 3), but a new radiolucent area was seen involving teeth 41, 31, and
the mesial root surface of tooth 32. These three teeth (and 42) tested vital, and the

2014 International Endodontic Journal. Published by John Wiley & Sons Ltd

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CASE REPORT

Figure 1 Periapical radiograph at initial visit. A radiolucent lesion is seen at apex of tooth 42 (osteolytic stage).

Figure 2 Eight-month recall: note significant reduction in lesion size associated with tooth 42.

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CASE REPORT

Figure 3 One year 3-month recall: tooth 42 lesion is less radiolucent but now it is surrounded by
dense bone (cementoblastic stage). Note new radiolucency involving the apices of teeth 41, 31 and
32 (osteolytic stage).

Figure 4 One year 10-month recall: tooth 42 lesion unchanged; lucency involving teeth 41, 31 and
32 replaced with dense bone (mature stage).

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Figure 5 Two years 6-month recall: tooth 42 lesion appears slightly larger and more radiolucent
compared to the previous recall. Note a new radiolucency at the apex of tooth 32.

clinical examination was within normal limits. At 1 year 10 months, the lesion with
tooth 42 remained unchanged and the radiolucent area with teeth 41, 31 and 32 had
completely disappeared with the resultant bone pattern appearing more radiopaque and
with diminished bone trabeculae (Fig. 4). At 2 years 6 months, lesion on tooth 42 was
more radiolucent and a new lesion appeared at the apex of 32 (Fig. 5). At 3 years
9 months, the lesions associated with teeth 32 and 42 became less radiolucent and
more radiopaque as compared to the previous recall (Fig. 6). Also, the bone trabecular
pattern in relation to teeth 31 and 41 was returning to a normal appearance (Fig. 6). At
6 years, lesion on tooth 42 remained unchanged but the lesion on tooth 32 healed completely with an almost normal trabecular pattern of bone (Fig. 7). At 8 years, the lesion
on tooth 42 had been mostly replaced with denser bone but a circular radiolucent area
re-appeared with tooth 32 (Fig. 8). At the 12-year recall, a normal trabecular pattern of
bone could be seen with all teeth except for a small radiolucent area on the distal surface of the root apex of tooth 32 (Fig. 9).

Discussion
The prevalence of PCOD has been reported to be between 0.24% and 5.9% (Stafne
1934, Chaudry et al. 1958, Neville & Albenesius 1986, Vicci & Capelozza 2002, Pereira
et al. 2008). The studies reporting a higher percentage included African American
women whereas those with a Caucasian population had a lower percentage of PCOD.
A high percentage of PCOD does occur in middle-aged, African American women but
there is enough evidence to show that they also occur at a younger age and in other
races as well. The case reported here is of a 26-year-old white female. The characteristic features of PCOD seen in this case were an asymptomatic female, with a welldefined radiolucency at the apex of a tooth with a vital pulp located in the anterior

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Figure 6 Three years 9-month recall: bone appearance of 31 and 41 appears normal. That of 32
and 42 appears to be in the cementoblastic stage.

Figure 7 Six-year recall: tooth 42 lesion unchanged. Note an almost normal pattern of bone trabeculae associated with 32.

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CASE REPORT

Figure 8 Eight-year recall: note somewhat denser bone at the apex of 42 (Mature stage). Tooth 32
lesion has a well-defined circular outline of what may be the cementoblastic stage of PCOD.

Figure 9 Twelve-year recall: bone surrounding all teeth (except 32) appears normal. 32 appears to
have a small radiolucent area on the distal surface of the root apex.

