EPIDERMAL INCLUSION CYST
Epidermal inclusion cysts are the most common benign cysts derived from the skin. They are also known as epidermoid cysts or follicular infundibular cysts. The name “sebaceous cyst” has been used to describe these cysts, although this is a misnomer, because epidermal inclusion cysts are not derived from sebaceous epithelium. The cysts can occur anywhere on the body except the palms, soles, glans, and vermilion border.
Clinical Findings: Most epidermal inclusion cysts are subcutaneous nodules that vary in size from 5 mm to more than 5 cm. They have no race predilection but are seen more commonly in men than in women. Onset most commonly occurs during the third decade of life. The nodules characteristically have an overlying central punctum. From this punctum, drainage of white, cheese-like material, which represents a buildup of macerated keratin debris, can occur. Most small epidermal inclusion cysts are asymptomatic, and they rarely cause a problem.
Larger epidermal inclusion cysts can become irritated and inflamed. If the inflammation is severe enough, the cyst wall ruptures. When the cyst contents enter the dermis, the keratin sets off a massive inflammatory reaction, which manifests clinically as edema, redness, and pain. Once this has occurred, patients often seek medical advice.
The main differential diagnosis for a ruptured epidermal inclusion cyst is a boil or furuncle. Ruptured epidermal inclusion cysts are almost never infected, although infection can occur within a longstanding ruptured cyst that has not been treated. The main differential diagnosis of an unruptured, noninflamed epidermal inclusion cyst is a pilar cyst. Pilar cysts do not have an overlying central punctum, and this is the easiest means of differentiating the two cyst types. Pilar cysts are also more common on the scalp. Milia are considered to be tiny epidermal inclusion cysts.
Histology: The epidermal inclusion cyst is a true cyst with an epithelial lining of stratified squamous epithelium and an associated granular cell layer. The central cavity is filled with keratin debris. The cyst is derived from follicular epithelium.
Pathogenesis: The epidermal inclusion cyst is derived from the infundibulum of the hair follicle. Epidermal inclusion cysts occur as the result of direct implantation of epidermis into the underlying dermis; from there, the epidermal component continues to grow into the cyst lining. Many researchers have looked at the roles of ultraviolet light and human papillomavirus infection in the etiology, but no definitive conclusions on either have been drawn.
Treatment: Small cysts that are asymptomatic do not need to be treated. One should advise patients not to manipulate or squeeze the cysts. Such trauma could cause rupture of the cyst wall and set off an inflammatory reaction. Small cysts can be cured by a complete elliptical excision, making sure to remove the entire cyst wall. If a small portion of the cyst wall is left behind, the cyst is likely to recur.
Inflamed cysts should be treated initially with an incision and drainage technique. The region is anesthetized and then incised with a no. 11 blade. The resulting cheesy-white macerated keratin debris is removed with lateral pressure, and a curette is used to break apart internal loculations. The drainage material has a pungent odor. The resulting cyst cavity can be packed or left open until the patient returns in 2 to 3 weeks for definitive removal of the cyst lining by excision. Intralesional triamcinolone is very effective in decreasing the inflammation and pain in these inflamed cysts. Long-standing cysts should be cultured and the patient given the appropriate antibiotic therapy based on the culture results.