Magnesium alloy AZ91 exhibits antimicrobial properties in vitro but not in vivo.

Magnesium alloys hold great promise for developing orthopedic implants that are biocompatible, biodegradable, and mechanically similar to bone tissue. This study evaluated the in vitro and in vivo antimicrobial properties of magnesium-9%aluminum-1%zinc (AZ91) and commercially pure titanium (cpTi) against Acinetobacter baumannii (Ab307). The in vitro results showed that as compared to cpTi, incubation with AZ91 significantly reduced both the planktonic (cpTi = 3.45e8, AZ91 = 8.97e7, p < 0.001) colony forming units (CFU) and biofilm-associated (cpTi = 3.89e8, AZ91 = 1.78e7, p = 0.01) CFU of Ab307. However, in vivo results showed no significant differences in the CFU enumerated from the cpTi and AZ91 implants following a 1-week implantation in an established rodent model of Ab307 implant associated infection (cpTi = 5.23e3, AZ91 = 2.46e3, p = 0.29). It is proposed that the in vitro results were associated with an increased pH in the bacterial culture as a result of the AZ91 corrosion process. The robust in vivo buffering capacity likely diminished this corrosion associated pH antimicrobial effect. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 106B: 221-227, 2018.

Influence of MC3T3-E1 preosteoblast culture on the corrosion of a T6-treated AZ91 alloy.

This study investigated the corrosion of artificially aged T6 heat-treated Mg-9%Al-1%Zn (AZ91) for biomedical applications. Corrosion tests and surface analysis were completed both with and without a monolayer of mouse preosteoblast MC3T3-E1 cells cultured on the sample. Electrochemical impedance spectroscopy (EIS) and inductively coupled plasma mass spectroscopy (ICPMS) were used to explore the corrosion processes after either 3 or 21 days of AZ91 incubation in cell culture medium (CCM). The EIS showed both the inner layer resistance (Rin ) and outer layer resistance (Rout ) were lower for samples without cells cultured on the surface at 3 days (Rin = 2.64 e4 Ω/cm(2) , Rout = 140 Ω/cm(2) ) compared to 21 days (Rin = 3.60 e4 Ω/cm(2) , Rout = 287 Ω/cm(2) ) due to precipitation of magnesium and calcium phosphates over time. Samples with preosteoblasts cultured on the surface had a slower initial corrosion (3 day, Rin = 1.88 e5 Ω/cm(2) , Rout = 1060 Ω/cm(2) ) which was observed to increase over time (21 day, Rin = 2.99 e4 Ω/cm(2) , Rout = 287 Ω/cm(2) ). Changes in the corrosion processes were thought to be related to changes in the coverage provided by the cell layer. Our results reveal that the presence of cells and biological processes are able to significantly influence the corrosion rate of AZ91.

Cathodic voltage-controlled electrical stimulation of titanium implants as treatment for methicillin-resistant Staphylococcus aureus periprosthetic infections.

Effective treatment options are often limited for implant-associated orthopedic infections. In this study we evaluated the antimicrobial effects of applying cathodic voltage-controlled electrical stimulation (CVCES) of -1.8 V (vs. Ag/AgCl) to commercially pure titanium (cpTi) substrates with preformed biofilm-like structures of methicillin-resistant Staphylococcus aureus (MRSA). The in vitro studies showed that as compared to the open circuit potential (OCP) conditions, CVCES of -1.8 V for 1 h significantly reduced the colony-forming units (CFU) of MRSA enumerated from the cpTi by 97% (1.89 × 106 vs 6.45 × 104 CFU/ml) and from the surrounding solution by 92% (6.63 × 105 vs. 5.15 × 104 CFU/ml). The in vivo studies, utilizing a rodent periprosthetic infection model, showed that as compared to the OCP conditions, CVCES at -1.8 V for 1 h significantly reduced MRSA CFUs in the bone tissue by 87% (1.15 × 105 vs. 1.48 × 104 CFU/ml) and reduced CFU on the cpTi implant by 98% (5.48 × 104 vs 1.16 × 103 CFU/ml). The stimulation was not associated with histological changes in the host tissue surrounding the implant. As compared to the OCP conditions, the -1.8 V stimulation significantly increased the interfacial capacitance (18.93 vs. 98.25 µF/cm(2)) and decreased polarization resistance (868,250 vs. 108 Ω-cm(2)) of the cpTi. The antimicrobial effects are thought to be associated with these voltage-dependent electrochemical surface properties of the cpTi.

Folate exacerbates the effects of ethanol on peripubertal mouse mammary gland development.

Alcohol consumption is linked with increased breast cancer risk in women, even at low levels of ingestion. The proposed mechanisms whereby ethanol exerts its effects include decreased folate levels resulting in diminished DNA synthesis and repair, and/or acetaldehyde-generated DNA damage. Based on these proposed mechanisms, we hypothesized that ethanol would have increased deleterious effects during periods of rapid mammary gland epithelial proliferation, such as peripuberty, and that folate deficiency alone might mimic and/or exacerbate the effects of ethanol. To test this hypothesis, weight-matched 28-35 day old CD2F1 female mice were pair-fed liquid diets ±3.2% ethanol, ±0.1% folate for 4 weeks. Folate status was confirmed by assay of liver and kidney tissues. In folate deficient mice, no significant ethanol-induced changes to the mammary gland were observed. Folate replete mice fed ethanol had an increased number of ducts per section, due to an increased number of terminal short branches. Serum estrogen levels were increased by ethanol, but only in folate replete mice. These results demonstrate that folate deficiency alone does not mimic the effects of ethanol, and that folate deficiency in the presence of ethanol blocks proliferative effects of ethanol on the mammary ductal tree.