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J Oral Maxillofac Surg60:756-761, 2002

The Surgical Treatment of Central Giant

Cell Granuloma of the Mandible

Anwar B. Bataineh, BDS, MScD, CSOS, MDSc,*

Taiseer Al-Khateeb, BDS, MScD, FDSRCS(Ed), FFDRCS(Ir),

and Maamon A. Rawashdeh, BDS, MScD, FDSRCS(En)

Purpose: The objective of this study was to report and evaluate our experience in the surgicaltreatment of mandibular central giant cell granuloma by resection without continuity defect and

peripheral ostectomy.

Methods: A retrospective analysis was conducted of patients with central giant cell granuloma of themandible who were treated between 1991 and 2000, in the Oral and Maxillofacial Surgery Unit at JordanUniversity of Science and Technology. A uniform surgical technique was used in all cases. The compactbone composed of the lower border of the mandible and/or posterior border of the ascending ramus,

together with the nutrient periosteum attached to it, was preserved. All soft tissues in contact with oroverlying the lesion and a margin of cancellous bone related to the lesion were excised. All patients were

reviewed annually for a follow-up period of 1 to 9 years (mean, 3.9 years).

Results: Eighteen patients with central giant cell granuloma were included, (9 males and 9 females).Their age ranged from 10 to 46 years, with 89% younger than 40 years. Five (28%) lesions were in theincisor-canine region, 2 (11%) were confined to the premolar region, 4 (22%) were in the premolar-molar

region, and 7 (39%) were in the molar-ramus region. All patients had aggressive central giant cellgranulomas with pain, tooth mobility, and rapidly enlarging swelling. The initial diameter of lesionsranged from 2.7 to 10 cm. During the follow-up period, there was 1 case of recurrence, 2 (11%) patients

had permanent lower lip paraesthesia, and no patient had obvious facial deformity.

Conclusion: Our results suggest that resection without a continuity defect and peripheral osteoctomyis a satisfactory method in the treatment of central giant cell granuloma of the mandible, with no or a verylow recurrence rate and favorable postoperative function. 2002 American Association of Oral and Maxillofacial Surgeons

J Oral Maxillofac Surg 60:756-761, 2002

The central giant cell granuloma (CGCG) of the jaws

is a common benign lesion accounting for approxi-

mately 7% of all benign tumors of the jaws.1 The

histologic features of CGCG have been extensively

discussed,2-6 and it is defined by the World Health

Organization as an intraosseous lesion consisting of

cellular fibrous tissue that contains multiple foci of

hemorrhage, aggregations of multinucleated giant

cells, and, occasionally, trabeculae of woven bone.7

The clinical behavior of CGCG ranges from a slowly

growing asymptomatic swelling to an aggressive lesion

that manifests with pain, local destruction of bone, rootresorption, or displacement of teeth. Aggressive sub-

types of CGCG have a tendency to recur after exci-sion.5,8 CGCG usually occurs in patients younger than

30 years, is more common in females than in males, and

is more common in the mandible than in the maxilla.9,10

The lesion has frequently been reported to be confinedto the tooth-bearing areas of the jaws2,11 and is morecommon in the anterior portion of the mandible, often

crossing the midline.2,10

The radiologic features of the CGCG have not beenclearly defined, and conflicting descriptions appear in

various textbooks and articles.9,10,12-15 The lesion mayappear as a unilocular or multilocular radiolucency,

with well-defined or ill-defined margins and varying

degrees of expansion of the cortical plates. It is im-portant to remember that the radiologic appearance

Received from the Department of Oral and Maxillofacial Surgery,

Faculty of Dentistry, Jordan University of Science and Technology,Irbid, Jordan.

*Associate Professor.

Assistant Professor.

Assistant Professor.

Address correspondence and reprint requests to Dr Bataineh:

Jordan University of Science and Technology, Faculty of Dentistry,

PO Box 3030, Irbid, Jordan; e-mail: anwar@just.edu.jo

2002 American Association of Oral and Maxillofacial Surgeons

0278-2391/02/6007-0006$35.00/0

doi:10.1053/joms.2002.33241

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of the lesion is not pathognomonic and may be con-

fused with that of many other lesions of the jaws.16,17

The traditional treatment of CGCG is surgical re-

moval. However, the extent of tissue removal rangesfrom simple curettage to en bloc resection. Curettage

has also been supplemented with cryosurgery18 andperipheral ostectomy.19 CGCG has also been treated

by nonsurgical methods such as radiotherapy,19 dailysystemic doses of calcitonin,20,21 and intralesional in- jection with corticosteroids.22

The purpose of this study was to report and evalu-ate our experience in the surgical treatment of man-

dibular CGCG by resection without continuity defectand peripheral ostectomy.

