J Oral Maxillofac Surg 60:756-761, 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)
The objective of this study was to report and evaluate our experience in the surgical treatment 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 the mandible who were treated between 1991 and 2000, in the Oral and Maxillofacial Surgery Unit at Jordan University of Science and Technology. A uniform surgical technique was used in all cases. The compact bone 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 or overlying 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 the incisor-canine region, 2 (11%) were conned 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 cell granulomas with pain, tooth mobility, and rapidly enlarging swelling. The initial diameter of lesions ranged 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 osteoctomy is a satisfactory method in the treatment of central giant cell granuloma of the mandible, with no or a very low 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 approximately 7% of all benign tumors of the jaws.1 The histologic features of CGCG have been extensively discussed,2-6 and it is dened by the World Health Organization as an intraosseous lesion consisting of cellular brous 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, root resorption, or displacement of teeth. Aggressive subtypes of CGCG have a tendency to recur after excision.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 conned to the tooth-bearing areas of the jaws2,11 and is more common in the anterior portion of the mandible, often crossing the midline.2,10 The radiologic features of the CGCG have not been clearly dened, and conicting descriptions appear in various textbooks and articles.9,10,12-15 The lesion may appear as a unilocular or multilocular radiolucency, with well-dened or ill-dened margins and varying degrees of expansion of the cortical plates. It is important to remember that the radiologic appearance 756
Purpose:

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

BATAINEH, AL-KHATEEB, AND RAWASHDEH

757 After reection of the soft tissue, a reciprocating saw or ssure bur is used to cut the cortical bone around the lesion approximately 0.5 cm from its margin. The lesion is reected in toto with the associated tissues and is removed en bloc. The bony cavity is then saucerized by reducing the height of its osseous walls, to facilitate visual and mechanical access. Peripheral ostectomy is subsequently performed by trimming the cancellous bone at each end of the bony defect, using coarse surgical or acrylic burs, to a depth of at least 1 cm or until the inner surface of compact bone is macroscopically free of the lesion. The condensed bone surrounding the inferior alveolar canal appears to afford some protection to the neurovascular bundle. After thorough debridement, the cavity is packed with ribbon gauze soaked in either Whiteheads varnish or iodoform paste that is retained in situ with loose sutures for 5 to 8 days after surgery, to protect the wound from food and other debris and allow healing by secondary intention. The patient is instructed to use frequent hot saline rinses starting the day after surgery to keep the wound free of food debris. If there is a risk of fracture of either the thin lower border of the mandible or the posterior border of the ascending ramus, eyelit wires are placed bilaterally and maxillomandibular xation is used for 2 weeks after surgery. All treated patients are regularly reviewed until healing is complete, and then they are reviewed both radiographically and clinically on an annual basis.

of the lesion is not pathognomonic and may be confused with that of many other lesions of the jaws.16,17 The traditional treatment of CGCG is surgical removal. However, the extent of tissue removal ranges from simple curettage to en bloc resection. Curettage has also been supplemented with cryosurgery18 and peripheral ostectomy.19 CGCG has also been treated by nonsurgical methods such as radiotherapy,19 daily systemic doses of calcitonin,20,21 and intralesional injection with corticosteroids.22 The purpose of this study was to report and evaluate our experience in the surgical treatment of mandibular CGCG by resection without continuity defect and peripheral ostectomy.

Patients and Methods

Data for this retrospective study were collected from records of all patients with CGCG of the mandible who had been treated in the Oral and Maxillofacial Surgery Unit of the Faculty of Dentistry of Jordan University of Science and Technology between 1991 and 2000. Data were analyzed with reference to age, gender, size of lesion, anatomic location, and follow-up period. In every case included, the clinical diagnosis of CGCG was conrmed on incisional biopsy before denitive surgery. The levels of serum calcium, phosphorus, and alkaline phosphatase were measured in all cases to exclude hyperparathyroidism, and only those cases that had normal levels were included in this study. Eighteen cases were included and followed up annually, by clinical and radiographic examination, for a period ranging from 1 to 9 years (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 adequately remove the CGCG while preserving the continuity of the mandible.
THE SURGICAL TECHNIQUE

