Is there an association between frontal fibrosing alopecia (FFA) and the pathogenesis of androgenetic alopecia (Androgenic Alopecia) and autoimmune alopecia?

From the Guidelines

There is an association between frontal fibrosing alopecia (FFA), androgenic alopecia, and autoimmune alopecia in terms of their pathogenesis, though they are distinct conditions. The pathogenesis of FFA appears to involve both hormonal and autoimmune mechanisms, while androgenic alopecia is primarily hormone-driven, and autoimmune alopecia involves T-cell mediated attack on hair follicles. The overlap between these conditions is seen in several ways:

• FFA patients often have concurrent androgenic alopecia;
• hormonal factors influence both FFA and androgenic alopecia;
• and all three conditions involve inflammation around hair follicles, though through different mechanisms. This association explains why some treatments may work across multiple forms of hair loss, such as anti-androgens (finasteride, dutasteride) or anti-inflammatory agents. However, treatment approaches must be tailored to the specific diagnosis, as the underlying mechanisms differ despite these associations, as noted in studies such as 1. Additionally, the role of micronutrients, including vitamin D and iron, has been explored in the context of alopecia areata, with some studies suggesting a potential link between deficiencies and the development of the condition, as discussed in 1. It is essential to consider these factors when developing treatment plans for patients with FFA, androgenic alopecia, or autoimmune alopecia. Key points to consider include:
• The potential for concurrent conditions, such as androgenic alopecia in FFA patients;
• the role of hormonal factors in FFA and androgenic alopecia;
• the involvement of inflammation in all three conditions;
• the potential benefits of anti-androgens or anti-inflammatory agents in treating these conditions;
• the need for tailored treatment approaches based on the specific diagnosis;
• the potential link between micronutrient deficiencies and the development of alopecia areata. By considering these factors and staying up-to-date with the latest research, clinicians can provide effective treatment and management strategies for patients with FFA, androgenic alopecia, and autoimmune alopecia.

From the Research

Association between Frontal Fibrosing Alopecia and Other Forms of Alopecia

• There is evidence to suggest an association between frontal fibrosing alopecia (FFA) and autoimmune disorders, including autoimmune alopecia 2.
• FFA has also been linked to androgenetic alopecia, with studies showing that men with FFA often have androgenetic alopecia or hair loss on eyebrows or extremities 3.
• The pathogenesis of FFA is complex and multifactorial, involving immune-mediated, genetic, hormonal, and environmental factors 4.
• The frequent onset of FFA in post-menopausal women and its similar patterning to female pattern hair loss suggest a role for sex steroid hormones in its pathogenesis 4.

Pathogenesis of Frontal Fibrosing Alopecia

• The current evidence suggests that FFA is characterized by Th1-mediated inflammation, collapse of hair follicle immune privilege, and bulge epithelial stem cell destruction 4.
• Peroxisome proliferator-activated receptor gamma (PPAR-γ) depletion and epithelial-mesenchymal transition are also key events leading to permanent hair follicle destruction in FFA 4.
• Genetic or epigenetic mechanisms may play a role in the pathogenesis of FFA, as suggested by familial reports of the disease 4.

Treatment of Frontal Fibrosing Alopecia

• Various treatment options have been suggested for FFA, including 5 alpha-reductase inhibitors, topical calcineurin inhibitors, hydroxychloroquine, peroxisome proliferator-activated receptor gamma agonists, and oral retinoid agents 5.
• Other potential treatment strategies and drugs, such as phototherapy, Janus kinase inhibitors, dehydroepiandrosterone, sirolimus, cetirizine, and rituximab, may also be effective in mitigating disease progression, but require further evaluation in clinical trials 5.