A total of 13 dogs have been reported to have presented with one or more primary bone sarcomas (Table 53-1) in conjunction with multifocal intramedullary bone infarction.(4,9) Twelve of the thirteen had osteosarcomas, and one had fibrosarcoma involving bone. All of these dogs originally presented to the veterinarian for problems referable to the bone tumors, and the bone infarction was discovered radiographically.

The breeds, weights, and sites of tumor development of dogs with tumors and bone infarction differ from those of dogs with osteosarcomas without bone infarction. Five of the thirteen dogs were miniature schnauzers, and all of the remaining eight were mixed breed dogs. Osteosarcoma not associated with bone infarction is exceedingly rare in miniature schnauzers, and only 11% So of dogs with osteosarcoma are mixed breeds.(1) The average weight of dogs with bone infarctions was less than 12 kg, and the largest dog weighed 27.7 kg. None of the dogs with bone infarction were giant breeds. In nine of eleven dogs with a solitary primary osteosarcoma associated with bone infarctions, the tumor was in the bones of the rear leg. In the general population of dogs with osteosarcoma, the primary tumor occurs most frequently in the front leg. The ratio of front leg tumors to hind leg tumors in dogs with osteosarcomas not related to bone infarction is about 1:5:1.(1) Two dogs were identified radiographically as having multifocal medullary bone infarction without coexistent neoplasm. One of these dogs subsequently developed bone tumors. There are no clinical problems that can be attributed directly to the bone infarctions.

Four of the dogs had multiple osteosarcomas. In one dog two tumors were discovered at the time of initial examination, and in three others tumors occurred in bones elsewhere in the body following amputation. Other than this, the osteosarcomas in dogs with infarction were indistinguishable morphologically and in their biologic behavior from osteosarcomas not related to bone infarction.

The distribution of the intramedullary infarction was variable, but it was always seen in the limb bones distal to the distal third of the femur and distal to the elbow. Radiographically the medullary infarctions were characterized by irregularly demarcated areas of radiopacity in the medullary cavities (Fig. 53-1).

Histopathologically several abnormalities were found in the medullary cavities of bones with infarctions. Muscular arteries in the medullary cavities of all involved, bone showed a loss of the normal structures. There was a replacement of the wall of this artery and occlusion of the lumen by a concentric deposition of poorly cellular collagen (Fig. 53-2). Occasionally, foamy macrophages were seen. The vascular change was seen only in intramedullary arteries. Perfusion of postmortem specimens with latex showed a lack of filling of the nutrient arteries.

FIG. 53-1 Radiograph of the left radius and ulna shows osteosarcoma of distal radius. Infarcts are visible in the medullary cavity of the radius (arrow). (Dubielzig RR, Biery DN, Brodey RS: Bone sarcomas associated with multifocal medullary bone infarction in dogs. J Am Vet Med Assoc 179:64-68, 1981)

Some bone sections showed a deposition of poorly organized proliferative osteoid on the endosteal surface of the bone (Fig. 53-3). Osteoid of this type is typically produced in reaction to hypoxia. The radiopaque lesions seen in the medullary cavity correspond to these proliferative lesions. This proliferative osteoid resists complete decalcification in 15% formic acid. Some sections show vascular occlusion and proliferative hypoxic osteoid surrounded by viable bone marrow. The most severely diseased sections show coagulation necrosis of the bone marrow in addition to the other changes. In these areas there is often necrosis of trabecular bone and necrosis of the proliferative osteoid.

TABLE 53-1 Clinicopathologic Findings in 13 Dogs With Bone Sarcomas Associated With Bone Infarction

FIG. 53-2 Intramedullary artery from dog 8 shows laminar deposition of collagen occluding the lumen. Note duplication of the internal elastic lamina (straight arrow) and red blood cells trapped in the collagenous material (curved arrows). (VerhoeffFs elastic stain, x 100) (Dubielzig RR, Biery DN, Brodey RS: Bone sarcomas associated with multifocal medullary bone infarction in dogs. J Am vet Med Assoc 179:64 68, 1981

FIG. 53-3 Photomicrograph of bone specimen from dog 9 shows proliferation of abnormal osteoid (PO) on the endosteal surface of the laminar osteoid (LO). (Verhoeff's elastic stain, x 40) (Dubielzig RR, Biery DN, Brodey RS: Bone sarcomas associated with multifocal medullary bone infarction in dogs. J Am Vet Med Assoc 179:64-68, 1981)

These findings suggest a progression of lesions from vascular disease with no necrosis to hypoxia and subsequent reactive hyperplasia and finally infarction as evidenced by bone marrow and bone necrosis. It is not known if the infarction is a direct result of the vascular occlusion or results in part from pressure necrosis due to the proliferation of osteoid in the confined spaces of the marrow cavity.

The underlying problem appears to be the fibrosis and occlusion of the nutrient arteries. Morphologically this vascular disease is unlike vascular lesions seen in association with thrombosis, hypertension, atherosclerosis, and amyloidosis. No other vessels were involved in affected dogs.

In humans, bone infarction has been associated with trauma, fat embolization, hyperadrenal corticism, hyperviscosity, sickle-cell anemia, and alcoholism.(7,8) Bone infarction is an occupational hazard among workers exposed to dysbaric conditions, such as deep-sea divers and test pilots.(2) Idiopathic osteonecrosis occurs in mice, rats, hamsters, and guinea pigs. (10) In humans, bone sarcomas have been associated with preexisting medullary bone infarction.(3,5,6)

The etiology of the disease is unknown. Studies to date have failed to demonstrate predisposing diseases similar to those found in humans. Several of the dogs at one point or another had lipemia, and studies are in progress to study the fat metabolism of an affected dog.



1. Brodey RS, Riser WM: Canine osteosarcoma: A clinicopathologic study of 194 cases. Clin Orthop 62:54, 1969
2. Chryssanthou CP: Dysbaric osteonecrosis. Clin Orthop 130:94, 1978
3. Dorfman MD, Norman A, Wolff H: Fibrosarcoma complicating bone infarctions in a caisson worker. J Bone Joint Surg 48A:477, 1965
4. Dubielzig RR, Biery DN, Brodey RS: Bone sarcomas associated with multifocal bone infarction in dogs. J Am Vet Med Assoc 179:64, 1981
5. Furney JG, Ferrer-Torells M, Reagan JW: Fibrosarcoma arising at the site of bone infarcts. J Bone Joint Surg 42A:802, 1960
6. Galli SJ, Weintraub MP, Proppe KH: Malignant fibrous histiocytoma and pleomorphic sarcoma in association with medullar bone infarcts. Cancer 41:607, 1978
7. Jacobs B: Epidemiology of traumatic and non-traumatic osteonecrosis. Clin Orthop 130:51, 1978
8. Jones JP: Editorial comment: Osteonecrosis. Clin Orthop 130:2, 1978
9. Riser WH, Brodey RS, Biery DN: Bone infarctions associated with malignant bone tumors in dogs. J Am Vet Med Assoc 160:411, 1972
10. Sokoloff L, Havermann RT: Idiopathic necrosis of bone in small laboratory animals. Arch Pathol 65 :323, 1958