Quantification of Cellular Proliferation in Acne Using the Monoclonal Antibody Ki-67

The mechanism by which ductal hypercornification occurs in acne is uncertain. We investigated proliferation in normal and acne follicles and in the interfollicular epidermis using the monoclonal antibody Ki-67, which reacts with a nuclear antigen expressed by cells in the G1, S, M, and G2 phases of the cell cycle. Cryostat sections of biopsies from the interscapular region from acne patients and from normal volunteers were stained with Ki-67 antibody and counterstained with 2% methyl green. The number of Ki-67-positive nuclei in the basal layer were counted and expressed as a percentage of the total number of basal nuclei in the ductal or interfollicular epithelia. The data was expressed as mean percent ± SD. In normal follicles from acne-affected sites 17.40% ± 1.86% (n = 8) of the nuclei were Ki-67 positive. This was significantly higher (p <0.01) than follicles from an area of skin unaffected by acne (11.01% ± 6.16%, n = 8). In the follicular epithelia of non-inflamed lesions, the percentage of Ki-67 positive nuclei was 23.44% ± 8.36% (n = 15). It was impossible to count the nuclei of follicular epithelium of inflamed lesions because little of this remained intact. In normal interfollicular epidermis, Ki-67-positive nuclei represented 5.33% ± 3.36% (n = 8) of the total. This value was not significantly different from the value obtained for interfollicular epidermis near non-inflamed lesions (10.46% ± 4.45%, n = 15). However, the number of Ki- 67-positive nuclei in the interfollicular epidermis near inflamed lesions was significantly higher than either of these two values: 25.26% ± 6.83%, n = 13, p < 0.05. Our results with Ki-67 confirm that ductal hyperproliferation occurs in acne and shows that normal follicles from acne skin may be “acne-prone.