Extended report
Effect of osteoprotegerin and osteoprotegerin ligand on
osteoclast formation by arthroplasty membrane derived macrophages
I Itonagaa, A Sabokbara, D W Murraya, N A Athanasoub
a Nuffield Department
of Orthopaedic Surgery, University of Oxford, Oxford, b Department
of Pathology, Nuffield Orthopaedic Centre, Windmill Road, Headington,
Oxford OX3 7LD
Correspondence to: Dr Athanasou
Accepted for publication 12 October 1999
OBJECTIVE
Osteoprotegerin
ligand (OPGL) is a newly discovered molecule, which is expressed by
osteoblasts/bone stromal cells. This ligand and M-CSF are now known to
be essential for osteoclast differentiation from marrow and circulating
precursors. This study examined whether OPGL and its soluble receptor
osteoprotegerin (OPG), influenced osteoclast formation from human
arthroplasty derived macrophages, to determine if the effects of OPGL
and OPG on these cells could contribute to the osteolysis of aseptic loosening.
METHODSOPGL (± dexamethasone/M-CSF) was added to cultures of macrophages isolated from
the pseudomembrane of loosened hip arthroplasties incubated on
glass coverslips and dentine slices. OPG was added to cocultures of
arthroplasty derived macrophages and UMR106 osteoblast-like cells.
Osteoclast differentiation in long term cultures was assessed by
expression of macrophage (CD14) and osteoclast markers (tartrate resistant acid phosphatase (TRAP), vitronectin receptor (VNR) and
lacunar resorption).
RESULTSIn the absence
of osteoblastic cells, the addition of OPGL alone was sufficient to
induce differentiation of macrophages (CD14+,
TRAP-, VNR-) into TRAP+ and
VNR+ multinucleated cells, capable of extensive lacunar
resorption. OPG was found to inhibit osteoclast formation by
arthroplasty macrophages in a dose dependent manner. OPG (100 ng/ml)
more than halved the formation of TRAP+ and
VNR+ cells and the extent of lacunar resorption in
co-cultures of UMR106 cells and arthroplasty macrophages.
CONCLUSIONSThis study
has shown that macrophages, isolated from the pseudomembrane
surrounding loose arthroplasty components, are capable of
differentiating into osteoclastic bone resorbing cells and that OPGL is
required for this to occur. OPG inhibits this process, most probably by
interrupting the cell-cell interaction between osteoblasts and
mononuclear phagocyte osteoclast precursors present in the pseudomembrane.
© 2000 by Annals of the Rheumatic Diseases
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