Changes in Femoral Head Blood Supply and Vascular Endothelial Growth Factor in Rabbits with Steroid-induced Osteonecrosis

Wang, G; Zhang, CQ; Sun, Yuan; Feng, Yong; Sb, Chen; Cheng, XG; Zeng, Botao

doi:10.1177/147323001003800333

Cited by 44 publications

(47 citation statements)

References 18 publications

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“…This likely translates into the protection by ACTH of glucocorticoidinduced osteonecrosis in a rabbit model [87]. An independent report with consistent findings was recently published [88]. We speculate that VEGF suppression secondary to ACTH suppression may contribute to the bone damage with long-term glucocorticoid therapy.…”

Section: Adrenocorticotrophic Hormonesupporting

confidence: 51%

Pituitary-bone connection in skeletal regulation

Zaidi

Sun

Liu

et al. 2016

Hormone Molecular Biology and Clinical Investigation

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Pituitary hormones have traditionally been thought to exert specific, but limited function on target tissues. More recently, the discovery of these hormones and their receptors in organs such as the skeleton suggests that pituitary hormones have more ubiquitous functions. Here, we discuss the interaction of growth hormone (GH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH), prolactin, oxytocin and arginine vasopressin (AVP) with bone. The direct skeletal action of pituitary hormones therefore provides new insights and therapeutic opportunities for metabolic bone diseases, prominently osteoporosis.

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Section: Adrenocorticotrophic Hormonesupporting

confidence: 51%

Pituitary-bone connection in skeletal regulation

Zaidi

Sun

Liu

et al. 2016

Hormone Molecular Biology and Clinical Investigation

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“…Wang et al reported significantly lower VEGF protein and mRNA levels and decreased femoral head blood supply in rabbits after 6 weeks of GC treatment [43]. Jiang el al.…”

Section: Discussionmentioning

confidence: 99%

A Novel Hybrid Compound LLP2A-Ale Both Prevented and Rescued the Osteoporotic Phenotype in a Mouse Model of Glucocorticoid-Induced Osteoporosis

et al. 2016

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Prolonged glucocorticoid (GC) administration causes secondary osteoporosis (GIOP) and non-traumatic osteonecrosis. LLP2A-Ale is a novel bone seeking compound that recruits mesenchymal stem cells to the bone surface, stimulates bone formation, and increases bone mass. The purpose of this study was to determine if treatment with LLP2A-Ale alone or in combination with parathyroid hormone (PTH) could prevent or treat GIOP in a mouse model. Four month old male Swiss-Webster mice were randomized to a prevention study with placebo, GC (day 1 – 28), and GC + LLP2A-Ale (IV, day 1) or a treatment study with placebo, GC (day 1 – 56), GC + LLP2A-Ale (IV, day 28), GC + PTH, and GC + LLP2A-Ale + PTH (day 28 – 56). Mice were sacrificed on day 28 (prevention study) or on day 56 (treatment study). The study endpoints included bone mass, bone strength, serum markers of bone turnover (P1NP and CTX-I) and angiogenesis (VEGF-A), surface-based bone turnover, and blood vessel density. LLP2A-Ale prevented GC-induced bone loss and increased mechanical strength in the vertebral body (day 28 and 56) and femur (day 56). LLP2A-Ale, PTH, and LLP2A-Ale + PTH treatment significantly increased the mineralizing surface, bone formation rate, mineral apposition rate, double labeled surface and serum P1NP level on day 56. LLP2A-Ale and PTH treatment increased femoral blood vessel density and LLP2A-Ale increased serum VEGF-A on day 28. Therefore, LLP2A-Ale monotherapy could be a potential option to both prevent and treat GC-induced osteoporosis and bone fragility.

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“…Growth factors are critical for osteoinduction, a central process for bone repair, as occurs in fracture healing. To ensure successful bone healing, the induction of angiogenesis is needed, and marrow stromal cells (MSCs) are also used to induce bone formation (15–20). Mesenchymal elements express factors like Vascular Endothelial Growth Factor (VEGF), and it has been demonstrated that MSCs from healthy subjects are characterized by a signature profile of VEGF expression distinct from patients affected by Osteonecrosis (ON) of the hip and by Osteoarthritis (OA) (14).…”

Section: Endothelial and Bone Cells The Molecular Basis Of Their Intmentioning

confidence: 99%

Bone Vascularization in Normal and Disease Conditions

Carulli¹,

Innocenti²,

Brandi³

2013

Front. Endocrinol.

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Bone vasculature is essential for many processes, such as skeletal development and growth, bone modeling and remodeling, and healing processes. Endothelium is an integral part of bone tissue, expressing a physiological paracrine function via growth factors and chemokines release, and interacting with several cellular lines. Alterations of the complex biochemical interactions between vasculature and bone cells may lead to various clinical manifestations. Two different types of pathologies result: a defect or an excess of bone vasculature or endothelium metabolism. Starting from the molecular basis of the interactions between endothelial and bone cells, the Authors present an overview of the recent acquisitions in the physiopathology of the most important clinical patterns, and the modern therapeutic strategies for their treatments.

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Changes in Femoral Head Blood Supply and Vascular Endothelial Growth Factor in Rabbits with Steroid-induced Osteonecrosis

Cited by 44 publications

References 18 publications

Pituitary-bone connection in skeletal regulation

Pituitary-bone connection in skeletal regulation

A Novel Hybrid Compound LLP2A-Ale Both Prevented and Rescued the Osteoporotic Phenotype in a Mouse Model of Glucocorticoid-Induced Osteoporosis

Bone Vascularization in Normal and Disease Conditions

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