Do fluoroscopic and radiographic images underestimate pin protrusion in paediatric supracondylar humerus and distal radius fractures? A synthetic bone model analysis.

PURPOSE: Fluoroscopy is commonly used to confirm acceptable position of percutaneously placed pins when treating paediatric fractures. There is a paucity of literature investigating the accuracy of fluoroscopic imaging when determining pin position relative to the far cortex of the fixated bone. The purpose of this study was to evaluate the accuracy of fluoroscopic and radiographic imaging in measuring smooth pin protrusion from the far cortex of a bone model. METHODS: Eight bone models were implanted with smooth pins and anteroposterior fluoroscopic and radiographic studies were obtained. All images were evaluated by orthopaedic attending physicians, residents and medical students. The length of pin protrusion from the model surface was estimated on fluoroscopic imaging and measured on radiographs and compared with actual lengths measured on the bone models. RESULTS: 20 evaluators took a total of 320 pin measurements on images of 8 models. There was a significant difference between fluoroscopic measurements compared to radiographic measurements and actual pin lengths. There was no significant difference between radiographic measurements and actual pin lengths. Level of training of examiner was not statistically significant. On average, fluoroscopic estimations of pin protrusion were 1.53 mm shorter than the actual measured length. CONCLUSION: Fluoroscopic images underestimate the length of smooth pins protruding from a bone model surface when compared with radiographs and actual measurements. Orthopaedic surgeons using fluoroscopy should be aware of this discrepancy when assessing intraoperative fluoroscopic images to decide on acceptable implant position. LEVEL OF EVIDENCE: Level V.

Cellular prion protein promotes post-ischemic neuronal survival, angioneurogenesis and enhances neural progenitor cell homing via proteasome inhibition.

Although cellular prion protein (PrP(c)) has been suggested to have physiological roles in neurogenesis and angiogenesis, the pathophysiological relevance of both processes remain unknown. To elucidate the role of PrP(c) in post-ischemic brain remodeling, we herein exposed PrP(c) wild type (WT), PrP(c) knockout (PrP-/-) and PrP(c) overexpressing (PrP+/+) mice to focal cerebral ischemia followed by up to 28 days reperfusion. Improved neurological recovery and sustained neuroprotection lasting over the observation period of 4 weeks were observed in ischemic PrP+/+ mice compared with WT mice. This observation was associated with increased neurogenesis and angiogenesis, whereas increased neurological deficits and brain injury were noted in ischemic PrP-/- mice. Proteasome activity and oxidative stress were increased in ischemic brain tissue of PrP-/- mice. Pharmacological proteasome inhibition reversed the exacerbation of brain injury induced by PrP-/-, indicating that proteasome inhibition mediates the neuroprotective effects of PrP(c). Notably, reduced proteasome activity and oxidative stress in ischemic brain tissue of PrP+/+ mice were associated with an increased abundance of hypoxia-inducible factor 1α and PACAP-38, which are known stimulants of neural progenitor cell (NPC) migration and trafficking. To elucidate effects of PrP(c) on intracerebral NPC homing, we intravenously infused GFP(+) NPCs in ischemic WT, PrP-/- and PrP+/+ mice, showing that brain accumulation of GFP(+) NPCs was greatly reduced in PrP-/- mice, but increased in PrP+/+ animals. Our results suggest that PrP(c) induces post-ischemic long-term neuroprotection, neurogenesis and angiogenesis in the ischemic brain by inhibiting proteasome activity.