Table S1

Patient informatio

Comparison of the general information between the first and second surgery in staged TKA.

<p>Comparison of the general information between the first and second surgery in staged TKA.</p

Comparison of VAS scores in rest position between two TKA surgeries.

<p>*P<0.05.</p

Comparison of ΔVAS in different time intervals.

<p>* Statistically significant between less than 6 months group and 6–12 months group (LSD-t test).</p><p>* Statistically significant between less than 6 months group and more than 12 months group (LSD-t test).</p><p>Comparison of ΔVAS in different time intervals.</p

Comparison of VAS scores in maximum flexion position between two TKA surgeries.

<p>*P<0.05.</p

Additional file 5 of Identification and development of the novel 7-genes diagnostic signature by integrating multi cohorts based on osteoarthritis

Additional file 5. Tableshowing that in the three datasets, 136 differentially expressed genes wereobtained, of which 45 were downregulated in the normal grou

Additional file 2 of Identification and development of the novel 7-genes diagnostic signature by integrating multi cohorts based on osteoarthritis

Additional file 2. Tableshowing the 648 differentially expressed genes in the GSE57218 dataset, ofwhich 309 were upregulated and 339 were downregulate

Additional file 1 of Identification and development of the novel 7-genes diagnostic signature by integrating multi cohorts based on osteoarthritis

Additional file 1. Tableshowing the 268 differentially expressed genes in the GSE129147 dataset, ofwhich 188 were upregulated and 80 were downregulate

Safranin O/Fast green (A, C, E) and Alcian blue/Fast nuclear red (B, D, F) staining of the KGN bead implanted sites in rat Achilles tendons <i>in vivo</i>.

Note that C is an enlargement of the rectangled region in A. Arrows point to the area outside the KGN-bead implantation site that appears normal. D is an enlargement of the yellow box in B. Triangles indicate the normal areas outside the KGN-bead implantation site. Positive staining was observed only in the KGN bead implanted sites (A, B, C, D) indicating the presence of glycosaminoglycan rich matrix representing chondrogenesis only at these sites. The DMSO bead implanted tissue sections stained minimally for these stains (E, F). Bar– 100 μm.</p

Table1_Disulfiram Suppressed Peritendinous Fibrosis Through Inhibiting Macrophage Accumulation and Its Pro-inflammatory Properties in Tendon Bone Healing.XLSX

The communication between macrophages and tendon cells plays a critical role in regulating the tendon-healing process. However, the potential mechanisms through which macrophages can control peritendinous fibrosis are unknown. Our data showed a strong pro-inflammatory phenotype of macrophages after a mouse tendon–bone injury. Moreover, by using a small-molecule compound library, we identified an aldehyde dehydrogenase inhibitor, disulfiram (DSF), which can significantly promote the transition of macrophage from M1 to M2 phenotype and decrease macrophage pro-inflammatory phenotype. Mechanistically, DSF targets gasdermin D (GSDMD) to attenuate macrophage cell pyroptosis, interleukin-1β, and high mobility group box 1 protein release. These pro-inflammatory cytokines and damage-associated molecular patterns are essential for regulating tenocyte and fibroblast proliferation, migration, and fibrotic activity. Deficiency or inhibition of GSDMD significantly suppressed peritendinous fibrosis formation around the injured tendon and was accompanied by increased regenerated bone and fibrocartilage compared with the wild-type littermates. Collectively, these findings reveal a novel pathway of GSDMD-dependent macrophage cell pyroptosis in remodeling fibrogenesis in tendon–bone injury. Thus, GSDMD may represent a potential therapeutic target in tendon–bone healing.</p