Updated: Oct 1, 2007
A chondroblastoma is a rare benign cartilaginous neoplasm that characteristically arises in the epiphysis of a long bone in young patients.1,2 (Also see the eMedicine Orthopedic Surgery article Chondroblastoma.)
Chondroblastomas consist of chondroblasts, which are round or oval primitive cells of the epiphyseal cartilage plate that contain dense eosinophilic cytoplasm. Cellular areas are surrounded by variable amounts of dense eosinophilic matrix and may contain coarse calcifications or calcifications in a chicken-wire pattern. Mitotic figures and cytologic atypia are rare. Cystic changes may simulate those of aneurysmal bone cysts (see Image 22), especially when the tumor occurs in the patella, talus, or calcaneus.3
Chondroblastomas represent less than 1% of all primary bone tumors.1,2 These lesions are less common than enchondromas and osteochondromas but more common than chondromyxoid fibromas.
The worldwide data for chondroblastomas are the same as those in the United States.
Complications associated with chondroblastomas include pathologic fractures (see Images 18-19) and, rarely, malignant transformation. Fractures are uncommon and proportionally more likely to occur in tumors of increasing size. Without surgical excision, the tumor may extend into the adjacent soft tissues or synovium and metastasize to distant organs. Metastasis, when it occurs, most frequently involves the lungs and tends to occur at the time of primary tumor recurrence.4,5 Widespread metastases and death have been reported.4,5,6
There is a male preponderance for chondroblastomas. The male-to-female ratio is 2-3:1.
Chondroblastomas generally occur in those aged 10-30 years; in the literature, the age range of affected patients has been 3-73 years for tumor occurrence. About 90% of the tumors occur in those aged 5-25 years.
Chondroblastomas typically occur in the epiphysis or apophysis of a long tubular bone, and the tumor is confined to the epiphysis in 40% of cases. In the remainder of the cases, the tumor extends to the adjacent metaphysis. Rarely, chondroblastomas arise in the metaphysis and, even less frequently, in the diaphysis.
The most commonly affected site is the lower extremity (72% of cases), in which 50% of the chondroblastomas occur around the knee (see Images 1 and 5). The femur is involved in 33% of cases; the humerus, in 20%; and the tibia, in 18%. Lesions in the proximal femur are 3 times more likely to occur in the greater trochanter than in the femoral head (see Image 8). About 90% of the lesions in the humerus occur in the proximal humeral head (see Image 10).
Approximately 10% of all chondroblastomas occur in the small bones of the hands and feet; the talus and calcaneus are common sites (see Image 13). Other rare sites include the para-acetabular innominate bone, ribs, skull, mandible, maxillae, vertebrae, scapulae, patellae, and sternum (see Images 14, 18, and 20). Case reports describe occurrences in the temporal bone7 and thoracic spine.8
The symptoms and signs of chondroblastomas are nonspecific and include local pain, tenderness, swelling, and muscle wasting. Joint effusion occurs in approximately 30% of patients. Symptoms may vary in duration (months to years) before diagnosis.
A relatively high rate of tumor recurrence (10-35%) has been reported for chondroblastomas.6 Risk factors for recurrence include a larger-than-average lesion (>3.7 cm), a secondary aneurysmal bone cyst, and a location in the proximal femur or pelvis.6 The recurrence with the last factor may be due to the difficulty in gaining surgical access in these locations and to cautiousness in removing the lesion to avoid compromising the blood supply to the femoral head.
The preferred modalities for evaluation of chondroblastomas are standard radiography and either computed tomography (CT) scanning or magnetic resonance imaging (MRI).
Underexposed radiographs may fail to depict a chondroblastoma. CT scanning may be useful for the better definition of possible cortical erosion and matrix mineralization, although this modality is usually inferior to MRI in the evaluation of transphyseal or transcortical extension, both of which are important factors in preoperative planning. Other modalities may be useful on a case-by-case basis.
