Gentamicin coating of plasma chemical oxidized titanium alloy prevents implant-related osteomyelitis in rats.

Implant related infection is one of the most feared and devastating complication associated with the use of orthopaedic implant devices. Development of anti-infective surfaces is the main strategy to prevent implant contamination, biofilm formation and implant related osteomyelitis. A second concern in orthopaedics is insufficient osseointegration of uncemented implant devices. Recently, we reported on a macroporous titanium-oxide surface (bioactive TiOB) which increases osseointegration and implant fixation. To combine enhanced osseointegration and antibacterial function, the TiOB surfaces were, in addition, modified with a gentamicin coating. A rat osteomyelitis model with bilateral placement of titanium alloy implants was employed to analyse the prophylactic effect of gentamicin-sodiumdodecylsulfate (SDS) and gentamicin-tannic acid coatings in vivo. 20 rats were randomly assigned to four groups: (A) titanium alloy; PBS inoculum (negative control), (B) titanium alloy, Staphylococcus aureus inoculum (positive control), (C) bioactive TiOB with gentamicin-SDS and (D) bioactive TiOB plus gentamicin-tannic acid coating. Contamination of implants, bacterial load of bone powder and radiographic as well as histological signs of implant-related osteomyelitis were evaluated after four weeks. Gentamicin-SDS coating prevented implant contamination in 10 of 10 tibiae and gentamicin-tannic acid coating in 9 of 10 tibiae (infection prophylaxis rate 100% and 90% of cases, respectively). In Group (D) one implant showed colonisation of bacteria (swab of entry point and roll-out test positive for S. aureus). The interobserver reliability showed no difference in the histologic and radiographic osteomyelitis scores. In both gentamicin coated groups, a significant reduction of the histological osteomyelitis score (geometric mean values: C = 0.111 ± 0.023; D = 0.056 ± 0.006) compared to the positive control group (B: 0.244 ± 0.015; p < 0.05) was observed. The radiographic osteomyelitis scores confirmed these histological findings.

Vitamin C attenuates the cytotoxic effects of Porphyromonas gingivalis on human gingival fibroblasts.

OBJECTIVE: Periodontitis is induced by an imbalance between bacterial virulence and host defense ability involving increased levels of oxidative stress. The aim of this study was to investigate the influence of vitamin C on the cytotoxic effects of Porphyromonas gingivalis on human gingival fibroblasts (HGF). METHODS: This in vitro study observed the interaction between HGF and P. gingivalis. HGF were cultured with medium containing vitamin C and exposed to P. gingivalis ATCC 33277 for a maximum of 180 min. The assessment of cell viability was followed by a 3-(4,5-dimethylthiazol-2-ly)-2,5-diphenyltetrazolium-bromide (MTT) assay. The apoptosis rate was detected by flow cytometry using Annexin-V-FITC and propidium iodide. Superoxide as an oxidative stress factor was measured photometrically by the reduction of ferricytochrome C. RESULTS: Vitamin C reduced the cytotoxic effects of P. gingivalis on HGF. Vitamin C-treated HGF showed significantly higher cell viability rates (89.0+/-5.7%) in comparison to untreated HGF (77.0+/-5.0%; p<0.05). In vitamin C-treated HGF, lower apoptosis rates (40.0+/-2.2%) were observed after P. gingivalis exposure than in untreated HGF (66.1+/-1.6%; p<0.05). The exposure of HGF to P. gingivalis led to a significant increase of superoxide concentration, but this effect was not influenced by vitamin C. CONCLUSION: Vitamin C reduces the cytotoxic and apoptotic effects of P. gingivalis on HGF in vitro. These results suggest that the benefit of vitamin C should be further investigated clinically.