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Quantification of cellular proliferation in acne using the monoclonal antibody Ki-67
H E Knaggs1, D B Holland, C Morris
1Department of Dermatology, General Infirmary, Leeds, England.
Insights
Acne involves increased cell proliferation in hair follicles, suggesting a "prone" state even in normal-appearing skin. This study used Ki-67 antibody to measure cell growth in acne patients, revealing heightened activity in affected follicles and surrounding epidermis.
Area of Science:
- Dermatology
- Cell Biology
- Histology
Background:
- The exact cause of ductal hypercornification in acne remains unclear.
- Understanding cellular proliferation is key to understanding acne pathogenesis.
Purpose of the Study:
- To investigate and quantify cell proliferation in acne follicles and interfollicular epidermis.
- To determine if normal follicles in acne-affected skin exhibit increased proliferation.
Main Methods:
- Utilized the Ki-67 monoclonal antibody to identify proliferating cells (G1, S, M, G2 phases).
- Analyzed cryostat sections of skin biopsies from acne patients and normal volunteers.
- Quantified Ki-67 positive nuclei in basal layers of follicular and interfollicular epithelia.
Main Results:
- Significantly higher Ki-67 positivity in normal follicles from acne sites compared to unaffected skin (17.4% vs 11.0%).
- Follicular epithelia of non-inflamed acne lesions showed elevated proliferation (23.4%).
- Interfollicular epidermis near inflamed lesions demonstrated significantly increased proliferation (25.3%) compared to normal epidermis (5.3%).
Conclusions:
- Confirms ductal hyperproliferation as a feature of acne.
- Suggests that normal follicles on acne-prone skin exhibit increased proliferation, indicating an 'acne-prone' state.
- Highlights increased epidermal proliferation near inflamed lesions in acne patients.
Abstract:
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."
