The etiology and pathogenesis of both granulomatous mastitis and plasma cell mastitis are unclear, but the factors associated with the pathogenesis have been studied in great depth. It is now believed that plasmacytoid mastitis is associated with impaired ductal drainage, abnormal hormonal stimulation of ductal secretion, and anaerobic bacterial infection.
The accumulation of epithelial cell debris and lipid-containing secretions fills the subareolar milk ducts, causing them to expand, resulting in thickening of the surrounding fibrous tissue and the decomposition of lipid-like substances accumulated in the lumen of the ducts. The lesion is centered on the milk ducts. Granulomatous mastitis is generally considered to be an autoimmune disease, associated with the patient’s use of birth control pills; it has also been reported in the literature to be associated with Corynebacterium infection; there is also evidence of a lactation-induced immune response and local hypersensitivity.
There are also experimental data confirming the association of the disease with hormonal imbalance in the body such as hyperprolactinemia or inflammation of lobular granulomas caused by infection, trauma, or chemical irritation; in addition, granulomatous mastitis has been associated with mycobacterial and actinomycotic infections. The lesions are centered on the lobules of the breast and are multifocal in distribution.
Plasmacytoid mastitis is commonly seen in middle-aged women with a history of childbearing and breastfeeding and may have a history of nipple dysplasia, poor or interrupted breastfeeding. Plasmacytoid mastitis often begins with nipple discharge or, in some patients, with a lump.
The mass is often located under the areola and its long axis is usually in line with the ducts of the breast. Most lumps have a long history and change slowly, remaining stationary for months or years, or suddenly increasing or decreasing in size, but rarely disappearing.
In most patients, there is localized skin flushing, softening of the mass, pain or vague tenderness, but there is no obvious throbbing pain during the suppurative phase, and the pus is often interspersed with pimple-like material after rupture, and a fistula is formed leading to the foramen ovale, and the wound does not converge for a long time or repeatedly ulcerates. Most patients with granulomatous mastitis are married women who have given birth, and most have breastfeeding experience. Granulomatous mastitis often occurs unilaterally in all parts of the breast except the areola area, but it is more common in the upper quadrant, and large lumps may involve the entire breast.
The lump is usually a single breast lump, painless or slightly painful, hard, with a length of 1.5 to 50 px, with unclear borders and a non-smooth surface, and may adhere to the skin or surrounding tissues.
Systemic symptoms are not obvious, and a few may be accompanied by fever. The lump increases rapidly and if left untreated, a breast abscess may develop within a short period of time, forming a sinus tract after ulceration and remaining untreated for a long time.
Ultrasound diagnosis of plasmacytoid mastitis shows an internally heterogeneous, non-enveloped hypoechoic lesion with a superficial location close to the skin; the echogenic intensity of the lesion is lower than that of the subcutaneous fat; blood flow signal is seen in the lesion, but the blood supply is not abundant; the pulsed Doppler spectrum is characterized by a low-velocity, low-resistance type; the ducts are cystically dilated, especially with strings of bead-like dilatation, which can be considered as plasmacytoid mastitis.
Ultrasound of granulomatous mastitis showed irregular lesion morphology, blurred borders, and uneven distribution of internal echogenicity. Color Doppler flow imaging showed moderate blood flow signal, and the pulsed Doppler spectrum was characterized by a low-velocity high-resistance spectrum with a high resistance index.
Mammography mammograms of plasmacytoid mastitis have faint or no mass shadows. X-rays show lesion areas of similar density to the surrounding glands, with fine burrs, small circles or rods of calcified foci around the ducts, uniform needle-like or linear calcified foci within the ducts, and sparse distribution of calcified foci. Mammography of granulomatous mastitis was nonspecific, showing dense shadows of limited structural disorganization with gross infiltration of the margins, limited turbidity of the fat layer, and thickened skin.
Pathologic and cytologic examination revealed that lesions of plasmacytoid mastitis were mostly located in deep subareolar breast tissue without obvious boundaries with surrounding tissues and showed extensive yellow-white structures and dilated ducts and cystic cavities filled with yellow-brown creamy or tofu-like material, smooth cystic lining, and hyperplastic and hard ductal connective tissue or inflammatory reaction.
Microscopic observation.
In the early stage, only ductal dilatation was seen. As the disease progressed, the epithelial cells of the dilated ducts atrophied and had loss, the lumen of the ducts had exfoliated epithelial cells and lipid-containing secretions, and the periductal tissues were accompanied by fibrosis and obvious thickening, and lymphocyte infiltration. The typical changes in the later stage were necrotic foci in the fatty tissue around the ducts and destruction of the lobular structure of the breast. The necrotic tissue is surrounded by a large number of plasma cells, lymphocytes, and a small number of histiocytes, neutrophils, and multinucleated giant cells, with plasma cell infiltration predominating.
Histological examination of granulomatous mastitis reveals diffuse distribution of dark red nodules of corn to soy size on the cut surface, with small cystic cavities visible in the center of some nodules. Microscopically, the lesions are seen to be multifocal, centered on the lobules of the breast, with most of the terminal ducts or alveoli of the lobules disappearing, and neutrophilic foci, or microabscesses, are common. Occasionally, small focal necrosis was seen, but no caseous necrosis was present.
Antacid staining does not reveal Mycobacterium tuberculosis, and there are no obvious foam cells or dilated ducts. Cytologic examination reveals more neutrophils, lymphocytes, Langan giant cells or foreign body giant cells, nuclear debris, and epithelial cells.
The breast is a structure unique to humans and mammals and is an ectodermal organ. It originates from the skin and is formed by local thickening of the epidermis. Its structure is similar to that of the sebaceous glands, a variant of the sweat glands, and its functional activity is similar to that of the sweat glands.
The breast develops through different stages such as embryonic, infantile, adolescent, menstrual, pregnancy, lactation, weaning, menopause and old age.
As the target organ of endocrine hormones, the breast is under the influence of endocrine hormones, especially sex hormones, in each period.
The clinical incidence of non-lactating breast inflammatory diseases has increased with the adjustment of dietary structure and the acceleration of life rhythm. Therefore, the prevention, treatment and care measures of non-lactating breast inflammation are beneficial to promote women’s physical and mental health and improve their quality of life.