ABSTRACT
HYPOTHESIS: Cultured fibroblasts derived from experimental gerbil cholesteatoma tissue exhibit an invasive phenotype in comparison with normal fibroblasts. BACKGROUND: Aural cholesteatomas are enlarging accumulations of keratin debris caused by keratinizing squamous epithelium in the middle ear. They characteristically result in the destruction of adjacent tissues, specifically bone erosion. The mechanisms by which cholesteatomas relentlessly invade the structures of the temporal bone are varied, but it has been suggested that one factor contributing to the aggressive nature of cholesteatomas is the transformation of resident fibroblasts into an invasive phenotype. METHODS: The ability of cultured normal and cholesteatoma fibroblasts to invade a basement membrane matrix in a Boyden chamber assay was examined. RESULTS: Less than 1% of gerbil fibroblasts invaded the matrix, compared with almost 10% of the invasive HT-1080 fibrosarcoma cells. Normal and cholesteatoma fibroblasts did not differ from each other in their invasive potential. CONCLUSION: Normal fibroblasts and fibroblasts from induced cholesteatomas do not exhibit the invasive phenotype characteristic of true neoplastic cells.
Subject(s)
Cholesteatoma, Middle Ear/pathology , Disease Models, Animal , Fibroblasts/pathology , Animals , Bone Resorption/metabolism , Bone Resorption/pathology , Cell Movement/physiology , Cells, Cultured , Cholesteatoma, Middle Ear/metabolism , Fibroblasts/metabolism , Gerbillinae , Keratins/metabolism , Temporal Bone/metabolism , Temporal Bone/pathology , Tympanic Membrane/metabolism , Tympanic Membrane/pathologyABSTRACT
From 1981 through June 1989, 59 children had surgery for a complete atrioventricular (AV) canal defect at Oregon Health Sciences University. We compared the morbidity, mortality, and hemodynamic status of 47 children with and 12 without Down's syndrome through review of operative, clinical, and cardiac catheterization records. Overall, 10 children with Down's syndrome have died, nine from cardiac cause within 90 days of surgery. The 2-year survival of these children was 77 +/- 6% as compared to 100% in children without Down's syndrome (p = 0.08). Early age at surgery, the surgical anatomy of the AV canal, and gender had no significant effect on survival. Before surgery, the hemodynamic status of Down's syndrome and non-Down's syndrome children did not differ; in a small group of post-operative catheterization, right heart pressures and pulmonary vascular resistance remained significantly higher in the Down's syndrome as compared to non-Down's syndrome children. These trends to higher mortality and poorer postoperative hemodynamics in children with Down's syndrome may necessitate closer follow-up if confirmed in other cohorts.
