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BONE-FORMING TUMORS

Common to all these neoplasms is the production of bone by the neoplastic cells. The tumor bone is usually deposited as woven trabeculae (except in osteomas) and is variably

mineralized.

Osteoma

Osteomas are bosselated, round to oval sessile tumors that project from the subperiosteal or endosteal surfaces of the cortex. Subperiosteal osteomas most often arise on or inside the

skull and facial bones. They are usually solitary and are detected in middle-aged adults. Multiple osteomas are seen in the setting of Gardner syndrome ( Chapter 17 ). They are

composed of woven and lamellar bone that is frequently deposited in a cortical pattern with haversian-like systems. Some variants contain a component of trabecular bone in which the

intertrabecular spaces are filled with hematopoietic marrow. Histologically the reactive bone induced by infection, trauma, or hemangiomas may simulate an osteoma and should be

considered in the differential diagnosis.

Osteomas are generally slow-growing tumors of little clinical significance except when they cause obstruction of a sinus cavity, impinge on the brain or eye, interfere with function of

the oral cavity, or produce cosmetic problems. Osteomas do not transform into osteosarcoma.

Osteoid Osteoma and Osteoblastoma

Osteoid osteoma and osteoblastoma are terms used to describe benign bone tumors that have identical histologic features but that differ in size, sites of origin, and symptoms. Osteoid

osteomas are, by definition, less than 2 cm in greatest dimension and usually occur in patients in their teens and twenties. Seventy-five per cent of patients are under age 25, and men

outnumber women 2:1. Osteoid osteomas can arise in any bone but have a predilection for the appendicular skeleton. Fifty percent of cases involve the femur or tibia, where they

commonly arise in the cortex and less frequently within the medullary cavity. Osteoid osteomas are painful lesions. The pain, which is caused by excess prostaglandin E2 produced by

the proliferating osteoblasts, is severe in relation to the small size of the lesion, is characteristically nocturnal, and is dramatically relieved by aspirin.[33] Osteoblastoma differs from

osteoid osteoma in that it more frequently involves the spine; the pain is dull, achy, and not responsive to salicylates; and it does not induce a marked bony reaction.

Morphology.

Grossly, both osteoid osteoma and osteoblastoma are round to oval masses of hemorrhagic gritty tan tissue. Histologically, they are well circumscribed and composed of a morass of

randomly interconnecting trabeculae of woven bone prominently rimmed by osteoblasts ( Fig. 26-21 ). The stroma surrounding the tumor bone consists of loose connective tissue that

contains many dilated and congested capillaries. The relatively small size and well-defined margins of these tumors in combination

Figure 26-21Osteoid osteoma composed of haphazardly interconnecting trabeculae of woven bone that are rimmed by prominent osteoblasts. The intertrabecular spaces are filled by



vascular loose connective tissue.

Figure 26-22Specimen radiograph of intracortical osteoid osteoma. The round radiolucency with central mineralization represents the lesion and is surrounded by abundant reactive

bone that has massively thickened the cortex.

Figure 26-23Major sites of origin of osteosarcomas. The numbers are approximate percentages.

Figure 26-24Osteosarcoma of the upper end of the tibia. The tan-white tumor fills most of the medullary cavity of the metaphysis and proximal diaphysis. It has infiltrated through the

cortex, lifted the periosteum, and formed soft tissue masses on both sides of the bone.

Figure 26-25Osteosarcoma. Coarse, lacelike pattern of neoplastic bone produced by anaplastic malignant tumor cells. Note the mitotic figures.

Figure 26-26Distal femoral osteosarcoma with prominent bone formation extending into the soft tissues. The periosteum, which has been lifted, has laid down a proximal triangular

shell of reactive bone known as a Codman triangle (arrow).

Figure 26-27Schematic of the development over time of an osteochondroma, beginning with an outgrowth from the epiphyseal cartilage.

Figure 26-28Enchondroma with a nodule of hyaline cartilage encased by a thin layer of reactive bone.

Figure 26-29Enchondroma of the phalanx with a pathologic fracture. The radiolucent nodules of hyaline cartilage scallop the endosteal surface.

Figure 26-30Chondroblastoma with scant mineralized matrix surrounding chondroblasts in a chicken wire-like fashion.

Figure 26-31Chondromyxoid fibroma with prominent stellate and spindle cells surrounded by myxoid matrix. Occasional osteoclast-type giant cells are also present.

Figure 26-32Chondrosarcoma with lobules of hyaline and myxoid cartilage permeating throughout the medullary cavity, growing through the cortex, and forming a relatively wellcircumscribed

soft tissue mass.

Figure 26-33Anaplastic chondrocytes within a chondrosarcoma.

Figure 26-34Nonossifying fibromas of the distal tibial metaphysis, producing an eccentric lobulated radiolucency surrounded by a sclerotic margin.

Figure 26-35Storiform pattern created by benign spindle cells with scattered osteoclast-type giant cells characteristic of a fibrous cortical defect and nonossifying fibroma.

Figure 26-36Fibrous dysplasia composed of curvilinear trabeculae of woven bone that lack conspicuous osteoblastic rimming and arise in a background of fibrous tissue.

Figure 26-37Ewing sarcoma composed of sheets of small round cells with small amounts of clear cytoplasm.

Figure 26-38Benign giant cell tumor illustrating an abundance of multinucleated giant cells with background mononuclear stromal cells.

Figure 26-39Magnetic resonance image of a giant cell tumor that replaces most of the femoral condyle and extends to the sub-chondral bone plate.

Figure 26-40Severe osteoarthritis with small islands of residual articular cartilage next to exposed subchondral bone. 1, Eburnated articular surface. 2, Subchondral cyst. 3, Residual

articular cartilage.

Figure 26-41Severe osteoarthritis of the hip. The joint space is narrowed, and there is subchondral sclerosis with scattered oval radiolucent cysts and peripheral osteophyte lipping

(arrows).

Figure 26-42Rheumatoid arthritis. A, Schematic view of the joint lesion. (Modified from Feldmann M: Development of anti-TNF therapy for rheumatoid arthritis. Nat Rev Immunol

2:364, 2002.) B, Low magnification reveals marked synovial hypertrophy with formation of villi. C, At higher magnification, subsynovial tissue containing a dense lymphoid aggregate

is seen.

Figure 26-43Subcutaneous rheumatoid nodule with an area of necrosis (top) surrounded by a palisade of macrophages and scattered chronic inflammatory cells.

Figure 26-44Immunopathogenesis of rheumatoid arthritis.

Figure 26-45Rheumatoid arthritis. A, Early disease, most marked in the second metacarpophalangeal joint, where there is narrowing of joint space and marginal erosions on both radial

and ulnar aspects of the proximal phalanx (see inset). B, More advanced disease with loss of articular cartilage, narrowing of joint spaces of virtually all the small joints, and ulnar

deviation of the fingers. There is dislocation of the second, third, and fourth proximal phalanges produced by advanced articular disease. (Courtesy of Dr. John O'Connor, Boston

University Medical Center, Boston, MA.)

TABLE 26-7-- Classification of Gout


Date: 2016-04-22; view: 713


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