Pathology in Scleritis: The Massachusetts Eye and Ear Infirmary Experience

Abstract

The histopathological aspects of scleral inflammation have been studied extensively in the past. Although certain inferences can be drawn from these descriptions, terms such as “chronic nonspecific inflammation,” or even “chronic granulomatous inflammation,” only camouflaged our ignorance about the possible pathogenic roles that cells might play. Even sophisticated techniques such as electron microscopy provided limited insights into the delineation of the distinctive composition of the cellular infiltrates as well as into the components of the matrix during inflammation. It was not until the relatively recent development of immunohistochemistry, particularly the exploitation of monoclonal antibody technology, that the etiology and pathogenesis of scleral diseases have become less obscure and intimidating. Our ability to characterize cells and determine extracellular matrix changes during inflammatory reactions contributes to the understanding of mechanisms of lesion production and thereby to the development of treatment options most likely to succeed. Thus it is possible to distinguish between T and B lymphocytes, to determine mononuclear subsets (T helper, T cytotoxic/suppressor, natural killer, macrophages, and Langerhans’ cells), and to detect HLA-DR glycoproteins in scleral inflammation; it is now possible to identify and further characterize different types of components of extracellular matrix (collagen, glycosaminoglycans, and glycoproteins) during inflammatory reactions; it is also possible to localize specific antigens (herpes simplex virus) in inflamed tissue.