Periapical cemento-osseous dysplasia: a case report with twelve

CASE REPORT

Periapical cemento-osseous dysplasia:a case report with twelve-yearfollow-up and review of literature

E. S. Senia1 & M. S. Sarao2

1Department 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 cemen-

to-osseous dysplasia by observing the radiographic changes that took place over a per-

iod 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 subse-

quently 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 nor-

mal 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 loca-

tions 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 End-

odontics, 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: [email protected]).

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

doi:10.1111/iej.12417

1

Keywords: benign fibro-osseous lesions, cementoma, periapical cemental dyspla-

sia, 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 classifica-

tion and nomenclature of FOLs. Many authors attempted to classify FOLs but Wal-

dron’s classification has been widely accepted and referenced. Waldron classified FOLs

into three groups: (i) fibrous dysplasia, (ii) reactive (dysplastic) lesions and (iii) fibro-osse-

ous neoplasms (Waldron 1993).

Periapical cemento-osseous dysplasia (PCOD) has been described as a reactive or dys-

plastic 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 dyspla-

sia (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 13–73 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

radiolucent–radiopaque 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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© 2014 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal2

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 radiolu-

cent–radiopaque or radiopaque lesion associated with one or more vital and asymptom-

atic 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 ori-

gin. Histologically, the tissue consists primarily of cellular connective tissue replacing

normal trabecular bone with calcified structures of insufficient size to be evident radio-

graphically. (ii) Cementoblastic stage follows the initial lytic phase and is characterized

by the presence of radiolucent areas containing nodular radiopaque deposits. Histologi-

cally, 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 character-

ized 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 full-

mouth 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 2–3 mm pocket depths. Palpation and percussion gave no evi-

dence of swelling, bony expansion or pain. Tooth 42 responded to cold, heat and elec-

tric 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 examina-

tion were within normal limits. The results of the radiographic findings (Figs. 2–9) 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

CASE

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© 2014 International Endodontic Journal. Published by John Wiley & Sons Ltd International Endodontic Journal 3

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

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

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Figure 3 One year 3-month recall: tooth 42 lesion is less radiolucent but now it is surrounded bydense bone (cementoblastic stage). Note new radiolucency involving the apices of teeth 41, 31 and32 (osteolytic stage).

Figure 4 One year 10-month recall: tooth 42 lesion unchanged; lucency involving teeth 41, 31 and32 replaced with dense bone (mature stage).

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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 com-

pletely 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 sur-

face 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 characteris-

tic features of PCOD seen in this case were an asymptomatic female, with a well-

defined radiolucency at the apex of a tooth with a vital pulp located in the anterior

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

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

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

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Figure 8 Eight-year recall: note somewhat denser bone at the apex of 42 (Mature stage). Tooth 32lesion 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 tohave a small radiolucent area on the distal surface of the root apex.

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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 pre-

dominant region associated with PCOD was the mandibular premolar–molar 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 con-

fined 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 develop-

ment 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 pat-

tern 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 pro-

gressive deposition of cementum-like calcifications, which increases the risk of second-

ary 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

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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 extrac-

tion of teeth associated with COD. As the development and maturation of COD is self-

limiting, treatment is usually not performed unless the patient is symptomatic (Goncal-

ves 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 persis-

tence of swelling, pain and delayed healing (Roghi et al. 2014).

In this case, the initial diagnosis was straightforward. The involved tooth had a well-

circumscribed 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 patient’s subjective symp-

toms, history, clinical findings and follow-up radiographic examinations. A definitive diag-

nosis 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 & Sla-

ter 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 den-

sity, 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, relation-

ship 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, dif-

ferentiation 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 path-

osis 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 ce-

mento-ossifying fibroma (Su et al. 1997), Paget’s 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. Paget’s 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 associ-

ated 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 associa-

tion 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 mandi-

ble, the mean age was 40 years, 15 of 16 cases were females and the SBCs occurred

mainly in the mandibular premolar–molar 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 extract-

ing 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.

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This case emphasizes the importance of patient history, quality radiographs and accu-

rate 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 misdiag-

nosed 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 report’s unique finding of an almost normal radiographic appearance

of the bone architecture after viewing the various stages of PCOD for 12 years, long-

term 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 clinician’s

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 nec-

essarily represent best practice, or the views of the IEJ Editorial Board, or of its affili-

ated Specialist Societies.

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Periapical cemento-osseous dysplasia: a case report with twelve