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2014 International Endodontic Journal. Published by John Wiley & Sons Ltd

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CASE REPORT

mandible. Tanaka et al. (1987) reported three cases and reviewed a total of 26 cases of
PCOD in a Japanese population. They concluded that in a Japanese population the predominant region associated with PCOD was the mandibular premolarmolar region and
not the anterior mandible as seen in other ethnic groups.
The aetiopathogenesis of PCOD is unclear and has been a topic of discussion for
many years. The most widely accepted hypothesis for the tissue of origin has been the
periodontal ligament (Kramer et al. 1992, Waldron 1993, Summerlin & Tomich 1994).
The progenitor role of periodontal ligament fibroblasts for adjacent hard-tissue cells has
been proposed (Cho et al. 1988). Robinson theorized that occlusal forces could cause
local tissue injury, initiating replacement of bony trabeculae with fibrous tissue followed
by the formation of immature bone and cementum-like deposits (Robinson 1956). This
theory was challenged by Melrose (1976) who pointed out that uncomplicated PCOD
did not show signs of an inflammatory process as existing lesions failed to heal even
after removing known irritants. He also noted that lesions developed in edentulous
areas, and there was a significant gender and racial predilection. Melrose (1976)
observed that PCOD lesions were always associated with teeth and exclusively confined to the alveolar process superior to the inferior alveolar canal, strongly suggesting
an odontogenic origin. Considering the high prevalence of PCOD in middle-aged
females, Zegarelli et al. (1964) suggested a hormonal imbalance as a likely causative or
contributory factor. Young et al. (1989) and Thakkar et al. (1993) independently reported
cases of autosomal patterns of inheritance of familial PCOD.
It is uncommon to see a case of PCOD with a long-term follow-up that demonstrated
all three of its stages. Manganaro & Millett (1996) reported a case of PCOD showing
the evolution of lesions from purely radiolucent to radiopaque over a 13-year period.
The case presented in this report shows the lesions progressing through all three
stages. The appearance and resolution of lesions involving 4 teeth and the radiographic
appearance of bone returning to an almost normal trabecular pattern at 12 years were
observed.
Based on radiographic and histologic findings, Thoma (1937) described the development of PCOD in three stages; osteolytic, cementoblastic and mature. In the present
report, the initial radiographic presentation (Fig. 1) of a well-defined radiolucency at the
root apex of a mandibular incisor represents the first stage of PCOD (osteolytic). The
8 month and 1 year 3-month recalls (Figs. 2 and 3) show the lesion around tooth 42
becoming less radiolucent and more radiopaque, indicative of the cementoblastic stage
of PCOD. The 1 year 3 month radiograph (Fig. 3) also shows a new radiolucent area in
relation to teeth 41, 31 and 32 representing the osteolytic stage of PCOD. Six months
later (Fig. 4), the radiolucent area around teeth 41, 31 and 32 has been replaced with
dense bone representing the mature stage. The mature stage can also be seen in the
radiograph taken at 8 years in relation to tooth 42 (Fig. 8). The final radiograph (Fig. 9)
taken at 12 years shows an almost normal trabecular pattern of bone except for tooth
32. This appears to be a feature not shown previously in the literature.
It would be interesting to know the histologic features of the tissue after the third
stage of PCOD. In this report, the radiographic appearance of PCOD after the third
stage revealed less radiopacity than the mature stage and a more normal trabecular pattern of bone. If the fibro-vascular and osseous components of the tissue resume their
almost normal proportions after the third stage of PCOD, there might be a reduced risk
of secondary infection. The hallmark of lesion maturation is considered to be the progressive deposition of cementum-like calcifications, which increases the risk of secondary infection and osteomyelitis (Alsufyani & Lam 2011). The degree of vascularization of
the dysplastic tissue, the extent of fibrosis and hyalinization, and the amount of calcific
deposits is determined to a great extent by the stage of PCOD. The greater the

