Multiple cartilaginous exostosis (MCE) is considered a developmental condition of growing dogs. There is evidence that the etiology of this condition may have a heritable component.332,358 The actual incidence of MCE is difficult to determine because affected dogs may show no signs and the diagnosis is often incidental. Lesions occur by the process of endochondral ossification when new bone is formed from a cartilage cap analogous to a physis. Lesions are located on bones, which form from endochondral ossification, and lesions stop growing at skeletal maturity. Malignant transformation of MCE lesions has been reported, but generally, they remain as unchanged, mature, bony projections from the surface of the bone from which they arose.333
Dogs typically present because of a nonpainful or moderately painful palpable mass on the surface of a bone or bones. The pain and lameness is thought to be due to mechanical interference of the mass with the overlying soft tissue structures. In the case of MCE of vertebral bodies, animals can present with clinical signs associated with spinal cord impingement. Radiographically, there is a bony mass on the surface of the affected bone, which has a benign appearance with fine trabecular pattern in the body of the mass (Figure 24-14). To obtain a histologic diagnosis, biopsy material must be collected so sections can include the cartilaginous cap and the underlying stalk of bone. Histologically, this cartilaginous cap gives rise to an orderly array of maturing bone according to the sequence of endochondral ossification. The cortical bone surfaces of the mass and the adjacent bone are confluent.331 A strong presumptive diagnosis is made by evaluation of the physical findings, history, and radiographic findings.
Figure 24-14 Lateral radiograph of a multiple cartilaginous exostosis lesion of the dorsal spinous process in a dog (A).
Treatment involves conservative surgical excision, but this is only necessary if signs do not abate after the dog is skeletally mature. Because of the likelihood of a heritable etiology, affected dogs should not be bred. Owners should also be advised of the possibility of late malignant transformation. Dogs with a previous history of MCE should be carefully evaluated for bone malignancy if signs return later in life.
Cysts are rare, benign lesions of bone. The majority of the veterinary literature pertaining to bone cysts centers on several small series of cases or single case reports.359-363 Affected animals are often young and present because of mild or moderate lameness; however, pathologic fracture can occur through cystic areas of long bones, leading to severe lameness. There appears to be a familial tendency in Doberman pinschers and Old English sheepdogs. The nomenclature in various reviews of canine bone cysts is confusing. By definition, a cyst is a fluid-filled sac lined by epithelium. The only true cyst of primary intraosseous origin is a simple bone cyst (SBC, or unicameral bone cyst). These lesions are usually in metaphyseal regions of long bones, and they can adjoin an open growth plate. Sometimes, however, unicameral bone cysts can be diaphyseal or epiphyseal. Neither the etiology nor the pathogenesis is known, but it is speculated that the lesions may be the result of trauma to the growth plate interfering with proper endochondral ossification. Others have theorized that with the rapid resorption and deposition of bone occurring in the metaphysis of a young animal, a cyst might develop if resorption is so rapid that a focus of loose fibrous tissue forms. The focus of fibrous tissue may then obstruct the thin-walled sinusoids, causing interstitial fluid to build up and form a cyst. The theory that appears to be partially substantiated is the synovial “rest” thesis. It is suggested that during fetal development a “rest” of synovial or perisynovial tissue becomes misplaced or incorporated into the adjacent osseous tissue. If this tissue remains or becomes functional, subsequent synovial secretion results in a cyst developing in the bone. Cysts have been described in bone just below articular cartilage (subchondral bone cysts or juxtacortical bone cysts).361,362,364 In these, it has often been possible to demonstrate direct communication with the articular synovial membrane. Radiographically, SBCs are single or, more commonly, multilocular, sharply defined, centrally located, radiolucent defects in the medullary canal of long bones. Variable degrees of thinning of the cortex with symmetric bone “expansion” are often a feature of the radiographs (Figure 24-15). The diagnosis cannot be reliably made from interpretation of radiographs alone. Lytic OS can be misdiagnosed as SBC. Diagnosis of an SBC relies on the histologic finding of a thin, fibrous wall lined by flat to slightly plump layers of mesothelial or endothelial cells. Treatment consists of meticulous curettage and packing the space with autogenous bone graft.
