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MUSCULOSKELETAL RADIOLOGY Table of Contents   
Year : 2001  |  Volume : 11  |  Issue : 3  |  Page : 119-126
Pictorial essay : Giant cell tumor of bone


Department of Surgery, Tata Memorial Hospital, Parel, Mumbai 400012, India

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Keywords: Bone neoplasm, giant cell tumor, CCT

How to cite this article:
Pardiwala D N, Vyas S, Puri A, Agarwal M G. Pictorial essay : Giant cell tumor of bone. Indian J Radiol Imaging 2001;11:119-26

How to cite this URL:
Pardiwala D N, Vyas S, Puri A, Agarwal M G. Pictorial essay : Giant cell tumor of bone. Indian J Radiol Imaging [serial online] 2001 [cited 2019 Jul 22];11:119-26. Available from: http://www.ijri.org/text.asp?2001/11/3/119/28389
Giant cell tumor (GCT) of the bone is a benign, but locally aggressive and destructive lesion. It is composed of primitive histiocytes and diffuse, large, multinucleated giant cells.

Epidemiology: In the Orient, GCT may account for 20% of all primary skeletal neoplasms [1]. Generally occurring in skeletally mature individuals with its peak incidence in the third decade of life [2], less than 2% are found in patients with open epiphyses [3]. There is a slight female predominance (56.4% in one large series) [2]. GCTs of the small bones of the hand and foot seem to occur at a slightly younger age group and demonstrate a higher incidence of multicentricity than that in other locations [4],[5].

Skeletal distribution: Almost always a mono-ostotic process, the most common sites include the distal femur, proximal tibia and distal radius. The sacrum, distal tibia, proximal humerus, proximal femur, pelvis and proximal fibula are not infrequent sites. Rarely bones of the hand and feet, vertebral bodies and ribs may be involved [2],[6],[7].

Pathology: On gross pathology, GCT typically involves the epi-physio-metaphyseal region of long bones. The tumor almost always extends up to the adjacent articular cartilage, which remains intact and, rarely, when neglected, it may involve the diaphysis because it may attain immense size. The tumor is usually eccentric to the long axis of the bone but may be centrally located. Predominant metaphyseal involvement with epiphyseal extension through the growth plate has been noted in a small number of skeletally immature patients [28]. The overlying cortex has usually undergone resorption and the contour of the bone is expanded by the tumor, which is covered by a thin shell of subperiosteal new bone. Areas of necrosis and hemorrhage may result in cystification of the tumor, which may be so prominent as to mimic aneurysmal bone cyst [2],[7],[9],[10].

Histopathology: Histologically the lesion is composed of osteoclast-like multinucleated giant cells in a moderately vascularized network of proliferating round, oval or spindle shaped stromal cells. Ossification and osteoid production are noted in small foci at the periphery of the lesions, particularly in soft tissue extensions [2],[7],[9],[10],[11].

Clinical behavior: Giant cell tumors are prone to local recurrence. Although benign, in 3.5% of patients they shows metastases to the lungs and more rarely to other sites, where the secondary tumors are histologically benign and identical to the primary lesion [9],[12],[13]. Metastases may also be related to previous surgical intervention or irradiation of the primary lesion [14],[15].

A sarcoma may occur in conjunction with a histologically benign GCT or it may develop at the site of a previously treated GCT after a prolonged interval, usually following irradiation. This occurrence is generally known as a malignant giant cell tumor in which the malignancy is usually an osteosarcoma, a malignant fibrous histiocytoma or a fibrosarcoma [2].

Treatment: The treatment of GCT is directed towards local control without sacrificing joint function. This has traditionally been achieved by intralesional curettage with autograft reconstruction by packing the cavity of the excised tumor with morselised iliac cortico-cancellous bone. Regardless of how thoroughly performed, intralesional excision leaves microscopic disease in the bone and hence has a recurrence rate as high as sixty-percent [16]. "Extended intralesional excision" by cementation using polymethylmethacrylate (bone cement) has reduced the incidence of local recurrence to less than ten percent [16]. Although a marginal or wide excision of the involved bone is curative if contamination is avoided, it is associated with reconstruction and disability problems.

GCTs can produce wide-ranging appearances depending on the site, complications such as hemorrhage or pathological fracture and after surgical intervention. This pictorial review demonstrates a spectrum of these features.


   Radiographic Features Top


The typical giant cell tumor of the epiphysis is a solitary, relentlessly growing neoplasm that results in extensive bone resorption. On rare occasions, it may present in multiple bones.


   Long And Tubular Bones Top


Epiphyseal location: GCT demonstrates an osteolytic lesion centered in the epiphysis but involving the metaphysis and extending at least in part to the adjacent articular cortex [Figure - 1]. Less than 2% present in the metaphysis or diaphysis [17] and in such instances the pathologist must prove that the lesion is not a giant cell rich osteosarcoma or a bone lesion of hyperparathyroidism.

