期刊文献+

眼睑无力综合征的发病机制:基质金属蛋白酶在弹性纤维降解中的作用 被引量:2

The pathogenesis of floppy eyelid syndrome: Involvement of matrix metalloprotein ases in elastic fiber degradation
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摘要 Objective: To investigate histopathologic alterations of eyelid biopsy specime ns from patients with floppy eyelid syndrome (FES) with special regard to elasti c fiber content and ultrastructure as well as to the expression of elastin-degr ading enzymes to elucidate the pathogenesis of this disorder. Design: Retrospect ive, interventional case series. Participants and Controls: Eleven consecutive p atients with FES and 10 age-matched control patients with basal cell carcinoma of the eyelid. Methods: Horizontal pentagonal eyelid resections of 16 upper lids were performed in 11 patientswith FES. Full-thickness eyelid biopsy specimens from study and control patients were examined by light and transmission electron microscopy, semiquantitative morphometry, and immunohistochemistry using antibo dies against matrix metalloproteinase (MMP)-2, MMP-7, MMP-9, and MMP-12 and neutrophil elastase. Results: All patients treated with surgical horizontal eyel id shortening were asymptomatic at follow-up. Histopa- thologic analysis of the surgical specimens showed, apart from unspecific sign s of chronic in-flammation, a significant decrease in the amount of elastin wit hin the tarsal plate and eyelid skin as compared with controls. Residual elastic fibers revealed an abnormal ultrastructure with a diminished elastin core. Immu nohistochemistry demonstrated an increased immunoreactivity for elastolytic prot eases, particularly MMP-7 and MMP-9, in areas of elastin depletion in FES spec imens as compared with controls. Conclusions: The findings indicate that upregul ation of elastolytic enzymes, most probably induced by repeated mechanical stres s, participates in elastic fiber degradation and subsequent tarsal laxity and ey elash ptosis in FES. Objective: To investigate histopathologic alterations of eyelid biopsy specime ns from patients with floppy eyelid syndrome (FES) with special regard to elasti c fiber content and ultrastructure as well as to the expression of elastin-degr ading enzymes to elucidate the pathogenesis of this disorder. Design: Retrospect ive, interventional case series. Participants and Controls: Eleven consecutive p atients with FES and 10 age-matched control patients with basal cell carcinoma of the eyelid. Methods: Horizontal pentagonal eyelid resections of 16 upper lids were performed in 11 patientswith FES. Full-thickness eyelid biopsy specimens from study and control patients were examined by light and transmission electron microscopy, semiquantitative morphometry, and immunohistochemistry using antibo dies against matrix metalloproteinase (MMP)-2, MMP-7, MMP-9, and MMP-12 and neutrophil elastase. Results: All patients treated with surgical horizontal eyel id shortening were asymptomatic at follow-up. Histopa- thologic analysis of the surgical specimens showed, apart from unspecific sign s of chronic in-flammation, a significant decrease in the amount of elastin wit hin the tarsal plate and eyelid skin as compared with controls. Residual elastic fibers revealed an abnormal ultrastructure with a diminished elastin core. Immu nohistochemistry demonstrated an increased immunoreactivity for elastolytic prot eases, particularly MMP-7 and MMP-9, in areas of elastin depletion in FES spec imens as compared with controls. Conclusions: The findings indicate that upregul ation of elastolytic enzymes, most probably induced by repeated mechanical stres s, participates in elastic fiber degradation and subsequent tarsal laxity and ey elash ptosis in FES.
出处 《世界核心医学期刊文摘(眼科学分册)》 2005年第11期56-56,共1页 Digest of the World Core Medical Journals:Ophthalmology
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