The American journal of otology · 2000
Treatment with dexamethasone arrests the development of myringosclerosis after myringotomy.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Mattsson C, Stierna P, Hellström S
Аннотация
HYPOTHESIS: To attempt to inhibit the development of myringosclerosis by intraperitoneal injection of dexamethasone.
BACKGROUND: The authors' earlier report showed that the development of myringosclerosis after myringotomy was associated with an inflammatory reaction. The present study was performed to secure evidence for this hypothesis.
METHODS: Three groups of bilaterally myringotomized rats were treated at 12-hour intervals with intraperitoneal injection of dexamethasone, RU486 (a glucocorticoid receptor antagonist), and saline, respectively. At 6, 12, 24, and 48 hours after the myringotomy, 2 animals were anesthetized on each occasion and examined otomicroscopically. The animals were then killed, and the tympanic membranes were excised and prepared for light microscopic studies.
RESULTS: Dexamethasone treatment retarded and diminished the development of sclerotic lesions markedly. Moreover, no inflammatory signs were seen in the flaccida specimens. When the RU486-treated animals were compared with the animals in the control group, there were no evident differences concerning the development of myringosclerosis or the extent of the inflammatory reaction.
CONCLUSION: These findings confirm the earlier hypothesis that an inflammatory reaction in collagen tissue is involved in the mechanism that causes the development of myringosclerosis.
BACKGROUND: The authors' earlier report showed that the development of myringosclerosis after myringotomy was associated with an inflammatory reaction. The present study was performed to secure evidence for this hypothesis.
METHODS: Three groups of bilaterally myringotomized rats were treated at 12-hour intervals with intraperitoneal injection of dexamethasone, RU486 (a glucocorticoid receptor antagonist), and saline, respectively. At 6, 12, 24, and 48 hours after the myringotomy, 2 animals were anesthetized on each occasion and examined otomicroscopically. The animals were then killed, and the tympanic membranes were excised and prepared for light microscopic studies.
RESULTS: Dexamethasone treatment retarded and diminished the development of sclerotic lesions markedly. Moreover, no inflammatory signs were seen in the flaccida specimens. When the RU486-treated animals were compared with the animals in the control group, there were no evident differences concerning the development of myringosclerosis or the extent of the inflammatory reaction.
CONCLUSION: These findings confirm the earlier hypothesis that an inflammatory reaction in collagen tissue is involved in the mechanism that causes the development of myringosclerosis.