THE CELLULAR EFFECTS OF ORTHOPEDIC IMPLANT WEAR PARTICLES ON OSTEOBLAST FUNCTION

Abstract

Purpose: Peri-implant osteolysis after total joint arhtro-plasty (TJA) is a major cause of implant loosening. Cellular responses to wear particles have been reported to play a role in asceptic loosening due to their cytotoxic nature to cellular components. Purpose of this study is to evaluate the effect of orthopedic implant wear particles on immature osteoblasts in an in-vitro setting in order to further understand the mechanisms involved in asceptic loosening of implants.

Methods: Stromal cells from femurs of 30 day-old Swiss Webster Mice were isolated, cultured in-vitro, and incubated with Titanium and Ceramic (smooth and angular) particles in the micrometer size range. After 9 days of incubation the cells were assessed for Alkaline phosphatase (ALP) activity or stained for cellular changes consistent with apoptosis.

Results: Here we report both a dose-dependent decrease (P< 0.05) in ALP activity and a significant increase in programmed cell death when murine stromal cells were cultured with orthopedic implant wear particles of differing compositions. Ceramic wear particles were consistently less toxic at lower concentrations (1 x 107 to 2 x 107 particles/ml) than were wear particles composed of titanium. However, at high concentrations (4 x 107 particles/ml) all particles regardless of composition were equally toxic. These findings suggest that ceramic particles may be less cytotoxic to bone marrow stromal cells/osteoblasts than are titanium particles.

Conclusions: Previous studies have suggested that inflammatory responses to orthopedic wear particles are responsible for the asceptic loosening of orthopedic implants. In the current study however, we found that wear particles may also induce cellular apoptosis of primary bone forming cells. This suggests that the asceptic loosening of orthopedic implants may be independent of inflammatory processes, and that implant material selection should be directed, in part, by its inability to cause programmed cell death.