The gross appearance of sclerosing adenosis depends on the size and microscopic composition of the lesion. Since the majority of sclerosing adenosis lesions are small and have a combination of stromal and glandular components, they are imperceptible on macroscopic evaluation. If a lesion has extensive fibrosis, it may appear as white and vaguely nodular (Fig. 5.2). Lesions composed predominantly of glandular components with epithelial proliferation may appear as circumscribed, rubbery, pale tan nodules.

Sclerosing adenosis is characterised by enlarged lobular units due to nodular proliferation of ducts and acini that are compressed and distorted by stromal collagen (Figs. 5.3, 5.4, and 5.5) [4, 7]. The normal lobular appearance is distorted by fibrosis, particularly in the centre of the lesion, where distorted glands may have an angulated appearance and mimic invasive carcinoma (Fig. 5.6). However, the lobulocentric nature of the lesion, which is best appreciated on low magnification, is maintained and can be the most important histologic feature to differentiate it from invasive cancer (Fig. 5.6). The ducts have both luminal epithelial and peripheral myoepithelial cells. Although the presence of a dual cell population is easy to appreciate on haematoxylin and eosin (H&E) sections in most cases, confirmation by immunohistochemistry may be helpful in selective instances to illustrate the preservation of myoepithelial cells (Fig. 5.7). The ratio of epithelial and myoepithelial cells can vary significantly from case to case (Fig. 5.8).

In some cases, there is significant epithelial atrophy and preferential proliferation of myoepithelial cells. In others, both epithelial and myoepithelial components appear hyperplastic. The basement membrane around glands of sclerosing adenosis is usually thickened and prominent. Occasionally, both epithelial and myoepithelial cells undergo metaplastic changes. Apocrine metaplasia of epithelium, spindle cell morphology, and myoid differentiation of myoepithelium are commonly seen in sclerosing adenosis. The term apocrine adenosis is used when the entire lesion of sclerosing adenosis shows apocrine metaplasia (Fig. 5.9) [8–10]. Microcalcifications are a common microscopic feature of sclerosing adenosis and can be present either in fibrotic stroma or in ductal lumens. Atypical ductal and atypical lobular hyperplasia or in situ carcinoma may involve sclerosing adenosis. These may cause major diagnostic difficulties, especially on core needle biopsies. Involvement of sclerosing adenosis by ductal carcinoma in situ may mimic invasive carcinoma, and it is one of thecommonly mistaken diagnoses on core needle biopsies. Ductal carcinoma in situ involving sclerosing adenosis can be high grade and arise within sclerosing adenosis. The integrity of the individual acini and preservation of myoepithelium may be difficult to appreciate on H&E sections alone (Figs. 5.10, 5.11, and 5.12). Lobulocentric architecture of sclerosing adenosis versus infiltrative growth pattern of invasive carcinoma, a background of dense fibrotic stroma of sclerosing adenosis versus the more cellular (desmoplastic) stroma of invasive carcinoma, should be useful in arriving at the correct diagnosis. Using immunohistochemical stains to highlight myoepithelial cells will be helpful [11–14].

Perineural pseudoinvasion has been reported in 2 % of sclerosing adenosis cases (Fig. 5.13) [15]. Sclerosing adenosis glands and ducts may be present around nerves, most commonly in the perineurium, but rarely in nerve fibres. The benign appearance of the glands and the preserved myoepithelial layer around the ducts will be helpful to differentiate these glands from invasive carcinoma.