Patients and Methods

Data for this retrospective study were collectedfrom records of all patients with CGCG of the mandi-

ble who had been treated in the Oral and MaxillofacialSurgery Unit of the Faculty of Dentistry of JordanUniversity of Science and Technology between 1991

and 2000. Data were analyzed with reference to age,gender, size of lesion, anatomic location, and fol-

low-up period. In every case included, the clinicaldiagnosis of CGCG was confirmed on incisional bi-opsy before definitive surgery. The levels of serum

calcium, phosphorus, and alkaline phosphatase weremeasured in all cases to exclude hyperparathyroid-

ism, and only those cases that had normal levels wereincluded in this study. Eighteen cases were included

and followed up annually, by clinical and radio-graphic examination, for a period ranging from 1 to 9years (mean, 3.9 years). In an attempt to eliminate the

lesion while minimizing deformity, loss of function,and the need for complex reconstructive surgery, we

advocated a treatment method designed to adequatelyremove the CGCG while preserving the continuity of

the mandible.

THE SURGICAL TECHNIQUE

The standard treatment for preoperatively diag-nosed CGCG was resection without a continuity de-fect and peripheral ostectomy, via an intraoral ap-

proach under general anesthesia. Considerable bloodloss may occur during surgery and blood should be

available; arrangement for autotransfusion is advanta-geous.

Because all soft tissues involved in the lesion mustbe removed, it is imperative that soft tissue incisionsare made through them down to bone. To facilitate

this, a sharp probe is used to determine and mark outthe extent of the bony defect. Incisions are subse-

quently made at least 1 cm away from the margins ofthe bony defect.

After reflection of the soft tissue, a reciprocating

saw or fissure bur is used to cut the cortical bonearound the lesion approximately 0.5 cm from its mar-

gin. The lesion is reflected in toto with the associatedtissues and is removed en bloc.

The bony cavity is then saucerized by reducing theheight of its osseous walls, to facilitate visual and

mechanical access. Peripheral ostectomy is subse-quently performed by trimming the cancellous boneat each end of the bony defect, using coarse surgical

or acrylic burs, to a depth of at least 1 cm or until theinner surface of compact bone is macroscopically free

of the lesion. The condensed bone surrounding theinferior alveolar canal appears to afford some protec-

tion to the neurovascular bundle. After thorough de-bridement, the cavity is packed with ribbon gauzesoaked in either Whiteheads varnish or iodoform

paste that is retained in situ with loose sutures for 5 to8 days after surgery, to protect the wound from food

and other debris and allow healing by secondary in-tention. The patient is instructed to use frequent hot

saline rinses starting the day after surgery to keep thewound free of food debris. If there is a risk of fractureof either the thin lower border of the mandible or the

posterior border of the ascending ramus, eyelit wiresare placed bilaterally and maxillomandibular fixation

is used for 2 weeks after surgery. All treated patientsare regularly reviewed until healing is complete, and

then they are reviewed both radiographically andclinically on an annual basis.

Results

During the study period from 1991 to 2000, eigh-teen patients with CGCG of the mandible were

treated. Nine (50%) were males and nine (50%) werefemales. The age of patients ranged from 10 to 46years (mean, 23.4 years); the age and gender distribu-

tion is shown in Table 1. Sixteen patients (89%) wereyounger than 40 years; of these, 7 (39%) were in the

second decade, 6 (33%) were in the third decade, and3 (17%) were in the fourth decade of life. The side,

anatomic location, distribution, and postoperative fol-

Table 1. THE AGE AND GENDER DISTRIBUTION OF18 PATIENTS WITH CENTRAL GIANT CELLGRANULOMA OF THE MANDIBLE

Age Range(yr)

No. of Cases

Males Females Total

10-19 4 3 7 (39%)20-29 2 4 6 (33%)30-39 2 1 3 (17%)40-50 1 1 2 (11%)Total 9 9 18 (100%)

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low-up period of the 18 CGCGs is shown in Table 2.

