No abstract available

No abstract available

[en] Within a colony of beagle dogs that had received intravenous injections of ₂₂₆Ra there was a subgroup of dogs, each of which developed a painful lesion of a long bone. These bone lesions had their inception in bizarre, progressively expansile resorption cavities in which the process of normal bone tissue replacement was defective. On occasion, bone sarcomas arose in some of the sites of perturbed bone repair. This radiation-induced disturbance of the normal bone remodeling process with its preneoplastic spectrum of radiographic and histologic lesions was termed radiation-osteodystrophy. Lesions were studied by sequential radiography prior to the onset of clinical signs. Because of the painful nature of the lesion and difficulty experienced by the dogs in walking, full leg amputations were performed. This not only provided relief from clinical signs, but also permitted the dog to continue to live, allowing study of subsequently identified radiation-induced lesions

[en] Critical-point-drying of tumor tissue fixed in a glutaraldehyde-paraformaldehyde solution and viewed by scanning electron microscopy (SEM) provides a 3-dimensional view of tumor cells and their matrices. This report describes the SEM appearance of three primary bone tumors: a canine osteosarcoma of the distal radius, a feline chondrosarcoma of the proximal tibia and a canine fibrosarcoma of the proximal humerus. The ultrastructural morphology is compared with the histologic appearance of each tumor

[en] The distribution of ²²⁶Ra-induced bone sarcomas in beagles is discussed. Diagrams of skeletons are presented to show distribution of tumors in the axial and appendicular bones

No abstract available

[en] Radiographic and histologic findings from a mid-level group (38 dogs) of radium toxicity dogs showed 49 primary bone tumors with a high frequency of tumors within the axial skeleton. Additional primary bone tumors, bone tumors metastatic to bone, soft tissue metastases, and lung metastases were detected. No bone tumors were identified in 3 dogs. Lesions described as radiation osteodystrophy were found in all but 2 dogs

[en] This report concerns radiation-induced bone lesions in both the axial and appendicular skeleton in a group of 41 beagle dogs (R20), each of which received a total injected dose of 0.376 μCi ²²⁶Ra/kg body weight

No abstract available

[en] Shoulder joints of 149 Beagles over 8 years old at the time of death (mean age, 13.8 years +/- 3.21), were examined radiographically throughout their life-times for the frequency of degenerative joint disease (DJD). Clinical histories revealed no underlying cause for DJD. The shoulder joints of a subgroup of 18 dogs were examined at necropsy, and thin sections of the joints were evaluated radiographically and histologically. Serial clinical radiographic studies indicated that normal shoulder joint development during the first year of life was followed by the appearance of subchondral bone sclerosis and bony remodeling of normal joint contour, and by the formation of periarticular osteophytes and enthesiophytes. All changes were progressive with age and typical for DJD in dogs. Bilateral involvement was common. Evaluation of specimens obtained at necropsy revealed: articular cartilage change with roughening of the surface layer, degeneration and death of superficial chondrocytes, exposure of deeper layers of chondrocytes that had proliferated with fissuring of the damaged cartilage, total cartilage loss with polishing of the exposed subchondral bone, mixed patterns of subchondral bone sclerosis and osteoporosis, change in contour of the articular surfaces, and formation of periarticular osteophytes and enthesiophytes. Joint capsule thickening, synovitis, pannus formation, and synovial chondroma formation were observed. Because of the available clinical information, in addition to the typical changes of DJD, it was thought that the changes were primary. Instability appeared to play a role in the pathogenesis of the joint disease described; however, it was not clear whether the instability caused abnormal forces on healthy cartilage or whether the primary cartilage wear caused the instability