CELLULAR FIBRONECTIN AND TENASCIN IN EXPERIMENTAL PERFORATING SCLERAL WOUNDS WITH INCARCERATION OF THE VITREOUS

Background: Posterior perforating eye injury carries a high risk of visual loss due to the formation of intravireal and epiretinal scar tissue. Intraocular scar formation in patients with retinal detachment has been shown to be associated with elevated intravitreal FN levels. The extracellular matrix glycoproteins fibronectin (FN) and tenascin (TN) have been located in epiretinal scar membranes. As both FN and TN are also involved in healing of cutaneous and corneal wounds, we undertook to study their expression in rabbit perforating scleral wounds with vitreous incarceration. Methods: A perforating scleral wound was produced and sutured without removal of vitreous from the wound in 18 pigmented rabbits. The rabbits were killed at various times (1 h to 21 days) after the operation, and the indirect immunohistochemical method was used for demonstration of FN and TN. Monoclonal mouse hybridoma antibodies 52 DH1 and 100 EB2, recognizing the cellular form of FN (cFN) and TN, respectively, were used. Results: During the first pest-operative week immunoreaction for glycoproteins, both the locally produced cFN and TN, were observed at the scar tissue containing the prolabed vitreous and the adjacent sclera. Subsequently, the reaction gradually shifted to the vitreal side of the wound, and 3 weeks after the operation it was almost completely restricted to a separated mass of vitreous beneath the scar. Conclusion: The expression of cFN and TN in the scleral scar and vitreous is indicative of their local synthesis. The shift of the expression of those proteins to the vitreal side of the wound with time suggests that the scarring process in the vitreous is delayed compared to the sclera.