CASE REPORT
10

hard-tissue component, the less the vascularization and the greater the risk of necrosis
and infection (Baden & Saroff 1986).
The concomitant occurrence of osteomyelitis with cemento-osseous dysplasia (COD)
has been reported (Groot et al. 1996, Kawai et al. 1999, Alsufyani & Lam 2011) and is a
risk in PCOD cases. In COD cases, it is recommended to avoid any type of surgical
intervention such as extraction, periodontal surgery and implant placement. Waldron
et al. (1975) reported poor socket healing and sequestrum formation following extraction of teeth associated with COD. As the development and maturation of COD is selflimiting, treatment is usually not performed unless the patient is symptomatic (Goncalves et al. 2005, Ogunsalu & Miles 2005, MacDonald-Jankowski 2008). There is a recent
PCOD case report of a 55-year-old Caucasian woman who presented with moderate
swelling and mobility of teeth 32, 33 and 34. Extraction of these teeth led to persistence of swelling, pain and delayed healing (Roghi et al. 2014).
In this case, the initial diagnosis was straightforward. The involved tooth had a wellcircumscribed apical radiolucent lesion located in the anterior mandible. It was caries
free, tested vital and there was no history of trauma or orthodontic treatment; all being
characteristic features of PCOD. The diagnosis was confirmed by the recall visits.
Arriving at definitive diagnosis requires the correlation of a patients subjective symptoms, history, clinical findings and follow-up radiographic examinations. A definitive diagnosis of FOLs becomes important when one realizes that it represents a diverse group
of processes. FOLs may have similar histologic and radiographic appearances but they
require different treatment approaches (Margo et al. 1985, Pecaro 1986, Musella & Slater 1989, Slootweg & Muller 1990, Waldron 1993). Brannon & Fowler (2001) in their
review of current concepts of benign FOLs, proposed the following Keys to diagnosis
of PCOD. (i) Predilection for middle-aged black females; (ii) one or more (0.5 cm or less)
circumscribed lesions in periapical areas of vital teeth; (iii) painless, nonexpansile, usual
location in anterior mandible; (iv) radiographic features can be radiolucent, mixed density, or opaque with radiolucent rim; and (v) cellular fibrous stroma with woven and/or
oval calcifications.
As determining pulp vitality plays a significant role in arriving at a diagnosis of PCOD,
Doppler flowmetry to evaluate blood flow in suspected teeth has been recommended
(Chandler et al. 1999). Taki et al. (1995) reported the use of scintigraphy to aid in the
diagnosis of PCOD. They reported a case of multiple PCOD which showed intense
accumulation on both Tc-99 m MDP and Ga-67 scinitgraphy. Smeele et al. (1991) in
their report of an unusual behaviour of PCOD showed that Technetium bone scan
revealed a hot spot in the maxilla and an increased uptake in the mandible.
More recently, the use of limited-field cone beam computed tomography (CBCT) has
increased in the endodontic community. CBCT provides valuable information regarding
the location of PCOD lesions relative to the buccal and lingual cortical plates, relationship of the lesion to the involved root apices, expansion and/or thinning of the cortical
plates and the status of the periodontal ligament and lamina dura. The use of CBCT to
aid in the definitive diagnosis of PCOD is recommended. Eskandarloo & Yousefi (2013)
reported on the CBCT findings of PCOD. They proposed that with the use of CBCT, differentiation of PCOD from other benign FOLs with similar calcifications on conventional
radiography would be more accurate. Several cases of misdiagnosis of COD have been
reported. The importance of a correct diagnosis to avoid incorrect treatment cannot be
overemphasized (Wilcox & Walton 1989, Koehler 1994, Smith et al. 1998, Galgano
et al. 2003, Islam et al. 2008, Resnick & Novelline 2008).
The differential diagnosis of PCOD varies with the stage of the lesion. In the early
osteolytic stage, PCOD must be differentiated from apical periodontitis. The majority of
misdiagnosed cases reported in the literature occur in this stage of PCOD (Wilcox &

