Treatment Of Intramedullary Infection Research Articles

The Potential Role of Increasing the Release of Mouse β- Defensin-14 in the Treatment of Osteomyelitis in Mice: A Primary Study

Mammalian β-defensins are small cationic peptides that have been implicated in mediating innate immune defenses against microbial infection. Mouse β-defensin-14 (MBD-14), based on structural and functional similarities, appears to be an ortholog of human β-defensin-3 (HBD-3). Previous studies identified signaling pathway p38 mitogen-activated protein kinase (MAPK) that contributed to the expression of MBD-14 in mouse osteoblasts upon contacted with methicillin-resistance Staphylococcus aureus (MRSA) supernatant, which provided a theoretical basis as a promising therapeutic target in the treatment of intramedullary infection with MRSA in vivo. In this study, the medullary cavities of tibiae were contaminated with MRSA 103 colony forming units and different doses of p38 MAPK agonists anisomycin were followed as group III or IV in 30 mice. Fifteen animals that received phosphate- buffered saline served as group II and 15 mice were not contaminated with MRSA and received phosphate-buffered saline served as controls (group I). Follow-up was 7 days. In day 1, day 4 and day 7 postoperatively, infection was evaluated by blood routine, microbiological and histological analyses after sacrifice. All animals of group II developed microbiological and histological signs of infection. Histological signs of infection, white blood counts and cultures of group III and IV showed significantly reduced bacterial growth compared to cultures of group II. Simultaneously, different doses of anisomycin significantly induced the expression of osteoblast-associated genes, including alkaline phosphatase, osteocalcin and collagen type I. In addition, the expression of HBD-3 in human interfacial membranes around infected periprosthetic joint by staphylococcus contaminated was evaluated, and the expression pattern changed with significant induction of HBD-3 in infected periprosthetic joint compared with aseptic loosening under inflammatory conditions. Our primary study indicated that the potential antibacterial role of increased MBD-14 in the osteomyelitis mouse model.

Staphylococcus aureus supernatant induces the release of mouse β-defensin-14 from osteoblasts via the p38 MAPK and NF-κB pathways

Mammalian β-defensins are small cationic peptides of approximately 2-6 kDa that have been implicated in mediating innate immune defenses against microbial infection. Previous studies have reported that mouse β-defensin-14 (MBD‑14), based on structural and functional similarities, appears to be an ortholog of human β-defensin-3 (HBD-3). The aim of this study was to identify the signaling pathways that contribute to the expression of MBD-14 in mouse osteoblasts (OBs) upon contact with methicillin-resistant Staphylococcus aureus (S. aureus) supernatant (SAS) to provide a theoretical basis for the use of MDB-14 as a therapeutic agent in the treatment of intramedullary infection with S. aureus in vivo. The bacterial exoproducts released by S. aureus mainly include a large amount of enterotoxins. Using mouse OBs, the release and regulation of MBD-14 was evaluated by real-time polymerase chain reaction (PCR) and enzyme‑linked immunosorbent assay (ELISA) following exposure to SAS. The activation of the p38 mitogen‑activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB) pathways was determined by western blot analysis. OBs treated with lipopolysaccharide (LPS) were used as the positive control. The results revealed that SAS significantly promoted the phosphorylation of p38 MAPK, NF-κB and the inhibitory subunit of NF-κBα (IκBα) in a time-dependent manner. The treatment of OBs with SB203580 (an inhibitor of p38 MAPK) and pyrrolidine dithiocarbamate (PDTC, an inhibitor of NF-κB) prior to stimulation with SAS significantly inhibited the phosphorylation and mRNA expression of p38 MAPK and NF-κB p65, simultaneously reducing the release of MBD-14. Our findings suggest that the release of MBD-14 is mediated at least in part through the activation of p38 MAPK and NF-κB in response to S. aureus‑secreted bacterial exoproducts. Moreover, our data demonstrate the innate immune capacity of OBs under conditions of bacterial challenge to enhance the local expression of this MBD-14, a peptide with anti‑staphylococcal activity.

Use of antibiotic cement rod to treat intramedullary infection after nailing: preliminary study in 19 patients

The treatment of intramedullary infections after nailing usually includes removal of the nail, debridement, and, in some cases, insertion of antibiotic-impregnated cement beads. We use this self-made antibiotic cement rod to treat intramedullary infections. Compared with the beads, it provides some limited mechanical support and can be preserved in the canal for a long time. We reviewed 19 infected patients who underwent removal of the nails, excision of sinus tracks, debridement of the canal and insertion of the rods. No recurrent infection occurred in 18 cases and 11 cases achieved bone healing, 6 cases achieved partial union. One patient had nonunion and one patient underwent amputation because of severe primary trauma and long-term infection. The rod was removed between 35 and 123 days after implantation. We conclude that the antibiotic cement rods could be a relatively effective, simple and inexpensive method of treating intramedullary infections after nailing.

Treatment of intramedullary infection with instability using antibiotic cement rod

Treatment of intramedullary infection with instability using antibiotic cement rod