Gynecomastia is defined as benign proliferation of male breast (ductal tissue, stroma, and/or fat) [1–4]. The term gynecomastia is derived from Greek words gyne, women, and mastos, breast [5]. Reported incidence of gynecomastia is different, and it ranges from 32 to 36% and up to 65% [1, 5–8]. Gynecomastia can be confused with pseudogynecomastia (accumulation of subareolar fat without real proliferation of glandular tissue, usually in the presence of general obesity) [3, 5, 7, 9].

The breast originates from the ectoderm, and the connective tissue is derived from the mesoderm [2, 5–8]. By the tenth week of gestation, the upper and lower part of milk line (from the primitive axilla to the primitive groin) disappears, and the limited portion at the level of the fourth intercostal space of embryo remains and forms the basis for development of the neonatal breast [5–8]. By birth, neonatal mammary tissue becomes functional; it grows proportionally with the child during childhood [8]. Until the puberty, the growth of breast is identical for males and females [2, 5, 6].

In adults, breasts are in position between the second and third and seventh and eighth rib; medially, there are sternal edge and laterally midaxillary line [5, 8]. Besides the skin and subcutaneous tissue, the breast is made up of parenchymatous and stromal tissue [5, 7, 8]. The breast is supplied by a vascular network consisting of the internal mammary, lateral thoracic, and intercostal arteries [5, 8]. Sensory supply of the breast is provided by T3–T5 nerve roots; the superior portion of the breast is supplied by supraclavicular nerve, and the nipple receives sensory innervation from T4 [7].

The etiology of gynecomastia is not completely understood [2]. It is thought to be the result of an imbalance of estrogen action relative to androgen action at the breast tissue level [3, 5, 10–12].

Gynecomastia can be classified as asymptomatic (with high incidence) and symptomatic (it is rare) [3, 5, 7]. Bailey et al. categorized gynecomastia in four groups: physiologic, pathologic, pharmacologic, and idiopathic [13].

Most commonly, gynecomastia is idiopathic [3, 10].

Physiologic (asymptomatic) gynecomastia is very common; it is related to hormonal changes; and it has three peaks of occurrence in neonatal, pubertal (in almost 66% of adolescent boys), and old age period (older than 65 years) [1–3, 5, 7, 8, 10, 11]. Leptin may play role in the development of physiologic gynecomastia [2].

Pathologic (symptomatic) gynecomastia is very rare, and it can be caused by increase in estrogen, a decrease in testosterone, medication, or drug use, or it may be idiopathic [2, 10].

Elevated serum estrogen levels may be a result of estrogen-secreting neoplasms or their precursors or with increase extragonadal conversion of androgens to estrogens by tissue aromatase [2, 5]. Increase aromatization of the precursors of the estrogen can result in the elevation of the estrogens (testicular germ cell tumors, liver disease, hyperthyroidism, Klinefelter syndrome) [2, 3, 12]. Levels of free serum testosterone are decreased in patients with gonadal failure [1–3, 9]. Serum levels of sex hormone-binding globulin (SHBG) can affect the estrogen/androgen balance in hyperthyroidism and chronic liver disease [1, 3, 9, 10].

Drugs may be associated with gynecomastia (pharmacologic gynecomastia) [1–3, 5–7, 10]. The use of medications such as hormones (antiandrogens, anabolic steroids, estrogen), antibiotics (metronidazole, ketoconazole, isoniazid), antiulcer medications (cimetidine, omeprazole, ranitidine), chemotherapeutic agents (methotrexate), cardiovascular drugs (digoxin, nifedipine, verapamil, spironolactone), psychoactive agents (diazepam, haloperidol), and marihuana is believed to cause gynecomastia [3, 9, 10, 12].

There is no increased risk of breast cancer in patients with gynecomastia when compared to the unaffected male population (with the exception of patients with Klinefelter syndrome) [1, 2, 9].

Three types of gynecomastia have been described: florid, fibrous, and intermediate [1, 5, 9]. The florid type is characterized by an increase in ductal tissue and vascularity with a variable amount of fat, the fibrous type has more stromal fibrosis and few ducts, and the intermediate type is a mixture of the two [7, 11]. Florid gynecomastia is usually seen when the duration is 4 months or less, the fibrous type is usually present after duration of 1 year, and the intermediate type is usually seen between 4 and 12 months [8, 11].

Various classification schemes have been proposed for gynecomastia [11, 14–16]. There are two classifications of gynecomastia mostly used in practice presented by Simon and Rohrich [11, 16]. Simon et al. proposed a qualitative classification of volume and skin redundancy dictating treatment: grade I, small enlargement, no skin excess; grade IIA, moderate enlargement, no skin excess; grade IIB, moderate enlargement with extra skin; and grade III, marked enlargement with extra skin (Fig. 6.1a–d) [7, 11, 17].

Rohrich’s classification is based on the amount of tissue mass requiring excision (adipose versus fibrous tissue predominance): grade I, minimal hypertrophy (<250 g of breast tissue) without ptosis, (IA primarily glandular, IB primarily fibrous); grade II, moderate hypertrophy (250–500 g of breast tissue) without ptosis (IIA primarily glandular, IIB primarily fibrous); grade III, severe hypertrophy (>500 g of breast tissue) with grade I ptosis (glandular or fibrous); and grade IV, severe hypertrophy with grade II or III ptosis (glandular or fibrous) [11, 16].

Gynecomastia is usually bilateral (it may also appear as asymmetrical or unilateral) [1, 3, 10]. On examination, gynecomastia presents as palpable, firm, tender, mobile, mound of tissue [1, 3, 9, 10].

There is positive family history in more than half of patients with persistent pubertal gynecomastia [3]. The testicular exam should be included in physical examination since it may reveal presence of malignancy or varicoceles [1, 3, 7, 8].