The effect of core decompression on femoral head blood flow in steroid-induced avascular necrosis of the femoral head.

Wang, G J; Dughman, S S; Reger, Steven I.; Stamp, Warren G.

doi:10.2106/00004623-198567010-00015

Cited by 67 publications

(36 citation statements)

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“…18 In the rigid intraosseous compartment, growth of fat cells may cause a rise in intraosseous pressure, and thereby compress the thin-walled sinusoids, with a subsequent decrease in bone blood flow. 3 We have found, however, decreased blood flow in the cortical bone of the proximal femur which does not contain sinusoids within the vascular bed. 19 Degenerative changes in the arteries and arterioles of the capsule of the hip and the femoral head have been found in cadavers of renal transplant patients without clinical hip symptoms.…”

Section: Discussionmentioning

confidence: 51%

“…Reduction of blood flow in the femoral head has been suggested as a mechanism. In one study in rabbits blood flow in the femoral head was shown to decrease after 6, 8 and 10 weeks of treatment with steroids, 3 and in another investigation multifocal osteonecrosis was shown to be present four weeks after treatment with a bolus of steroid. 4 A statistically significant correlation was found between the cumulative dose of methylprednisolone in the first month after heart transplantation and the development of avascular necrosis.…”

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confidence: 95%

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Selective reduction of bone blood flow by short-term treatment with high-dose methylprednisolone

Drescher

Schneider

Becker

et al. 2001

The Journal of Bone and Joint Surgery. British volume

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T reatment with corticosteroids is a risk factor for non-traumatic avascular necrosis of the femoral head, but the pathological mechanism is poorly understood. Short-term treatment with high doses of methylprednisolone is used in severe neurotrauma and after kidney and heart transplantation. We investigated the effect of such treatment on the pattern of perfusion of the femoral head and of bone in general in the pig.We allocated 15 immature pigs to treatment with high-dose methylprednisolone (20 mg/kg per day intramuscularly for three days, followed by 10 mg/kg intramuscularly for a further 11 days) and 15 to a control group. Perfusion of the systematically subdivided femoral head, proximal femur, acetabulum, humerus, and soft tissues was determined by the microsphere technique. Blood flow in bone was severely reduced in the steroid-treated group. The reduction of flow affected all the segments and the entire epiphysis of the femoral head. No changes in flow were found in non-osseous tissue. Short-term treatment with high-dose methylprednisolone causes reduction of osseous blood flow which may be the pathogenetic factor in the early stage of steroid-induced osteonecrosis.

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Section: Discussionmentioning

confidence: 51%

mentioning

confidence: 95%

Selective reduction of bone blood flow by short-term treatment with high-dose methylprednisolone

Drescher

Schneider

Becker

et al. 2001

The Journal of Bone and Joint Surgery. British volume

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show abstract

“…Hypertrophy and proliferation of fat cells, diminished hematopoiesis, lipid deposition in osteocytes, fatty degeneration of osteocytes, marrow necrosis, and thinner and sparse trabeculae are histopathologic changes occurring in the early stages of steroid-and alcohol-induced ON of the femoral head [9,19,22,23,36,47,50,57]. Several hypotheses have been proposed in the literature, including the increased size and number of fatty cells, increased intraosseous pressure, fatty degeneration of osteocytes, fat embolism, and extraosseous arterial occlusion due to abnormal changes in histologic features, hemodynamics, metabolism, and biochemical features within the femoral head [1,10,17,23,24,35,39,48]. Studies on primary and cloned MSCs have demonstrated differentiation into a large number of adipocytes increased while levels of ALP activity and osteocalcin decreased with longer durations of exposure and with higher concentrations of steroid or ethanol [8,10,28,56].…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of Puerarin on Alcohol-induced Osteonecrosis

Wang

Yin

et al. 2008

Clinical Orthopaedics &Amp; Related Research

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Alcohol can induce adipogenesis by bone marrow stromal cells and may cause osteonecrosis of the femoral head. Currently, there are no medications available to prevent alcohol-induced osteonecrosis. We hypothesized puerarin, a Chinese herbal medicine with antioxidative and antithrombotic effects, can prevent alcohol-induced adipogenesis and osteonecrosis. Both bone marrow stromal cells (in vitro) and mice (in vivo) were treated either with ethanol or with ethanol and puerarin, with an untreated group serving as a control. In the in vitro study, the number of adipocytes, contents of triglycerides, and levels of PPARc mRNA expression were decreased and alkaline phosphatase activity, contents of osteocalcin, and levels of osteocalcin mRNA expression were increased in cells treated with both alcohol and puerarin, compared with cells treated with alcohol only. In the in vivo study, marrow necrosis, fat cell hypertrophy and proliferation, thinner and sparse trabeculae, diminished hematopoiesis, and increased empty osteocyte lacunae in the subchondral region of the femoral head were observed in mice treated with alcohol. However, no such changes were seen in femoral heads of mice treated with alcohol and puerarin. The data suggest puerarin can inhibit adipogenic differentiation by bone marrow stromal cells both in vitro and in vivo and prevents alcohol-induced osteonecrosis in this model.

