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Giant-cell reparative granuloma of the temporal bone: a case report and review of the literature.

Abstract

Giant-cell reparative granuloma (GCRG) is an unusual, non-neoplastic fibrous lesion that most often arises in the mandible and maxilla. GCRG of the temporal bone is exceedingly rare. To the best of our knowledge, only 17 cases have been previously reported in the international medical literature. Although no case of metastasis has been reported, this malignancy can be locally aggressive, and it often recurs following incomplete excision. We report the case of a young woman with a very large GCRG of the right temporal bone. We discuss the clinical picture, differential diagnosis, histologic evaluation, appearance on computed tomography and magnetic resonance imaging, and treatment options. We also review the cases of temporal bone GCRG that have been reported in the literature so far.

Introduction

The term giant-cell reparative granuloma (GCRG) was introduced by Jaffe in 1953 to describe a lesion of the mandible and maxilla that occurred following a trauma-induced intraosseous hemorrhage. (1) He also distinguished GCRG, which is not a true neoplasm, from giant-cell tumor. Since 1953, GCRG has been reported in many other sites, including the axial skeleton and long bones, (2) the hands and feet, (3) the facial bones, (4) the cranial vault, (5) the sphenoid and ethmoid bones, (6-8) the orbit, (9) and the nose. (10) GCRG of the temporal bone was first described by Hirschl and Katz in 1974. (11) Up to now, only 16 other cases have been published in the international medical literature (table).

Although GCRG of the temporal bone has been purported to be a reaction to cranial trauma, (1,2,11,12) its pathogenesis remains unclear. (13,14) It can occur at any age, and there does not appear to be a clear gender predilection. (13) Reported symptoms include hearing loss, tinnitus, a palpable mass, pain, vertigo, and facial weakness. (14) Complete surgical excision is regarded as the treatment of choice. (12-14) Curettage of the lesion is not sufficient. (13,14) Whenever complete removal is not possible, radiotherapy should be considered. (13-15) Following complete excision, the prognosis is good, and reported recurrence rates have ranged from 10 to 15% in most studies. (11,16-18)

In this article, we report a new case of temporal bone GCRG, in which a large tumor infiltrated the sphenoid bone, infratemporal fossa, pterygoid fossa, temporomandibular joint, middle cranial fossa, and temporal lobe. To our knowledge, infiltration of the temporal lobe by a temporal bone GCRG has not been previously described in the literature.

Case report

A 17-year-old girl came to the Department of Otorhinolaryngology-Head and Neck Surgery in October 1998 with a 2-month history of hearing loss in her right ear. She reported no other symptoms, and she had no history of head or acoustic trauma or exposure to ototoxic agents. Her family history was negative for hearing loss.

Examination of the head and neck revealed that a mass was obstructing the right auditory canal and had almost completely occluded the lumen. Pure-tone audiometry revealed normal function in the right inner ear and a 20 dB air-bone gap at all frequencies tested. Serum levels of calcium, alkaline phosphatase, phosphorus, and parathyroid hormone were within normal limits. Computed tomography (CT) demonstrated a 4-cm osteolytic lesion of the right temporal bone and infratemporal fossa with intracranial but extradural extension. The temporomandibular joint was not involved. On magnetic resonance imaging (MRI), the lesion reflected low-intensity signals on both T1- and T2-weighted images, but there was some strong enhancement following the application of gadolinium contrast.

Because of the contrast enhancement, a preoperative embolization of the lesion was performed. Intraoperative rapid section revealed a tumor of unclear dignity. For that reason, the operation was abandoned after the mastoidectomy and without complete removal of the tumor. The definitive histology revealed that the tumor was a GCRG. The patient was scheduled to undergo a complete removal of the lesion, but unfortunately she and her mother refused the recommended surgery.

In February 2001, the young woman returned to our institution. Since her initial treatment, time tumor had grown significantly and the patient was experiencing total right-sided sensorineural deafness, intermittent vertigo, tinnitus, facial weakness (House-Brackmann grade II-III), and paresthesia in the area of the right mandibular nerve.

CT and MRI showed a very large tumor in the right temporal bone that involved the sphenoid bone, infratemporal fossa, pterygoid fossa, temporomandibular joint, and middle cranial fossa with extension into the right temporal lobe (figure 1). There were erosions of the labyrinth and the bony canal of the internal carotid artery as well as destruction of the right cochlea.

