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首页> 外文期刊>Acta biomaterialia >Chronic inflammation in biomaterial-induced periprosthetic osteolysis: NF-κB as a therapeutic target
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Chronic inflammation in biomaterial-induced periprosthetic osteolysis: NF-κB as a therapeutic target

机译：生物材料引起的假体周围骨质溶解的慢性炎症：NF-κB作为治疗靶标

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摘要

Biomaterial-induced tissue responses in patients with total joint replacement are associated with the generation of wear particles, which may lead to chronic inflammation and local bone destruction (periprosthetic osteolysis). Inflammatory reactions associated with wear particles are mediated by several important signaling pathways, the most important of which involves the transcription factor NF-κB. NF-κB activation is essential for macrophage recruitment and maturation, as well as the production of pro-inflammatory cytokines and chemokines such as TNF-α, IL-1β, IL-6 and MCP1. In addition, NF-κB activation contributes to osteoclast differentiation and maturation via RANK/RANKL signaling, which increases bone destruction and reduces bone formation. Targeting individual downstream cytokines directly (such as TNF-α or IL-1β) may not effectively prevent wear particle induced osteolysis. A more logical upstream therapeutic approach may be provided by direct modulation of the core IκB/IKKα/ β/NF-κB signaling pathway in the local environment. However, the timing, dose and strategy for administration should be considered. Suppression of chronic inflammation via inhibition of NF-κB activity in patients with malfunctioning joint replacements may be an effective strategy to mitigate wear particle induced periprosthetic osteolysis.
机译：全关节置换患者中由生物材料引起的组织反应与磨损颗粒的产生有关，这可能导致慢性炎症和局部骨破坏（假体周围骨溶解）。与磨损颗粒相关的炎症反应是由几种重要的信号通路介导的，其中最重要的涉及转录因子NF-κB。 NF-κB激活对于巨噬细胞募集和成熟以及促炎性细胞因子和趋化因子（如TNF-α，IL-1β，IL-6和MCP1）的产生至关重要。此外，NF-κB的活化通过RANK / RANKL信号传导促进破骨细胞的分化和成熟，从而增加了骨的破坏并减少了骨的形成。直接靶向单个下游细胞因子（例如TNF-α或IL-1β）可能无法有效防止磨损颗粒引起的骨溶解。可以通过在局部环境中直接调节核心IκB/IKKα/β/NF-κB信号通路来提供更合乎逻辑的上游治疗方法。但是，应考虑给药的时间，剂量和策略。在关节置换不良的患者中，通过抑制NF-κB活性来抑制慢性炎症可能是减轻磨损颗粒引起的假体周围骨溶解的有效策略。

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