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Malignant Tumors of Jaw


Malignant Tumors of Jaw
Malignant tumors involving the jawbones are nearly always epidermoid carcinomas, which are formed from peripheral epithelium and invade the bones secondarily. Malignant transformation of a benign neoplasm, particularly of a mixed tumor of salivary tissue, is sometimes seen. Metastases of primary carcinoma of the thyroid, breast, or prostate to the jaws via the blood-stream are very rare, and so are malignant primary tumors of odontogenic, osteogenic, or other origin.

Though osteogenic sarcoma is the most common and most malignant of bone tumors, only 2% to 3% of cases appear in the jawbones. Trauma is believed to play a role in its etiology, as evidenced by clinical histories and experimental production in  animals.  It is  a  solitary growth, which differentiates it from various tumors of nonosteogenic origin (e.g., endothelioma, multiple myeloma). The maxillary tumor illustrated has caused wide, mottled destruction of bone, as revealed by radiographic findings. The classic “sun-ray” pattern seen in the long bones is seldom appreciated in the jaws, although new bone formation may be noted. The swelling can involve the entire maxilla and portions of the palate, with invasion into the antrum. Pain, paresthesia, swelling, tenderness, and displacement of teeth, with disturbed mastication, are associated symptoms. Hematologic metastasis can be an early phenomenon.
Malignant Tumors of Jaw

The histopathologic picture shows immature cells, which are pleomorphic and hyperchromatic, with some admixture of stroma, myxomatous tissue, cartilage, and osteoid tissue. Pathologic descriptions sometimes refer to osteolytic, osteoblastic, and telangiectatic (vascular) types. The osteoblastic variety tends to grow more slowly than the vascular type.
Fibrosarcoma may be formed peripherally and invade the jaws, or centrally from tissues of the tooth, germ or other mesenchymal enclaves, or connective tissue elements of the nerves and blood vessels. In the case of rapidly advancing osteolytic lesions, clinical recognition is usually delayed until loosening of the teeth, encroachment on the antrum or nose, or perforation of the cortical plate has occurred. No evidence of periosteal activity is noted, as is sometimes the case with osteosarcoma. Frequently, proud flesh in the socket of an extracted tooth is the first sign of an underlying malignancy. In the mandibular tumor chosen for illustration, pathologic fracture was caused by the widespread destruction of medullary bone. The tumor mass has perforated the lingual wall of the mandible, with invasion of soft tissues in the floor of the mouth and neck. Radiographic examination showed a blurred, diffuse osteolytic area, denoting an invasive rather than an expansile growth. The microscopic picture reveals spindle-shaped cells, with anaplasia and varying amounts of intercellular collagenous tissue; in the rapidly growing forms, a plump cellular shape with frequent mitoses is seen, but little intercellular material is present.
Carcinoma invading the mandible is illustrated in a lesion of the anterior floor of the mouth. The tumor here is a grade III malignancy, causing early infiltration of cortical bone, with progress along the haversian canals and destruction of a large portion of cancellous bone. At the same time, extension occurs through the lymph channels  to involve the submandibular and cervical nodes, as well as the soft tissues contiguous to the tumor. The base of the tongue has become fixed and immobile. A fungating tumor mass is observed in the floor of the mouth, which is secondarily infected and extremely painful, with a foul exudate and odor.