Knee osteoarthritis (KOA) is a common and severe disease characterized by articular cartilage degeneration, subchondral bone remodeling and inflammation. The purpose of this study was to investigate the therapeutic effects of high fibular osteotomy (HFO) in a KOA rabbit model and to examine the molecular mechanisms involved in medial compartment KOA protective effects. Our data showed that HFO delayed the progression of articular cartilage damage and suppressed subchondral bone remodeling in destabilization of the medial meniscus (DMM)-induced KOA model. HFO also decreased MMP-1, MMP-3, MMP-13 and ADAMTS-5 expression, and increased Col2 and aggrecan expression. In parallel, HFO attenuated the expression of IL-1β, IL-6 and TNF-α. Furthermore, HFO suppressed DMM-mediated NFκB activation, which suggested that the molecular mechanism underlying the protective effect of HFO in medial compartment KOA may be related to the NFκB signaling pathway. Collectively, our data indicated that HFO may be a therapeutic approach to treating medial compartment KOA.

膝关节骨关节炎（KOA）是一种常见且严重的疾病，其特征是关节软骨退变、软骨下骨重塑和炎症。本研究的目的是研究高位腓骨截骨术 (HFO) 在 KOA 兔模型中的治疗效果，并检查内侧间室 KOA 保护作用的分子机制。我们的数据显示，在内侧半月板 (DMM) 诱导的 KOA 模型不稳定中，HFO 延迟了关节软骨损伤的进展并抑制了软骨下骨重塑。HFO 还降低了 MMP-1、MMP-3、MMP-13 和 ADAMTS-5 的表达，并增加了 Col2 和蛋白聚糖的表达。同时，HFO 减弱了 IL-1β、IL-6 和 TNF-α 的表达。此外，HFO 抑制了 DMM 介导的 NFκB 激活，这表明 HFO 在内侧间室 KOA 中保护作用的分子机制可能与 NFκB 信号通路有关。总的来说，我们的数据表明 HFO 可能是治疗内侧隔室 KOA 的一种治疗方法。