Intramedullary eccentric versus central location: In the major long bones such as the femur and tibia, all lesions begin in the intramedullary region. Most are eccentric, but become symmetric and centrally located with growth [Figure - 1]. In the thin long bones, such as the fibula or radius, most lesions are centrally placed from initial presentation [Figure - 2].

Geographical destruction: Most cases of GCT show circumscribed borders or so-called geographical destruction [Figure - 1]. In about 10% the edges may appear permeative to moth-eaten [18]. These differences reflect the variability in the lesions' growth rates. The pathologist must exclude a giant cell rich osteosarcoma or aneurysmal bone cyst engrafted on a GCT in all these cases.

Confinement to bone: Early lesions are contained within the original bone contours. With growth, the tumor usually bulges beyond the confines of the cortex, which undergoes varying degrees of resorption. A significant percentage may cause eccentric or concentric cortical erosion and extend into soft tissues [Figure - 3].

Extension to articular cartilage: Most GCTs abut a border of the articular cartilage (subchondral bone) in one or more planes [Figure - 1],[Figure - 2].

Lysis with and without trabeculation: Lysis is common to all GCTs, probably due to massive osteoclastic proliferation. Peripheral bony ridges of a lobulated tumor give the radiographic appearance of trabeculations [Figure - 1]. These trabeculations appear as filigree of coarse to fine honeycomb-like patterns.

Absence of benign host bone sclerosis: The margins of the lesion bordering the adjacent cancellous bone may be well defined or ill defined and seldom a thin shell of reactive bone may be present. Less than 5% of GCT have a rind of benign host bone sclerosis and these may represent rare, older to regressing forms of GCT [18].

Absence of punctate calcifications, intralesional bone formation or periosteal reaction: Apart from a thin shell of subperiosteal new bone outlining the outer surface of the tumor, no periosteal reactions are appreciated unless a pathological fracture is present. There is no mineralized tumor matrix.


   Spine And Flat Bones Top


The radiographic features of GCT at sites other than the long bones are non-specific and not unlike those of other osteolytic processes.

GCT of the spine almost always begins in the vertebral body and may lead to vertebral collapse or extend into the intervertebral disc, adjacent vertebral body and spinal canal or paraspinal soft tissue [19].

Sternal and sacral lesions are osteolytic and owing to a large size and a soft tissue component, may simulate the appearance of a malignant neoplasm. In the sacrum, transarticular extension of the tumor may be noted.


   Multicentric Giant Cell Tumor Top


Rarely two or more bones may be involved by GCT [20]. In Mirra's series the incidence was 1.3% of conventional GCT [18].


   Conventional Tomography Top


Better delineation of the osseous margins of the lesion and the status of the cortex including that subjacent to the articular cartilage is possible with conventional tomography. However, it may suggest disruption of a thinned, but continuous cortex and therefore may be misleading [21]. Computed tomography will rarely add additional information that changes the differential diagnosis [22]. However, CT is superior to conventional radiography and tomography in outlining the extent of the tumor [Figure - 4], especially its extra-osseous portion and its relationship to adjacent structures, as well as evaluation of cortical integrity and determination of tumor recurrence [21],[23]. The expanded and thinned cortex is vividly demonstrated and the presence or absence of matrix calcification can be assessed. Fluid levels may be seen [8],[24] secondary to an aneurysmal bone cyst component or due to intratumoral hemorrhage. Reactive changes and edema on the outer cortical surface or the synovium may mimic tumor extension. The axial slices provided by CT do not allow accurate evaluation of the subarticular cortex because of volume averaging.

The advent of color volume rendered 3-dimensional CT with video files allows evaluation of multiple tissues at the same time. The spatial depiction of the tumor along with surrounding anatomical relationships such as vessels and ureter make this a useful preoperative imaging modality in cases of pelvic GCT [Figure - 5]. Manipulation and rotation of the 3D images through 360 degrees allows the surgeon a better understanding of the extent of the mass and anticipated surgical complexities.


   Magnetic Resonance Imaging Top


MRI is currently the best imaging modality for GCT because of its superior contrast resolution and multiplanar imaging capabilities that allow accurate tumor delineation [22],[25]. MRI is useful in determining extra-osseous extent and articular surface involvement [26], however subtle cortical destruction is better demonstrated by CT [Figure - 6].

GCT shows low intensity on T1W and heterogeneous high intensity on T2W images. Therefore intramedullary tumor is best seen on T1W, while its extra-osseous portion is best appreciated on T2W images [26],[27]. The hypervascular stroma contains sinusoidal vessels, which predispose to hemorrhage [28]. The phagocytosed erythrocytes lead to iron deposition in the form of hemosiderin [29]. GCT's often have extensive hemosiderin deposition within tumor tissue, resulting in very low signal intensity on all pulse sequences [29]. This is seen in upto 60% of patients [29]. Low signal areas may also be due to collagen deposition secondary to surgery or trauma [29]. Gadolinium enhancement reveals areas of hypervascularity and enhancement with a very heterogeneous signal pattern [30].


