4.4 Article

Marsupialization inhibits interleukin-1α expression and epithelial cell proliferation in odontogenic keratocysts

Journal

JOURNAL OF ORAL PATHOLOGY & MEDICINE
Volume 31, Issue 9, Pages 526-533

Publisher

BLACKWELL MUNKSGAARD
DOI: 10.1034/j.1600-0714.2002.00029.x

Keywords

immunohistochemistry; in situ hybridization; interleukin-1 alpha (IL-1 alpha); Ki-67; marsupialization; odontogenic keratocyst

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Background: Marsupialization results in the reduction of odontogenic cyst size. Interleukin-1alpha (IL-1alpha) is thought to play a crucial role for the expansion of odontogenic keratocysts. The aim of this study was to investigate the effects of marsupialization on the expression of IL-1alpha and on the proliferating activity of a lining epithelium in odontogenic keratocysts. Methods: The concentrations of IL-1alpha, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in the intracystic fluids of odontogenic keratocysts were measured by the enzyme-linked immunosorbent assay (ELISA). The expression of IL-1alpha mRNA in odontogenic keratocysts was measured before and after marsupialization by in situ hybridization. The expression of IL-1alpha and epithelial cell-proliferating activities in odontogenic keratocysts were also measured by immunohistochemistry using antibodies for human IL-1alpha and Ki-67 antigen, respectively. Results: The intracystic fluid levels of IL-1alpha were significantly higher than those of IL-6 and TNF-alpha in odontogenic keratocysts. In situ hybridization and immunohistochemistry showed that strong expression of IL-1alpha mRNA and protein was mainly detected in the epithelial cells of odontogenic keratocysts. After marsupialization, the signal intensities for IL-1alpha mRNA and protein were significantly decreased. In addition, the Ki-67 labeling index of the epithelial cells was decreased proportionally with the grade of IL-1alpha mRNA expression after the marsupialization. Conclusion: Our findings suggest that marsupialization may reduce the size of odontogenic keratocyst by inhibiting IL-1alpha expression and the epithelial cell proliferation.

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