INTERLEUKIN-1 CAUSING BONE DESTRUCTION IN MIDDLE-EAR CHOLESTEATOMA

We previously reported the localization of interleukin 1 in the epithelial layer of human cholesteatomas. On the basis of other studies that showed interleukin 1 can stimulate fibroblasts and macrophages to produce collagenases and prostaglandins, we then proposed that interleukin 1 may play an important role in cholesteatoma-related bone resorption, also. Our immunocytochemical study involving more human cholesteatoma samples revealed the presence of interleukin 1 in bone cells and monocytes in the region of active bone destruction. In the present study, the effect of interleukin 1 on these cells found at the bone resorption site was examined. By radioimmunoassay, interleukin 1 was shown to stimulate the production of prostaglandin E2 by osteoblasts in vitro. Interleukin 1 also promoted the migration and multinucleation of bone marrow-derived monocytes. These osteoclast-like cells formed from monocytes contained tartrate-resistant acid phosphatase, and caused the resorption of the devitalized bone in vitro. Above findings suggest that interleukin 1 could cause the bone destruction in cholesteatomas, not only by stimulating the local bone cells, but also by recruiting monocytes for osteoclastic bone resorption.