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

Rene Olivares-Navarrete, Sharon L. Hyzy, Paul J. Slosar, Jennifer M. Schneider, Zvi Schwartz, Barbara D. Boyan

Research output: Contribution to journalArticle

49 Scopus citations

Abstract

Study Design. An in vitro study examining factors produced by human mesenchymal stem cells on spine implant materials. Objective. The aim of this study was to examine whether the inflammatory microenvironment generated by cells on titanium-aluminum-vanadium (Ti-alloy, TiAlV) surfaces is affected by surface microtexture and whether it differs from that generated on poly-ether-ether-ketone (PEEK). Summary of Background Data. Histologically, implants fabricated from PEEK have a fibrous connective tissue surface interface whereas Ti-alloy implants demonstrate close approximation with surrounding bone. Ti-alloy surfaces with complex micron/submicron scale roughness promote osteoblastic differentiation and foster a specific cellular environment that favors bone formation whereas PEEK favors fibrous tissue formation. Methods. Human mesenchymal stem cells were cultured on tissue culture polystyrene, PEEK, smooth TiAlV, or macro-/micro-/nano-textured rough TiAlV (mmnTiAlV) disks. Osteoblastic differentiation and secreted inflammatory interleukins were assessed after 7 days. Fold changes in mRNAs for inflammation, necrosis, DNA damage, or apoptosis with respect to tissue culture polystyrene were measured by low-density polymerase chain reaction array. Data were analyzed by analysis of variance, followed by Bonferroni's correction of Student's t-test. Results. Cells on PEEK upregulated mRNAs for chemokine ligand-2, interleukin (IL) 1β, IL6, IL8, and tumor necrosis factor. Cells grown on the mmnTiAlV had an 8-fold reduction in mRNAs for toll-like receptor-4. Cells grown on mmnTiAlV had reduced levels of proinflammatory interleukins. Cells on PEEK had higher mRNAs for factors strongly associated with cell death/apoptosis, whereas cells on mmnTiAlV exhibited reduced cytokine factor levels. All results were significant (P < 0.05). Conclusion. These results suggest that fibrous tissue around PEEK implants may be due to several factors: reduced osteoblastic differentiation of progenitor cells and production of an inflammatory environment that favors cell death via apoptosis and necrosis. Ti alloy surfaces with complex macro/micro/nanoscale roughness promote osteoblastic differentiation and foster a specific cellular environment that favors bone formation.

Original languageEnglish (US)
Pages (from-to)399-404
Number of pages6
JournalSpine
Volume40
Issue number6
DOIs
StatePublished - Mar 15 2015

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Keywords

  • PEEK
  • Ti6Al4V
  • fibrosis
  • implant surface
  • inflammatory mediators
  • interbody spine cage
  • mRNA array
  • mesenchymal stem cells
  • osteogenesis

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Clinical Neurology

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