Solid-solid displacive, structural phase transformations typically undergo a discrete structural change from a parent to a product phase. Coupling electron microscopy, three-dimensional atom probe, and first-principles computations, we present the first direct evidence of a novel mechanism for a coupled diffusional-displacive transformation in titanium-molybdenum alloys wherein the displacive component in the product phase changes continuously with changing composition. These results have implications for other transformations and cannot be explained by conventional theories.
Periprosthetic joint infections (PJI) occurring after artificial joint replacement is a major clinical issue requiring multiple surgeries and antibiotic interventions. Staphylococcus aureus is the common bacteria responsible for PJI. Recent in vitro research has shown that staphylococcal strains rapidly form aggregates in the presence of synovial fluid (SF). We hypothesize that these aggregates provide early protection to bacteria entering the wound site allowing the bacteria time to attach to the implant surface leading to biofilm formation. Thus, understanding attachment kinetics of these aggregates is critical in understanding the aggregates adhesion on various biomaterial surfaces. In this study, the number, size and surface area coverage of aggregates as well as of single cells of S. aureus were quantified at various conditions on different orthopedic materials relevant to orthopedic surgery; Stainless steel (316L), Titanium (Ti), Hydroxyapatite (HA), and Polyethylene (PE). It was observed that, regardless of the material type, SF induced aggregation resulted in reduced aggregate surface attachment and greater aggregate size than the single cell populations under various shear stresses. Additionally, the surface area coverage of bacterial aggregates on PE was relatively high when compared to other materials, which could potentially be due to the rougher surface of PE. Furthermore, increasing shear stress to 78 mPa decreased aggregates attachment on Ti and HA while increasing the aggregates average size. Therefore, this study demonstrates that the SF induced inhibition of aggregates attachment on all materials suggesting that the biofilm formation is initiated by lodging of aggregates on the surface features of implants and host tissues.
IMPORTANCE
Periprosthetic joint infections occurring after artificial joint replacement is a major clinical issue that require repeated surgeries and antibiotic interventions. Unfortunately, 26% of the patients die within 5 years of developing these infections. Staphylococcus aureus is the common bacteria responsible for this problem that can form biofilm to provide protection from antibiotics as well as the immune system. Although biofilms are evident on the infected implants, it is unclear how these are attached on the surface in the first place. Recent in vitro research investigations have shown that staphylococcal strains rapidly form aggregates in the presence of synovial fluid and provides protection to bacteria and, therefore, allows time to attach to the implant surface leading to biofilm formation. Thus, in this study, we investigated the attachment kinetics of Staphylococcus aureus aggregates on different orthopedic materials. The information presented in this article will add knowledge in surgical management and implant design.
Periprosthetic joint infections occurring after joint replacement are a major clinical problem requiring repeated surgeries and antibiotic interventions.
Staphylococcus aureus
is the most prominent bacterium causing most implant-related infections.
S. aureus
can form a biofilm, which is defined as a group of attached bacteria with the formation of an envelope that is resistant to antibiotics. The attachment and retention of these bacteria on implant surfaces are not clearly understood.
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