Summary. Coagulase-negative staphylococci, including S. epidermidis, have emerged as the leading pathogens of hospital-acquired biomaterial-related infections. These infections can be clinically indolent and challenging also for diagnostic imaging. In the current model of catheter-related infections, . 68. Ga-labeled Siglec-9 PET/CT imaging was able to detect peri-implant S. epidermidis bone infections. Introduction. Coagulase-negative staphylococci, including S. epidermidis, have emerged as the leading pathogen of nosocomial (hospital-acquired) biomaterial-related infections, including periprosthetic infections and intravascular catheter-related bloodstream infections. Pathogenic S. epidermidis strains exhibit robust attachment to implant surfaces and subsequent biofilm formation. By nature, the clinical picture of periprosthetic S. epidermidis infections can be indolent with vague signs of infection. These infections are also highly challenging for diagnostic imaging and microbiologic studies. Our recent experimental study of . 18. F-FDG-PET/CT confirmed that subacute peri-implant S. epidermidis infections, reflecting limited inflammatory reaction, are characterised by low . 18. F-FDG uptake. Vascular adhesion protein-1 (VAP-1) is an inflammation inducible endothelial protein, which controls leukocyte migration to sites of inflammation and infection. Siglec-9 is a leukocyte ligand of VAP-1. We hypothesised that . 68. Ga-labeled Siglec-9, developed for PET imaging of inflammation and cancer, could be a novel tracer also for early defection of S. epidermidis peri-implant bone infections. Material & Methods. Thirty adult male Sprague-Dawley rats were randomised into three groups (n=10/group). A clinical intravenous polymer catheter was introduced into the medullary cavity of the left tibia followed by injections of a clinical isolate of S. epidermidis (T-54580, 3 × 10. 8. CFU/mL) and an adjunct sodium morrhuate. In the positive control group, a clinical isolate of S. aureus (52/52A/80, 3 × 10. 5. CFU/mL) with sodium morrhuate was injected. In the negative control group, equal amount of sterile saline was injected via the catheter. The catheter, cut at the level of tibial tuberosity, was left in situ to serve as the implant. Two weeks after surgery, PET imaging with . 68. Ga-DOTA-Siglec-9 was performed with quantitative analysis of the standardised uptake value (SUV) in the region of interests both in vivo and ex vivo. SUV ratio between the operated and contralateral intact tibia was calculated. The presence of infections and the absence of contamination in the negative control group were verified by separate microbiological analyses of bone samples and retrieved implants. The presence of microbial biofilms on catheters was verified ex vivo with fluorescence microscope. Histologic inflammatory reaction was graded using a scoring system. Intergroup differences were tested by means of ANOVA with a post-hoc test. Results. Both staphylococcal strains caused histologically acute osteomyelitic changes. In . 68. Ga-DOTA-Siglec-9 PET/CT imaging of the negative control group, there was a significant difference (29.5%, p<0.001) in the SUV ratio of the operated and contralateral tibia, demonstrating aseptic inflammatory reaction to catheter implantation. The corresponding SUV ratio values were 58.1% in the S. epidermidis group and 41.7% in the S. aureus group. The uptake in the S. epidermidis group was significantly (p=0.009) higher than in the negative control group. Discussion/Conclusion. The animal model was reproducible in creation of culture-positive biomaterial-related infections. . 68. Ga-labeled Siglec-9 PET/CT imaging was able to demonstrate aseptic inflammation in the negative control group and the tracer also detected peri-implant bone infections caused by S. epidermidis

Platelet-rich plasma is a new inductive therapy which is being increasingly used for the treatment of the complications of bone healing, such as infection and nonunion. The activator for platelet-rich plasma is a mixture of thrombin and calcium chloride which produces a platelet-rich gel.

We analysed the antibacterial effect of platelet-rich gel in vitro by using the platelet-rich plasma samples of 20 volunteers. In vitro laboratory susceptibility to platelet-rich gel was determined by the Kirby-Bauer disc-diffusion method. Baseline antimicrobial activity was assessed by measuring the zones of inhibition on agar plates coated with selected bacterial strains.

Zones of inhibition produced by platelet-rich gel ranged between 6 mm and 24 mm (mean 9.83 mm) in diameter. Platelet-rich gel inhibited the growth of Staphylococcus aureus and was also active against Escherichia coli. There was no activity against Klebsiella pneumoniae, Enterococcus faecalis, and Pseudomonas aeruginosa. Moreover, platelet-rich gel seemed to induce the in vitro growth of Ps. aeruginosa, suggesting that it may cause an exacerbation of infections with this organism. We believe that a combination of the inductive and antimicrobial properties of platelet-rich gel can improve the treatment of infected delayed healing and nonunion.