[FIGURE 1 OMITTED]

The lesion was resected via a combined pterional and infratemporal approach. The operation was performed in cooperation with the Department of Maxillofacial Surgery and the Department of Neurosurgery, and we were continuously assisted by computer-navigation control (Stryker Leibinger Navigation System; Freiburg, Germany). The tumor had damaged a large portion of the right temporal bone. The internal carotid artery, the facial nerve, and the mandibular nerve were ensheathed. During the operation, large portions of time temporal bone (including the cochlea and the labyrinth) and the temporomandibular joint (including the articular disk, masseter, and medial pterygnid muscle), parts of the temporal muscle, the greater wing of the sphenoid, the adventitia of the internal carotid artery, the maxillary artery, the mandibular nerve, parts of the temporal dura, and a small part of the caudal temporal lobe had to be resected. By performing such a radical operation, we were able to remove all tumor tissue as well as a margin of grossly uninvolved tissue. We were able to spare the facial nerve, and we treated it with a nerve stimulator at the completion of surgery. We reconstructed the dura with fascia lata and temporal muscle. Finally, we used a titanium mesh to restore the integrity of the middle cranial fossa and the temporal calotte.

The excised lesion was light brown and had a soft, friable consistency. Histologically, there was a fibroplastic proliferation with osteoclast-like polynuclear giant cells, newly formed osteoid trabeculae, lymphocytic infiltrates, macrophages, and hemosiderin deposits (figure 2, A). Immunohistochemical studies yielded positive vimentin staining of the fibroblastic spindle cells. The osteoclastic origin of the giant cells was confirmed by positive staining with tartrate-resistant acid phosphatase (figure 2, B) in combination with negative reactions for S100 and CD1a; these findings also excluded Langerhans'-cell histiocytosis.

[FIGURE 2 OMITTED]

Coronal MRI with gadolinium contrast 2 weeks following surgery revealed no signs of residual tumor (figure 3). Postoperatively, the patient exhibited a profound weakness of the right facial nerve (House-Brackmann grade V), but she gradually experienced a complete recovery within 6 months. Her vertigo gradually resolved over 4 weeks. During the first 12 months postoperatively, she complained that her powers of concentration had diminished. She also reported a permanent numbness in the area of the right mandibular nerve and total right-sided deafness.

In view of the size of the tumor and the involvement of bone, muscle, connective tissue, the mandibular joint, the dura mater, and the brain, postoperative radiation was recommended by the Department of Radiation Therapy, but the patient declined. Further treatment of the altered occlusion of her mouth was administered in the Department of Maxillofacial Surgery. The most recent MRI was conducted in March 2003, and there was no sign of recurrence.

Discussion

GCRG is a rare, benign, granulomatous lesion. (19) When it does occur, it most often arises in the mandible and maxilla; it can also involve any other bone in the jaw, cheek, and extragnathic region. (20) Including our patient, only 18 cases of GCRG of the temporal bone have been reported in the international medical literature (table). This group includes 6 females and 12 males, aged 4 months to 72 years (mean: 30.2 yr). Although different authors have reported that GCRG of the jaw has a predilection for females, (1,17,21,22) such does not appear to be the case for GCRG of the temporal bone. Even so, because of the small number of cases that have been reported, it is not possible to speculate whether there is a true gender predilection for temporal bone GCRG.

Among the 13 cases in which the authors specified the length of follow-up, monitoring time ranged from 10 months to 15 years (mean: 3.8 yr). Three reports contained no information on the length of follow-up, and two contained no information on follow-up at all. Of the 16 patients who were followed up after treatment, only two (12.5%) experienced a recurrence.

Symptoms. The reported symptoms of GCRG of the temporal bone include heating loss, tinnitus, a palpable mass, pain, vertigo, and facial weakness. Conductive hearing loss was the most common symptom, occurring in 12 of the 18 patients (66.7%). Tinnitus and a palpable mass were noted in 5 patients each (27.8%), pain in 3 (16.7%), and vertigo and facial weakness in 2 each (11.1%). One patient (5.6%) also complained of dysphagia and protrusion.

