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涎腺肿大症的发病机制:功能缺陷性肌上皮细胞的可能作用。

Pathogenesis of sialadenosis: possible role of functionally deficient myoepithelial cells.

作者信息

Ihrler Stephan, Rath Christian, Zengel Pamela, Kirchner Thomas, Harrison John D, Weiler Christoph

机构信息

Institute of Pathology, Ludwig Maximilian University, Munich, Germany.

出版信息

Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010 Aug;110(2):218-23. doi: 10.1016/j.tripleo.2010.03.014. Epub 2010 Jun 26.

DOI:10.1016/j.tripleo.2010.03.014
PMID:20580282
Abstract

OBJECTIVES

The pathogenesis of acinar enlargement in sialadenosis is obscure. As myoepithelial cells had been reported to show degenerative changes, we decided to investigate the possible role of functionally deficient myoepithelial cells in the development of sialadenosis.

STUDY DESIGN

This study was a morphometric analysis of glands immunohistochemically stained for CK14, alpha-actin, and Ki67 in 10 cases of sialadenosis and 11 normal parotids.

RESULTS

In sialadenosis, acini were much larger; there was a minor decrease in the density of the distribution of myoepithelial cells stained for CK14 and a major decrease in the density of the distribution and thickness of the myofilament component of myoepithelial cells stained for alpha-actin; and the proliferation of acinar and myoepithelial cells was reduced.

CONCLUSIONS

Our results demonstrate a major loss and thinning of the myofilament component of the myoepithelial cells and thereby a loss of mechanical support for the acini in sialadenosis. This possibly allows acinar cells to expand as secretory granules accumulate intracellularly to produce the great acinar enlargement. This functional myoepithelial insufficiency is possibly a consequence of an autonomic neuropathy secondary to severe metabolic or hormonal disorders.

摘要

目的

涎腺肿大症中腺泡肿大的发病机制尚不清楚。由于有报道称肌上皮细胞会出现退行性改变,我们决定研究功能缺陷的肌上皮细胞在涎腺肿大症发展过程中可能发挥的作用。

研究设计

本研究对10例涎腺肿大症患者和11例正常腮腺进行了免疫组织化学染色,分别检测CK14、α-肌动蛋白和Ki67,并对腺体进行形态计量分析。

结果

在涎腺肿大症中,腺泡明显更大;CK14染色的肌上皮细胞分布密度略有下降,α-肌动蛋白染色的肌上皮细胞肌丝成分分布密度和厚度大幅下降;腺泡细胞和肌上皮细胞的增殖减少。

结论

我们的结果表明,涎腺肿大症中肌上皮细胞的肌丝成分大量丢失且变薄,从而导致腺泡失去机械支撑。这可能使得腺泡细胞随着细胞内分泌颗粒的积累而扩张,从而导致腺泡显著肿大。这种功能性肌上皮功能不全可能是严重代谢或激素紊乱继发自主神经病变的结果。

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