Background: Recently, arthroscopic ankle arthrodesis has been performed for moderate-to-severe varus-deformed ankle osteoarthritis. However, the effect of osteophyte resection in the lateral gutter in arthroscopic ankle arthrodesis has not been clarified. We hypothesized that a varus-deviated ankle with lateral gutter osteophytes can be corrected by osteophyte resection. Methods: Thirty-nine ankles of 38 patients were included. The mean age of patients was 70.0 (45-83) years. The patients were divided into the following groups: group with an osteophyte in the lateral gutter (osteophyte) and group with no osteophytes (nonosteophyte). Preoperative and postoperative tibiotalar angle, tibial plafond angle, and tibiotalar angle under valgus stress, as well as the Japanese Society for Surgery of the Foot (JSSF) ankle/hindfoot scale, were recorded. Twelve ankles underwent lateral gutter osteophyte resection, whereas the other 27 ankles did not require osteophyte resection. Results: Preoperative tibiotalar angle was higher in the osteophyte group than in the nonosteophyte group (21.8 vs 11.2 degrees, P = .01). The tibiotalar angle in the preoperative valgus stress imaging was higher in the osteophyte group (12.9 vs 5.7, P < .01). However, the postoperative tibiotalar angle was similar between the 2 groups (7.1 vs 5.4, P = .183). JSSF ankle/hindfoot scale improved in both groups. Conclusion: Lateral gutter osteophyte resection enabled correction of the varus malalignment in arthroscopic ankle arthrodesis. Level of Evidence: Level III, retrospective comparative series.

Level III, retrospective comparative series.

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We investigated the expression and localization of the receptor activator nuclear factor κB ligand (RANKL) in cartilage from patients with rheumatoid arthritis (RA) of relevance to cartilage degeneration. We also examined the role of exogenous lymphotoxin (LT)-α on RANKL expression in human chondrocytes and its effect on in vitro osteoclast differentiation. Cartilage and synovial fluid samples were obtained from 45 patients undergoing total joint replacement surgery or joint puncture, including 24 patients with osteoarthritis (OA) and 21 patients with RA. RANKL expression in articular cartilage was examined by immunohistochemistry. LT-α concentrations in synovial fluid were measured using an enzyme-linked immunosorbent assay (ELISA). Normal human chondrocytes were stimulated with LT-α, and the relative mRNA levels of RANKL, osteoprotegerin (OPG), matrix metalloproteinase-9, and vascular endothelial growth factor were examined by real-time polymerase chain reaction. Soluble RANKL protein in culture media was measured using ELISA, and membrane-bound RANKL protein in cells was examined by western blotting. Co-cultures of human chondrocytes with peripheral blood mononuclear cells (PBMCs) were stimulated with macrophage-colony stimulating factor and LT-α, and osteoclast differentiation was evaluated by staining for tartrate-resistant acid phosphatase. LT-α concentrations were higher in RA synovial fluid than in OA samples. The population of RANKL-positive chondrocytes of RA cartilage was higher than that of OA cartilage, and correlated with cartilage degeneration. Stimulation of cultured human chondrocytes by LT-α increased RANKL expression, the RANKL/OPG ratio, and angiogenic factors. Membrane-bound RANKL in chondrocytes was up-regulated after stimulation of LT-α, whereas soluble RANKL in culture medium did not increase. Co-cultures of human chondrocytes and PBMCs demonstrated that LT-α stimulated human chondrocytes to produce RANKL and induced osteoclastic differentiation of PBMCs. RANKL produced by chondrocytes may contribute to cartilage destruction during RA and LT-α could promote the expression of RANKL in human chondrocytes.

We investigated the effects of adipose-derived extract (AE) on cultured chondrocytes and in vivo cartilage destruction. AE was prepared from human adipose tissues using a nonenzymatic approach. Cultured human chondrocytes were stimulated with interleukin-1 beta (IL-1β) with or without different concentrations of AE. The effects of co-treatment with AE on intracellular signaling pathways and their downstream gene and protein expressions were examined using real-time PCR, Western blotting, and immunofluorescence staining. Rat AE prepared from inguinal adipose tissues was intra-articularly delivered to the knee joints of rats with experimental osteoarthritis (OA), and the effect of AE on cartilage destruction was evaluated histologically. In vitro, co-treatment with IL-1β combined with AE reduced activation of the p38 and ERK mitogen-activated protein kinase (MAPK) pathway and nuclear translocation of the p65 subunit of nuclear factor-kappa B (NF-κB), and subsequently downregulated the expressions of matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4, IL-6, and IL-8, whereas it markedly upregulated the expression of IL-1 receptor type 2 (IL-1R2) in chondrocytes. Intra-articular injection of homologous AE significantly ameliorated cartilage destruction six weeks postoperatively in the rat OA model. These results suggested that AE may exert a chondroprotective effect, at least in part, through modulation of the IL-1β-induced inflammatory signaling pathway by upregulation of IL-1R2 expression.