Abstract
Aseptic loosening subsequent to periprosthetic osteolysis is the leading cause for the revision of arthroplasty failure. The biological response of macrophages to wear debris has been well established, however, the equilibrium of bone remodeling is not only dictated by osteoclastic bone resorption but also by osteoblast-mediated bone formation. Increasing evidence shows that wear debris significantly impair osteoblastic physiology and subsequent bone formation. In the present review, we update the current state of knowledge regarding the effect of biomaterial implant wear debris on osteoblasts. The interaction of osteoblasts with osteoclasts and macrophages under wear debris challenge, and potential treatment options targeting osteoblasts are also presented.
Highlights
Total joint arthroplasty (TJA) has been widely and successfully applied for surgical management of severe trauma or arthritic joint diseases
Scanning electron microscopy has revealed that particulate materials generated from implant wear vary more greatly in shape than commercially available particles, and are more detrimental or inflammatory to osteoblasts (Dean et al, 1999b)
We briefly introduce the general cellular response of osteoblasts to various biomaterial wear particles and discuss the interactions between osteoblasts and macrophages/osteoclasts
Summary
Total joint arthroplasty (TJA) has been widely and successfully applied for surgical management of severe trauma or arthritic joint diseases. It has been demonstrated that IL-8 and MCP-1 mRNA expression and protein secretion were up-regulated when osteoblasts were exposed to implant particles, in a time- and concentrationdependent manner in vitro (Fritz et al, 2002, 2006; Queally et al, 2009; Lochner et al, 2011; Yang et al, 2015), and that this upregulation was dependent on particle-induced NF-κB-mediated transcriptional activation These chemokines play critical roles in the initiation of inflammation processes by local and systemic recruitment of inflammatory cells
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