Results
During the study period from 1991 to 2000, eighteen patients with CGCG of the mandible were treated. Nine (50%) were males and nine (50%) were females. The age of patients ranged from 10 to 46 years (mean, 23.4 years); the age and gender distribution is shown in Table 1. Sixteen patients (89%) were younger than 40 years; of these, 7 (39%) were in the second decade, 6 (33%) were in the third decade, and 3 (17%) were in the fourth decade of life. The side, anatomic location, distribution, and postoperative fol-

The standard treatment for preoperatively diagnosed CGCG was resection without a continuity defect and peripheral ostectomy, via an intraoral approach under general anesthesia. Considerable blood loss may occur during surgery and blood should be available; arrangement for autotransfusion is advantageous. Because all soft tissues involved in the lesion must be removed, it is imperative that soft tissue incisions are made through them down to bone. To facilitate this, a sharp probe is used to determine and mark out the extent of the bony defect. Incisions are subsequently made at least 1 cm away from the margins of the bony defect.

Table 1. THE AGE AND GENDER DISTRIBUTION OF 18 PATIENTS WITH CENTRAL GIANT CELL GRANULOMA OF THE MANDIBLE

Age Range (yr) 10-19 20-29 30-39 40-50 Total

No. of Cases
Males Females Total

4 2 2 1 9

3 4 1 1 9

7 (39%) 6 (33%) 3 (17%) 2 (11%) 18 (100%)

758 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 conned 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 orthopantomograms, 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 dened as multilocular or unilocular radiolucent areas; their borders were generally well dened in 7 cases and poorly dened in 9 cases. The inferior and/or posterior mandibular borders appeared intact in every case. All cases were treated by resection without continuity defect and peripheral ostectomy (Fig 1C), leaving the lower and/or the posterior border of the mandible intact. In 16 cases (89%), the inferior alveolar nerve was identied and appeared to be intact but merely displaced by the lesion. In 2 cases (11%), the inferior alveolar nerve was difcult to identify. Six patients complained of lower lip paresthesia, which resolved after 2 to 5 months in 4 patients, and no lingual paresthesia was detected. The healing was uneventful (Fig 2C), and no other complications were encountered.

CENTRAL GIANT CELL GRANULOMA

Table 2. THE SIDE, ANATOMIC LOCATION DISTRIBUTION, AND POSTOPERATIVE FOLLOW-UP PERIOD OF 18 CASES OF MANDIBULAR CENTRAL GIANT CELL GRANULOMA

No. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

Side L R L R L R R R R R R L L R R R R R

Region Molar Premolar-molar Molar Incisor-canine Premolar-molar Incisor-canine Molar-ramus Molar-ramus Incisor-canine Incisor-canine Molar Canine-premolar Canine-premolar Molar-ramus Molar-ramus Premolar Premolar Incisor-canine

Follow-up Period (yr) 9 9 7 7 6 4 2 2 3 3 3 3 3 2 2 2 2 1

FIGURE 1. A, Preoperative orthopantomograph showing a welldened radiolucent lesion central giant cell granuloma of mandible from right second premolar to left rst premolar with displacement of teeth. B, The lesion viewed from the lateral aspect depicting its relationship to adjacent teeth. Note the extreme expansion of the mandible and its overlying tissue. C, Postoperative orthopantomograph shows the resection 3 months after surgery.

Patients with preoperative infection in the area of the lesion were given antibiotics before, during, and after surgery. During the follow-up period of 1 to 9 years (mean, 3.9 years) (Table 2), evidence of local recurrence was found in 1 case (6%) at 3 months after initial resection. Surgery was repeated with wider excision and peripheral ostectomy, and no further recurrence has so far been detected.

