Surgical masks (SMs) are used to reduce bacterial shedding from the mouth, nose and face. This study aimed to investigate whether SMs may be a potential source of bacterial shedding leading to an increased risk of surgical site infection. Bacterial contamination of the SMs was tested by making an impression of the external surface of the mask on sterile culture media immediately. We investigated the difference in bacterial counts between the SMs worn by surgeons and those placed unused in the operating room (OR), and the bacterial count variation with indicated wearing time. Moreover, the difference in bacterial counts on the external surface between the first and second layers of double-layered SMs was also assessed. The bacterial count on the surface of SMs increased with extended operating times; significant difference was found between the 4- to 6-hour and 0-hour groups (p < 0.05). When we analysed the bacterial counts from the same surgeon, a significant increase was noted in the 2-hours group. Moreover, the bacterial counts were significantly higher among the surgeons than the OR. Additionally, the bacterial count of the external surface of the second mask was significantly higher than that of the first one. The source of bacterial contamination in SMs was the body surface of the surgeons rather than the OR environment. Moreover, we recommend that surgeons should change the mask after each operation, especially those beyond 2 hours. Double-layered SMs or those with excellent filtration function may also be a better alternative. This study provides strong evidence for the identification that SMs as source of bacterial contamination during operative procedures, which should be a cause for alarm and attention in the prevention of surgical site infection in clinical practice.

Background: Surgical site infection (SSI) continues to be one of the most common postoperative complications. In our previous study, surgical mask (SM) bioburden was identified to be a potential source of SSI. In the present study, we investigated the factors involved in SM bioburden. Methods: Bioburdens of the disposable SM (A: medical mask; B: medical surgical mask) and newly laundered cloth SM (C) were tested by immediately making an impression of the external surface of the mask on sterile culture media. SM microstructure was observed using a scanning electron microscope (SEM). Filtering efficiency and airflow resistance were evaluated with TSI Automated Filter Tester 8130 (TSI Incorporated) according to GB/19083-2010. Whether speaking during operation and washing the face pre-operatively affect SM bioburdens was also evaluated. Surgical procedures were performed in a dynamic operation room. Fifty cases of mask use were enrolled in this study. Results: The bioburden of mask A was the highest. The bioburden of mask B was the lowest. Mask C possessed the lowest filtering efficiency and the highest airflow resistance. SM bioburden was higher in the speaking group. SM bioburden showed no significant difference after washing the face, despite the finding that washing could significantly reduce facial bioburden. Conclusions: Multiple factors influence SM bioburdens. Mask B showed the lowest bioburden and best protection effects. Mask C is not recommended to be used, especially considering that surgeons do not wash the cloth masks daily. Unnecessary talking during operation is not recommended, and washing the face before surgery is not strictly necessary.

Osteoarthritis (OA) is a degenerative joint disease with an immense unmet medical need. FGF18 protein is a potential regenerative factor for cartilage repair. However, traditional protein delivery methods have limited efficacy due to the short lifetime and shallow infiltration. In this work, we discovered that lipid nanoparticle (LNP) can infiltrate and deliver FGF18 mRNA deeper in the cartilage than proteins. After mRNA UTR optimization and chemical modification, the expression of FGF18 can last up to 6 days in the cartilage. Furthermore, delivering FGF18 mRNA activates FOXO3a-autophagy pathway, which protects against chondrocyte degeneration and senescence. Local intra-articular injection of FGF18 mRNA-LNP significantly alleviates OA symptoms in DMM and senile OA models. Sustained expression and accessibility of FGF18-mRNA to deeper chondrocytes makes LNP-mRNA more effective than FGF18 recombinant protein. In summary, this study presents a novel approach superior to recombinant protein alone and holds promise as a new therapeutic strategy for OA.

Surface modification of titanium has been a hot topic to promote bone integration between implants and bone tissue. Titanium dioxide nanotubes fabricated on the surface of titanium by anodic oxidation have been a mature scheme that has shown to promote osteogenesis in vitro. However, mechanisms behind such a phenomenon remain elusive. In this study, we verified the enhanced osteogenesis of BMSCs on nanotopographic titanium in vitro and proved its effect in vivo by constructing a bone defect model in rats. In addition, the role of the mechanosensitive molecule Yap is studied in this research by the application of the Yap inhibitor verteporfin and knockdown/overexpression of Yap in MC3T3-E1 cells. Piezo1 is a mechanosensitive ion channel discovered in recent years and found to be elemental in bone metabolism. In our study, we preliminarily figured out the regulatory relationship between Yap and Piezo1 and proved Piezo1 as a downstream effector of Yap and nanotube-stimulated osteogenesis. In conclusion, this research proved that nanotopography promoted osteogenesis by increasing nuclear localization of Yap and activating the expression of Piezo1 downstream.

The central physiological role of the bone marrow renders bone marrow stromal cells (BMSCs) particularly sensitive to aging. With bone aging, BMSCs acquire a differentiation potential bias in favor of adipogenesis over osteogenesis, and the underlying molecular mechanisms remain unclear. Herein, we investigated the factors underlying age-related changes in the bone marrow and their roles in BMSCs’ differentiation. Antibody array revealed that CC chemokine ligand 3 (CCL3) accumulation occurred in the serum of naturally aged mice along with bone aging phenotypes, including bone loss, bone marrow adiposity, and imbalanced BMSC differentiation. In vivo Ccl3 deletion could rescue these phenotypes in aged mice. CCL3 improved the adipogenic differentiation potential of BMSCs, with a positive feedback loop between CCL3 and C/EBPα. CCL3 activated C/EBPα expression via STAT3, while C/EBPα activated CCL3 expression through direct promoter binding, facilitated by DNA hypomethylation. Moreover, CCL3 inhibited BMSCs’ osteogenic differentiation potential by blocking β-catenin activity mediated by ERK-activated Dickkopf-related protein 1 upregulation. Blocking CCL3 in vivo via neutralizing antibodies ameliorated trabecular bone loss and bone marrow adiposity in aged mice. This study provides insights regarding age-related bone loss and bone marrow adiposity pathogenesis and lays a foundation for the identification of new targets for senile osteoporosis treatment.