Avascular necrosis of bone is a relatively common clinical condition caused by inflammatory conditions, steroid or other drug use, and trauma that affect many different sites in man. Revascularization of the necrotic bone is slow to occur, often resulting in bone resorption and eventual collapse of the involved bone. Rapid revascularization and subsequent bone remodeling may lead to improved outcomes.Surgical revascularization with arterovenous bundles (AV bundles) or vascularized bone grafts results in neoangiogenesis and bone remodeling. Gene transfer of an angiogenic factor to the vessel wall may be an additional strategy to further accelerate this process. In this study, we examined the effectiveness of vascular endothelial growth factor (VEGF) gene transfer to augment surgical revascularization of necrotic bone. An adenoviral vector, either with the VEGF gene (VEGF-A) or identical virus without the cDNA VEGF insert (ADV-AE1) was used to transduce endothelial cells in rabbit saphenous arteries. The artery was then placed with its venae comitantes as an AV bundle into necrotic iliac crest bone in vivo. Angiogenesis in the necrotic bone was quantified by bone blood flow measurement and assessment of vessel density following microangiography. The extent of neoangiogenesis was significantly greater in the VEGF group than the control group at 1 week postoperatively.
The ability of vascular endothelial growth factor (VEGF) to accelerate neoangiogenesis from implanted arterovenous (AV) bundles in necrotic bone was evaluated. A saphenous AV bundle was placed in a necrotic segment of rabbit ilium. In group II, VEGF (100 ng/h x 3 days) was administered by continuous infusion. Bone blood flow was measured with radioactive-labeled microspheres, and capillary density was determined by microangiography combined with Spälteholtz bone clearing at 1, 2, and 4 weeks. Neovascularization was observed along the implanted vascular bundle in both groups. One week after surgery, bone blood flow and vessel area were significantly higher in VEGF-treated animals (P < 0.05). No significant difference was observed at later times. Direct VEGF administration increased surgical angiogenesis and improved blood flow and neovascularization in necrotic bone 1 week after AV bundle implantation. Thereafter, a robust angiogenic response from the AV bundle was seen in both groups.
BackgroundPsoas abscess and pyogenic spondylitis are intractable diseases that require long-term treatment, but the clinical characteristics and causative organisms have not been fully investigated. Herein, we describe the clinical characteristics of these diseases and evaluate the factors associated with in-hospital mortality and the presence of gram-negative rods as causative microorganisms.MethodsAll patients diagnosed with pyogenic spondylitis or psoas abscesses at a tertiary hospital were included. We retrieved the clinical data (age, sex, outcome, length of hospital stay, disease, bacteria, medication, comorbidities, and treatment status), vital signs (blood pressure, heart rate, and body temperature), and laboratory test results (blood cell count, liver function, renal function, electrolytes, blood sugar, and C-reactive protein) of all patients. The outcomes were in-hospital deaths and positive cultures of gram-negative rods.ResultsWe analyzed 126 patients consisting of 69 (55%) men with a population mean age of 72 years. Seventy-two patients had pyogenic spondylitis and 54 had psoas abscesses. Eleven patients (8.3%) died during admission. The causative bacteria were gram-positive cocci in 63 patients (50%) and gram-negative bacteria in 19 patients (15%). The multivariate logistic model showed that blood urea nitrogen (BUN) (odds ratio [OR] 1.04, 95% confidence interval [CI] 1.02–1.06) and cardiovascular diseases (OR 7.02, 95% CI 1.55–31.8) were associated with in-hospital mortality. Platelets less than 150,000/μL (OR 3.14, 95% CI 1.02–9.65) and higher aspartic aminotransferase (OR 1.02, 95% CI 1.00–1.03) were associated with gram-negative rods.ConclusionsPatients with suspected psoas abscesses or pyogenic spondylitis having a high BUN level and a history of cardiovascular diseases have a higher risk of mortality.
To clarify the pathology of radial-sided wrist pain with inconclusive X-ray and MRI findings, we performed arthroscopic examinations of 11 wrists in 10 patients. Physical examination and various image investigations could not identify the cause of the pain. Arthroscopy revealed partial to complete tears of the scapho-lunate interosseous ligament and synovitis and/or chondral bone defects at the scaphotrapezio-trapezoidal joint in all 11 wrists. Surgical procedures consisted of eight simple synovectomies, two ligament reconstructions and one percutaneous pinning. Pain relief was achieved in 10 wrists. One wrist which had a simple synovectomy did not recover, so underwent secondary scaphotrapezio-trapezoidal fusion. In conclusion, we found that various degrees of scapholunate interosseous ligament tear and scaphotrapezio-trapezoidal joint osteoarthritis were the main causes of radial-sided wrist pain with inconclusive X-ray and simple MRI findings.
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