Osteoarthritis-like disorder in rats with vascular deprivation - Induced necrosis od the femoral head

Citation
D. Levin et al., Osteoarthritis-like disorder in rats with vascular deprivation - Induced necrosis od the femoral head, PATH RES PR, 195(9), 1999, pp. 637-647
Citations number
44
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
PATHOLOGY RESEARCH AND PRACTICE
ISSN journal
03440338 → ACNP
Volume
195
Issue
9
Year of publication
1999
Pages
637 - 647
Database
ISI
SICI code
0344-0338(1999)195:9<637:ODIRWV>2.0.ZU;2-K
Abstract
The reparative processes following vascular deprivation-induced necrosis of the femoral head were studied histologically in rats sacrificed 2, 7, 14, 21, 42 and 92 days postoperatively. The blood supply was severed by incisio n of the periosteum at the neck of the femoral head and transection of the ligamentum teres. Granulation tissue and a well-vascularized fibrous tissue originating from the joint capsule invaded the necrotic marrow spaces. Wit h progressive resorption of the necrotic tissues and osteoneogenesis, both appositional and intramembranous, within the fibrotic intertrabecular space s, the remodeling process led to a shift of the normal spongy architecture of the femoral head to a compacta-like one. In a few cases, osseous bridges bisected a necrotic physeal cartilage at the latest time intervals. The re modeling was associated with flattening of the femoral heads as well as wit h degenerative, regenerative and reparative alterations of the articular ca rtilage. In one of the two femoral heads obtained three months postoperativ ely, cystic spaces developed in the fibrous subchondral zone. Our findings are consistent with the view that ineffective attempts at restoring the pre necrotic state of the femoral head by replacing the necrotic with viable ti ssue triggers the collapse of the femoral head. Thickening and condensation of the subchondral bone, leading to increased stiffness of the subchondral zone, result in the osteoarthritis-like disorder. Mimicking the well-known phases of human osteonecrosis, the model readily allows for preclinical st udies of therapeutic regimens.