Etiology. The pathogenesis of GCRG is still controversial. (13,14) Jaffe wrote that the lesion represents a hyperplastic, reparative reaction to an intraosseous hemorrhage induced by trauma. (1) Many authors still share this opinion. (2,12) It must be mentioned, however, that there was no history of head trauma or previous surgery in 9 of the 18 cases of temporal bone GCRG. In another 5 cases, the authors did not report whether there had been any trauma. In fact, only 4 cases involved some previous trauma to the head. In one of those reports, the authors claimed that the lesion had occurred secondary to blunt trauma inflicted by a cricket bat. (19) However, the fact that this trauma had occurred only 6 weeks before the patient sought treatment for his tumor makes it most unlikely that the 3 x 2 x 1.5-cm GCRG had actually been caused by that particular trauma. Other causes that have been proposed include infections, (11) developmental anomalies, (17) and hormonal influences, (23) but no single theory has gained wide acceptance. (14)

Differential diagnosis. The diagnosis of GCRG is based on the combination of clinical information, radiologic data, histopathologic characteristics, and response to treatment. (13) GCRG must be differentiated from the brown tumor of hyperparathyroidism, aneurysmal bone cyst, chondroblastoma, fibrous dysplasia, cherubism, osteosarcoma, and true giant-cell tumor. (12-14,18)

Brown tumor of hyperparathyroidism. The histologic appearance of the brown tumor of hyperparathyroidism is often indistinguishable from GCRG. (10,13,14) Still, the differentiation between the two can be made without difficulty by measuring serum calcium, phosphorus, and alkaline phosphatase levels. (21) as well as phosphate clearance and levels of parathyroid hormone and urine hydroxyprotein. (13)

Aneurysmal bone cyst. Aneurysmal bone cyst is another non-neoplastic, reparative process with a giant-cell component. (13,24) A cystic blow-out of the bone is a typical finding on plain x-ray. (21) On MRI, aneurysmal bone cyst is usually not homogeneous and is characterized by a high signal intensity. (12,13) Histologically, it is characterized by thin-walled, blood-containing cystic cavities that are lined with flat fibroblastic cells and bony giant cells. (24) Aneurysreal bone cyst of the temporal bone is exceedingly rare, as only 10 cases have been reported in the literature. (24) Chondroblastoma. Chondroblastoma of the head and neck is most often located in the temporal bone. (20) It is characterized by local recurrence and metastasis, and it should be considered clinically to be a malignant tumor. (25) Its important histopathologic features are focal chondroid differentiation, intercellular calcification, and epitheliumlike cells in nodules and ribbons with scattered, multinucleated giant cells and granular hemosiderin pigments. (20,25,26) On CT, chondroblastoma appears as a high-density mass with mild contrast enhancement. (25)

Fibrous dysplasia. The typical histopathologic features of fibrous dysplasia are the presence of osteolysis, immature bone trabeculae, and fibro-osseous tissue in the affected part of the bone. (27) Its signal intensity is typically low on both T1 and T2-weighted MRI. (12) Fewer than 80 cases of temporal bone fibrous dysplasia have been reported in the international medical literature. (27)

Cherubism. Cherubism is a rare, benign, autosomaldominant inherited condition characterized by cystic proliferation of the mandible and maxilla in childhood. (28,29) Histologically, it features proliferating vascular fibrous tissue with osteoclastic, multinucleated giant cells. (28) Radiologically, there is a specific finding of bilateral, multilocular cystic expansion of the jaws. (28) Cherubism does not occur in the temporal bone.

Osteosarcoma. There might be a large, benign giant-cell component to osteosarcoma, but the presence of atypia of the mononucleated cells is a useful criterion in making the differential diagnosis between it and GCRG. (20)

Giant-cell tumor. Giant-cell tumor is often difficult to distinguish from GCRG. (13,14,20) Prior to Jaffe's report in 1953, (1) all giant-cell lesions were designated as giant-cell tumors.(14) GCRG has often been misdiagnosed as giant cell tumor, (14,21) especially during the years before the first reported case of temporal bone GCRG by Hirschl and Katz in 1974. (11) True giant-cell tumor is a real neoplasm, and it accounts for 3 to 7% of all primary bone tumors. (13) In most cases, it occurs at the ends of long bones. (20,30) Bertoni et al reviewed 2,046 cases of giant-cell tumor and found that only one had occurred in the temporal bone. (20)

