Implant materials generate different peri-implant inflammatory factors: poly-ether-ether-ketone promotes fibrosis and microtextured titanium promotes osteogenic factors.

Materials such as titanium-aluminum-vanadium alloy (Ti-6Al-4V, TiAlV) and poly-ether-ether-ketone (PEEK) are commonly used in spinal interbody fusion surgical procedures. These 2 materials, while used for similar clinical applications, have substantially different surface characteristics, especially on a micron scale. Poly-ether-ether-ketone is popular because its modulus of 3 to 4 GPa1,2 is close to that of native cortical bone, 14 to 18 GPa. In addition, PEEK is radiolucent, allowing surgeons to examine whether bone fills the intervertebral space. However, it is often encapsulated by fibrous tissue. The lack of bone integration can ultimately result in implant subsidence and nonunion. Ti alloys have higher elastic moduli than bone but have yielded successful results clinically.3,4 Studies in animal models show greater bone apposition to Ti and Ti alloy surfaces, particularly when the surfaces have a rough microtopography.5–7In vitro studies indicate that microtextured Ti and Ti alloy surfaces promote osteoblast differentiation and production of factors that favor bone formation in vivo, whereas PEEK does not.8–10 After a material is implanted into the body, the immune system initiates an immune response sequence.11 The inflammatory response to the biomaterial is mediated in large part by the local inflammatory microenvironment, which results in a cascade triggering migration of other cells to the vicinity. A high level of inflammation creates a longer resolution period. Fibroblasts initially produce extracellular matrix in an effort to support the damaged tissue; however, extended activation of macrophages and other immune cells leads to reduction in matrix remodeling and the fibrotic scar tissue that was formed in the support stage of wound healing, which remains. The persistence of fibrosis around PEEK implants in contrast to peri-implant bone formation around Ti alloy suggests that PEEK may stimulate formation of microenvironment consisting of specific inflammatory cytokines that enhance fibrous tissue formation, whereas micron-scale–roughened Ti alloy surfaces reduce production of these factors. To test this hypothesis, we cultured human mesenchymal stem cells (MSCs) on disks consisting of machined PEEK, machined Ti6Al4V, and microtextured Ti6Al4V, and examined their production of factors associated with inflammation, apoptosis, and necrosis.