Anin vitroinvestigation of bacteria-osteoblast competition on oxygen plasma-modified PEEK

Abstract

Polyetheretherketone (PEEK) films were oxygen plasma treated to increase surface free energy and characterized by X-ray photoelectron microscopy, atomic force microscopy, and water contact angles. A parallel plate flow chamber was used to measure Staphylococcus epidermidis, Staphylococcus aureus, and U-2 OS osteosarcomal cell-line adhesion to the PEEK films in separate monocultures. In addition, bacteria and U-2 OS cells were cocultured to model competition between osteoblasts and contaminating bacteria for the test surfaces. Plasma treatment of the surfaces increased surface oxygen content and decreased the hydrophobicity of the materials, but did not lead to a significant difference in bacterial or U-2 OS cell adhesion in the monocultures. In the S. epidermidis coculture experiments, the U-2 OS cells adhered in greater numbers on the treated surfaces compared to the untreated PEEK and spread to a similar extent. However, in the presence of S. aureus, cell death of the U-2 OS occurred within 10 h on all surfaces. The results of this study suggest that oxygen plasma treatment of PEEK may maintain the ability of osteoblast-like cells to adhere and spread, even in the presence of S. epidermidis contamination, without increasing the risk of preoperative bacterial adhesion. Therefore, oxygen plasma-treated PEEK remains a promising method to improve implant surface free energy for osseointegration.

Competitive colonization of prosthetic surfaces bystaphylococcus aureusand human cells

“…Contrary to this finding Subbiahdoss et al showed that cell death occurred irrespective of the concentration of surrounding bacteria . According to Rochford et al S. aureus in concentration of 10 4 CFU/mL produced the death of osteoblast in 10 h. However, in our study a high percentage of the cells were alive after 48 h. S. aureus is an aggressive pathogen, which actively releases cytotoxic products into the surrounding environment inducing apoptosis in osteoblasts. Alexander et al proposed that S. aureus ‐induced apoptosis of osteoblasts involves activation of caspase‐8, which is an initiator caspase activated in death receptor‐mediated apoptosis pathways .…”

“…Critical in the healing response of the host is the spread and proliferation of osteoblast cells on the implant surface even in presence of contamination . In our study, the presence of S. aureus diminished osteoblast adherence and viability and, as in other studies, the number and spreading area per cell decreased with increasing density of adhering staphylococci .…”

“…The effect of bacteria on the ability of human cells to attach to prostheses has, however, been largely neglected. In the co‐culture method used in other studies, bacteria were let to adhere prior to cell adhesion and spread . We evaluated whether in a simultaneous adherence of bacteria and human cells, the race is won by tissue.…”

Bacterial adhesion mechanisms on dental implant surfaces and the influencing factors

“…However, in the presence of S. aureus contamination, cell death of the U-2 OS occurred within 10 h on all surfaces. Therefore, they concluded oxygen plasma-treated PEEK may be a promising way to improve implant surface free energy for better osseointegration without leading to more bacteria adhesion [68].…”

Mechanism of cell integration on biomaterial implant surfaces in the presence of bacterial contamination

“…Furthermore, biomaterials have also been found on which low levels of contaminating bacteria counter‐intuitively stimulate adhesion and spreading of tissue cells. These observations were made on widely different materials, ranging from modified titanium alloy to oxygen plasma‐modified polyetheretherketone films when osteosarcomal cells were grown in presence of contaminating S. epidermidis and suggest that cells have an intrinsic mechanism to their disposal that allows them to deal effectively with low levels of bacterial contamination on an implant surface.…”