   Radionuclide Scintigraphy (Bone Scan) Top


GCT produces increased uptake of technitium-99m radio-pharmaceuticals. The pattern of increased uptake may be diffuse (40%) or peripheral with little central activity (60%) [31]. Extended uptake beyond the margins of the tumor precludes accurate definition of intramedullary extent [21]. Increased uptake in the bone across the adjacent joint and in other joints of the same extremity not involved by tumor may occur [32]. Therefore the role of bone scan in GCT is limited because it is non-specific and unreliable in defining the extent of the tumor [31]. It is however, helpful in evaluating the rare patient with multicentric GCT [Figure - 7].


   Angiography Top


Although angiography is seldom used as a diagnostic modality in the era of CT and MRI, it can determine the extra-osseous extent of the tumor and its relationship to major vessels. A majority of the GCTs are hypervascular, but 10% aneurysmal bone cyst component may be completely avascular. Reactive hyperemic synovium may mimic extra-osseous tumor extension [27].

The role of angiography today, in patients with GCT, is limited to a study of regional vascular anatomy and perhaps, transcatheter arterial embolisation in instances of unresectable neoplasms [33].

The role of embolisation for unresectable tumors

Unresectable giant cell tumors (e.g. certain sacral and pelvic tumors) can be managed with transcatheter embolization of their blood supply. Since flow reconstitution invariably occurs, embolization is performed at monthly intervals until significant pain palliation is achieved. Subsequent embolizations are performed when there is symptomatic or radiographic relapse of the tumor.


   Pet Scan Top


Positron emission tomography allows the visualization of the metabolic activity of disease. In orthopedic surgery it is of most help in the diagnosis of malignant tumors and their recurrence, the staging of tumors and the monitoring of their response to therapy. Although the role of PET in GCT is as yet to be defined, this imaging modality holds great promise. Definition of the primary tumor with a number of radiotracers will allow the determination of blood flow, the turnover of DNA, the turnover of amino-acids, hypoxia of the tumor and the glucose metabolism. This will enable metabolic staging of the tumor to be done, which may have a predictive value equal to or surpassing histological techniques [34].

Evaluation Of Local Recurrence

Local recurrences manifest themselves within three years in 80% to 90% of patients [6] and appear to be related to the surgical margin [6]. Clinically characterized by pain, the radiographic features include:

  1. Lysis of the bone graft, which may have become incorporated or in the adjacent cancellous bone, in patients having undergone intralesional curettage with bone grafting [Figure - 8].
  2. Following curettage and cementation an osteolytic zone caused by thermal injury measuring 2 mm surrounds the cement. This radiolucent zone is bordered by a thin outer sclerotic rim for about 6 months [Figure - 9] [14],[35]. Lysis or failed development of the sclerotic rim between the cement and cancellous bone suggests recurrence [Figure - 10][35].
  3. Although recurrence usually occurs in the parent bone, soft tissue implantation can occur at the time of surgery and may be the only site of disease [Figure - 11]. Soft tissue recurrence is visible on plain radiographs because of its tendency towards peripheral calcification [Figure - 12][11].


MR is the optimum technique for evaluation of recurrent or residual disease. Local postoperative high signal within the surgical bed that exhibits a rounded mass-like appearance with eccentric growth is highly suggestive of tumor [36]. Differentiation of recurrent tumor from cement related giant cell reaction could sometimes be difficult. Giant cell granulomas usually develop after several years while the majority of tumor recurrences occur within 18 months after the initial surgery. In addition, tumor recurrence grows more rapidly than giant cell granuloma. However, overlap of features between these two entities can occur and a CT-guided core biopsy may be needed

 
   References Top

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2.Dahlin DC, Unni KK. Bone tumors. General aspects and data on 8,542 cases. Springfield, IL, Charles C Thomas. 1986. p 507.   Back to cited text no. 2    
3.Picci P, Manfrini M, Zucchi V, et al . Giant cell tumor of bone in skeletally immature patients. J Bone Joint Surg 1983;65A:486-490.   Back to cited text no. 3    
4.Averill RM, Smith RJ, Campbell CJ. Giant cell tumors of the bones of the hand. J Hand Surg 1980;5:39-50.   Back to cited text no. 4  [PUBMED]  
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13.Szyfelbein WM, Schiller AL. Cytologic diagnosis of giant cell tumor metastatic to lung. A case report. Acta Cytol 1979;23:460-464.   Back to cited text no. 13    
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34.Smith MA, O'Doherty MJ. Positron emission tomography and the orthopaedic surgeon. J Bone Joint Surg 2000;82B:324-325.   Back to cited text no. 34    
35.Pettersson H, Rydholm, Persson B. Early radiologic detection of local recurrence after curettage and acrylic cementation of giant cell tumors. Eur J Radiol 1986;6:1-4.   Back to cited text no. 35    
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Correspondence Address:
D N Pardiwala
Department of Surgery, Tata Memorial Hospital, Dr Ernest Borges Road, Parel, Mumbai 400012
India
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Source of Support: None, Conflict of Interest: None


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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10], [Figure - 11], [Figure - 12]



 

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