Five (28%) were in the incisor/canine region (Figs 1A,

B), of which 3 (17%) were crossing the midline; 2

(11%) were confined to the premolar region, 4 (22%)

were in the premolar-molar region, and 7 (39%) were

in the molar/ramus region (Figs 2A, B). The diameter

of the lesions, as measured on the initial orthopanto-

mograms, ranged from 2.7 to 10 cm (Fig 3).All patients presented with pain, mobility of teeth,

and rapidly enlarging facial swelling. These features

alerted the clinician to the possibility of a malignant

tumor; cases were subsequently diagnosed as CGCG

on incisional biopsies. All cases were radiologically

investigated using orthopantamugrams. Lesions were

defined as multilocular or unilocular radiolucent ar-eas; their borders were generally well defined in 7

cases and poorly defined in 9 cases. The inferior

and/or posterior mandibular borders appeared intact

in every case.

All cases were treated by resection without conti-

nuity defect and peripheral ostectomy (Fig 1C), leav-

ing the lower and/or the posterior border of the

mandible intact. In 16 cases (89%), the inferior alve-

olar nerve was identified and appeared to be intact

but merely displaced by the lesion. In 2 cases (11%),

the inferior alveolar nerve was difficult to identify. Six

patients complained of lower lip paresthesia, which

resolved after 2 to 5 months in 4 patients, and nolingual paresthesia was detected. The healing was

uneventful (Fig 2C), and no other complications were

encountered.

Patients with preoperative infection in the area ofthe lesion were given antibiotics before, during, and

after surgery. During the follow-up period of 1 to 9years (mean, 3.9 years) (Table 2), evidence of local

recurrence was found in 1 case (6%) at 3 months afterinitial resection. Surgery was repeated with wider

excision and peripheral ostectomy, and no furtherrecurrence has so far been detected.

Discussion

The CGCG may occur at any age, but it is mostcommonly seen in the first 3 decades.23 In this study,

FIGURE 1. A, Preoperative orthopantomograph showing a well-defined radiolucent lesion central giant cell granuloma of mandiblefrom right second premolar to left first premolar with displacement ofteeth. B, The lesion viewed from the lateral aspect depicting its rela-tionship to adjacent teeth. Note the extreme expansion of the mandibleand its overlying tissue. C, Postoperative orthopantomograph showsthe resection 3 months after surgery.

Table 2. THE SIDE, ANATOMIC LOCATIONDISTRIBUTION, AND POSTOPERATIVE FOLLOW-UPPERIOD OF 18 CASES OF MANDIBULAR CENTRALGIANT CELL GRANULOMA

No. Side RegionFollow-up Period

(yr)

1 L Molar 92 R Premolar-molar 93 L Molar 74 R Incisor-canine 75 L Premolar-molar 66 R Incisor-canine 47 R Molar-ramus 28 R Molar-ramus 29 R Incisor-canine 3

10 R Incisor-canine 311 R Molar 312 L Canine-premolar 313 L Canine-premolar 314 R Molar-ramus 215 R Molar-ramus 216 R Premolar 217 R Premolar 218 R Incisor-canine 1

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it was found that 89% of cases occurred in patients

younger than 40 years, with no cases observed in the

first decade. This finding is in accordance with the age

distribution reported by other investigators.1,10,19,24 In

previously published series, significant female prepon-

derance was observed,2,24,25 but another reported only a

slight female predominance.23 We found a female-to-

male ratio of 1:1. One explanation for this ratio might be

the inclusion in this series of only cases of mandibular

CGCG.

The anterior part of the mandible has been identi-

fied as the most common location for CGCGs, with

some crossing the midline.10,24,26 CGCGs have been

thought to arise in regions of the jaw originally hous-

ing deciduous teeth.2 One study showed that 37.5% of

CGCGs were located in the incisor, canine, and pre-

molar regions.23 We found that 39% of our patients

CGCGs were located in the incisor, canine, and pre-molar regions. It is worth noting that more than 50%

of our cases involved the premolar-molar-ramus re-

gion. This has been previously reported19,23 and dis-

putes the predilection of CGCGs to the deciduous

tooth-bearing area.

CGCG of the jaw is usually unifocal. Multifocal

lesions should alert the clinician to the possibility of

hyperparathyroidism or, if bilateral, cherubism.19

CGCG should also be distinguished from giant cell

tumor of long bones. The latter is locally aggressive

with a high recurrence rate and a potential for malig-

nant transformation.27

Auclair et al28

showed thatcompared with CGCG, giant cell tumor shows more

evenly distributed giant cells, with a more marked

inflammatory cell infiltrate, and prominent regions of

tissue necrosis. Some CGCGs of the jaws, despite an

innocent histologic appearance, show an aggressive

behavior and a tendency to recur. Ficarra et al8 con-

sidered that these lesions should be defined as ag-

gressive giant cell granulomas of the jaws, rather

than giant cell tumor. Aggressive CGCG has a ten-

dency to recur if inadequately removed, and high

recurrence rates have been reported.5,25 It has been

shown that recurrence usually happens when the

FIGURE 2. A, Preoperative orthopantomograph showing a radiolu-cent lesion central giant cell granuloma of right ascending ramus andbody of the mandible with impacted and displaced second and thirdmolars. B, Intraoral view of the lesion is depicting its relationship toadjacent teeth. Note the expansion of the mandible and its overlyingtissue. C, Postoperative orthopantomograph showing extensive bonerepair and remodeling 1 year after surgery.

