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Mediates Orthopedic Implant Osteolysis
From the Departments of Orthopedic Surgery*
and
Pathology,
Washington University School of
Medicine, St. Louis, Missouri
Osteolysis complicating arthroplasty reflects progressive
generation of implant-derived wear particles, which prompt an
inflammatory reaction attended by recruitment of osteoclasts to
the prosthesis-bone interface. To identify a soluble mediator of
peri-prosthetic osteolysis we first showed that implant particles
induce c-src in murine bone marrow macrophages (BMMs), a
protein specifically expressed when these cells commit to the
osteoclast phenotype. The fact that tumor necrosis factor-
(TNF) is
a potent osteoclastogenic agent while at the same time is the only
soluble moiety known to be c-src inductive suggests that this cytokine
may mediate implant particle-induced osteoclastogenesis. Consistent
with this hypothesis, prosthesis-derived wear particles,
recovered at revision arthroplasty, dose-dependently prompt TNF
secretion by BMMs. Similarly, particulate
polymemthylmethacrylate, the major component of orthopedic
implant cement, induces BMM expression of TNF mRNA and protein
in a time- and dose-dependent manner. Furthermore, failure of
BMMs derived from mice deleted of both the p55 and p75 TNF receptors to
express c-src in response to polymemthylmethacrylate indicates TNF is
an essential mediator of particle induction of this osteoclast specific
protein. To test the hypothesis that TNF mediates implant
osteolysis, we established an in vivo murine
model of this condition that histologically mirrors that of man.
Verifying that TNF is essential to development of particle
osteolysis, mice failing to express both the p55 and p75 TNF
receptors are protected from the profound bone resorption attending
polymemthylmethacrylate particle implantation on calvariae of wild-type
animals. Finally, the protective effect of deletion of both TNF
receptors is recapitulated in mice lacking only the p55 receptor.
Thus, targeting TNF and/or its p55 receptor may arrest wear
particle osteolysis.
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