Journal of Indian Academy of Oral Medicine and Radiology

: 2016  |  Volume : 28  |  Issue : 1  |  Page : 98--101

Central giant cell granuloma: A case report with review of literature

Kamala A Kamble1, Sanketh S Guddad2, Sujith S Guddad3, Ashok Lingappa4,  
1 Department of Oral Medicine and Radiology, School of Dental Sciences, Krishna Institute of Medical Sciences Deemed University, Karad, Maharashtra, India
2 Department of Periodontology, School of Dental Sciences, Krishna Institute of Medical Sciences Deemed University, Karad, Maharashtra, India
3 Department of Periodontology, Coorg Institute of Dental Sciences, Virajpet, Karnataka, India
4 Department of Oral Medicine and Radiology, Bapuji Dental College and Hospital, Davangere, Karnataka, India

Correspondence Address:
Kamala A Kamble
Department of Oral Medicine and Radiology, School of Dental Sciences, KIMSDU, Karad - 415 110, Satara, Maharashtra


Central giant cell granuloma (CGCG) is an uncommon, benign, and proliferative lesion of the jaw with an unknown etiology. It is considered widely to be a nonneoplastic lesion. The actual etiology of CGCG is still unclear, although inflammation, hemorrhage, and local trauma have all been suggested. The incidence in the general population is very low, and patients are generally younger than 30 years. The biologic behavior of CGCG of the jaw ranges from quiescent to aggressive with destructive expansion. Here, we report a case of CGCG in an 18-year-old female patient with review of literature.

How to cite this article:
Kamble KA, Guddad SS, Guddad SS, Lingappa A. Central giant cell granuloma: A case report with review of literature.J Indian Acad Oral Med Radiol 2016;28:98-101

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Kamble KA, Guddad SS, Guddad SS, Lingappa A. Central giant cell granuloma: A case report with review of literature. J Indian Acad Oral Med Radiol [serial online] 2016 [cited 2022 Jul 4 ];28:98-101
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Central giant cell granuloma (CGCG) is a benign intraosseous lesion first described by Jaffe in 1953.[1] This is a relatively uncommon pathologic process accounting for <7% of all benign lesions of the jaws. The nature of this lesion is controversial; three competing theories prevailing are it being reactive, a developmental anomaly, or benign neoplasm. Neville et al.,[2] consider this entity to be a nonneoplastic lesion and the World Health Organization also classifies it as a bone-related lesion and not a tumor, although its clinical behavior and radiographic features often are those associated with a benign tumor. Another controversial issue is the relationship of CGCG of the jaws to the giant cell tumor that occurs in extragnathic location.[1] Occurrence of CGCG in patients with anomalies with a known genetic origin such as neurofibromatosis type 1, cherubism, and Noonan's syndrome indicates that a genetic-related etiology might also be possible. Here, we report a case of CGCG on the right side of the mandible.[3]

 Case Report

An 18-year-old female presented with a swelling on the right side of mandible for the past 5 months and associated with pain for 1 month. The pain was insidious in onset, mild, throbbing, intermittent, and nonradiating in nature. Past medical, dental and family histories were noncontributory. An intraoral examination [Figure 1] revealed a solitary swelling in the right lower buccal vestibule measuring approximately 2.5 × 2 cm extending from distal aspect of 31 to mesial aspect of 45 with significant vestibular obliteration in relation to 41–45. The overlying mucosa appeared pink to erythematous. The swelling was firm in consistency with expansion of buccal cortical plate and gingival recession with respect to 42 and 43 with Grade I mobility. Pulp vitality test showed positive response with 31, 41, 42, and 45 whereas 43 and 44 gave delayed response and fine needle aspiration cytology was nonproductive.{Figure 1}

Intraoral periapical radiograph [Figure 2]a revealed a unilocular radiolucency with displacement of the roots of 42 and 43. Occlusal radiograph [Figure 2]b showed thinning of cortical plate and perforation in addition to buccal cortical plate expansion in relation to 42, 43, and 44 regions. Panoramic radiograph (orthopantomogram) [Figure 3] showed a solitary radiolucent lesion in the right side of mandible extending from 42 to 45 with a fine granular bone pattern with mixture of straight and coarse faint wispy septa. The routine blood and urine investigations were within the normal limit. Patient underwent surgical curettage along with extraction of 42, 43 and 44 teeth [Figure 4]a and with placement of sutures [Figure 4]b. Subsequent histopathological examination [Figure 5]a - low power and [Figure 5]b - high power] showed a cellular connective tissue with abundant oval to spindle-shaped mesenchymal cells distributed throughout the stroma, irregular-shaped giant cells, and bone lined by osteoblasts, and a few osteoid areas were seen suggestive of CGCG. Follow-up of patient [Figure 6] with maintenance of 42, 43, and 44 teeth region was carried out up to 1 year, and there was no recurrence of the lesion. The patient was referred to the department of prosthodontics for fixed partial denture in the same region.{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Figure 6}