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Walton 1989, Koehler 1994, Smith et al. 1998, Galgano et al. 2003, Islam et al. 2008,
Resnick & Novelline 2008). The best tools to differentiate PCOD from a periapical pathosis originating from a tooth are pulp vitality tests. However, these important tests are
unavailable if the tooth has been endodontically treated. The clinician then has to rely
on patient history, signs and symptoms etc.
In the cementoblastic and mature stages, the differential diagnosis might include cemento-ossifying fibroma (Su et al. 1997), Pagets disease of bone (Su et al. 1997),
chronic sclerosing osteomyelitis (Alawi 2002) and cementoma (Konopka et al. 2012).
Cemento-ossifying fibromas (COF) do not show a female predilection, they occur in a
younger population and lesions are larger in size with more than half of the patients
exhibiting jaw expansion. The majority of cases do not show any relationship with teeth
apices or with previous extraction sites. Pagets disease of bone is more commonly
seen in males, has a higher occurrence in whites than blacks, affects maxilla more
commonly than mandible, is bilateral and patients have high serum levels of alkaline
phosphate and elevated urinary hydroxyproline levels. Chronic sclerosing osteomyelitis
is primarily an inflammatory disorder with cyclic episodes of pain and swelling and is
usually not restricted to tooth-bearing areas. Cementoma is usually seen in younger
female patients presenting as a well-defined radiopacity with a radiolucent rim associated with a tooth root showing signs of resorption.
In a low percentage of cases (8.5%), PCOD has been associated with simple bone
cysts (SBCs) (Alsufyani & Lam 2011). Melrose et al. (1976) first recognized an association between COD and SBCs in their study of 34 cases. They described the presence
of 17 SBCs in 14 of the 34 patients with florid COD. The relationship between COD
and SBCs is not well understood. The incidence of SBCs occurring in patients with
florid COD was found to be high, but not statistically significant. Rushton (1946) defined
SBCs as a vacant or fluid containing cystic lesions surrounded by a hard bony wall with
no epithelial lining and no evidence of infection. SBCs usually occur in the marrow
spaces, are solitary, not confined to tooth-bearing areas and about half of the cases are
associated with a traumatic event (Rubin & Murphy 1989, Shigematsu et al. 1994).
Mahomed et al. (2005) presented a series of 7 cases and analysed 9 additional cases
of COD associated with SBCs from the literature. All 16 cases occurred in the mandible, the mean age was 40 years, 15 of 16 cases were females and the SBCs occurred
mainly in the mandibular premolarmolar regions.
Visnapuu et al. (2007) presented a novel finding of an association between PCOD
and neurofibromatosis type 1 (NF1). In their study of 55 patients (29 females and 26
males) with NF1, 8 females had PCOD but none of the males had it. The 8 females
were between 20 and 60 years of age, and the PCODs were located in the mandible.
The occurrence of PCOD in female NF1 patients had not been previously reported.
Osseous dysplasias are common in NF1 patients. The oral manifestations include
impacted, displaced, supernumerary or missing teeth and overgrowth of the alveolar
ridge.
An accurate diagnosis of PCOD is essential to render appropriate treatment, which in
most cases is no treatment. To arrive at an accurate diagnosis of PCOD, the clinician
needs to have an open mind. He/she has to consider the possibility that a periapical
lesion may be of nonodontogenic origin. The clinician also needs to be skilful in extracting the relevant dental history from the patient, be proactive in utilizing diagnostic tools
including but not limited to cold, electric and heat pulp tests, and limited-field CBCT. In
the end, the thoughtful assimilation of all the pieces of the puzzle leads to an accurate
diagnosis. An astute clinician will be provoked to perform further evaluations if a piece
(s) of the puzzle does not fit.

11

CASE REPORT

This case emphasizes the importance of patient history, quality radiographs and accurate pulp testing for arriving at a correct diagnosis and the important role of follow-up
examinations to confirm the diagnosis. If the initial presenting lesion had been misdiagnosed and root canal treatment performed, needless retreatment, apical surgery or
even extraction may have followed as the endodontic lesion may not have healed as
expected. The varied radiographic appearances (stages) of PCOD depend on timing
as clearly demonstrated in this case. If the first radiographs had been taken 12 years
later the presence and long-term behaviour of PCOD would have remained unknown to
both patient and dentist.

Conclusion
Based on this case reports unique finding of an almost normal radiographic appearance
of the bone architecture after viewing the various stages of PCOD for 12 years, longterm evaluation of PCOD lesions is recommended. It would also be beneficial to study
the histology of these PCOD lesions after the resolution of the dense radiopaque areas
of bone. Reports on this aspect of PCOD would be a valuable addition to the clinicians
knowledgebase of COD lesions. It is important for the clinician to correctly identify and
differentiate COD lesions.

Disclaimer
Whilst this article has been subjected to Editorial review, the opinions expressed,
unless specifically indicated, are those of the author. The views expressed do not necessarily represent best practice, or the views of the IEJ Editorial Board, or of its affiliated Specialist Societies.

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