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Summary: A 7‐year‐old Holsteiner gelding was presented with a left common digital extensor sheath effusion of one‐year's duration. Radiographic examination revealed two extra‐articular mineralised bodies adjacent to the dorsolateral carpometacarpal joint. Ultrasonography confirmed an intrathecal location of one mineralised body in the common digital extensor sheath, palmar fraying of the common digital extensor tendon and tenosynovitis. Ultrasound could not confirm whether the second mineralised body was intrathecal or located external to the common digital extensor sheath. Common digital extensor tenoscopy facilitated removal of both mineralised bodies and revealed a fistula communicating with the carpometacarpal joint. The mineralised bodies, initially thought to be synovial osteochondromas, were histologically identified as para‐articular osteochondromas. There are no previously published reports of para‐articular chondroma/osteochondroma in the horse. Despite surgical removal of the para‐articular osteochondromas, concern for future extensor sheath distension remained given the communication between the carpometacarpal joint and common digital extensor sheath. [ABSTRACT FROM AUTHOR]

At the Laboratory for Energy-related Health Research at the University of California, Davis, semimonthly injections of 226Ra were given to a group of beagle dogs, and periodic skeletal radiography followed, as well as histological studies of the bones. At the Center for Human Radiobiology (Argonne National Laboratory, Massachusetts Institute of Technology, New Jersey Radium Research Project) measurements were made of radium body content in 2259 occupationally or iatrogenically exposed persons. Of these, 1768 had skeletal radiography (one or more times). In humans, the radiographic changes were, in decreasing order of frequency, osteolytic cortical and cancellous bone destruction, bone sclerosis, pathological fracture, and avascular necrosis of bone. In beagles, osteolytic destruction and pathological fractures were common, avascular necrosis was not observed, but there was frequently cortical thickening and new-bone formation in cancellous bone. In bath population groups, there was a high incidence of bone sarcoma. In the beagles, one high-dosage group numbering 38 dogs had 49 malignant bone tumors. Among the 2259 measured persons, there were 60 who had bone sarcoma, and 29 who had cancer of the mastoids or paranasal sinuses. No significant skeletal effects have been diagnosed radiologically in persons with systemic intakes of 226Ra or 228Ra below about 10 μCi or with skeletal doses below about 100 rad. In humans, the lowest skeletal dose at which a bone sarcoma has been diagnosed is 890 rad, and the lowest intake associated with a bone sarcoma is 96 μCi 226Ra or about 1.7 μCi per kg body weight. [ABSTRACT FROM AUTHOR]

Morphologic changes resulting from the effects of chronic radionuclide toxicity (226Ra) in the skeletons of workers in the radioluminescent dial painting industry with preterminal body burdens ranging from about 1.5 to 0.042 μCi were compared with the pathologic alterations in the skeletons of a group of 38 beagle dogs injected with 1.12 μCi/kg. Similarities observed in the skeletal responses of the two species were the presence of (1) dead bone tissue with delayed resolution, (2) a chronic disturbance in the remodeling mechanism of bone tissue, and (3) radiation-induced bone sarcomas. A detailed analysis of sequential changes in radiographic lesions arising in the beagle skeletons, complemented by histopathologic evaluation at the time of limb amputation or at necropsy, has enabled us to examine the disturbance in the bone remodeling process. The perturbation of critical importance in the generation of primary bone tumors appears to lie in the bone tissue formation and deposition phase of the bone remodeling process and gives rise to a spectrum of histologic patterns which we have termed “radiation osteodystrophy.” While some of the newly generated patterns demonstrate indolent behavior with fibrous tissue replacement and bone marrow refill, other sites of bone resorption are replaced by a unique fibro-osseous tissue response resembling fibrous dysplasia or osteoblastoma. Some of these proliferative lesions may. undergo progressive malignant degeneration. While the more indolent part of the spectrum was also seen in human skeletal tissues, only premalignant and early sarcomatous stages were seen in canine tissues. [ABSTRACT FROM AUTHOR]

Summary This paper reviews most of the important clinical syndromes currently considered as examples of articular osteochondroses based on the belief that they arise from a primary lesion in the articular cartilage that produces failure in endochondral ossification. Arguments are made why a number of syndromes are not osteochondroses. Because morphological lesions resembling osteochondrosis can be produced at osteochondral junctions from primary disorders centred in the growth cartilages (dyschondroplasia) or in the capillary bed that replaces the cartilage model during endochondral ossification, the definition of osteochondrosis in horses needs to be reexamined. Because the morphology of an individual lesion of osteochondrosis provides little insight into its fundamental cause, this paper suggests that the pattern of skeletal distribution of the lesions in affected individuals may help distinguish between foals with the idiopathic (constitutional defects in the cartilage model) and acquired forms of osteochondrosis. In foals with acquired osteochondrosis when the cause of the defect in endochondral ossification is known, the cause of the disorder should be included in naming the clinical syndrome, e.g. traumatic osteochondrosis or zinc-induced osteochondrosis. The search for the key to the pathogenesis of osteochondrosis in horses can only begin after the fundamental mechanisms causing perturbations of endochondral ossification are better understood. [ABSTRACT FROM AUTHOR]