Tuesday 13 September 2011
Following a variety of injuries to the mesothelium, including chemical or mechanical exfoliation, the proximity of an inflammatory or neoplastic process, or its exposure to asbestos fibers,there is an initial loss of the surface cell monolayer followed by the deposition of fibrin, leukocytes, and macrophages.
Soon, particularly when the irritative stimulus persists, layers of proliferating spindle-shaped cells, indistinguishable from fibroblasts but with a characteristic immunophenotype, appear underneath this layer off ibrin.
Evidence suggests that these fibroblast-like cells may play an important role in the restoration of the mesothelial surface layer.
Raftery provided evidence that perivascular cells resembling fibroblasts proliferate under areas of experimentally denuded peritoneum, suggesting that they are thef orerunners for a newly formed mesothelial layer.
Immunohistochemical studies with antibodies to keratins support this interpretation.
Bolen et al. found that normal surface mesothelium expressed both low–and high–molecular-weight keratins, where-as the resting submesothelial cells only expressed vimentin.
However, they also found that reactive, proliferating, subserosal fibroblast-like cells coexpressed low–molecular-weight keratins and vimentin.
During the process of mesothelial repair, these specialized fibroblast-like cells gradually acquire more cytoplasm and, as they approach the surface, become rounded and develop epithelial phenotypic and immunophenotypic charac-teristics, such as expression of high–andlow–molecular-weight keratins, and loss or reduction of vimentin expression.
This appears to be an exclusive property of the submesothelial mesenchyme. It is important to emphasize that these subserosal cytokeratin-expressing reactive cells, if not correctly identified, may be a source of diagnostic error, particularly in the distinction between desmoplastic malignant mesothelioma and fibrous pleurisy.