The 2011 Cicatricial Alopecia Symposium* was attended by approximately 90 members of the scientific community representing academia, industry, and government. The program was held over 2 days and included three keynote talks and six sessions: (i) Bench: “Mechanisms of inflammation”; (ii) Bedside: “Disease Presentation and Epidemiology”; (iii) Bench: “Nuclear Receptors and Lipids in Skin and Hair Disease”; (iv) Bedside: “Current and Emerging Therapies for Cicatricial Alopecia”; (v) Identifying Translational Opportunities in Cicatricial Alopecia; and (vi) Stem cells, Cicatricial Alopecia, and Hair Follicle Regeneration. In addition to major talks by invited speakers, the meeting included short talks selected from submitted abstracts, followed by panel discussions. The symposium culminated in a workshop composed of small discussion groups, each focusing on specific research questions and priorities.
Dr Stephen I Katz (NIAMS) discussed new directions at NIAMS and said that funding for hair research has steadily increased over the past 10 years. The symposium began with keynote addresses by David Norris (University of Colorado School of Medicine) and Frederick Miller (Environmental Autoimmunity Group, NIEHS). Dr Norris gave an overview of inflammatory alopecia and noted that alopecia areata and primary cicatricial alopecia (PCA) are the yin and yang of hair disorders. The inflammatory infiltrate targets the hair follicle (HF) bulb and spares the bulge stem cells in alopecia areata, whereas it targets the permanent, stem cell portion of the follicle in PCA, thereby making the hair loss permanent. He pointed out that factors driving the inflammatory reactions in PCA are poorly defined. He emphasized the recent associations reported in laboratory models of lipid abnormalities and hair loss. He noted that defined targets, such as peroxisome proliferator-activated receptor gamma (PPARγ) involvement in lichen planopilaris pathogenesis and treatment, have yet to be found in alopecia areata.
Dr Miller gave an overview of the role of environment in the pathogenesis of autoimmune diseases and emphasized the role of UV radiation in autoimmune diseases, which induces greater skin inflammation in female mice compared with male mice. His take-home message was that major risk factors for autoimmune diseases are both environmental and genetic, and that there is a clear gender bias in the prevalence of antinuclear antibodies and in the expression of estrogen and IFN-responsive genes. He suggested that it might be important to evaluate the incidence of each of the PCA subtypes in different parts of the world.