Background: Contracted socket is still a major problem for patients with anophthalmia. The main factor for this condition is inflammation and fibrosis, which result in conjunctival shortening. Myofibroblasts that express α-SMA are the primary mediators of anophthalmic socket contraction.
Methods: One healthy eye of a New Zealand white rabbit were randomly selected for evisceration and divided into four treatment groups, each with five rabbits. Each rabbit in the group received a single subconjunctival injection of a different agent. Group, I was the control group that received no injection, Group II received MMC 0.4 mg/ml, Group III received TCA 40 mg/ml, and Group 4 received fibrin glue. After 14 days, the animals were euthanized, and conjunctival samples were submitted for histopathological analysis. A monoclonal α-SMA antibody was applied, and pathologists provided the IRS score for each sample. The differences in α-SMA expression were statistically analyzed with a significant level of p <0.05
Result: All groups displayed a statistically significant decrease in α-SMA expression compared to the control group (p<0.05) as sorting as MMC group with p=0.007, TCA group with p=0.007, and fibrin glue with p= 0.009. MMC was the most effective at reducing α-SMA (p=0.004). Surprisingly, there were no statistically significant differences between MMC, TCA, and fibrin glue when they were evaluated independently.
Conclusion: A single subconjunctival injection of fibrin glue may be used as a novel treatment to prevent socket contracture in actively healing sockets.