Figure 24-15 Lateral radiograph of a distal radial bone lesion histologically confirmed as a simple bone cyst (SBC). Typical radiographic features include a multilocular, sharply defined, centrally located radiolucency, without evidence of cortical destruction.
Aneurysmal bone “cysts” (ABCs) are spongy, multiloculated masses filled with free-flowing blood. The walls of an ABC are rarely lined by epithelium, and the lesion is possibly an arteriovenous malformation. A proposed pathogenesis of ABCs is that a primary event such as trauma or a benign bone tumor occurs within the bone or periosteum. This event disrupts the vasculature, resulting in a rapidly enlarging lesion with anomalous blood flow, which damages the bone mesenchyme. The bone reacts by proliferating. As the vascular anomaly becomes stabilized, the reactive bone becomes more consolidated and matures. It is important to differentiate these lesions from OS or other malignant lesions of bone. The age of affected dogs ranges from 2 to 14 years, but it has been reported in a 6-month-old dog.360 Treatment can be achieved by en bloc resection and reconstruction, but extensive curettage with packing of the defect with autogenous bone graft can be effective.
Primary tumors involving the bones of cats are rare. An estimate of the incidence of all bone tumors in cats is 4.9 per 100,000.365 Between 67% and 90% of bone tumors in cats are histologically malignant. OSs are the most common primary bone tumor in cats accounting for 70% to 80% of all primary malignant cancer of cats. Feline OS occurs in appendicular or axial skeletal sites and extraskeletal sites. OS occurs in appendicular long bones approximately twice as often as in axial skeleton sites.366 However, in one study, 50 of 90 skeletal OS cases were appendicular and 40 of 90 were axial.367 Axial OS originates most commonly in the skull (especially oral cavity) and pelvis but is also reported in the ribs and vertebrae. The disease in cats differs from that in dogs in that the primary lesions occur more often in hind limbs in cats (distal femur and proximal tibia) and the disease is reported to be far less metastatic than in dogs.368 In a large feline OS case study, 56 of 146 cases were extraskeletal in origin, with the most commonly affected sites being those commonly used for vaccination: interscapular, dorsal lumbar, or thigh areas. Other locations included ocular/orbital, oral, intestinal, and mammary sites. No mention is made of any differences in the pathology of these tumors in comparison to skeletal sites.367 There are case reports of feline extraskeletal OSs in the flank, liver, and duodenum.369-371
OS generally affects older cats (reported mean ages of 8.5,366 10,368 10.2,368 and 10.7372 years), but the age range of reported cases is large (1 to 20 years), so bone lesions in younger cats cannot be ruled out as OSs based on age criteria alone. The age at presentation for axial OS is greater than appendicular OS.367 Conflicting reports on gender predisposition exist with either no difference between sexes or a slight male predisposition.366-368,372 OS was reported to arise after a limb fracture was repaired with an intramedullary pin in one cat and following RT in another.38
MCE is a disease that occurs after skeletal maturity in cats. This is in contrast to dogs in which exostoses develop before closure of growth plates. Also, in contrast to dogs, the lesions seldom affect long bones, are rarely symmetric, and are probably of viral rather than familial origin. There does not appear to be any breed or sex predisposition, although early reports of this condition were in the Siamese.373 Affected cats range in age from 1.3 to 8 years (mean 3.2 years).374 Virtually all cats with MCEs will test positive for feline leukemia virus (FeLV) antigenemia. This disease has an aggressive natural behavior.
The histologic characteristics of feline OS are similar to canine OS. OS of cats is composed of mesenchymal cells embedded in malignant osteoid. There may be a considerable amount of cartilage present, and osteoid may be scant. A feature of some feline OS cases is the presence of multinucleate giant cells, which may be numerous. Reactive host bone and remnants of host bone are often present in specimens. Tumors are seen to be invasive; however, some surrounding soft tissue may be compressed rather than infiltrated. There is often variation of the histologic appearance within the tumor, with some portions having a more fibrosarcomatous appearance and others more cartilaginous. Some authors have described subtypes that resemble those seen in dogs: chondroblastic, fibroblastic, and telangiectatic, as well as the giant cell variant. These histologic subtypes, however, do not appear to confer any prognostic predictive value.375,376 OSs in cats are locally aggressive but have a low metastatic rate compared to canine OS. Feline OS can be of the juxtacortical type.
