JOURNAL OF COSMETIC SCIENCE 26 metabolized by bacterial enzymes to glycerol and free fatty acids. Excessive sebum secretion and loosely bound corneocytes clog pores and create an anaerobic environment where anaerobic microorganisms multiply and eventually provoke infl ammatory reac- tions. Excessive sebum production has been attributed to androgen levels. Several clinical observations clearly indicate a causal role for androgens in acne. Androgens have been shown to increase the size and output of sebum of the sebaceous glands (1). Acne begins to develop with the increase in androgens during the prepubertal period. Conversely, antiandrogens have been shown to reduce sebum lipids and to alleviate acne. Acne is also characterized by improper epidermal differentiation of the lower portion of the infundibulum of the sebaceous follicle. The keratinocytes lining the infundibulum are hyperproliferative compared with normal skin. This improper epidermal differentia- tion leads to a clogged pore. This clogging of the pore creates a micro-environment favor- able for the growth of acne. The excessive lipids and improper differentiation of the keratinocytes in the follicle en- courage bacteria growth and cause a weakening of the skin barrier in this follicle. This allows the excessive bacteria to migrate into the skin and contribute to the infl ammation observed in the fi nal stages of the acne process (1,2). The primary pathogenic agent implicated in the development of infl ammatory as well as non-infl ammatory acne is Propionibacterium acnes (3). P. acnes is included in a family of anaerobic, non-spore-forming gram-positive rods. The 1960s saw the use of antibiotics to treat acne by reducing P. acnes however, in the last two decades several antibiotic-resistant strains have emerged (4,5). In addition to antibiotics, topical benzoyl peroxide and salicylic acid have consis- tently been found to be effective in reducing acne lesions (5,6). The fi nal phase of comedone formation is the infl amed lesion. The bacterial infi ltrate into the skin triggers infl ammatory mediator production and cellular infi ltrate. A variety of infl ammatory mediators have been described in the acne lesion. These include IL-1 alpha, IL-1 beta, and substance P (7). In addition, there is a reported increase in lymphocytic infi ltrate and neutrophil infi ltrate into the follicular region (8). This also contributes to the infl ammation associated with the acne lesion. Clinical assessment of the effi cacy of acne treatment has been largely based on global ex- pert assessment, lesion counts or patient assessment (7–9). These techniques have been enhanced with the use of modern photographic techniques. However, these clinical as- sessments still require the counting of lesions and the documentation of shifts in the total number of lesions to determine the effi cacy of a topical treatment. This requires many weeks of the continued use of a treatment modality to observed shifts in the total number of lesions. In order to speed the evaluation process we have developed a technique to evaluate individual lesions. MATERIALS AND METHODS The treatment regimen consisted of the following materials: a simple foam cleanser, a toner (2% salicylic acid), and an oil-in-water lotion containing benzoyl peroxide. All three products were designed to address the four components of acne: keratinization, bacteria, sebum control, and infl ammation. To address each of these issues we added the following ingredients: (a) n-acetyl glucosamine, used to accelerate desquamation (b) decanoic acid, used for its antimicrobial properties (c) saw palmetto extract, used to

RAPID ASSESSMENT OF ANTI-ACNE PRODUCT 27 suppress 5 alpha reductase and therefore sebum production (10) (d) hoelen extract, used to inhibit phospholipase A2 to suppress infl ammation (11) and (e) resveratrol, a cycloox- ygenase inhibitor, used to suppress infl ammation (12). This product also contained 2.5% benzoyl peroxide (13). CLINICAL Ten female volunteers, between the ages of 18 and 50, were recruited from the local population. All subjects were of normal health with no evidence of acute or chronic dis- ease other than acne. Written informed consent was obtained from each volunteer before entrance into the study. The panelists were not on any antibiotic, antihistamines, retin- oids, anti-infl ammatories, steroid therapy, or benzoyl peroxide and/or salicylic acid treat- ment for at least two weeks prior to commencement of this study. The subjects were not under the care of a dermatologist and were not on any acne treatment for at least one month before the study started. Pregnant or lactating females were excluded. The panelists exhibited acne with at least four acne lesions on the upper back, where the minimum distances between lesions was approximately 4–6 cm. Two infl amed acne lesions were selected for each treatment and one to be left untreated. Each lesion was marked, pho- tographed (14), and graded (15,16). A skin surface microscope (Scopeman) was used to vi- sualize, size, and grade the lesions by two MDs at the testing lab. The lesions were treated and photographed every day for seven days (excluding Saturday and Sunday). RESULTS The lesions were chosen for maximum erythema and size. Each of these immediately ap- peared to resolve and lessen with each 24 hours of observation. Within seven days the size and infl ammation was back to normal in the untreated lesions. The regimen containing multi-prong technologies caused a signifi cant immediate re- duction in the size of the individual lesions. As observed in Figure 1, there was a distinct reduction in acne lesion size in the individual lesions treated with the regimen. This reduction in size occurred within two to three days. Figure 1. Average size of individual acne lesions in millimeters. Measurements were taken daily for eight days (excluding Sunday) for a control untreated lesion (black bars) and a treated lesion (grey bars). The area under the curve was 10.68 cm for the treated lesion and 15.37 cm for the untreated lesion (p = 0.0076).