Objective: To better define the pathogenesis of acne keloidalis (AK).
Design: Prospective, blinded study of histologic material collected from 10 patients with clinically typical AK.
Setting: Outpatient dermatology clinic of a military tertiary care medical center.
Patients: Ten male volunteers 18 years or older with early AK lesions (1- to 4-mm firm papules on the lower occipital/nuchal region).
Data source: Biopsy specimens from small, early lesions and from clinically uninvolved skin, studied histologically with transverse sectioning.
Intervention: Three separate 4-mm punch biopsy specimens of the scalp (lesional, perilesional, and "normal" scalp) were obtained from each volunteer. The specimens were processed using transverse sectioning.
Main outcome measures: The primary variables for data analysis were the presence or absence of the following histologic features: premature loss of the inner root sheath; eccentric placement of shaft, with thinning of the outer root sheath; lamellar fibroplasia surrounding the follicle; loss of sebaceous glands; evidence of follicular destruction or scarring; inflammation; and intrafollicular or perifollicular microorganisms. The number and type of hairs were also recorded.
Results: The most common findings in the 19 histologically abnormal specimens were perifollicular, chronic (lymphocytic and plasmacytic) inflammation, most intense at the level of the isthmus and lower infundibulum; lamellar fibroplasia, most marked at the level of the isthmus; complete disappearance of sebaceous glands, associated with inflamed or destroyed follicles; thinning of the follicular epithelium, most marked at the level of the isthmus; and total epithelial destruction (superficial and deep), with residual "naked" hair fragments. Even some "normal" specimens contained true follicular scars, demonstrating that normal-appearing scalp skin had previously been affected by the disease.
Conclusions: Acne keloidalis is a primary form of scarring alopecia, and many of the histologic findings closely resemble those found in certain other forms of cicatricial alopecia. Extensive subclinical disease may be present in patients with AK and can account for some of the permanent hair loss. Overgrowth of microorganisms does not appear to play an important role in the pathogenesis of the disease. There is no etiologic relationship between AK and pseudofolliculitis barbae. Therapies found to be useful in other forms of inflammatory scarring alopecia are useful in the treatment of early AK.