Interest in sebaceous gland physiology and its diseases is rapidly increasing. We provide a summarized update of the current knowledge of the pathobiology of acne vulgaris and new treatment concepts that have emerged in the last 3 years (2005)(2006)(2007)(2008). We have tried to answer questions arising from the exploration of sebaceous gland biology, hormonal factors, hyperkeratinization, role of bacteria, sebum, nutrition, cytokines and toll-like receptors (TLRs). Sebaceous glands play an important role as active participants in the innate immunity of the skin. They produce neuropeptides, excrete antimicrobial peptides and exhibit characteristics of stem cells. Androgens affect sebocytes and infundibular keratinocytes in a complex manner influencing cellular differentiation, proliferation, lipogenesis and comedogenesis. Retention hyperkeratosis in closed comedones and inflammatory papules is attributable to a disorder of terminal keratinocyte differentiation. Propionibacterium acnes, by acting on TLR-2, may stimulate the secretion of cytokines, such as interleukin (IL)-6 and IL-8 by follicular keratinocytes and IL-8 and -12 in macrophages, giving rise to inflammation. Certain P. acnes species may induce an immunological reaction by stimulating the production of sebocyte and keratinocyte antimicrobial peptides, which play an important role in the innate immunity of the follicle. Qualitative changes of sebum lipids induce alteration of keratinocyte differentiation and induce IL-1 secretion, contributing to the development of follicular hyperkeratosis. High glycemic load food and milk may induce increased tissue levels of 5a-dihydrotestosterone. These new aspects of acne pathogenesis lead to the considerations of possible customized therapeutic regimens. Current research is expected to lead to innovative treatments in the near future. Biology of sebaceous glandsThe sebaceous gland is a holocrine gland, and its secretion is formed by the complete disintegration of the glandular cells. Excreting sebum is the major function of sebaceous glands (1), and increased sebum excretion is a major concurrent event that parallels the development of acne lesions. With the development of human sebaceous gland experimental models for in vitro studies (2-5), considerable progress has been made in our understanding of many new

Scientific advances are continually improving the knowledge of acne and contributing to the refinement of treatment options; it is important for clinicians to regularly update their practice patterns to reflect current standards. The Global Alliance to Improve Outcomes in Acne is an international group of dermatologists with an interest in acne research and education that has been meeting regularly since 2001. As a group, we have continuously evaluated the literature on acne. This supplement focuses on providing relevant clinical guidance to health care practitioners managing patients with acne, with an emphasis on areas where the evidence base may be sparse or need interpretation for daily practice.

Our findings provide support for the reliability and validity of the Korean JSPE-S and indicate that it can serve as a useful instrument for assessing empathy among Korean medical students.

Recent studies have suggested that dietary factors, specifically glycaemic load, may be involved in the pathogenesis of acne. The aim of this study was to determine the clinical and histological effects on acne lesions of a low glycaemic load diet. A total of 32 patients with mild to moderate acne were randomly assigned to either a low glycaemic load diet or a control group diet, and completed a 10-week, parallel dietary intervention trial. Results indicate successful lowering of the glycaemic load. Subjects within the low glycaemic group demonstrated significant clinical improvement in the number of both non-inflammatory and inflammatory acne lesions. Histopathological examination of skin samples revealed several characteristics, including reduced size of sebaceous glands, decreased inflammation, and reduced expression of sterol regulatory element-binding protein-1, and interleukin-8 in the low glycaemic load group. A reduction in glycaemic load of the diet for 10 weeks resulted in improvements in acne.

Acne vulgaris is a highly prevalent skin disorder characterized by hyperseborrhea, inflammation, and Propionibacterium acnes overgrowth. Only isotretinoin and hormonal therapy reduce sebum production. To identify a new drug candidate that modulates sebum, we examined the effects of EGCG, the major polyphenol in green tea, on human SEB-1 sebocytes and in patients with acne. In SEB-1 sebocytes, we found that EGCG reduced sebum by modulating the AMPK-SREBP-1 signaling pathway. EGCG also reduces inflammation by suppressing the NF-κB and AP-1 pathways. EGCG also induces cytotoxicity of SEB-1 sebocytes via apoptosis and decreases the viability of P. acnes, thus targeting almost all the pathogenic features of acne. Finally, and most importantly, EGCG significantly improved acne in an 8-week randomized, split-face, clinical trial, and was well tolerated. Our data provide a therapeutic rationale for the use of EGCG in acne.