Summary
The use of internal fixation devices for fracture repair induces profound changes
in the affected bone. The factors implicated in the development of implant induced
osteoporosis have been extensively studied. The processes following bone plate fixation
which results in vascular and structural changes to the bone have not been accurately
described. There are many inconsistencies in the design of experimental studies and
in data interpretation which confound the issue.
Implant induced osteoporosis appears to be a biphasic phenomenon following the application
of rigid internal fixation, with an early-onset osteonecrosis (8-12 weeks) elicited
through cortical vascular insufficiency, followed by osteoporosis (24-36 weeks) induced
by stress redistribution.
The development of implant induced osteoporosis appears to involve mechanical factors
(surgical trauma, screw placement, rigidity of the fixation device), acting in conjunction
with vascular insufficiencies related to the bone-plate interface contact area and
pressure distribution.
Whatever the pathogenesis, the end result is a thinning of the diaphyseal cortices.
Should implant removal be deemed necessary such osteoporosis is a cause for concern
in view of the bones predisposition to refracture following plate removal. The degree
of cortical osteoporosis observed appears to be time-dependent following internal
fixaton and as such the clinical outcomes, after implant removal, are also related
to the timing of removal.
Numerous factors have been implicated in the development of the vascular and structural
changes that follow the plating of bone. It appears that implant induced osteoporosis
has a multifactorial pathogenesis involving surgical trauma, screw placement and the
rigidity of the fixation device. Elements involved in the interface between plate
and bone, such as interface contact area and pressure, are also implicated in the
pathogenesis.
Keywords
Osteoporosis - internal fixation - stress protection