A Novel Method for Secondary Mandible Reconstruction to Re-Achieve a Native Condyle Position Comprising a New Design for Cutting Guides and New Positioning Devices.

Secondary mandibular reconstruction using fibular free flaps (FFF) is a technical challenge for surgeons. Appropriate operation planning is crucial for postoperative quality control and is notably necessary for the (re-) achievement of a physiological condylar position, and the sensible expansion and shaping of the transplant. Computer-assisted planning may help to reconstruct mandibular defects in a patient-specific and precise manner. Herein, we present a newly-developed workflow for secondary mandibular reconstruction using FFF; it comprises digital planning and in-house manufacturing to perform precise secondary mandible reconstruction. This method utilizes a newly designed positioning device to ensure the precise positioning of the fibula segments in relation to each other and the mandibular stumps. The presented in-house-printed positioning device made it possible to achieve digital planning with high precision during surgery.

Drug-induced Defibrinogenation as New Treatment Approach of Acute Hearing Loss in an Animal Model for Inner Ear Vascular Impairment.

OBJECTIVE: Disturbance of cochlear microcirculation is considered to be the final common pathway of various inner ear diseases. Hyperfibrinogenemia causing increased plasma viscosity is a known risk factor for sudden sensorineural hearing loss and may lead to a critical reduction of cochlear blood flow. The aim of this study was to evaluate the effect of a substantial reduction of plasma fibrinogen levels by drug-induced defibrinogenation for the treatment of acute hearing loss in vivo. METHODS: Acute hearing loss was induced by hyperfibrinogenemia (i.v. injection of 330 mg/kg BW fibrinogen), using a guinea pig animal model. Parameters of cochlear microcirculation and hearing thresholds were quantified by intravital microscopy and evoked response audiometry. After obtaining baseline values, the course of hearing loss and disturbances of microcirculation were investigated under influence of intravenous defibrinogenation therapy (ancrod), corticosteroid, or placebo treatment, using 5 animals/group. RESULTS: Acute hyperfibrinogenemia caused hearing loss from 10 ±â€Š7 to 26 ±â€Š10 dB SPL at baseline. Drug-induced reduction of fibrinogen levels showed a significant increase of cochlear microcirculation (1.6-fold) and recovered hearing threshold (11 ±â€Š6 dB SPL). Placebo or corticosteroid treatment had no effect on hearing loss (35 ±â€Š7 dB SPL and 32 ±â€Š18 dB SPL, respectively). CONCLUSION: Acute hyperfibrinogenemia resulted in hearing loss. Drug-induced reduction of elevated fibrinogen levels caused an increase in cochlear blood flow and a decrease in hearing thresholds. Placebo or corticosteroid treatment had no effect. Reduction of plasma fibrinogen levels could serve as a clinical treatment option for acute hearing loss.