Experimentally produced osteonecrosis as a result of fat embolism.
Jones-JP Jr.; Sakovich-L; Anderson-CE
NIOSH 1974 Jan; :117-132
Experimental studies on rabbits were made to test the hypothesis that fat embolism of bone may be an initiating event in producing osteonecrosis. Focal and minute regions of avascular necrosis in bone and marrow were produced in the metaphyseal and epiphyseal zones of the right femoral heads of rabbits by a single infusion of .12 milliliters of Lipiodol (iodized oil) into the distal aorta. Fat emboli persisted up to five weeks after infusion. The presence of osteonecrosis was determined by roentgenographic, histologic, and radioautographic methods. Slightly increased bone density of questionable significance was observed at six and ten weeks after infusion. It is speculated that the etiological agent in dysbaric osteonecrosis may not be reversible with decompression therapy alone, but may also require the use of various lipid-clearing agents.
Bone-disorders; Musculoskeletal-system-disorders; Skeletal-system-disorders; Decompression-sickness; Circulatory-system-disorders; Blood-disorders; Clots;
Dysbarism-Related Osteonecrosis, NIOSH (Proceedings of a Symposium on Dysbaric Osteonecrosis, Galveston, Texas, February, 1972)