Etiology and pathogenesis: Hemorrhage and thrombus formation in early experimental osteonecrosis

Published

Journal Article

The aim of the current study was to test the hypothesis that the induction of an underlying immunologic condition in rabbits may enhance the development of steroid-induced osteonecrosis. Thirty-five adult rabbits were divided into four groups. Group I: 10 rabbits were immunized at 15-day intervals for 2 months by murine anti-bodies to deoxyribonucleic acid autoantibodies. Four weeks after the end of the immunization, the animals received injections of methylprednisolone for 7 days and then prednisolone per os for 8 months. Group II: 10 animals only received immunizations according to the protocol used in Group I. Group III: 10 animals only were treated with corticosteroids according to the protocol used in Group I. Group IV: five animals were used as controls. Various changes were ob in the proximal metaphysis and diaphysis of the femur in eight of 10 animals in Group I (80%) and in five of 10 animals in Group II (50%) when compared with the animals in Group III and Group IV. The most common feature was evidence of new and old hemorrhage through the sinusoids, exudative reaction and thrombus formation in veins and small arteries. Focal necrotic areas of bone marrow showed an accumulation of cell debris, residue of hemorrhage, and disappearance of marrow elements. These findings suggest that (1) corticosteroids ay potentiate the effects of a preexisting condition to increase the risk of osteonecrosis; (2) immunologic reaction may be an important factor in the pathogenesis of necrotic lesions; and (3) repeated intramedullary hemorrhage and thrombus formation may represent early major pathologic findings in bone necrosis.

Duke Authors

Cited Authors

  • Korompilias, AV; Gilkeson, GS; Seaber, AV; Urbaniak, JR

Published Date

  • January 1, 2001

Published In

Start / End Page

  • 11 - 18

Electronic International Standard Serial Number (EISSN)

  • 1528-1132

International Standard Serial Number (ISSN)

  • 0009-921X

Citation Source

  • Scopus