Purpose: This study aimed to identify and prevent preoperative factors that can be influenced in preoperative planning to reduce postoperative malcorrections.Methods: The method used in this study was a retrospective two‐centre analysis of 78 pre and postoperative fully weight‐bearing radiographs of patients who underwent valgus osteotomy correction due to symptomatic medial compartment osteoarthritis. A computer software (TraumaCad^®) was used to aim for an intersection point of the mechanical tibiofemoral axis (mTFA) with the tibia plateau at 55–60% (medial = 0%, lateral = 100%). Postoperative divergence ± 5% of this point was defined as over‐ and undercorrection. Preoperative joint geometry factors were correlated with postoperative malcorrection. Planning was conducted using the established method described by Miniaci (Group A) and with additional correction of the joint line convergence angle (JLCA) using the formula JLCA‐2/2 (Group B). Additionally, in a small clinical case series, planning was conducted with JLCA correction. Statistical analysis was performed using (multiple) linear regression analysis and analysis of variance (ANOVA) with p < 0.05 considered significant.Results: In 78 analysed cases, postoperative malcorrection was detected in 37.2% (5.1% undercorrection, 32.1% overcorrection). Linear regression analysis revealed preoperative body mass index (BMI, p = 0.04), JLCA (p = 0.0001), and osteotomy level divergence (p = 0.0005) as factors correlated with overcorrection. In a multiple regression analysis, JLCA and osteotomy level divergence remained significant factors. Preoperative JLCA correction reduced the planned osteotomy gap (A 9.7 ± 2.8 mm vs B 8.3 ± 2.4 mm; p > 0.05) and postoperative medial proximal tibial angle (MPTA: A 94.3 ± 2.1° vs B 92.3 ± 1.5°; p < .05) in patients with preoperative JLCA ≥ 4°. The results were validated using a virtual postoperative correction of cases with overcorrection. A case series (n = 8) with a preoperative JLCA > 4 revealed a postoperative accuracy using the JLCA correction of 3.4 ± 1.9%.Conclusion: Preoperative JLCA ≥ 4° and tibial osteotomy level divergence were identified as risk factors for postoperative overcorrection. Preoperative JLCA correction using the formula JLCA‐2/2 is proposed to better control ideal postoperative correction and reduce MPTA. The intraoperatively realised osteotomy level should be precisely in accordance with preoperative planning.Level of evidence: III, cross‐sectional study.

A continuing challenge in cartilage tissue engineering for cartilage regeneration is the creation of a suitable synthetic microenvironment for chondrocytes and tissue regeneration. The aim of this study was to develop a highly tunable hybrid scaffold based on a silk fibroin matrix (SM) and a hyaluronic acid (HA) hydrogel. Human articular chondrocytes were embedded in a porous 3-dimensional SM, before infiltration with tyramine modified HA hydrogel. Scaffolds were cultured in chondropermissive medium with and without TGF-β1. Cell viability and cell distribution were assessed using CellTiter-Blue assay and Live/Dead staining. Chondrogenic marker expression was detected using qPCR. Biosynthesis of matrix compounds was analyzed by dimethylmethylene blue assay and immuno-histology. Differences in biomaterial stiffness and stress relaxation were characterized using a one-step unconfined compression test. Cell morphology was investigated by scanning electron microscopy. Hybrid scaffold revealed superior chondro-inductive and biomechanical properties compared to sole SM. The presence of HA and TGF-β1 increased chondrogenic marker gene expression and matrix deposition. Hybrid scaffolds offer cytocompatible and highly tunable properties as cell-carrier systems, as well as favorable biomechanical properties.

Platelet-released growth factors (PRGFs) or other thrombocyte concentrate products, e.g., Platelet-Rich Fibrin (PRF), have become efficient tools of regenerative medicine in many medical disciplines. In the context of wound healing, it has been demonstrated that treatment of chronic or complicated wounds with PRGF or PRF improves wound healing in the majority of treated patients. Nevertheless, the underlying cellular and molecular mechanism are still poorly understood. Therefore, we aimed to analyze if PRGF-treatment of human keratinocytes caused the induction of genes encoding paracrine factors associated with successful wound healing. The investigated genes were Semaphorin 7A (SEMA7A), Angiopoietin-like 4 (ANGPLT4), Fibroblast Growth Factor-2 (FGF-2), Interleukin-32 (IL-32), the CC-chemokine-ligand 20 (CCL20), the matrix-metalloproteinase-2 (MMP-2), the chemokine C-X-C motif chemokine ligand 10 (CXCL10) and the subunit B of the Platelet-Derived Growth Factor (PDGFB). We observed a significant gene induction of SEMA7A, ANGPLT4, FGF-2, IL-32, MMP-2 and PDGFB in human keratinocytes after PRGF treatment. The CCL20- and CXCL10 gene expressions were significantly inhibited by PRGF therapy. Signal transduction analyses revealed that the PRGF-mediated gene induction of SEMA7A, ANGPLT4, IL-32 and MMP-2 in human keratinocytes was transduced via the IL-6 receptor pathway. In contrast, EGF receptor signaling was not involved in the PRGF-mediated gene expression of analyzed genes in human keratinocytes. Additionally, treatment of ex vivo skin explants with PRGF confirmed a significant gene induction of SEMA7A, ANGPLT4, MMP-2 and PDGFB. Taken together, these results describe a new mechanism that could be responsible for the beneficial wound healing properties of PRGF or related thrombocytes concentrate products such as PRF.

Joint inflammation causes meniscus degeneration and can exacerbate post-traumatic meniscus injuries by extracellular matrix degradation, cellular de-differentiation and cell death. The aim of this study was to examine whether anti-inflammatory interleukin-10 exerts protective effects in an in vitro model of TNF-α-induced meniscus degeneration. Meniscus tissue was harvested from the knees of adult cows. After 24 h of equilibrium explants were simultaneously treated with bovine TNF-α and IL-10. After an incubation time of 72 h cell death was measured histomorphometrically (nuclear blebbing, NB) and release of glycosaminoglycans (GAG, DMMB assay) and nitric oxide (NO, Griess-reagent) were analysed. Transcription levels (mRNA) of matrix degrading enzymes, collagen type X (COL10A1) and nitric oxide synthetase 2 (NOS2) were measured by quantitative real time PCR. TNF-α-dependent formation of the aggrecanase-specific aggrecan neoepitope NITEGE was visualised by immunostaining. Differences between groups were calculated using a one-way ANOVA with a Bonferroni post hoc test. Administration of IL-10 significantly prevented the TNF-α-related cell death (P .001), release of NO (P .003) and NOS2 expression (P .04). Release of GAG fragments (P .001), NITEGE formation and expression of MMP3 (P .007), -13 (P .02) and ADAMTS4 (P .001) were significantly reduced. The TNF-α-dependent increase in COL10A1 expression was also antagonized by IL-10 (P .02). IL-10 prevented crucial mechanisms of meniscal degeneration induced by a key cytokine of OA, TNF-α. Administration of IL-10 might improve the biological regeneration and provide a treatment approach in degenerative meniscus injuries and in conditions of post-traumatic sports injuries.