The primary difference between giant-cell tumor and GCRG is the prognosis. (13) Giant-cell tumor is reported to have a higher incidence of recurrence than GCRG; reported recurrence rates of giant-cell tumor of the long bones range between 45 and 62%. (14) Giant-cell tumor may undergo malignant transformation, (13,14) and metastatic spread, usually to the lung, occurs in 1 to 6% of cases of giant-cell tumor of the extremities. (14,31) In giant-cell tumor of the craniofacial bones, only one case of lymph node metastasis and no case of pulmonary metastasis has been noted. (14)

On radiologic evaluation, giant-cell tumor and GCRG are indistinguishable. (13,14) On CT, both usually appear as a nonspecific lytic lesion. (13,14) On MRI, most lesions reflect a low signal intensity on T1-and T2-weighted imaging. (13,14) Both tumors enhance with gadolinium contrast; the degree of enhancement ranges from slight (12) to strong. (13)

Because of the nonspecific nature of the radiologic findings, the differentiation between giant-cell tumor and GCRG must be made histologically. Giant-cell tumor originates in the connective tissue of bone marrow, whereas GCRG arises from periosteal connective tissue. (13) Several histopathologic differences between the two lesions have been described in the literature. GCRG has been reported to contain fewer multinucleated giant cells than has giant-cell tumor. (14) The giant cells in giant-cell tumor tend to be more evenly distributed and have a more uniform appearance.(11,14,18) GCRG is associated with a greater degree of osteoid formation, hemorrhage, hemosiderin deposition, and inflammation. (14) The spindling quality of the cells that encircle the giant cells has been described as a consistent feature of GCRG. (4,18,20) In giant-cell tumor, typical findings are foci of necrosis and the presence of marked mitotic activity. (14)

There may be areas of a GCRG lesion that cannot be histologically differentiated from giant-cell tumor. (20) Ung et al recommended maintaining the current nomenclature of giant-cell tumor and GCRG whenever a clear distinction between the lesions can be made histologically. (14) In borderline cases, however, they preferred the term giant-cell lesion, which can be further classified as aggressive or nonaggressive on the basis of symptoms. (14) However, we agree with Bertoni et al that it is important to make every effort to separate giant-cell tumor of the skull from GCRG because the prognosis of giant-cell tumor is generally much worse. (20) Bertoni et al described 15 cases of giant-cell tumor of various skull bones; 3 of those patients died of giant-cell tumor. (20) To the best of our knowledge, there is not a single reported case of death caused by GCRG.

Treatment. Complete surgical excision is the therapy of choice for GCRG. (13,14) Some authors have claimed that curettage is sufficient for treatment. (1,15,21) However, Auclair et al noted that the recurrence rate following simple curettage of GCRG was 50%, compared with a recurrence rate of only 10% following complete surgical excision. (31) For large tumors, preoperative superselective intravascular embolization has been advocated. (32) Unlike giant-cell tumor, GCRG does not undergo malignant transformation, and there is not a single documented case of GCRG metastasis. (14)

Complete excision of giant-cell tumors of the long bones can usually be performed without major difficulty. However, the skull base, with its large number of vital structures, provides a significant challenge to complete surgical removal. (14) In cases where complete resection is not possible, postoperative radiation has been advocated. (13,16) Of the 18 patients who have had GCRG of the temporal bone, 3 underwent radiation therapy--2 after a complete resection and 1 after an incomplete resection. The size of the radiation doses varied greatly--from 600 and 5,000 cGy. Especially in young patients, radiation therapy for this primarily benign lesion should be performed only when complete resection is not possible or when the tumor has infiltrated many different structures, as happened in our patient. Keep in mind that any radiation therapy carries the potential risk of sarcomatous transformation in the decades to come. (14) On the other hand, patients with giant-cell tumor of the temporal bone should always undergo radiation following resection in light of the high risk of recurrence. (20)

De Lange et al (22) and Pogrel et al (33) reported a total of six patients with GCRG of the jaw who experienced a complete remission alter they were treated with calcitonin. Anti-inflammatory drugs may play a future role in the treatment of GCRG, but more data are needed, especially long-term results, before calcitonin treatment can be regarded as an adequate alternative to surgery. (13)
Table. Summary of all reported cases of temporal bone GCRG

