Extended reports
Bisphosphonates in bone cement inhibit PMMA particle induced bone
resorption
Nuffield Orthopaedic Centre, University of
Oxford, Oxford
Correspondence to: Dr N A Athanasou, Department of Pathology, Nuffield Orthopaedic Centre, Headington, Oxford, OX3 7LD.
Accepted for publication 29 July 1998
OBJECTIVE
Wear particle induced bone resorption is
thought to be one of the mechanisms that contribute to implant
loosening. It has previously been shown that macrophages, in response
to polymethylmethacrylate (PMMA) particles, differentiate into bone
resorbing osteoclasts, and that this process is inhibited by a
bisphosphonate, etidronate (EHDP). The aim of this study was to
determine whether incorporating EHDP in bone cement could reduce PMMA
associated bone resorption.
METHODS
Two concentrations of EHDP were mixed with
PMMA monomer before polymerisation. Particles of PMMA (1-10 µm) were
generated then added to mouse monocytes cocultured with UMR106 rat
osteoblast-like cells and the extent of osteoclast differentiation was
determined by assessing the extent of tartrate resistant acid
phosphatase (TRAP) staining and measuring the amount of lacunar bone resorption.
RESULTS
The addition of PMMA to
monocyte-UMR106 cocultures resulted in a marked increase in the number
of TRAP positive osteoclast-like cells and a significant increase in
the number of lacunar resorption pits compared with control cultures to
which no particles had been added. After the addition of particles of
PMMA + 20 mg EHDP, significantly fewer lacunar pits (p=0.00006) and
fewer TRAP positive cells were noted compared with cocultures
containing PMMA particles alone.
CONCLUSIONS
These results indicate that by
mixing a bisphosphonate with bone cement, it is possible to inhibit
PMMA particle induced bone resorption. This bisphosphonate inhibition
of PMMA biomaterial wear particle containing macrophage-osteoclast
differentiation and bone resorption may provide a possible therapeutic
strategy to prevent or to control the osteolysis of aseptic loosening.
© 1998 by Annals of the Rheumatic Diseases
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