The left atrial appendage (LAA) occluder is an important medical device for closing the LAA and preventing stroke. The device‐related thrombus (DRT) prevents the implantation of the occluder in exerting the desired therapeutic effect, which is primarily caused by the delayed endothelialization of the occluder. Functional coatings are an effective strategy for accelerating the endothelialization of occluders. However, the occluder surface area is particularly large and structurally complex, and the device is subjected to a large shear friction in the sheath during implantation, which poses a significant challenge to the coating. Herein, a hydrogel coating by the in situ UV‐triggered polymerization of double‐network polyelectrolytes is reported. The findings reveal that the double network and electrostatic interactions between the networks resulted in excellent mechanical properties of the hydrogel coating. The sulfonate and Arg‐Gly‐Asp (RGD) groups in the coating promoted hemocompatibility and endothelial growth of the occluder, respectively. The coating significantly accelerated the endothelialization of the LAA occluder in a canine model is further demonstrated. This study has potential clinical benefits in reducing both the incidence of DRT and the postoperative anticoagulant course for LAA closure.

Osteoarthritis (OA), which is principally featured by progressive joint metabolic imbalance and subsequent degeneration of articular cartilage, is a common chronic joint disease. Arctigenin (ATG), a dietary phyto‐oestrogen, has been described to have potent anti‐inflammatory effects. Nevertheless, its protective effects on OA have not been clearly established. The target of our following study is to evaluate the protective effects of ATG on IL‐1β–induced human OA chondrocytes and mouse OA model. Our results revealed that the ATG pre‐treatment effectively decreases the level of pro‐inflammatory mediators, such as prostaglandin E2 (PGE2), nitrous oxide (NO), inducible nitric oxide synthase (iNOS), cyclooxygenase‐2 (COX‐2), IL‐6 and tumour necrosis factor alpha (TNF‐α) in IL‐1β–induced human chondrocytes. In addition, ATG protects against the degradation of extracellular matrix (ECM) under the stimulation of IL‐1β and the possible mechanism might be connected with the inactivation of phosphatidylinositol‐3‐kinase (PI3K)/Akt/nuclear factor‐kappa B (NF‐κB) axis. Furthermore, a powerful binding capacity between ATG and PI3K was also uncovered in our molecular docking research. Meanwhile, ATG may act as a protector on the mouse OA model. Collectively, all these findings suggest that ATG could be utilized as a promising therapeutic agent for the treatment of OA.

Obesity is related to osteoarthritis (OA). Aberrant lipid metabolism results in increased levels of free fatty acids, such as palmitate (PA), leading to inflammatory responses and excess catabolism of chondrocytes. Asiatic acid (AA), a plant anti-inflammatory compound, has been reported to exert protective effects for several diseases, but its effect on obesity-related OA is still unclear. The aim of this study is to evaluate the chondro-protective effect of AA on PA-induced human chondrocytes and a high fat diet (HFD)-fed mouse cartilage degeneration model. In vitro, the levels of the inflammatory and extracellular matrix (ECM) markers of chondrocytes after being treated with PA (500 μM) and AA (2.5–10 μM) were determined using western blotting and immunofluorescence enzyme-linked immunosorbent assay (ELISA). In vivo, after the oral administration of HFD and AA, X-ray examination, safranin O staining, and ELISA assay were conducted to evaluate cartilage calcification and degeneration and cytokine and adipokine levels in the serum of mice. AA treatment eliminated the inflammation caused by PA and extracellular matrix degradation. Mechanistically, AA blocked the stimulation of the NF-κB pathway. Analysis with co-immunoprecipitation and molecular docking indicated that the MD-2/TLR4 complex was a target of AA. In vivo, AA treatment not only prevented HFD-induced OA changes but also reduced proinflammatory cytokine and adipokine production in obese mice. AA exerted a chondroprotective effect by inhibiting the TLR4/MD-2 axis, thus showing promise for treating obesity-related OA.

Purpose. The aim of this study was to report the histopathology of failed free vascularized fibular grafting (FVFG) for osteonecrosis of the femoral head (ONFH) after a mean follow‐up of 11.5 years (ranged from 10.6 to 14.2 years). Methods. Six hips of 5 patients with a history of steroid use, aged 34–67 years, were in stage II of ONFH as classified by the Ficat and Arlet classification at the time of FVFG treatment. Grafting failure led to osteoarthritis of the hip joint during a mean of 11.5 years of follow‐up. Femoral head specimens were first evaluated macroscopically. Bone specimens were sectioned into long strips, divided into necrotic, transitional, and healthy zones, and then prepared for nondecalcified and decalcified histopathological examination using hematoxylin and eosin (HE) staining, Goldner’s trichrome staining, and immunofluorescence (IF) staining. Results. Femoral head articular cartilage surfaces appeared thin, opaque, and partially cartilaginous missing, with gradual collapse detected in weight‐bearing areas. The interface with the fibular graft showed well union, with no obvious gaps between graft and host bone, as observed macroscopically. The necrotic area was filled with fibular graft, cancellous bone, and cartilaginous or soft tissue invasion. Histopathology results revealed well integration between fibular graft and host bone, with thickened trabecular bone. Gaps occurred in transitional and healthy zones. In the necrotic zone, cartilaginous or soft tissue invasion occurred, while thin or missing articular cartilage exposed subchondral bone to hip joint surfaces. By IF counterstaining with CD‐31 and α‐SMA, blood vessel transplanted during fibular grafting could be clearly observed along the graft from healthy to necrotic zones. In the necrotic zone, blood vessels presented obviously and spread into the surrounding area of the graft tip. Conclusion. After FVFG procedure with a mean follow‐up of 11.5 years, fibular grafts retained their integrity as viable, vascularized, cortical bone that fused well with host bone and formed thickened trabecular bone surrounding the surface of the graft. However, the revascularization of FVFG’s blood vessels spreading from the tip of the fibular graft into subchondral area of necrotic lesion did not improve significantly in these failure cases. The local necrotic lesion failed to be repaired as healthy trabecular bone to buttress articular surface and was occupied by soft tissues.