Hydraulic resistance: A measure of vascular outflow obstruction in osteonecrosis

Downey, Daniel J.; Simkin, Peter A.; Lanzer, William L.; Matsen, Frederick A.

doi:10.1002/jor.1100060215

Cited by 10 publications

(4 citation statements)

References 12 publications

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“…The femoral head is at an especially high risk of ischemic in-jury because of the absence of an effective collateral circulation [Downey et al, 1988]. Although different risk factors have been found that could lead to the disruption of the vascular supply, and several theories have been proposed and discussed elsewhere in detail [Lavernia et al, 1999;Assouline-Dayan et al, 2002], precise mechanisms still remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Changes in Bone Microarchitecture and Bone Mineral Density following Experimental Osteonecrosis of the Hip in Rabbits

Hofstaetter

Jin-Xi

Yan

et al. 2006

Cells Tissues Organs

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Background: Osteonecrosis of the femoral head is a common disorder which can lead to hip joint destruction usually necessitating total hip replacement. Methods: Quantitative micro-computed tomography, digital radiography and histology were used to characterize changes in bone microarchitecture and bone mineral density during the repair of the osteonecrotic femoral head as well as during the development of secondary osteoarthritis in the ipsilateral acetabulum. Osteonecrosis was induced surgically in 17 adult, male rabbits and the contralateral side was used as control. Results: At 4 weeks no changes in microarchitecture in the femoral head nor in the acetabulum were found. At 6 months the repair process led to an increase in bone mass in the trabecular region of the femoral head. However, a decrease in volumetric bone mineral density and an increase in apparent porosity were seen in the compact subchondral and cortical region of the osteonecrotic femoral head. At 6 months the subchondral bone of the osteoarthritic ipsilateral acetabulum was thicker, but had a lower volumetric bone mineral density and a higher apparent porosity. Conclusion: Resorption of necrotic compact bone may weaken the structural properties of the femoral head. Moreover, remodeling and resorption of subchondral bone may play a critical role in the disease process of osteoarthritis.

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Section: Introductionmentioning

confidence: 99%

Changes in Bone Microarchitecture and Bone Mineral Density following Experimental Osteonecrosis of the Hip in Rabbits

Hofstaetter

Jin-Xi

Yan

et al. 2006

Cells Tissues Organs

View full text Add to dashboard Cite

show abstract

“…Because of the absence of an effective collateral circulation, which could compensate for the severing of the primary blood supply, the femoral head is at an especially high risk of ischemic injury. 13…”

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confidence: 99%

Osteonecrosis of the Femoral Head of Laboratory Animals: The Lessons Learned from a Comparative Study of Osteonecrosis in Man and Experimental Animals

2003

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Animal models of osteonecrosis of the femoral head are indispensable to the understanding of successful treatment modalities for avascular necrosis of the femoral head in adults and in children with Legg-Calvé-Perthes disease. Many of these models adequately reflect the current "vascular deprivation" theory regarding the etiology of the disease. In addition to spontaneous occurrence, surgical- and corticosteroid-induced models are suitable, common experimental ones. Osteonecrosis of spontaneously hypertensive rats appears to be due to defective bone formation and compression of the arteries entering the femoral head at its lateral facets by daily weight-bearing loads. Successful modeling of surgical-induced femoral capital necrosis can be a challenge in animals with a dual epiphyseal blood supply. High doses of corticosteroids are a pivotal risk factor in the development of osteonecrosis. The pathogenesis of corticosteroid-induced osteonecrosis likely resides in reduced blood flow. Steroids may reduce blood flow by numerous mechanisms, including marrow adipocytic hypertrophy leading to sinusoidal compression, venous stasis and, eventually, obstruction of the arteries, and arterial occlusion by fat emboli and lipid-loaded fibrin-platelet thrombi. Other, less common varieties of osteonecrosis include those secondary to endotoxin-induced disseminated intravascular coagulation, immune reactions, immoderately low or high temperatures, and high-impact-related injuries. Common to these diverse forms of osteonecrosis are fibrin thrombi clogging arterioles and small arteries.

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“…Irrespective of where the blood flow is initially disrupted, i.e. at the level of arteries, veins, capillaries or sinusoids, the circulation in the arteries is ultimately arrested [3]. …”

Section: Introductionmentioning

confidence: 99%

Vasculature deprivation – induced osteonecrosis of the rat femoral head as a model for therapeutic trials

Bejar

Peled

Boss

2005

Theor Biol Med Model

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Experimental Osteonecrosis: The authors' experience with experimentally produced femoral capital osteonecrosis in rats is reviewed: incising the periosteum at the base of the neck of the femur and cutting the ligamentum teres leads to coagulation necrosis of the epiphysis. The necrotic debris is substituted by fibrous tissue concomitantly with resorption of the dead soft and hard tissues by macrophages and osteoclasts, respectively. Progressively, the formerly necrotic epiphysis is repopulated by hematopoietic-fatty tissue, and replaced by architecturally abnormal and biomechanically weak bone. The femoral heads lose their smooth-surfaced hemispherical shape in the wake of the load transfer through the hip joint such that, together with regressive changes of the joint cartilage and inflammatory-hyperplastic changes of the articular membrane, an osteoarthritis-like disorder ensues.Therapeutic Choices: Diverse therapeutic options are studied to satisfy the different opinions concerning the significance of diverse etiological and pathogenic mechanisms: 1. Exposure to hyperbaric oxygen. 2. Exposure to hyperbaric oxygen and non-weight bearing on the operated hip. 3. Medication with enoxaparin. 4. Reduction of intraosseous hypertension, putting to use a procedure aimed at core decompression, namely drilling a channel through the femoral head. 5. Medication with vascular endothelial growth factor with a view to accelerating revascularization. 6. Medication with zoledronic acid to decrease osteoclastic productivity such that the remodeling of the femoral head is slowed.Glucocorticoid-related osteonecrosis appears to be apoptosis-related, thus differing from the vessel-deprivation-induced tissue coagulation found in idiopathic osteonecrosis. The quantities of TNF-α, RANK-ligand and osteoprotegerin are raised in glucocorticoid-treated osteoblasts so that the differentiation of osteoclasts is blocked. Moreover, the osteoblasts and osteocytes of the femoral cortex mostly undergo apoptosis after a lengthy period of glucocorticoid medication.

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Hydraulic resistance: A measure of vascular outflow obstruction in osteonecrosis

Cited by 10 publications

References 12 publications

Changes in Bone Microarchitecture and Bone Mineral Density following Experimental Osteonecrosis of the Hip in Rabbits

Changes in Bone Microarchitecture and Bone Mineral Density following Experimental Osteonecrosis of the Hip in Rabbits

Osteonecrosis of the Femoral Head of Laboratory Animals: The Lessons Learned from a Comparative Study of Osteonecrosis in Man and Experimental Animals

Vasculature deprivation – induced osteonecrosis of the rat femoral head as a model for therapeutic trials

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