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Updated: Jun 11, 2026

Generation of Monocyte-Derived Dendritic Cells with Differing Sialylated Phenotypes
Published on: October 20, 2023
Pathogenesis of sialadenosis: possible role of functionally deficient myoepithelial cells
Stephan Ihrler1, Christian Rath, Pamela Zengel
1Institute of Pathology, Ludwig Maximilian University, Munich, Germany.
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.
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