Host response - Orthopaedic Biomaterials in Research and Practice - page 346

portion of the implant capsule or one side of a replaced joint and to
have the appearance of a sterile abscess. As discussed in Chapter 13,
causation of this process in TJRs is generally seen as dominated by
implant motion (“micromotion”); it is unclear which comes first: the
motion producing the debris or the biologic reaction leading to motion
and production of debris.
There is substantial in vitro evidence that stimulated macrophages
can attack bone directly and that, in addition, they release pro-inflam-
matory cytokines and other mediators of inflammation, which attracts
and stimulates osteoclasts. Animal studies suggest that TNF-α is a
key cytokine involved in osteolysis. The result may be a quick “dis-
secting” osteolysis that moves into the interface between normal
bone and the implant, leaving a broad (1-5 mm wide) lucent zone and
potentially leading to rapid clinical failure. There is an established
correlation between number of macrophages, volume of UHWMPE
wear debris, and osteolytic regions. Size and volume of particles are
determinant of resulting host response. In vitro studies of human and
murine macrophages have shown that the most biologically active size
range is 0.1 to 1.0 μm in terms of macrophages producing cytokines
and resulting in bone-resorbing activity. Osteolysis has been demon-
strated most graphically in the unfortunate use of a UHMWPE femo-
ral head in the Monk “soft-top” endoprosthesis, which bears directly
against bone in the acetabulum, leading to aggressive polyethylene
granulomatosis.

Infection Infection is the great enemy of the surgeon, rendering useless the best

reconstruction and hindering its revision. Implant site infections are a
major revision risk and can prolong hospital care, although their inci-
dence in previously uninfected sites rarely exceeds 1%. Infections may
be separated into early and late occurrence.
Early infections are generally due to the introduction of skin or air-
borne pathogens during surgery. The role of the implant in the estab-
lishment and maintenance of early infection appears to be largely
mechanical, in serving as a barrier to easy revascularization of the dam-
aged tissue immediately adjacent to the implant. Pre-existing sensitivity
to metal has also been implicated in the related problem of early infec-
tion of internal fracture fixation sites. However, animal studies suggest
that all commonly used prosthetic materials produce modest increased
infectability of the implant site by Staphylococcus aureus. However,
sites with PMMA polymerized in situ, as is the case in TJR arthroplasty,
are particularly sensitive, requiring as few as 1000 colony-forming units
of Staphylococcus epidermidis and Escherichia coli for infection. Any
particulate debris can act as a scaffold for bacterial adhesion and biofilm
growth and ultimately reduce the minimum number of bacteria needed
to cause an infection.
Late infection frequently has a hematogenous source, and thus
local vascular insufficiency seems a weak explanation for its tenacity.
However, in vitro studies demonstrate that stainless steel and cobalt-base
alloy constituents, in concentrations present in the immediate vicinity of