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“…BMSCs can be induced to differentiate into a large number of adipocytes and decreased number of osteoblasts if the cells are treated with longer durations and higher concentrations of steroids, and the levels of ALP activity and osteocalcin decrease (4,5,35,40,41). These findings indicate that steroids can increase adipogenesis and decrease osteogenesis in bone marrow stroma, and induce intracellular lipid deposition causing fat degeneration and the death of osteocytes, which may be associated with the development of osteonecrosis (3,7,8,26,28).…”

Section: Discussionmentioning

confidence: 90%

“…Although a number of studies have tried to protect the femoral head against ON, the mechanisms of ONFH remain unknown and presently there are no effective treatments for the condition (21,22). Several possible hypotheses of ON have been proposed in the literature, including an increase in the size and number of fatty cells, increased intraosseous pressure, fatty degeneration of osteocytes, fatty embolisms, and extraosseous arterial occlusions due to abnormal changes in histologic features, hemodynamics, metabolism, and biochemical features within the femoral head (3,4,(23)(24)(25)(26)(27)(28). Hypertrophy and proliferation of fat cells, diminished hematopoiesis, lipid deposition within osteocytes, fatty degeneration of osteocytes, marrow necrosis, and thinner or sparse trabeculae are histopathologic changes occurring throughout the early stages of steroid-induced ONFH (3,7,8,26,(29)(30)(31)(32)(33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

Preventive effects of siRNA targeting PPARγ gene on steroid-induced osteonecrosis in rabbits

Li²,

Wang

et al. 2014

Connective Tissue Research

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Purposes/Aim: Glucocorticoid steroids can induce expression of PPARg gene and enhance adipogenesis by bone marrow mesenchymal stem cells (BMSCs), which may result in osteonecrosis of the femoral head. Currently, there are no medications available to prevent steroid-induced osteonecrosis. We hypothesized that siRNA targeting PPARg gene may prevent steroid-induced adipogenesis and osteonecrosis in rabbit. The purpose of this study was to evaluate the preventive effects of siRNA targeting PPARg gene on steroid-induced adipogenesis and osteonecrosis. Methods: Forty-eight healthy New Zealand rabbits were randomized into four groups with Group M treated with dexamethasone only, Group S with dexamethasone and a recombinant adenovirus shuttle vector carrying siRNA targeting PPARg gene, Group Con with dexamethasone and a vector carrying irrelative sequence, and Group N with no treatment serving as control. Expressions of the PPARg, osteocalcin and Runx2 genes, as well as histopathologic changes were evaluated. Results: The levels of PPARg gene expression were decreased while the levels of osteocalcin and Runx2 gene expression were increased in rabbits treated with dexamethasone and recombinant adenovirus shuttle vector carrying siRNA targeting PPARg gene (Group S), compared to rabbits treated either with dexamethasone alone (Group M) or with both dexamethasone and a vector carrying irrelative sequence (Group Con). The marrow necrosis, adipocyte hypertrophy and proliferation, diminished hematopoiesis, thinner and sparse trabeculae, and increased empty osteocyte lacunae in the femoral head were observed in Group M and Group Con rabbits. However, no such changes were seen in Group S rabbits that were treated with dexamethasone and a recombinant adenovirus shuttle vector carrying siRNA targeting PPARg gene. Conclusion: siRNA targeting PPARg gene can inhibit adipogenic differentiation of BMSCs and prevent steroid-induced osteonecrosis in rabbit. The inhibition of bone-marrow adipogenesis and concomitant enhancement of osteogenesis with RNAi may provide a novel approach to the prevention of steroid-induced osteonecrosis.

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The effect of core decompression on femoral head blood flow in steroid-induced avascular necrosis of the femoral head.

Cited by 67 publications

References 0 publications

Selective reduction of bone blood flow by short-term treatment with high-dose methylprednisolone

Selective reduction of bone blood flow by short-term treatment with high-dose methylprednisolone

Preventive Effects of Puerarin on Alcohol-induced Osteonecrosis

Preventive effects of siRNA targeting PPARγ gene on steroid-induced osteonecrosis in rabbits

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