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Article type : Journal of Applied Microbiology Aspect ratio of nano/microstructures determines Staphylococcus aureus adhesion on PET and titanium surfaces

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Basic calcium phosphate (BCP)-based calcification of cartilage is a common finding during osteoarthritis (OA) and is directly linked to the severity of the disease and hypertrophic differentiation of chondrocytes. Chondrocalcinosis (CC) is associated with calcium pyrophosphate dihydrate (CPPD) deposition disease in the joint inducing OA-like symptoms. There is only little knowledge about the effect of CPPD crystals on chondrocytes and the signaling pathways involved in their generation. The aim of this study was to investigate the chondrocyte phenotype in CC cartilage and the effect of CPPD crystals on chondrocytes. Cartilage samples of patients with CC, patients with severe OA, and healthy donors were included in this study. The presence of CC was evaluated using standard X-ray pictures, as well as von Kossa staining of cartilage sections. OA severity was evaluated using the Chambers Score on cartilage sections, as well as the radiological Kellgren–Lawrence Score. Patients with radiologically detectable CC presented calcification mainly on the cartilage surface, whereas OA patients showed calcification mainly in the pericellular matrix of hypertrophic chondrocytes. OA cartilage exhibited increased levels of collagen X and matrix metalloproteinase 13 (MMP13) compared with CC and healthy cartilage. This observation was confirmed by qRT-PCR using cartilage samples. No relevant influence of CPPD crystals on hypertrophic marker genes was observed in vitro, whereas BCP crystals significantly induced hypertrophic differentiation of chondrocytes. Interestingly, we observed an increased expression of p16 and p21 in cartilage samples of CC patients compared with OA patients and healthy controls, indicating cellular senescence. To investigate whether CPPD crystals were sufficient to induce senescence, we incubated chondrocytes with BCP and CPPD crystals and quantified senescence using β-gal staining. No significant difference was observed for the staining, but an increase of p16 expression was observed after 10 days of culture. Primary chondrocytes from CC patients produced CPPD crystals in culture. This phenotype was stabilized by mitomycin C-induced senescence. Healthy and OA chondrocytes did not exhibit this phenotype. BCP and CPPD crystals seem to be associated with two different chondrocyte phenotypes. Whereas BCP deposition is associated with chondrocyte hypertrophy, CPPD deposition is associated with cellular senescence.

Aseptic loosening is the main reason for arthroplasty failure. The wear particles generated at the tribological bearings are thought to induce an inflammatory tissue response, leading to bone loss and the subsequent loosening of the implant. Different wear particles have been shown to activate the inflammasome, thereby contributing to an inflammatory milieu in the direct vicinity of the implant. The aim of this study was to investigate whether the NLRP3 inflammasome is activated by different metal particles in vitro and in vivo. Three different cell lines representing periprosthetic cell subsets (MM6, MG63 and Jurkat) were incubated with different amounts of TiAlV or CoNiCrMo particles. The activation of the NLRP3 inflammasome was determined through the detection of the caspase 1 cleavage product p20 in a Western blot. The formation of the inflammasome was also investigated in vivo using immunohistological staining for ASC in primary synovial tissues as well as tissues containing TiAlV and CoCrMo particles and in vitro after the stimulation of the cells. The results show that the CoCrMo particles induced ASC more markedly, as a readout for inflammasome formation in vivo, compared to TiAlV particular wear. The CoNiCrMo particles also induced ASC-speck formation in all the tested cell lines, which was not induced by the TiAlV particles. The Western blot shows that NRLP3 inflammasome activation, measured through caspase 1 cleavage, was increased only by the CoNiCrMo particles in the MG63 cells. We conclude from our data that the activation of the inflammasome is mainly driven by CoNiCrMo particles and less by TiAlV particles, indicating that different inflammatory pathways are activated by the different alloys.

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Fretting corrosion is associated with increased risk of premature implant failure. In this complex in vivo corrosion system, the contribution of static crevice corrosion of the joined metal alloys is still unknown. The aim of this study was to develop a methodology for testing crevice corrosion behavior that simulates the physiological conditions of modular taper junctions and to identify critical factors on corrosion susceptibility. Samples of medical grade CoCr28Mo6 cast and wrought alloy, TiAl6V4 wrought alloy and REX 734 stainless steel were prepared metallographically and the microstructure was investigated using scanning electron microscopy (SEM). Crevice formers that mimic typical geometries of taper junctions were developed. Crevice corrosion immersion tests were performed in different physiological fluids (bovine serum or phosphate buffered saline with additives of 30 mM H 2 O 2 at pH = 1) for 4 weeks at 37 C. SEM with energy dispersive X-ray spectroscopy as well as focused ion beam were used to characterize the surface morphology, investigate present damages and identify the chemical composition of residues. Macroscopic inspection showed increased crevice corrosion susceptibility of TiAl6V4 and REX 734 under severe simulated inflammatory conditions. CoCr28Mo6 cast alloy exhibited degraded areas next to Cr-and Mo-rich precipitations that were located within the opposed crevices. The results indicate that aggressive electrolyte composition and crevice heights of 50-500 μm are critical influencing factors on crevice corrosion of biomedical alloys. Furthermore, manufacturing-related microstructure of common implant alloys determines the deterioration of corrosion resistance. The developed method should be used to enhance the corrosion resistance of common implant biomaterials by an adapted microstructure.

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