osteonecrosis/نقص الأكسجة

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An association study between hypoxia inducible factor-1alpha (HIF-1α) polymorphisms and osteonecrosis.

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Bone hypoxia resulting from impaired blood flow is the final pathway for the development of osteonecrosis (ON). The aim of this study was to evaluate if HIF-1α, the major transcription factor triggered by hypoxia, is genetically implicated in susceptibility to ON. For this we analyzed frequencies of

Association study of hypoxia inducible factor 1alpha (HIF1alpha) with osteonecrosis of femoral head in a Korean population.

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OBJECTIVE Disruption of the vascular supply to the bone and subsequent hypoxia has been implicated in the pathogenesis of osteonecrosis (ON) of the femoral head (ONFH). To evaluate the genetic effect of HIF1alpha, a key transcription factor in controlling hypoxia condition, on ONFH, we analyzed

Hypoxia-inducible factor (HIF): how to improve osseointegration in hip arthroplasty secondary to avascular necrosis in sickle cell disease.

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Many studies in the literature have been carried out to evaluate the various cellular and molecular processes involved in osteogenesis.Angiogenesis and bone formation work closely together in this group of disorders. Hypoxia-inducible factor (HIF) which is stimulated in tissue hypoxia triggers a

MicroRNA-mediated interacting circuits predict hypoxia and inhibited osteogenesis of stem cells, and dysregulated angiogenesis are involved in osteonecrosis of the femoral head.

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OBJECTIVE MicroRNAs (miRNAs) are associated with various pathologic conditions and can serve as diagnostic or therapeutic biomarkers. This study tried to identify the differentially expressed miRNAs to predict the possible pathomechanisms involved in osteonecrosis of the femoral head

Hypoxia-inducible factor-1 is a positive regulator of Sox9 activity in femoral head osteonecrosis.

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Legg-Calve-Perthes disease (LCPD) is a juvenile form of ischemic osteonecrosis of the femoral head leading to femoral head deformity and premature osteoarthritis. Femoral head osteonecrosis occurs due to blood supply disruption which results in hypoxic injury to the femoral head. Hypoxia-inducible

Effects of hypoxia environment on osteonecrosis of the femoral head in Sprague-Dawley rats

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Introduction: Osteonecrosis of the femoral head (ONFH) is a disease in which the blood supply of the femoral head is interrupted or damaged, resulting in joint dysfunction. Hypoxic environments increase the expression of EPO, VEGF, and

Combined effect of tnf-α polymorphisms and hypoxia on steroid-induced osteonecrosis of femoral head.

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OBJECTIVE Tumor necrosis factor (TNF)-α is a proinflammatory cytokine, some studies reported that TNF-α gene plays important role in the pathogenesis of SONFH. And the polymorphisms of TNF-α were presented as risk factors for steroid-induced osteonecrosis of the femoral head (SONFH). Meanwhile,

Effects of hypoxia on osteogenic differentiation of mesenchymal stromal cells used as a cell therapy for avascular necrosis of the femoral head.

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Avascular necrosis of the femoral head (AVN) occurs as common result of various conditions or develops as a primary entity, with a high freqency in young adults. Because of its tendency toward osteoarthritis requiring total hip arthroplasty, alternative treatments are being advocated, including cell

Transplantation of hypoxia preconditioned bone marrow mesenchymal stem cells enhances angiogenesis and osteogenesis in rabbit femoral head osteonecrosis.

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OBJECTIVE Osteonecrosis of the femoral head may be a disease resulting from abnormal proliferation or differentiation of mesenchymal stem cells. The present investigation explored the novel strategy of hypoxia-preconditioned BMMSCs to reverse the impairment of osteonecrosis BMMSCs and enhance the

Genetic association of angiogenesis- and hypoxia-related gene polymorphisms with osteonecrosis of the femoral head.

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Multiple factors have been implicated in the development of osteonecrosis of the femoral head (ONFH). In particular, non-traumatic ONFH is directly or indirectly related to injury of the vascular supply to the femoral head. Thus, hypoxia in the femoral head caused by impaired blood flow may be an

Erythropoietin Enhances Bone Repair Effects via the Hypoxia-Inducible Factor Signal Pathway in Glucocorticoid-Induced Osteonecrosis of the Femoral Head.

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This study aimed to determine whether erythropoietin could repair glucocorticoid-induced osteonecrosis of the femoral head after the systemic or local administration of recombinant human erythropoietin. Gelatin microspheres were used to load recombinant human erythropoietin for local delivery.

Hypoxia-inducible factor prolyl hydroxylase inhibitor prevents steroid-associated osteonecrosis of the femoral head in rabbits by promoting angiogenesis and inhibiting apoptosis.

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The purpose of this study was to investigate the preventive effect of ethyl 3,4-dihydroxybenzoate(EDHB) on steroid-associated femoral head osteonecrosis(ONFH) in a rabbit model. New Zealand white rabbits were randomly divided into two groups (prevention group and model group), each containing 24

Discrepant hypoxia tolerance aggravates subchondral delamination in osteonecrosis of the femoral head.

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[Osteonecrosis in drepanocytemia (author's transl)].

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Aseptic osteonecrosis is due to local hypoxemia related to the sickling process. Its frequency in the U.S.A. is 8,5 p. 100 for heterozygotic patients and 0,2 p. 100 for homozygotic ones. It is rare in AS status but frequent in the double heterozygotism SC. Alcoholism, hyperlipidemia, hyperuricemia,

Different synovial vasculogenic profiles of primary, rapidly destructive and osteonecrosis-induced hip osteoarthritis. An immunohistochemistry study.

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To present a hypothesis regarding the pathways of angiogenesis in primary versus secondary hip osteoarthritis (OA). In synovial tissue samples provided by 57 consecutive patients who underwent hip arthroplasty, immunohistochemical examinations were performed using the following angiogenesis-related

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