Discussion
The CGCG may occur at any age, but it is most commonly seen in the rst 3 decades.23 In this study,

BATAINEH, AL-KHATEEB, AND RAWASHDEH

759 The anterior part of the mandible has been identied 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 housing deciduous teeth.2 One study showed that 37.5% of CGCGs were located in the incisor, canine, and premolar regions.23 We found that 39% of our patients CGCGs were located in the incisor, canine, and premolar regions. It is worth noting that more than 50% of our cases involved the premolar-molar-ramus region. This has been previously reported19,23 and disputes 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 malignant transformation.27 Auclair et al28 showed that compared with CGCG, giant cell tumor shows more evenly distributed giant cells, with a more marked inammatory cell inltrate, 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 considered that these lesions should be dened as aggressive giant cell granulomas of the jaws, rather than giant cell tumor. Aggressive CGCG has a tendency 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 radiolucent lesion central giant cell granuloma of right ascending ramus and body of the mandible with impacted and displaced second and third molars. B, Intraoral view of the lesion is depicting its relationship to adjacent teeth. Note the expansion of the mandible and its overlying tissue. C, Postoperative orthopantomograph showing extensive bone repair and remodeling 1 year after surgery.

it was found that 89% of cases occurred in patients younger than 40 years, with no cases observed in the rst decade. This nding is in accordance with the age distribution reported by other investigators.1,10,19,24 In previously published series, signicant female preponderance was observed,2,24,25 but another reported only a slight female predominance.23 We found a female-tomale ratio of 1:1. One explanation for this ratio might be the inclusion in this series of only cases of mandibular CGCG.

FIGURE 3. Size diameter (in centimeters) of 18 central giant cell granulomas of the mandible as measured in the initial orthopantomograms. Open bars denote the diameter of lesions crossing the midline.

760 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. Becelli et al29 described a case of excision of the lesion, reconstruction of the mandible via an autologous iliac crest bone graft, osseointegrated implants, and an overdenture prosthesis. Webb and Brockbank18 presented the treatment of an aggressive CGCG of the mandible by combined curettage and cryosurgery and a 5-year follow-up period without recurrence. Eisenbud et al19 advocated the technique of curettage or curettage plus peripheral ostectomy for the treatment of 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 without continuity defect and peripheral ostectomy. This relatively aggressive surgical modality is justied by the aggressiveness of the lesions, because all patients presented with alarming symptoms of pain, displacement of teeth, and rapidly increasing facial swelling. Chuong et al5 suggested that aggressive tumors that present with pain, rapid growth, facial swelling, or cortical perforation be treated with en bloc resection. It should also be noted that the diameter of the lesions in our study at the time of initial presentation ranged from 2.7 to 10 cm. These were large lesions that required hospitalization and endotracheal general anesthesia for surgical removal. The large size is also an indication of the aggressiveness of the lesions. In an attempt to distinguish aggressive and nonaggressive subtypes of CGCG and to predict the prognosis of newly diagnosed CGCGs, numerous studies have been conducted using cytometric and immunocytochemical methods. It has been shown that aggressive/recurring subtypes have a higher number and relative size index of giant cells and a greater fractional surface area occupied by giant cells.5,8 Furthermore, aggressive subtypes have been shown to express a greater count of nucleolar organization regions.10 These cytometric and immunocytochemical methods are not always available, especially in developing countries, and this invites the surgeon to use a relatively aggressive surgical technique. Surgical treatment of CGCGs can be associated with recurrence and serious facial mutilation and loss of teeth and tooth germs are also unavoidable. To avoid such disadvantages, an alternative treatment for the CGCG has recently been introduced, in which patients receive a daily dose of calcitonin. This treatment method also avoids the need for radiotherapy in growing children.20 CGCGs have been treated with calcitonin in various concentrations for at least 1 year; complete remission of CGCG has been observed without signs of recurrence.21,30 However, calcitonin therapy is complicated owing to the great amount of

CENTRAL GIANT CELL GRANULOMA

discomfort and the relatively long duration of treatment, which is more intolerable by some patients, especially children.21 CGCG has also been treated by weekly intralesional injection with corticosteroids; successful results have been reported.22,31 Corticosteroid therapy is, however, relatively contraindicated in certain medical conditions, such as diabetes mellitus, peptic ulcer, and generalized immunocompromised states.31 Nonsurgical treatment of CGCG is probably a good treatment option for small slowly enlarging lesions. Successful 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 does not invade perineural sheaths or spread via perineural spaces.19 In this study, the inferior alveolar nerve was identied and appeared in 16 cases (89%) to be merely displaced by the lesion but free of pathologic tissue. Therefore, it was possible to isolate and/or reposition the inferior alveolar bundle, preserving the sensation in the lower lip and chin and avoiding sequelae such as distressing paresthesia or painful dysesthesia.

References
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