Abstract

The purpose of this study was to describe the incidence of subsidence in patients with AO/OTA 41 (tibial plateau) fractures which were repaired with a novel fenestrated screw system to used to deliver CaPO4 bone substitute material to fill the subchondral void and support the articular reduction. Patients with unicondylar and bicondylar tibial plateau fractures were treated according to the usual technique of two surgeons. After fixation, the Zimmer Biomet N-Force Fixation System®, a fenestrated screw that allows for the injection of bone substitute was placed and used for injection of the proprietary calcium phosphate bone graft substitute into the subchondral void. For all included patients, demographic information, operative data, radiographs, and clinic notes were reviewed. Patients were considered to have articular subsidence if one or more of two observations were made when comparing post-operative to their most recent clinic radiographs: > 2mm change in the distance between the screw and the lowest point of the tibial plateau, > 2mm change in the distance between the screw and the most superior aspect of the plate. Data were analyzed to determine if there were any identifiable risk factors for complication, reoperation, or subsidence using logistic regression. Statistical significance was set at p < 0.05. 34 patients were included with an average follow-up of 32.03 ± 22.52weeks. There were no overall differences between height relative to the medial plateau or the plate. Two patients (5.9%) had articular subsidence. Six patients (15.2%) underwent reoperation, two (6%) for manipulations under anaesthesia due to arthrofibrosis, and four (12%) due to infections. There were 6 (19%) total infections as 2 were superficial and required solely antibiotics. One patient had early failure. Use of a novel fenestrated screw system for the delivery of CaPO4 BSM results in articular subsidence and complication rates similar to previously published values and appears to be a viable option for addressing subchondral defects in tibial plateau fractures. IV.

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