Hofman Martijn, Koopmans Guido, Kobbe Philipp, Poeze Martijn, Andruszkow Hagen, Brink Peter R G, Pape Hans-Christoph
Department of Orthopaedic Trauma, University of Aachen Medical Center, Pauwelsstrasse 30, 52074 Aachen, Germany.
Algiax Pharmaceuticals GmbH, Max-Planck-Strasse 15a, 40699 Erkrath, Germany.
Mediators Inflamm. 2015;2015:204842. doi: 10.1155/2015/204842. Epub 2015 Mar 22.
Over the last 3 decades, scientific evidence advocates an association between traumatic brain injury (TBI) and accelerated fracture healing. Multiple clinical and preclinical studies have shown an enhanced callus formation and an increased callus volume in patients, respectively, rats with concomitant TBI. Over time, different substances (cytokines, hormones, etc.) were in focus to elucidate the relationship between TBI and fracture healing. Until now, the mechanism behind this relationship is not fully clarified and a consensus on which substance plays the key role could not be attained in the literature. In this review, we will give an overview of current concepts and opinions on this topic published in the last decade and both clinical and pathophysiological theories will be discussed.
在过去三十年中,科学证据表明创伤性脑损伤(TBI)与骨折愈合加速之间存在关联。多项临床和临床前研究分别显示,伴有TBI的患者和大鼠的骨痂形成增强且骨痂体积增加。随着时间的推移,不同物质(细胞因子、激素等)成为研究重点,以阐明TBI与骨折愈合之间的关系。到目前为止,这种关系背后的机制尚未完全阐明,文献中也未就哪种物质起关键作用达成共识。在本综述中,我们将概述过去十年发表的关于该主题的当前概念和观点,并讨论临床和病理生理学理论。