ascorbic-acid and Myringosclerosis

In the present study, tympanic membranes (TM) harvested from myringotomized rats were analyzed histopathologically to compare the systemic and local effects of ascorbic acid on the development of myringosclerosis.. Forty male Wistar-Albino rats weighing between 350-400 g were included in this study. Under otomicroscopic examination, a standard 2-mm myringotomy incision was made on the posteroinferior quadrant of the TM of both ears. Rats were randomized into five groups as control, topical ascorbic acid 50 mg/kg, systemic ascorbic acid 50, 100, and 200 mg/kg groups, each group containing eight rats. On the 15th day of the study, the rats were decapitated, and bullas of the rats were extracted. Sections were stained with hematoxylin-eosin and examined through light microscopy. Inflammation, distribution width of plaques, edema, and neovascularization were observed on the lamina propria. Thickness of the TM was evaluated under the microscope and scored semiquantitatively.. When intergroup comparisons of parameters related to total TM thickness were performed, differences between the control group and topical AA (ascorbic acid) or systemic treatment groups were found to be statistically significant (p<0.005). A statistically significant difference was detected among control, topical and systemic 200 mg/kg ascorbic acid groups for the edematous lamina propria (p=0.003 and p<0.05, respectively).. For the total TM thickness, systemic and topical ascorbic acid use was effective when compared with the control group. It has been concluded that systemic use of higher doses of (200 mg/kg) ascorbic acid is beneficial in the resolution of the edematous lamina propria.

Topics: Administration, Topical; Animals; Antioxidants; Ascorbic Acid; Disease Models, Animal; Dose-Response Relationship, Drug; Injections, Intraperitoneal; Male; Myringosclerosis; Rats; Rats, Wistar; Tympanic Membrane; Tympanic Membrane Perforation; Wounds and Injuries

This study investigated the effects of ascorbic acid and N-acetyl cysteine (NAC) antioxidants on the development of myringosclerosis (MS) in an experimental model.. Myringotomies were performed in the ears of 15 guinea pigs, and Spongostan pieces were placed on the perforated regions of the tympanic membrane. The subjects were divided randomly into three groups and treated with three different solutions on the Spongostan-group 1: (control, 0.9% saline), group 2 (ascorbic acid), and group 3 (NAC). On day 15 after treatment, specimens from the tympanic membranes were obtained and examined via light microscopy. Sclerosis and inflammation scores and the tympanic membrane thicknesses were evaluated. Immunohistochemical methods were used to evaluate the expression of VEGF, TGF-β, iNOS, and IL1-β in all groups.. Lower sclerosis and inflammation scores and reduced tympanic membrane thicknesses were observed in groups treated with NAC or ascorbic acid compared with the control group. Immunohistochemical studies revealed significantly less expression of VEGF, TGF-β, and iNOS in groups 2 and 3 compared with group 1. Additionally, IL1-β expression was significantly less in group 3 than in group 1. Compared with group 1, group 2 animals exhibited reduced inflammation in the lamina propria, fewer active fibroblasts, less leukocyte infiltration, and decreased thickness of the vessels; group 3 animals exhibited decreased numbers of active fibroblasts and collagen fibers in the lamina propria.. Inflammation scores, cellular infiltration, and expression of VEGF, TGF-β, and iNOS were reduced by ascorbic acid and/or NAC treatments, thereby decreasing MS development. Decreased expression of IL1-β was observed only in animals treated with NAC.

Topics: Acetylcysteine; Animals; Antioxidants; Ascorbic Acid; Disease Models, Animal; Female; Fibrin Foam; Fibroblasts; Free Radical Scavengers; Guinea Pigs; Hemostatics; Immunohistochemistry; Inflammation; Leukocytes; Microscopy; Mucous Membrane; Myringosclerosis; Nitric Oxide Synthase; Random Allocation; Transforming Growth Factor beta; Tympanic Membrane; Vascular Endothelial Growth Factor A