Osteochondroma may occur as a solitary lesion in cats, but there is a form that is multicentric (osteochondromatosis). The lesions are composed of hard, irregular exostoses with a fibrous and cartilaginous cap.377 Endochondral ossification occurs from the cartilage cap, which extends to a variable thickness. This cap tends to blend with adjacent tissue, making its surgical removal difficult. Cats usually develop multiple sites of disease, and there is a potential for malignant transformation and metastasis. The presence of FeLV antigenemia is also a foreboding prognostic finding for these cats.
The most common signs of OS are lameness, swelling, and deformity, depending on the location of the lesion. The lesions may appear radiographically similar to the OS in dogs with mixed osteoblastic and osteolytic aggressive bone lesion with an ill-defined zone of transition between normal and tumor-affected bone; however, some cats have lesions arising from the periosteal surface (juxtacortical OS).366 Tumors can reach a large size without evidence of severe clinical signs. It is rare for cats to have metastatic OS at presentation.
Cats with viral-associated MCE have rapidly progressing, conspicuous, hard swellings over affected sites causing pain and loss of function. Common sites for lesion development are the scapula, vertebrae, and mandible; however, any bone can become affected. Radiographically, the lesions are either sessile or pedunculated protuberances from bone surfaces with indistinct borders with the normal bone. There may be a loss of smooth contour with evidence of lysis, particularly if there is malignant transformation.
Both OS and MCE may be suspected, based on the radiographic appearance of the lesions and the FeLV status of the cat. Definitive diagnosis is made by histopathologic evaluation of properly collected biopsy tissue. Metastatic rates for cats with primary bone tumors are low compared to dogs (5% to 10% versus >90%), and three-view thoracic radiographs are recommended as part of the staging process. Presurgical evaluation with a CBC, chemistry profile, and urinalysis is recommended to rule out concurrent disease.
Amputation is the recommended treatment for feline appendicular OS in which there are no clinically detectable metastatic lesions. Complete surgical excision of the primary tumor is prognostic for increased survival time, DFI, and recurrence-free interval.372 Due to the low metastatic rate and prolonged MSTs of 24 to 44 months with amputation alone,366,368 adjuvant chemotherapy is not indicated or recommended in cats, which is in contrast to the situation in dogs. No adjuvant therapy is known to be efficacious in extending survival time in cats. The MST for feline OS in axial sites (6.7 months) is lower than that of appendicular and extraskeletal OS sites.367 This likely reflects the difficulty of achieving complete resection and local tumor control in these anatomic sites rather than a difference in biologic behavior. A combination of surgical resection and RT may be appropriate in these cases. SRT has been used in several cats for local tumor control in appendicular and axial sites.
Histologic grade, using a grading scheme that evaluates tumor vascular invasion, pleomorphism, mitotic index, and tumor matrix and cell necrosis, is prognostic for survival.372 Specifically, tumors with high number of mitoses have a higher hazard ratio for decreased recurrence-free intervals. The metastatic potential of OS in cats (5% to 10%) is much less than for the same disease in dogs or humans. Reported anatomic sites for metastases are lung, kidney, liver, brain, and spleen. Cats with MCE have a guarded prognosis. Lesions may be removed surgically for palliation; however, local recurrences are common, or new, painful, debilitating lesions may occur. No reliably effective treatment is known for this condition in cats.
Non-OS primary bone tumors in cats are rare. Fibrosarcoma is the second most common primary bone tumor of cats.375 Chondrosarcoma is reported to be next in terms of frequency, and hemangiosarcomas rarely involve bones of cats.368 Little is known about the biologic behavior of these rare lesions. Aggressive surgical resection is the preferred treatment for these tumors. The metastatic rate is low; however, metastases have been seen in cats with chondrosarcoma and hemangiosarcoma.368,376
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