THE EXPRESSION OF TENASCIN AND FIBRONECTIN IN KERATOCONUS, SCARRED AND NORMAL HUMAN CORNEA

Background: The etiology and pathogenesis of keratoconus remain unclea r, and therefore we decided to study the distribution of different iso forms of tenascin (Tn) and fibronectin (Fn) in normal human corneas an d in those obtained from penetrating keratoplasty for keratoconus and corneal scarring. Methods: Frozen sections of human cornea and conjunc tiva were stained by immunohistochemical methods with a panel of monoc lonal antibodies (MAbs) against different isoforms of Tn and Fn. Resul ts: In the normal human eve, Tn was found in the limbal and conjunctiv al basement membrane region, in the conjunctival blood vessels and at the junction of the cornea and sclera, but no immunoreaction was seen in the normal cornea. In the corneas from the keratoconus patients, a clear immunoreaction for Tn was seen in the defects of Bowman's membra ne as well as in the distorted stroma beneath the defects. In some of the keratoconus corneas, basement membrane adjacent to the defects als o showed reactivity for Tn, and in clinically and histologically scarr ed keratoconus corneas the scars expressed Tn. In the scarred corneas, only blood vessels in the posterior portion of the cornea showed immu noreactivity for Tn, while no Tn was noted in the scar area or in Bowm an's membrane. No major differences were noticed in the reactivity of different MAbs against Tn isoforms. Fn, extradomain A Fn (EDA-Fn) and oncofetal Fn (onc-Fn) were found in the basement membrane of the centr al cornea of the normal eye. In keratoconus corneas, the defects and c linical end histological scars bound MAbs against Fn, EDA-Fn and onc-F n, but in the scarred corneas no enhancement in the expression of Fns was noted. Extradomain B cellular Fn (EDB-Fn) was not expressed in any of the eyes studied. Conclusions: The results suggest that the anteri or portion of the cornea is involved in the pathogenesis of keratoconu s. Furthermore, it seems that the expression of Tn and Fns in the clin ically scarred keratoconus corneas is due to a process in which both r epairing and scar-forming mechanisms operate at the same time. However , the origin of the defects in Bowman's membrane seen in keratoconus s till remains unclear. They may be minor scars due to the disease or pr imary defects in the process leading to keratoconus.