Accumulation of lipid peroxide in the content of comedones may be involved in the progression of comedogenesis and inflammatory changes in comedones.
BACKGROUND
Previous studies reported that lipid peroxide (LPO) caused by oxidation of sebum is associated with the progression of acne vulgaris, and that therapy with antioxidative ingredients is efficacious for treatment. In this study, we hypothesized that lipid accumulation in comedones induces progression of comedogenesis and inflammatory changes in comedones, and investigated the possible role of accumulated LPO in comedogenesis and its inflammatory changes.


METHODS
We first sampled comedones and the stratum corneum from patients with acne vulgaris. The quantities of LPO, interleukin-1-alpha (IL-1alpha), and NF-kappa-B (NF-kappaB) in comedones and in the stratum corneum from each patient were measured for comparison. Next, comedones were sampled again from the same patients and classified into five groups: microcomedo (MC), noninflammatory open comedo (NIOC), noninflammatory closed comedo (NICC), inflammatory open comedo (IOC), and inflammatory closed comedo (ICC). We measured quantities of LPO in each group.


RESULTS
The quantities of LPO, IL-1alpha, and NF-kappaB were significantly higher in the content of comedones than those in the stratum corneum. The quantities of LPO in the content of IOC and ICC were significantly higher than those of MC, NIOC, and NICC; however, there were no significant differences in quantities of LPO between the content of MC, NIOC, and NICC.


CONCLUSIONS
We conclude that the accumulation of a certain amount of LPO in the content of comedones may play an important role in the progression of comedogenesis and the excessive accumulation of LPO may be involved in inflammatory changes in comedones.
Tochio
Takumi
T
Research Laboratories, Nippon Menard Cosmetic Co., Ltd., 2-7, Torimi-cho, Nishi-ku, Nagoya 451-0071, Japan. tochio.takumi@menard.co.jp
Tanaka
Hiroshi
H
Nakata
Satoru
S
Ikeno
Hiroshi
H
D000152:Acne Vulgaris / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D015415:Biomarkers / Q000032:analysis; D002518:Ceramides / Q000032:analysis; D002784:Cholesterol / Q000032:analysis; D005230:Fatty Acids, Nonesterified / Q000032:analysis; D006801:Humans; D053582:Interleukin-1alpha / Q000032:analysis; D015227:Lipid Peroxidation; D008054:Lipid Peroxides / Q000032:analysis*; D008055:Lipids / Q000032:analysis; D016328:NF-kappa B / Q000032:analysis*; D012629:Sebum / Q000737:chemistry
D015415:Biomarkers; D002518:Ceramides; D005230:Fatty Acids, Nonesterified; D053582:Interleukin-1alpha; D008054:Lipid Peroxides; D008055:Lipids; D016328:NF-kappa B; D002784:Cholesterol