Biology of the hair follicle – Bianca Maria Piraccini (Italy)
Why does a clinician need to know about the biology of hair follicles? Because the understanding of hair diseases cannot avoid the understanding of hair follicle anatomy and physiology.
New insights into the molecular pathophysiology of some types of alopecia has led to the development of new drugs and understanding their mechanism of action is mandatory for proper prescription and correct patient management.
The hair follicle is a unique organ that periodically regenerates itself by spontaneously undergoing repetitive cycles of growth (anagen), apoptosis-driven regression (catagen), and relative quiescence (telogen). During the anagen phase the follicles produce the hair shaft, which consists of terminally differentiated keratinocytes. The hair shaft is pigmented, as melanocytes of the hair follicle matrix produce melanin and transfer it to keratinocytes, with gradual slowing down and stop of activity with age, leading to hair graying.
What are the mechanisms and the molecules that regulate the alternance of the different phases of the hair cycles? This is one of the most studied topics in the field of hair diseases. Discovering the molecules that promote/inhibit hair growth may explain the pathogenesis of hair disorders and may also help the development of new therapeutical options. During cycling, the hair follicle undergoes important anatomical/biochemical changes without being aggressed by the immune system. This immune privilege is unique of the hair follicle and, when lost, may explain the onset of autoimmune conditions, such as alopecia areata.
Discovering the causes of loss of immune privilege and the ways to restore it are another important field of research in alopecia areata.
Frontal fibrosing alopecia – Ramon Grimalt (Spain)
Frontal fibrosing alopecia (FFA), a cicatricial type of alopecia, is increasing in prevalence worldwide.
FFA patients typically present with hair loss in the frontal scalp region and eyebrows. An early diagnosis and treatment are important to prevent permanent hair loss. Etiopathogenesis remains unknown, as well as which cutaneous comorbidities might be associated with this pathology.
In the literature, some articles report the association of FFA with some autoimmune cutaneous diseases, such as discoid lupus or vitiligo, but so far there’s no clear association.
The aim of the talk will be to analyze the frequency of cutaneous conditions that could be associated with FFA and try to understand better the relation with emollients, sunscreens or other factors, as well as discuss about the best treatment options.
New drugs in alopecia areata – Antonella Tosti (United States)
Alopecia Areata (AA) is the second most common non-scarring hair loss disorder, with a prevalence of 1 in 1000 and a lifetime incidence of 2% worldwide. No specific treatment for AA has been approved for AA thus far.
Due to the autoimmune etiology of AA, the most employed treatments for severe AA are “non-specific” immunosuppressants that shut down the entire immune system such as steroids, methotrexate, and cyclosporine.
The AA community has witnessed great advances in the treatment of AA in the last 10 years, with the development of tailored drugs aimed at the specific pathophysiology of AA with a good safety profile. AA has a T cell-mediated autoimmune etiology, that starts with disruption of the hair follicle immune-privilege. In AA hair follicular epithelial cells produce IL 15. This cytokine recruits and activate cytotoxic T cells that produce IFN-γ, which activates the JAK-STAT pathway in the follicular cells leading to increased production of IL-15, with a chronic persistent inflammation.
Tofacitinib, that was approved for rheumatoid arthritis in 2012, was the first JAK inhibitor to be shown to induce regrowth in AA and since then research on other JAKS has grown dramatically.
In addition to Tofacitinib, Ruxolitinib and Baricitinib are currently marketed (even if not worldwide), and have been utilized “off label” for the treatment of alopecia areata. Baricitinib has just completed a phase 2/3 clinical trial and might be soon approved by health authorities. Several other JAK inhibitors are currently undergoing clinical trials.
Although Jak inhibitors are a very effective treatment, efficacy is not 100%, and other pathways besides the JAK/STAT probably need to be targeted.
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