History
A 3-year-old sexually intact male Golden Retriever was evaluated for mild bilateral hind limb ataxia of 2 years' duration that had become worse during the 3 weeks prior to evaluation and multiple firm masses over the thorax and vertebral column. On physical examination, the dog was normothermic. Abnormal findings detected during neurologic examination included ataxia, conscious proprioceptive deficits, and hyper-reflexive to normal with-drawal and patellar reflexes in both hind limbs. Hyperesthesia was detected during palpation of the thoracic and lumbar portions of the vertebral column. Neuroanatomic lesion localization was compatible with a T3 through L3 myelopathy. No clinically important abnormalities were detected on CBC and serum biochemical analyses. Radiographs of the thorax were obtained (Figure 1).
Radiographic Findings and Interpretation
Multiple expansile osseous lesions ranging in size from 3 to 5 cm are evident on multiple ribs (Figure 2). Additional expansile lesions are evident on the spinous processes of the thoracic vertebrae with the largest lesion seen at the level of the second and third thoracic vertebrae. Radiographic findings are compatible with a diagnosis of multiple cartilaginous exostoses (MCE).
Comments
Multiple cartilaginous exostoses is a benign proliferative bone and cartilage disease that is seen more commonly in skeletally immature animals with growth typically stopping with skeletal maturation.1 Growth after maturity suggests neoplastic transformation. Bones that develop by endochondral ossification are most often affected, and multiple bone involvement is common. Dogs may have a familial tendency for MCE; however, no breed or sex predilections have been identified.1 Displacement of chondrocytes from the physis, creating a physis-like structure perpendicular to the long axis of the bone, has been implicated in the etiopathogenesis of MCE; however, the exact mechanism is not known.1
Clinical signs are caused by anatomic malformations, disfigurement, and compression of surrounding structures. Neurologic abnormalities are caused by proliferation of bony tissue causing compression of neural structures. Diagnosis is dependent on radiography of the entire skeleton and biopsy of lesions; however, the radiographic appearance of circumscribed, benign-appearing exostosis on multiple bones is pathognomonic for this unusual condition.1 In the dog of this report, results of myelography of the thoracic and lumbar portions of the vertebral column confirmed spinal cord compression at 2 thoracic sites from osseous proliferation associated with the spinous process (Figure 3).
Back-scattered scanning electron microscopy of biopsy specimens has recently been described as aiding in the histologic diagnosis of MCE2; the centripetal calcification pattern, composition, and maturity of the trabeculae can only be distinguished by this technique.2
Treatment in dogs with subclinical disease is not necessary because the disease is usually self-limiting after skeletal maturity. Radiographic monitoring is recommended because malignant transformation to chondrosarcoma or osteosarcoma has been reported.1 In dogs developing clinical disease, excision or decompression is indicated. The prognosis for severely affected or clinically affected growing dogs is guarded to poor. The prognosis has been reported as favorable in skeletally mature dogs with subclinical disease without evidence of neoplastic transformation.3
Because of the guarded to poor prognosis for the dog in this report, the owner chose to have the dog euthanized. Necropsy and histologic examination of lesions confirmed a diagnosis of MCE.
References
- 1.↑
Pool RR, Thompson KG. Tumors of bones. In: Meuten DJ, ed. Tumors in domestic animals. 4th ed. Ames, Iowa: Iowa State Press, 2002;245–317.
- 2.↑
Franch J, Font J, Ramis A, et al. Multiple cartilaginous exostoses in a Golden Retriever cross-bred puppy. Vet Comp Orthop Traumatol 2005;18:189–193.
- 3.↑
Gambardella PC, Osborne CA, Stevens JB. Multiple cartilaginous exostoses in the dog. J Am Vet Med Assoc 1975;166:761–768.