Pathogenesis of sialadenosis: possible role of functionally deficient myoepithelial cells

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.