A particularly salient test of biological reactivity depends on replicating the conditions under which devices will perform over a longer term in an appropriate experimental animal model. Thus, in a series of nine cats, devices were implanted in paraspinal muscles around lumbar vertebrae and in tibialis anterior muscles of the hindlimb for survival periods of one, six, and thirteen months. Different sites in the paraspinal muscles of the same animals were also implanted with negative control articles, including USP-recommended polyethylene rods, silicone rods custom-fabricated to reproduce the form of the tested devices, and BIONs whose glass package was sheathed in thin-walled silicone tubing (0.1 mm wall thickness). Each test and control article was inserted into a small pocket made in the muscle with the tips of fine scissors. The insertion sites of the devices were closed and marked with 6-0 multistranded polybutylate-coated polyester nonresorbable suture (Ethicon Ethi-bond). This suture also provided a test article against which the bioreactivity of the tested devices could be compared (Figures 3.4 and 3.5).
After all tested survival times, implant sites were evaluated histologically in fixed sections stained using haematoxylin and eosin, and in frozen sections reacted for adenosine triphosphatase activity (Figure 3.4). None of the implanted articles were found to change the enzyme reactivity of surrounding muscle fibers. No obvious difference could be found in the degree of inflammatory reaction around the devices and the negative control articles when the implant sites were evaluated according to their contents of inflammatory cells of different types and the extent of fibrotic and necrotic change using scales similar to those described elsewhere.17 In addition, the thicknesses of capsules around the implants were measured and found to be similar around devices and control articles (Figure 3.5). In the first few months, implants were surrounded by a loosely structured connective tissue capsule about 100-500 microns thick that contained many inflammatory cells. In longer-term implants of 6-13 months, capsules were much thinner and were composed of flattened connective tissues with few associated inflammatory cells. No obvious difference was observed between reactions around the devices at six and thirteen months, suggesting that the use of a six-month survival period may be adequate to establish a stable interface between the device and the biological tissue. Interestingly, the reactions around suture material appeared to be greater than those around devices and control articles; capsules were somewhat thicker and less organized, and inflammatory cells could be identified in close approximation to strands of suture even at the longest survival times. The somewhat heightened reaction might have resulted because the braided material of the suture was more difficult to encapsulate cleanly by a muscle scar.
FIGURE 3.4 Histological appearance of the connective tissue capsules around long-term implants removed from cat muscles. A. Encapsulation around silicone rod (6 month survival). Note the dense inner capsule and loose connective tissue around the implant site. B. Fibrosis in interstices between muscle fibers close to implant site (13 month survival). C. Capsule around non-coated BION (6 month survival). D. Capsule around non-coated BION (13 month survival); tissue stained with ATPase to show reactivities typical of normal muscle fibers.
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