Hypertrophy and Atrophy in a Lobular Unit

A 68 year old woman underwent an excisional biopsy because of architectural distortion.

Image 1.  The biopsy specimen contains sclerosing adenosis, characterized by a proliferation of small, elongated glandular structures that are arranged parallel to each other.  At low power, the maintenance of a lobulocentric configuration is evident. 

Image 3. Myoid hypertrophy is prominent, and in longitudinal sections the epithelial component of sclerosing adenosis is inconspicuous.

Image 5.  Immunohistochemistry using antibodies to smooth muscle actin highlights prominent myoid component in a longitudinally cut terminal duct.

Image 2.  The acini of sclerosing adenosis are compressed, and the intralobular connective tissue is sclerotic.  Calcifications are frequently associated with sclerosing adenosis.

Image 4.  The original lobular units and terminal duct are evident, although the myoid component predominates. 

Image 6.  A lobular unit cut in cross section shows strong expression of smooth muscle actin, by the myoid component, which encircles the residual luminal epithelial cells.

Image 7.  Residual luminal epithelial cells are highlighted using antibodies to cytokeratin.

Diagnosis:  Sclerosing adenosis with prominent myoid component. 

Discussion: The normal lobular unit is composed of luminal and myoepithelial cells (MEC), the latter containing microfilaments, cell matrix adherens junctions and smooth muscle specific cytoskeletal proteins.  MECs are true epithelial cells, however, because the major components of their intermediate filament system are cytokeratins 5 and 14, because they form desmosomes, hemidesmosomes, and cadherin-mediated cell-cell junctions, and because they are permanently separated from the connective tissue by underlying basement membrane.  (Deugnier, M-A, et al.  The importance of being a myoepithelial cell.  Breast Cancer Research 2002, 4:224).

Myoepithelial cells may show prominent myoid component, sometimes referred to as myoid hypertrophy, and this phenomenon can cause dramatic atrophy of the luminal component (so-called myoid atrophy).  This finding is of no clinical significance, but makes for pleasing microscopic images.