Non-epithelial Lesions

Abstract

Mammary fat necrosis is an important benign lesion because of its ability to mimic cancer both clinically and mammographically. Fat necrosis is associated with trauma, especially in women with pendulous breasts. However, a history of trauma is present in only up to 65 % of cases (Bilgen et al. 2001). Other causes of fat necrosis include seat-belt trauma, cyst aspiration, needle core biopsy, lumpectomy, radiation therapy, reduction mammoplasty, breast reconstruction with transverse rectus abdominis myocutaneous flap, removal of implant and anticoagulant therapy (Hogge et al. 1995; Di-Piro et al. 1995). Microscopically, fat necrosis is caused by sterile inflammation resulting from leakage of fatty acids from the adipocytes, leading to a polymorph, lymphocytic and macrophage infiltrate with associated giant cell reaction. Saponification by blood and tissue lipases leads to formation of vacuoles surrounded by macrophages. Clinically, fat necrosis can present with a firm and fixed lump, with or without skin or nipple retraction. Lanyi (1986) succinctly illustrated stages in the pathogenesis of fat necrosis as follows:

• 1. Lesion phase — damage to the fat cells with leakage of the neural fat.

• 2. Absorption phase — lipophages remove the liberated neutral fat leading to formation of fat vacuoles with macrophage, plasma cell and other inflammatory cell infiltrate.

• 3. Repair phase — increasing numbers of fibroblasts follow the absorption phase, walling off a cavity with a dense capsule or scar formation. Calcium salts or haemosiderin deposition may occur in the fibrosis. The calcification of the oil cyst may exhibit an eggshell appearance.

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