Chondrosarcoma
Eosinophilic Granuloma, Skeletal
Giant Cell Tumor
Hemangioma, Bone
Osteomyelitis
Degenerative cysts of osteoarthritis (eg, subchondral cysts, geodes)
Intraosseous ganglion
Avascular necrosis
The radiographic appearance of chondroblastomas is reflected by the benign, slow-growing nature of these lesions. The tumors typically arise in the epiphysis of a long bone, most commonly in the lower extremities. They are usually round or oval, geographic, lucent lesions with sharply marginated borders (see Image 1). The rim may be sclerotic, nonsclerotic, or incompletely sclerotic. About 80% of chondroblastomas are 1-4 cm in diameter, although lesions as large as 13 cm have been reported. An eccentric position of the tumor in the epiphysis is most common, but central locations sometimes occur. Approximately 40-50% of chondroblastomas are confined to the epiphysis, with the remainder demonstrating metaphyseal extension (see Images 1-4).
Chondroblastomas have variable matrix mineralization patterns. About 40% are uniformly lucent, and 60% have a mottled opacity due to amorphous calcification or peripheral septae. The calcifications occur less often in the punctate, "rings and arcs" form. Opacity due to septae and calcification is best differentiated on CT scans.
With increasing size, chondroblastomas may extend into the metaphysis and cause endosteal scalloping, bulging of the overlying cortex, and/or periosteal reaction. Periosteal reaction occurs in 15-30% of cases and may be solid or laminated (see Image 21), but it never occurs in the aggressive sunburst or Codman triangle pattern. The longer the lesion is present, the more likely the presence of periosteal reaction and matrix mineralization. Periosteal reaction may be distant from the actual tumor; this finding is not completely understood.
CT scanning with a review of the soft-tissue and bone windows is rarely necessary. Typically, this modality is reserved for the evaluation of aggressive or recurrent tumors. CT scans can depict matrix mineralization, soft-tissue extension, and cortical erosion, if present. A fluid-fluid level may be identified; this is a nonspecific finding that also occurs with aneurysmal bone cysts, giant cell tumors, and telangiectatic osteosarcoma. Coronal and sagittal reconstructions, like conventional CT scans, can be used to assess extension across the physeal plate (see Image 2).
MRI provides useful information regarding the extent of the tumor when a chondroblastoma extends to the metaphysis. The signal-intensity characteristics of the chondroblastoma reflect the prominent cellular stroma of the tumor, which has low signal intensity on T1-weighted images and variable signal intensity on T2-weighted images (see Images 4, 7, and 9).9 Foci of hypointense signals in the lesion on T2-weighted images are purportedly correlated with the histologic findings of abundant immature chondroid matrix, chondroblastic hypercellularity, calcification, and hemosiderin deposition.9 Occasionally, the hypointensity is uniform throughout the lesion. As with CT scans, MRIs may show fluid-fluid levels (see Image 22).
In contrast to chondroblastomas, the signal intensities of enchondromas, osteochondromas, and well-differentiated osteosarcomas tend to be high on T2-weighted images. Clear cell chondrosarcomas, however, show characteristics similar to those of chondroblastomas, and the signal intensity on T2-weighted images varies with the cellularity of the tumor and the extent of the adjacent inflammatory change. (Also see the eMedicine Radiology articles Enchondroma and Enchondromatosis, Osteochondroma and Osteochondromatosis, Osteosarcoma, Classic, and Osteosarcoma, Variants.)
The adjacent inflammatory changes, not seen with standard radiography or CT scans, are usually hyperintense on T2-weighted MRIs. This adjacent signal-intensity abnormality may be misleading because its extent is discordant with the radiographic appearance. When such discordance is encountered, the radiographic findings should be the basis for the diagnosis.
Ultrasonography currently has no role in the evaluation of chondroblastomas.