FIGURE 3. Size diameter (in centimeters) of 18 central giant cellgranulomas of the mandible as measured in the initial orthopantomo-grams. Open bars denote the diameter of lesions crossing the midline.

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lesion perforates the cortical plates to involve the

surrounding soft tissue.26

CGCGs have traditionally been treated surgically.22

The common therapy is curettage or resection. Be-celli et al29 described a case of excision of the lesion,

reconstruction of the mandible via an autologous iliaccrest bone graft, osseointegrated implants, and an

overdenture prosthesis. Webb and Brockbank18 pre-sented the treatment of an aggressive CGCG of themandible by combined curettage and cryosurgery and

a 5-year follow-up period without recurrence. Eisen-bud et al19 advocated the technique of curettage or

curettage plus peripheral ostectomy for the treatmentof CGCG. Their results showed no evidence of disease

in 21 of 23 cases followed up for 2 or more years.All of our patients were treated by resection with-

out continuity defect and peripheral ostectomy. This

relatively aggressive surgical modality is justified bythe aggressiveness of the lesions, because all patients

presented with alarming symptoms of pain, displace-ment of teeth, and rapidly increasing facial swelling.

Chuong et al5 suggested that aggressive tumors thatpresent with pain, rapid growth, facial swelling, orcortical perforation be treated with en bloc resection.

It should also be noted that the diameter of the lesionsin our study at the time of initial presentation ranged

from 2.7 to 10 cm. These were large lesions thatrequired hospitalization and endotracheal general an-

esthesia for surgical removal. The large size is also anindication of the aggressiveness of the lesions.

In an attempt to distinguish aggressive and nonag-

gressive subtypes of CGCG and to predict the prog-

nosis of newly diagnosed CGCGs, numerous studieshave been conducted using cytometric and immuno-cytochemical methods. It has been shown that aggres-

sive/recurring subtypes have a higher number andrelative size index of giant cells and a greater frac-tional surface area occupied by giant cells.5,8 Further-

more, aggressive subtypes have been shown to ex-press a greater count of nucleolar organization

regions.10 These cytometric and immunocytochemi-cal methods are not always available, especially in

developing countries, and this invites the surgeon touse a relatively aggressive surgical technique.

Surgical treatment of CGCGs can be associated

with recurrence and serious facial mutilation and lossof teeth and tooth germs are also unavoidable. To

avoid such disadvantages, an alternative treatment forthe CGCG has recently been introduced, in which

patients receive a daily dose of calcitonin. This treat-ment method also avoids the need for radiotherapy ingrowing children.20 CGCGs have been treated with

calcitonin in various concentrations for at least 1 year;complete remission of CGCG has been observed with-

out signs of recurrence.21,30 However, calcitonin ther-apy is complicated owing to the great amount of

discomfort and the relatively long duration of treat-

ment, which is more intolerable by some patients,especially children.21

CGCG has also been treated by weekly intralesionalinjection with corticosteroids; successful results have

been reported.22,31 Corticosteroid therapy is, how-ever, relatively contraindicated in certain medical

conditions, such as diabetes mellitus, peptic ulcer,and generalized immunocompromised states.31 Non-surgical treatment of CGCG is probably a good treat-

ment option for small slowly enlarging lesions. Success-ful treatment of painful, large, and rapidly growing

lesions is more likely achieved by surgical removal.Although CGCG is expansive in its growth, it does

not grow around or invade nerve trunks. It also doesnot invade perineural sheaths or spread via perineuralspaces.19 In this study, the inferior alveolar nerve was

identified and appeared in 16 cases (89%) to bemerely displaced by the lesion but free of pathologic

tissue. Therefore, it was possible to isolate and/orreposition the inferior alveolar bundle, preserving the

sensation in the lower lip and chin and avoidingsequelae such as distressing paresthesia or painfuldysesthesia.

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