Search

Bone destruction is one of the clinical features of chronic otitis media with cholesteatoma. Bone resorption may be due to the epithelial debris accumulated in the cholesteatoma epidermal sac that acts as foreign body material inducing a destructive granulation tissue and creates pressure on the bony middle ear. This compressive force then induces bone resorption. The present study was designed to replicate certain conditions similar to those in cholesteatoma leading to bone resorption. Four types of materials were implanted into the middle ear cavity of rats: (1) laminaria, an expandable seaweed material, (2) preswollen laminaria, (3) keratin powder suspension, and (4) surgical grade silicone, which when bent exerts pressure on the bulla wall. The placement of laminaria segments in the middle ear cavity of rats was followed by swelling of the implanted materials within 7 days. The bulla bone response was by neo-osteogenesis as well as active bone resorption. The new bone was observed on the external and/or internal surface of the tympanic bone. The cochlear bone also showed extensive bone resorption in the animals. Osteogenesis was rarely observed on the capsule of the cochlea. We also observed no bone resorption at sites without presence of inflammatory connective tissue between laminaria and bone. The typical multinucleated osteoclasts were often seen at the resorption area but the majority of bone resorption sites were characterized by the presence of mononuclear cells and other inflammatory cells. Preswollen laminaria, keratin powder, and silicone strips induced minimal bone resorption. No resorption was observed in the bony cochleas of these experimental groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibronectin was localized in human cholesteatoma tissues by immunohistochemical methods. The avidin-biotin-peroxidase complex staining method was used with specific fibronectin antibody. Fibronectin appeared to be localized in the matrix of the cholesteatoma studied, particularly on the surface of the cell membranes and the nuclei of the basal cells and in connective tissue. Fibronectin was not seen in the granular layer or in the keratin area. Fibronectin was found on the surface of granulation tissue, mononuclear cells, fibroblasts and endothelial cells of blood vessels. These findings were confirmed by the immunofluorescent staining method. Our previous study showed that fibronectin induced a migration of keratinocytes, macrophages and fibroblasts demonstrated by the Boyden's chamber chemotaxis assay. Macrophages and fibroblasts were shown to produce collagenase, a bone resorption factor, in cholesteatomatous tissue. The present study showed the presence of fibronectin in the matrix of cholesteatoma and granulation tissue, suggesting that fibronectin might play an important role in the clinical development and invasive behavior of cholesteatoma.