Nuclear medicine studies have limited value in the evaluation of chondroblastomas. Avid uptake of the bone-seeking radiopharmaceutical may, in part or in whole, be due to the regional hyperemia of the tumor (see Image 12). In the presence of a periosteal reaction, radionuclide uptake may extend beyond the lesion margins (see Image 23). If radionuclide uptake is present in multiple areas, chondroblastomas are less likely than enchondromas or osteochondromas, which are more frequently multiple.
Angiography may be used to create a vascular road map of the chondroblastoma for surgical planning, but the angiograms usually show no vascular abnormality. A periosteal reaction and neovascularity at the cortical surface near the tumor site or in the adjacent synovium have been described. Vascular displacement may be present if the tumor is large.
The therapy of choice is extended surgical curettage and packing with a bone graft or polymethylmethacrylate (PMMA). In skeletally immature patients, filling of the defect with PMMA is recommended because the polymer agent may allow continued skeletal growth — a concern in young patients — while residual tumor cells are destroyed. In older patients in whom skeletal growth is not an issue, bone grafting is recommended for smaller lesions. For large lesions, excision and cementation or reconstruction may be required.
PMMA packing is recommended over bone grafting after the removal of recurrent lesions or lesions that are likely to recur. If a secondary aneurysmal bone cyst is present, the use of phenol or cryosurgery should be considered because of the higher local recurrence rate that has been reported with these lesions.
Angiographic embolotherapy has no role in cases of chondroblastomas, although image-guided percutaneous therapy for difficult surgical cases may become more common in the future.
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Jambhekar NA, Desai PB, Chitale DA, Patil P, Arya S. Benign metastasizing chondroblastoma: a case report. Cancer. Feb 15 1998;82(4):675-8. [Medline]. [Full Text].
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Atalar H, Basarir K, Yildiz Y, Erekul S, Saglik Y. Management of chondroblastoma: retrospective review of 28 patients. J Orthop Sci. Jul 2007;12(4):334-40. [Medline].
Brien EW, Mirra JM, Kerr R. Benign and malignant cartilage tumors of bone and joint: their anatomic and theoretical basis with an emphasis on radiology, pathology and clinical biology. I. The intramedullary cartilage tumors. Skeletal Radiol. Jun 1997;26(6):325-53. [Medline].
Keenan S, Bui-Mansfield LT. Musculoskeletal lesions with fluid-fluid level: a pictorial essay. J Comput Assist Tomogr. May-Jun 2006;30(3):517-24. [Medline].
Tins B, Cassar-Pullicino V, McCall I, et al. Radiofrequency ablation of chondroblastoma using a multi-tined expandable electrode system: initial results. Eur Radiol. Apr 2006;16(4):804-10. [Medline].
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Codman tumor, cartilage-containing giant cell tumor, calcified giant cell tumor, epiphyseal chondromatous giant cell tumor, epiphyseal tumors, benign cartilaginous neoplasms, chondroclasts
Bonnie P Fines, MD, Consulting Staff, Department of Radiology, St Cloud Hospital
Bonnie P Fines, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, and Radiological Society of North America
Disclosure: Nothing to disclose.
Gregory Scott Stacy, MD, Assistant Professor, Department of Radiology, University of Chicago Hospitals
Gregory Scott Stacy, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Roentgen Ray Society, Radiological Society of North America, and Society of Skeletal Radiology
Disclosure: Nothing to disclose.
Michael A Bruno, MD, Associate Professor, Departments of Radiology and Medicine, Pennsylvania State University College of Medicine; Director, Radiology Quality Management Services, Milton S Hershey Medical Center, Pennsylvania State University College of Medicine
Michael A Bruno, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, and Society of Skeletal Radiology
Disclosure: Nothing to disclose.
Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
Murali Sundaram, MBBS, FRCR, FACR, Consulting Staff, Department of Diagnostic Radiology, The Cleveland Clinic Foundation
Disclosure: Nothing to disclose.
Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.
Felix S Chew, MD, MBA, EdM, Professor, Department of Radiology, Vice Chairman for Radiology Informatics, Section Head of Musculoskeletal Radiology, University of Washington
Felix S Chew, MD, MBA, EdM is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.
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