Gynecomastia is caused by stromal prominence and a proliferation of ducts. The stroma may be edematous or with a more long standing condition, become fibrotic.
The ducts often show micropapillary hyperplasia. There is fibrosis compatible with a more long standing lesion.
Gynecomastia is felt to be related to an imbalance of estrogens and androgens, with a decreased testosterone-to-estradiol ratio. Etiologies include idiopathic gynecomastia, pubertal forms, medication, anabolic steroids, cirrhosis, primary hypogonadism, and testicular tumors, among others.
Gynecomastia can be divided into two histological types: florid type and fibrous type. The florid type exhibits mild to moderate epithelial hyperplasia with fingerlike protrusions into the lumen. The stroma of the florid type is celullar and edematous. The fibrous type has an overall picture of atrophy with minimal epithelial proliferation and a fibrous, aceullar stroma.
Note that traditionally, the florid type was termed "early type" and the fibrous was termed "late type". However, studies have shown that they do not reliably predict the duration of the lesion and both types may co-exist in the same specimen. Therefore, the terms "florid" and "fibrous" are now preferred.1
Gynecomastia is enlargement of the male breast due to proliferation of the glandular and stromal tissues. It is common in infancy, adolescence, and in middle-aged to elderly men. In contrast, enlargement in obese men due to deposition of fatty tissue, is referred to as pseudogynecomastia, and it is devoid of ductal proliferation.
Treatment should primarily be focused on the underlying cause of the gynecomastia.
1 O'Malley FP, Pinder SE. Breast Pathology: Foundations in Diagnostic Pathology. Philadelphia, PA: Elvesier; 2006:303-7.