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Basilar skullfractures: the petrous bone., Objectives: to provide suggestions for the management of three of the most dangerous or important lesions (internal carotid artery lesions, cerebrospinal fluid leaks and facial nerve paralysis) associated with the petrous part of basilar skull fractures, thereby trying to assess categories of evidence and determine strengths of recommendation., Methodology: A PubMed-based literature review was carried out, as well as a consultation of online sources as encountered in the literature review. Also, a non-systematic search of chapters of well-known books dealing with the subject of temporal bone traumata was conducted., Results: Specific levels of evidence and/or strength of recommendation can be retrieved from the literature, but only with respect to the prophylactic use of antibiotics, the prescription of antithrombotic medications and the indications for angiography., Conclusion: The ample amount of available literature allows for sound management decisions, with reference made to algorithms when available in the literature. Nevertheless, for most of the management/search questions, categories of evidence and strength of recommendation are low or lacking.

Cerebrospinal fluid rhinorrhea is a serious and potentially fatal condition because of an increased risk of meningitis and brain abscess. Approximately 80% of all cases occur in patients with head injuries and craniofacial fractures. Despite technical advances in the diagnosis and management of CSF rhinorrhea caused by craniofacial injury through the introduction of MRI and endoscopic extracranial surgical approaches, difficulties remain. The authors review here the pathophysiology, diagnosis, and management of CSF rhinorrhea relevant exclusively to traumatic anterior skull base injuries and attempt to identify areas in which further work is needed.

A 29-year-old man presented with skull base fractures involving the bilateral petrous bones and clivus to the posterior clinoid process manifesting as bilateral abducens nerves palsy. Conservative treatment resulted in residual bilateral abducens nerves palsy. Posterolateral impact probably resulted in strain-stress in the neighborhood of the foramen lacerum, resulting in a clivus fracture of the posterior clinoid process and bilateral petrous bone fractures. Chalasia of Gruber's ligament then exerted mechanical pressure on the bilateral abducens nerves.

The present study was designed to investigate whether hydrolysis of synthetic octacalcium phosphate (OCP) into hydroxyapatite affects bone formation. Mouse bone marrow stromal ST-2 cells and primary calvarial osteoblastic cells were cultured on the dishes pre-coated with OCP or its hydrolyzed Ca-deficient hydroxyapatite (OCP hydrolyzate; HL). The capacity of proliferation and differentiation was determined up to day 20. Granules of OCP and HL were implanted into critical-size rat calvaria defects for 4 and 12 weeks, and then bone formation was measured by histomorphometry. Structural changes of incubated and implanted OCP were determined by X-ray diffraction (XRD) and Fourier transform infrared spectroscopy (FTIR). The proliferation of both ST-2 and primary osteoblasts cultured on OCP or HL was initially inhibited, whereas their differentiation to osteoblasts was promoted at last. Implantation of OCP in bone defect more significantly enhanced bone formation than that of HL until 12 weeks. OCP tended to convert to apatite in vitro and in vivo. The conversion of the implanted OCP was ascertained to advance gradually with implantation periods. Taken together, these results suggest that OCP supports appositional bone formation and OCP-apatite conversion may be involved in this stimulatory capacity of OCP.