The incidence of CGCG in the general population is estimated to be 0.0001% with 60% of cases occurring before the age of 30. Gender predilection reports are variable, but the majority of them occur in females with a female:male ratio 2:1.[1] It has been noted that the development of CGCG occasionally coincides with the onset of pregnancy or menarche.[4] CGCG is more prevalent in the anterior than the posterior jaws, often crossing the midline (50%), and the mandible is more commonly affected than the maxilla and confined to the tooth-bearing areas of the jaws.[1],[4] In this case, the right side of the mandible was affected. In most of the cases, the lesion presents as a painless, slow-growing swelling of the jaw. Intraorally, swelling with sometime bluish brown discoloration can be observed. Most common complaint is pain, paresthesia, and displacement of teeth which frequently leads to malocclusion. Swelling results in facial asymmetry and difficulty in mastication. In this case, the patient had diffuse swelling of the right side of the mandible associated with pain.[3],[4]

Radiographically, the lesion commonly presents as a solitary radiolucency with a multilocular appearance or, less commonly, a unilocular appearance. Lesions develop twice as often in the mandible with an epicenter anterior to the first molar in young patients, and there is tendency for the epicenter to occur in the posterior aspect of the jaws after the first two decades of life. In the maxilla, the epicenter is more commonly anterior to the canine. The borders may be well-defined or ill-defined and show variable expansion and destruction of the cortical plates. The internal structure may show granular pattern of calcification which is organized into ill-defined, wispy septa which emanate at right angles to the periphery of the lesion. Displacement and resorption of teeth are also evident.[1],[5] The present case exhibited unilocular radiolucency with coarse faint septa, corticated borders, root displacement, and cortical plate expansion.

CGCG should be differentiated from odontogenic keratocyst (OKC), unicystic ameloblastoma, and aneurismal bone cyst (ABC). OKC can be differentiated from CGCG, as it is asymptomatic, occurs 65% in mandibular third molar region, has an epicenter superior to alveolar canal, presents as a multilocular radiolucency with scalloped borders, and high-recurrence rate. Unicystic ameloblastoma is asymptomatic, occurs in mandibular third molar region, and radiographically appears unilocular with thinning and expansion of the cortical plates. ABC affects mandible (ramus and molar area) more than the maxilla, is symptomatic, seen in younger age group, and radiographically appears unilocular with thinning, and cortical plate expanision.[6]

Clinical and radiographic features are not definitive diagnosis in CGCG. Two major histological features are diagnostic in CGCG. There is highly cellular, fibroblastic stroma with plump, spindle-shaped cells with high-mitotic rate. The multinucleated giant cells are irregularly distributed and are prominent throughout the fibroblastic stroma. Histologically, the features of CGCG are indistinguishable from brown tumor of hyperparathyroidism and giant cell lesions, but biochemical tests such as serum calcium, phosphorus, and alkaline phosphatase can be taken into consideration to rule out these lesions.[3],[4] Based on the clinical, radiographical, and histological features, several groups of investigators have suggested that central giant cell lesions of the jaw may be divided into two categories, aggressive and nonaggressive, and the difference between these two lesions is illustrated in [Table 1].[3],[7]{Table 1}

The treatment of the CGCG ranges from curettage to resection. Surgical treatment such as simple curettage, curettage with peripheral ostectomy, enucleation, and en bloc resection can be carried out. Aggressive lesions should be corrected and treated with curettage.[7],[8] Intralesional injection of corticosteroids (triamcinolone hexacetonide 20 mg/ml diluted in anesthetic solution of 2% of lidocaine twice weekly for 6 weeks) has been used successfully.[9] Calcitonin therapy (salmon calcitonin nasal spray 200 IU/day) controls the osteoclastogenesis and interferon alpha (INF-α injection, 3 × 106 IU/day) injection, used as adjunct to surgery, acts as antiangiogenic and inhibits bone resorption.[10],[11] Recurrence rates have been reported to range between 11% and 49% for curettage alone and can be as high as 72% for aggressive subtypes.[1],[12]


CGCGs are benign, but occasionally they can be aggressive lesions developing in the jaws. Although simple curettage is effective in treatment for the majority of CGCG of the jaws, aggressive lesions should be treated by surgical resection along with curettage. Use of INF-α and intralesional corticosteroid therapy are the latest therapeutic approaches available at this time. Further studies should be encouraged to clarify the etiopathogenesis of the disease and various treatment modalities and also to create awareness among our professional colleagues.

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Conflicts of interest

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