Abstract
Purpose Knee osteoarthritis (KOA) is a common and severe disease characterized by articular cartilage degeneration, subchondral bone remodeling and inflammation. This study aimed 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.Methods A rabbit model of destabilization of the medial meniscus was used to induce post-traumatic KOA. The effectiveness of HFO on protection against KOA was tested. Hematoxylin and eosin staining, Safranin O/Fast green staining and micro-CT analysis were performed to evaluate structural and morphological changes. The expression of metalloproteinase (MMP)-1, MMP-3, MMP-13, collagen type II (Col2), a disintegrin and metalloproteinase domain with thrombospondin motifs (ADAMTS)-5, aggrecan, interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α was assessed by real time PCR, western blotting and enzyme-linked immunosorbent assay. Additionally, western blotting was performed to test the expression of NFκB p65, phospho-IκBα and IκBα. Results HFO delayed the progression of articular cartilage damage and suppressed subchondral bone remodeling. 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, the molecular mechanism underlying the protective effect of HFO in medial compartment KOA was related to the NFκB signaling pathway. Conclusion HFO may be a novel therapeutic approach to treating medial compartment KOA.
High fibular osteotomy ameliorates medial compartment knee osteoarthritis in a rabbit model
