Abstract
We report a study on how the bone-implant interface of 20 T.H.A. failed because of aseptic loosening. The aim of this study was to look for the mechanism that promotes the activation of the cell-population located in the tissues at the interface. We have demonstrated, with the help of cytochemical and enzymatic techniques, that cell-activation can be supported by similar agents for every type of implant (cemented or cementless). We believe that these agents could be identified with lymphokines, particularly with Interleukin 1 (IL-1), and that the production of these factors is stimulated by mechanical factors. These results evidence the importance of debris, in addition to micromotion, at the beginning of the process of aseptic loosening.
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