 Age/ Initial
Author(s) sex Trauma symptoms

Hirschl and Katz, (11) 36/F Yes Hearing loss
 1974

Colclasure et al, (34) 1981 10/M NR * Hearing loss

 22/M NR Hearing loss,
 mass

Tesluk et al, (18) 1989 56/M No Mass, pain

Ciappetta et al, (15) 1990 25/M Yes Dysphagia, pain,
 protrusion

Cohen and ([dagger])/F No Mass
 Granda-Ricart, (35) 1993

Lewis et al, (12) 1994 32/F Yes Hearing loss

Nemoto et al, (36) 1995 36/M No Hearing loss,
 tinnitus

 28/M No Hearing loss,
 tinnitus

Maruno et al, (37) 1997 3/F No Facial weakness,
 hearing loss

Ung et al, (14) 1998 36/F No Hearing loss

Liu et al, (13) 2001 44/M No Hearing loss,
 tinnitus

 72/M No Hearing loss

Khodaei et al, (38) 2001 36/M NR Pain, tinnitus,
 vertigo

Sharma et al, (19) 2002 12/M Yes Facial weakness,
 hearing loss,
 mass, tinnitus,
 vertigo

Matsui et al, (32) 2002 41/M NR Mass

Yoshimura et al, (39) 2002 38/M NR NR

Boedeker et al, ([double 17/F No Hearing loss
 dagger]) 2003

Author(s) Therapy Follow-up

Hirschl and Katz, (11) Biopsy plus radiation Well at 17 mo
 1974 (2,500 cGy)

Colclasure et al, (34) 1981 Total resection Well at 6 yr

 Total resection plus Well at 7 yr
 radiation (600 cGy)

Tesluk et al, (18) 1989 Total resection Well at 1 yr

Ciappetta et al, (15) 1990 Total resection Well at 15 yr

Cohen and Total resection NR
 Granda-Ricart, (35) 1993

Lewis et al, (12) 1994 Total resection Well; length of
 follow-up NR

Nemoto et al, (36) 1995 Total resection Well; length of
 follow-up NR

 Total resection Well; length of
 follow-up NR

Maruno et al, (37) 1997 Total resection Recurrence at 1 yr

Ung et al, (14) 1998 Total resection Recurrence at 4 yr

Liu et al, (13) 2001 Total resection plus Well at 3 yr
 radiation (5,000 cGy)

 Total resection Well at 21 mo

Khodaei et al, (38) 2001 Total resection Well at 3 yr

Sharma et al, (19) 2002 Total resection Well at 10 mo

Matsui et al, (32) 2002 Total resection NR

Yoshimura et al, (39) 2002 Total resection Well at 4 yr

Boedeker et al, ([double Biopsy initially, Well at 2 yr
 dagger]) 2003 total resection
 3 yr later

* NR = not reported; ([dagger]) Age: 4 mo.;
([double dagger]) Present report.


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(36.) Nemoto Y. Inoue Y. Tashiro T, et al. Central giant cell granuloma of the temporal bone. AJNR Am J Neuroradiol 1995;16:982-5.

(37.) Maruno M. Yoshimine T, Kubo T, Hayakawa T. A case of giant cell reparative granuloma of the petrous bone: Demonstration of the proliferative component. Surg Neurol 1997:48:64-8.

(38.) Khodaei I. Rowley 11, Farrell M. et al. An unusual cause for tinnitus, Ir Med J 2001;94:312-13.

(39.) Yoshimura J. Onda K, Tanaka R. Takahashi H. Giant cell reparative granuloma of the temporal bone: Neuroradiological and immunohistochemical findings. Neurol Med Chir (Tokyo) 2002; 42:510-15.

From the Department of Otorhinolaryngology-Head and Neck Surgery (Dr. Boedeker, Dr. Ridder, Dr. Maier, and Dr. Schipper), and the Department of Pathology (Dr. Kayser), University of Freiburg, Freiburg, Germany.

Reprint requests: Carsten Christof Boedeker, MD, Department of Otorhinolaryngology-Head and Neck Surgery, University of Freiburg, Killianstrasse 5, 79106 Freiburg, Germany. Phone: 49-761-270-4201; fax: 49-761-270-4075; e-mail: boedeker@ hno.ukl.uni-freiburg.de
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Title Annotation:Original Article
Author:Schipper, Jorg
Publication:Ear, Nose and Throat Journal
Geographic Code:4EUGE
Date:Dec 1, 2003
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