The impact of topical and systemic enoxaparin sodium use on traumatic tympanic membrane perforation and myringosclerosis.

The objective of this study is to investigate the effect of topical and systemic enoxaparin sodium on the healing pattern of experimentally induced tympanic membrane perforation and formation of myringosclerosis. A total of 24 Wistar-Albino strain rats were included in the study. Standard myringotomies were performed on each rat. In the first group, isotonic serum physiologic was dropped on external ear canal (control group). Topical enoxaparin was dropped on external ear canal and daily topical doses of enoxaparin were dropped on external ear canal of the rats for 14 days (topical treatment group). Third group received subcutaneous injections of enoxaparin for 14 days (systemic treatment group). Five micrometer thick sections of the bullae of the rats were stained with H&E. Inflammation, edema and sclerotic lesions and neovascularization observed in the lamina propria layer of the tympanic membrane, and total thickness of the tympanic membrane were evaluated. In intergroup comparisons, significant difference in the distribution pattern of severity of inflammation in all three groups was not observed (p = 0.784, p > 0.05). Total TM thickness differed among all three groups (p = 0.028, p < 0.05). A statistically significant difference was observed between the systemic enoxaparin and the control groups (p = 0.022, p < 0.05). A statistically significant difference was observed between the topical enoxaparin and the control groups (p = 0.037, p < 0.05). However, comparison between the topical and systemic treatment groups could not reveal any statistically significant intergroup difference (p = 0.682, p > 0.05). A significant difference was not observed among three groups as for the distribution of myringosclerotic plaques, severity of edema and neovascularization in the lamina propria (p = 0.539, p > 0.05), (p = 0.063, p > 0.05), (p = 0.152, p > 0.05). Topical and systemic enoxaparin treatment did not prevent formation of sclerotic plaques; however, it decreased TM thickness significantly in comparison with the control group.