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Radiologic-Pathologic Conferences of The University of Texas M.D. Anderson Cancer Center |
1
Department of Diagnostic Radiology, Box 57, The University of Texas M. D.
Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030.
2
Department of Pathology, The University of Texas M. D. Anderson Cancer Center,
Houston, TX 77030.
Received November 23, 1999;
accepted after revision January 4, 2000.
From the weekly radiologic—pathologic correlation conferences
conducted by Gary J. Whitman.
Introduction
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Osteosarcoma is the most common primary malignant tumor of the skeleton after multiple myeloma. Craniofacial lesions account for fewer than 10% of lesions [1,2,3]. Fifty percent of lesions are mandibular, and 25% are maxillary [1]. Typically, the body of the mandible or alveolar ridge of the maxilla is affected in a man in his third or fourth decade [1,2,3]. Painful local swelling is the presenting symptom in 50% of patients [3], but maxillary and skull lesions are usually painless [2]. Dental symptoms occur in 25%, and cervical adenopathy is often absent [2, 3].
Osteosarcoma may arise de novo or in association with well-recognized precursors such as Paget's disease, radiation injury, bone infarcts, osteomyelitis, and certain clinical syndromes [1, 3]. Osteosarcoma after radiation typically develops after a latency period of 5-10 years after doses in excess of 3000 Gy [1]. These tumors characteristically occur at the edge of the radiation field because the administered radiation is unable to cause cell death but is sufficient to induce malignant transformation [2]. Osteosarcoma is also the most common second malignant neoplasm in survivors of familial or bilateral retinoblastoma [4, 5]. This disease is caused by a genetic mutation found in the tumor suppressor gene RB1 on chromosome 13, which not only increases the risk of de novo osteosarcoma but also potentiates the osteosarcoma-inducing ability of ionizing radiation [1, 4, 5]. Seventy percent of second malignant neoplasms occur within the field of therapeutic radiation [4, 5].
Histologically, osteosarcoma contains two basic components: proliferating tumor cells arising from undifferentiated bone-forming mesenchyma and an extracellular osteoid matrix [1, 2, 5]. On microscopy, a great morphologic variability is found, and division into osteoblastic, chondroblastic, or fibroblastic subtypes can be made on the basis of dominant differentiated element and matrix product [1,2,3].
Both CT and MR imaging are excellent for revealing tumor extent and as aids in presurgical planning. CT is superior in localizing matrix mineralization, periosteal bone reaction, and cortical destruction, whereas MR imaging is better in delineating soft-tissue and marrow infiltration and in differentiating tumor from sinus secretions [2, 3]. Craniofacial osteosarcomas are predominantly osteolytic with the exception of mandibular lesions, which are osteoblastic in 50% of patients [2]. Periosteal reaction is rare and found in mandibular lesions [2]. Tumor matrix mineralization and aggressive bone destruction is strongly suggestive of osteosarcoma [2, 3]. Presence of matrix mineralization and periosteal new bone formation favors a diagnosis of osteosarcoma over metastatic carcinoma, lymphoma, and myeloma; a destructive mass is generally not found in radiation osteitis. A less aggressive osteosarcoma may be radiologically indistinguishable from chondrosarcoma [2, 3].
The mainstay of treatment is surgical resection with negative margins [5]. The success of adjunct chemotherapy and radiation therapy is unproven, although they should be considered in view of the poor prognosis [5]. Mandibular osteosarcoma recurs locally in 50% of patients, and the rates are higher for maxillary and skull lesions [1]. The 5-year survival rates range from 23% to 59% [1, 3, 5].
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