AimRadiotherapy is associated with cell depletion and loss of blood supply, which are linked to compromised bone healing. However, the molecular events underlying these effects at the tissue–implant interface have not been fully elucidated. This study aimed to determine the major molecular mediators associated with compromised osseointegration due to previous exposure to radiation.Materials and MethodsTitanium implants were placed in rat tibiae with or without pre‐exposure to 20 Gy irradiation. Histomorphometric, biomechanical, quantitative polymerase chain reaction (qPCR) and enzyme‐linked immunosorbent assay analyses were performed at 1 and 4 weeks after implantation.ResultsThe detrimental effects of irradiation were characterized by reduced bone–implant contact and removal torque. Furthermore, pre‐exposure to radiation induced different molecular dysfunctions such as (i) increased expression of pro‐inflammatory (Tnf) and osteoclastic (Ctsk) genes and decreased expression of the bone formation (Alpl) gene in implant‐adherent cells; (ii) increased expression of bone formation (Alpl and Bglap) genes in peri‐implant bone; and (iii) increased expression of pro‐inflammatory (Tnf) and pro‐fibrotic (Tgfb1) genes in peri‐implant soft tissue. The serum levels of pro‐inflammatory, bone formation and bone resorption proteins were greater in the irradiated rats.ConclusionsIrradiation causes the dysregulation of multiple biological activities, among which perturbed inflammation seems to play a common role in hindering osseointegration.

中文翻译：

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照射骨骨结合不良的分子机制：大鼠胫骨模型的体内研究


目的放疗与细胞耗竭和血液供应丧失有关，这与骨骼愈合受损有关。然而，组织-植入物界面上这些影响背后的分子事件尚未完全阐明。本研究旨在确定与由于先前暴露于辐射而导致的骨结合受损相关的主要分子介质。材料和方法将钛植入物放置在大鼠胫骨中，有或没有预暴露于 20 Gy 照射。在植入后 1 周和 4 周进行组织形态学、生物力学、定量聚合酶链反应 （qPCR） 和酶联免疫吸附测定分析。结果照射的有害影响以骨与植入物接触和移除扭矩降低为特征。此外，辐射前诱导了不同的分子功能障碍，例如 （i） 促炎 （Tnf） 和破骨细胞 （Ctsk） 基因的表达增加，以及骨形成 （Alpl） 基因在植入贴壁细胞中的表达降低;（ii） 种植体周围骨中骨形成 （Alpl 和 Bglap） 基因的表达增加;（iii） 种植体周围软组织中促炎 （Tnf） 和促纤维化 （Tgfb1） 基因的表达增加。照射大鼠血清促炎蛋白、骨形成蛋白和骨吸收蛋白水平较高。结论照射导致多种生物活性失调，其中炎症扰动似乎在阻碍骨整合方面起着共同的作用。