In order to repair critical‐sized bone defects, various polylactic acid‐glycolic acid (PLGA)‐based hybrid scaffolds are successfully developed as bone substitutes. However, the byproducts of these PLGA‐based scaffolds are known to acidify the implanted site, inducing tiresome acidic inflammation. Moreover, these degradation productions cannot offer an osteo‐friendly microenvironment at the implanted site, matching natural bone healing. Herein, inspired by bone microenvironment atlas of natural bone‐healing process, an osteo‐microenvironment stage‐regulative scaffold (P80/D10/M10) is fabricated by incorporating self‐developed decellularized bone matrix microparticles (DBM‐MPs) and multifunctional magnesium hydroxide nanoparticles (MH‐NPs) into PLGA with an optimized proportion using low‐temperature rapid prototyping (LT‐RP) 3D‐printing technology. The cell experiments show that this P80/D10/M10 exhibits excellent properties in mechanics, biocompatibility, and biodegradability, meanwhile superior stimulations in osteo‐immunomodulation, angiogenesis, and osteogenesis. Additionally, the animal experiments determined that this P80/D10/M10 can offer an osteo‐friendly microenvironment in a stage‐matched pattern for enhanced bone regeneration, namely, optimization of early inflammation, middle neovascularization, and later bone formation. Furthermore, transcriptomic analysis suggested that the in vivo performance of P80/D10/M10 on bone defect repair is mostly attributed to regulating artery development, bone development, and bone remodeling. Overall, this study reveals that the osteo‐microenvironment stage‐regulative scaffold provides a promising treatment for bone defect repair.

To report the diagnosis, injury mechanisms, and imaging characteristics of hyperextension bicondylar tibial plateau fractures and examine the indications and feasibility of the modified anterior midline incision as a treatment strategy. We performed a retrospective analysis of 11 cases of hyperextension bicondylar tibial plateau fractures who were treated with open reduction and internal fixation, predominantly via an anterolateral and posteromedialdouble incision or a modified anterior midline incision. Radiological and functional evaluations were performed. Eleven patients were followed-up for a mean period of 11.5 months (range 3–24 months). The mean time to radiographic bony union was 12.5 weeks (range 10–26 weeks). At final follow-up, the average Rasmussen functional score was 26.8 (range 24 − 29); five patients had an excellent rating, and six a good rating. The average range of motion of the affected knees was 3.4–130° postoperatively. Fixation failure was not observed in any of the treated fractures. Hyperextension bicondylar tibial plateau fractures show a special Tiankeng-like collapse characteristic, while the changes in posterior tibial slope angle are easy to overlook. The modified anterior midline incision is a safe and effective approach for treatment of hyperextension bicondylar tibial plateau fractures with less rear displacement. Open reduction and double plating for the treatment of hyperextension bicondylar tibial plateau fractures provides excellent results.

Background: Rheumatoid arthritis (RA) is a globally prevalent chronic inflammatory disease. Environmental exposures, such as air pollution and smoking, are considered potential risk factors. However, the causal relationships and underlying mechanisms between these factors and RA are not fully understood. Methods: This study utilized large-scale genome-wide association studies (GWASs) from European ethnic backgrounds and employed bidirectional two-sample Mendelian randomization (MR) to investigate the relationships between air pollution, smoking, and RA. Genetic correlations were assessed using linkage disequilibrium score regression (LDSC). Furthermore, mediation analysis was conducted to evaluate the potential mediating roles of iron metabolism and urinary biomarkers in these relationships. Results: The MR analysis revealed that genetically predicted lifetime smoking intensity was associated with an 85% increased risk of RA. Subgroup analysis differentiating between seropositive RA (SPRA) and seronegative RA (SNRA) showed a causal association with SPRA, but not with SNRA. C-reactive protein was identified as a mediator in the relationship between lifetime smoking and both RA and SPRA, mediating 18.23% and 32.45% of the effects, respectively. Genetic correlation analysis further confirmed a positive genetic association between smoking and both RA and SPRA. Conclusions: This study provides significant insights into the genetic and causal connections between air pollution, smoking, and the development of RA, highlighting the mediating role of C-reactive protein. These findings not only offer new perspectives on how smoking might enhance RA risk through inflammatory pathways but also underscore the importance of reducing smoking exposure in public health strategies.