Arthroscopic Repair for the Anterior Horn of the Lateral Meniscus With Suture Anchor.

The anterior horn tear of the lateral meniscus, often accompanied with local parameniscal cysts, is usually managed by cysts debridement and meniscus repair with the outside-in technique (OIT). However, a big gap between the meniscus and anterior capsule would be produced after cysts debridement and be difficult to be closed by the OIT. Or, the OIT would result in knee pain because of the overly tight knots. Therefore, we devised an anchor repair technique. Following the cysts resection, the anterior horn of the lateral meniscus (AHLM) is fixed at the anterolateral edge of the tibial plateau with 1 suture anchor, and then followed by suturing the AHLM with the surrounding synovium to promote healing. We recommend this technique as an alternative method for repairing an AHLM tear accompanied with local parameniscal cysts.

Inhibition of fibroblast activation protein ameliorates cartilage matrix degradation and osteoarthritis progression.

Fibroblast activation protein (Fap) is a serine protease that degrades denatured type I collagen, α2-antiplasmin and FGF21. Fap is highly expressed in bone marrow stromal cells and functions as an osteogenic suppressor and can be inhibited by the bone growth factor Osteolectin (Oln). Fap is also expressed in synovial fibroblasts and positively correlated with the severity of rheumatoid arthritis (RA). However, whether Fap plays a critical role in osteoarthritis (OA) remains poorly understood. Here, we found that Fap is significantly elevated in osteoarthritic synovium, while the genetic deletion or pharmacological inhibition of Fap significantly ameliorated posttraumatic OA in mice. Mechanistically, we found that Fap degrades denatured type II collagen (Col II) and Mmp13-cleaved native Col II. Intra-articular injection of rFap significantly accelerated Col II degradation and OA progression. In contrast, Oln is expressed in the superficial layer of articular cartilage and is significantly downregulated in OA. Genetic deletion of Oln significantly exacerbated OA progression, which was partially rescued by Fap deletion or inhibition. Intra-articular injection of rOln significantly ameliorated OA progression. Taken together, these findings identify Fap as a critical pathogenic factor in OA that could be targeted by both synthetic and endogenous inhibitors to ameliorate articular cartilage degradation.

Depletion of circ_0128846 ameliorates interleukin-1ß-induced human chondrocyte apoptosis and inflammation through the miR-940/PTPN12 pathway.

BACKGROUND: Previous evidence has suggested that circular RNA (circRNA) is abnormally expressed in osteoarthritis (OA). However, the underlying mechanism of circRNA in OA progression remains unclear. The study aims to reveal the mechanism of circ_0128846 regulating OA. METHODS: Human chondrocytes (C28/I2 cells) were treated with interleukin-1ß (IL-1ß) to mimic an OA cell model. The expression levels of circ_0128846, miR-940 and protein tyrosine phosphatase 12 (PTPN12) were detected by qRT-PCR. Protein expression was checked by Western blotting. Cell viability, proliferation, and apoptosis were analyzed by a cell counting kit-8 assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay and flow cytometry analysis, respectively. The production of tumor necrosis factor-α (TNF-α) and IL-6 was determined by an enzyme-linked immunosorbent assay (ELISA). The binding relationship between miR-940 and circ_0128846 or PTPN12 was identified by dual-luciferase reporter assay and RNA immunoprecipitation assay. RESULTS: Circ_0128846 and PTPN12 expression were significantly upregulated, whereas miR-940 was downregulated in the cartilage tissues of OA patients and IL-1ß-treated C28/I2 cells compared with controls. IL-1ß treatment inhibited C28/I2 cell proliferation and induced cell apoptosis and the production of inflammatory factors, TNF-α and IL-6; however, these effects were partly reversed after circ_0128846 depletion. In terms of mechanism, circ_0128846 acted as a miR-940 sponge, and miR-940 combined with PTPN12. Also, circ_0128846 depletion partly ameliorated IL-1ß-induced C28/I2 cell disorders through miR-940. PTPN12 overexpression also partly relieved miR-940-mediated effects in IL-1ß-treated C28/I2 cells. Further, circ_0128846 induced PTPN12 expression by interacting with miR-940. CONCLUSION: Circ_0128846 regulated human chondrocyte proliferation, apoptosis and inflammation through the miR-940/PTPN12 pathway in OA.

Adipose-derived stem cell exosomes facilitate rotator cuff repair by mediating tendon-derived stem cells.

Aim: To evaluate the potential capability of adipose-derived stem cell exosomes (ADSC-exos) on rotator cuff repair by mediating the tendon-derived stem cells (TDSCs) and explored the mechanism. Methods: First, we investigated the growth, survival and migration of TDSCs in the presence of ADSC-exos in vitro. Using a rat rotator cuff injury model to analyze the ability of the ADSC-exos to promote rotator cuff healing in vivo. Results: The hydrogel with ADSC-exos significantly improved the osteogenic and adipogenesis differentiation and enhanced the expression of RUNX2, Sox-9, TNMD, TNC and Scx and the mechanical properties of the articular portion. Conclusion: The ADSC-exos have the potential to promote the rotator cuff repair by mediating the TDSCs.

[Effect of continuous passive motion on basic fibroblast growth factor expression during tendon-bone repair after surgical repair of acute rupture of the supraspinatus tendon in rabbits].

OBJECTIVE: To study the effect of continuous passive motion (CPM) on basic fibroblast growth factor (b-FGF) expression during tendon-bone repair in rabbits and explore the role of stress in the postoperative repair after acute rotator cuff injury. METHODS: Sixteen rabbits randomized into CPM group (n=8) and non-CPM group (n=8) were subjected to surgically induced acute rupture of the supraspinatus tendon and subsequent surgical repair, with another two rabbits serving as the control. Two weeks after the operation, the rabbits in CPM group underwent CPM training, and those in non-CPM group were normally fed only. At 2, 4, 6, and 8 weeks after the operation, 2 rabbits from each group were sacrificed and the tissue samples were obtained for detecting the changes in b-FGF expression. RESULTS: Two weeks after the operation, b-FGF expression was detected in both groups, and the CPM group showed slightly higher and more diffusive expression. At 4 weeks, b-FGF expression was significantly higher and distributed over a greater area in CPM group and in the non-CPM group. A large number of fibroblasts positive for b-FGF expression were identified in CPM group, aligning in parallel with the tendon membrane. At 6 weeks, b-FGF in the CPM group showed no obvious changes but that in the non-CPM group became lightened. At 8 weeks, b-FGF expression was reduced in both groups, which was more obvious in the non-CPM group. CONCLUSION: CPM can promote b-FGF expression to enhance type III collagen synthesis at the tendon-bone interface in early stage of tendon-bone repair following acute rupture of supraspinatus tendon in rabbits, thereby contributing to tendon-bone recovery after rotator cuff injury.