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Abstract
Frontal Fibrosing Alopecia (FFA) is primary cicatricial alopecia characterized by progressive loss of the frontal hairline and eyebrows, which is prevalent most commonly in post-menopausal women but can also affect men and pre-menopausal women. Genes and autoimmunity are thought to play a role in the pathogenesis.

Research gaps and future directions for FFA are discussed in this systematic review, which examines the clinical features, pathogenesis, and management strategies of the disease.

Introduction
Originally described in 1994 by Kossard, Frontal Fibrosing Alopecia (FFA) is an inflammatory condition derived from primary cicatricial alopecia (PCA) [1]. It appears that environmental or lifestyle factors may be contributing to the increase since Kossard’s discovery [2]. Female postmenopausal women are most commonly affected by FFA, but males and younger women can also be affected [3]. In this review, a summary of the current understanding of FFA's clinical features, pathogenesis, and management strategies, including hormonal, genetic, and autoimmune factors will be provided.

Literature Findings
Clinical Implications
Perifollicular erythema and hyperkeratosis accompany progressive frontal hairline recession in FFA [4]. Postmenopausal women account for the majority of cases (80-90%); younger women and men account for the remainder [5]. The most common symptom of FFA is marginal hair loss in the frontal region, which can sometimes extend to the temporal region. In addition to the hairline recession, loss of eyebrows (madarosis) is also a common occurrence [6]. Other areas of the body, particularly the extremities, can also be affected by hair loss [7].

It has been reported that up to 50% of patients develop extra-follicular manifestations, including facial papules and macules [8]. Upon histological examination, a lymphocytic infiltrate targets the follicular unit's isthmus and infundibulum in a "lichenoid" pattern [9]. In the end, this leads to permanent hair loss due to follicular dropout and fibrosis [10].

Pathogenesis
The mechanism of FFA may be influenced by several factors: hormonal, genetic, and autoimmune factors, although the etiology is vastly unknown.

Hormonal: There may be a hormonal etiology since 51% of female patients report a history of gynecological issues [11]. Furthermore, it has been suggested that FFA is associated with androgenetic alopecia, as many patients with FFA have elevated androgen levels [12].

Genetic: Five loci were significantly associated with FFA in a genome-wide association study, including variants in genes known to be associated with PCA [13]. However, it is still unclear what genetic underpinnings of FFA exist due to the lack of large-scale familial studies.

Autoimmune: There is a high prevalence of autoimmune diseases in patients with FFA, especially thyroid disorders [14]. There was found to be a significant increase in Th1 and Th17 cytokines in patients with FFA, which is suggestive of a T-cell-mediated immune response [15]. In addition, studies have demonstrated CD8+ T-cell presence in histopathology, supporting the concept that immune-mediated processes play a role in disease progression [16].

Management & Treatment
There is no golden standard of care for patients with FFA, however, hair regrowth can be stimulated by some management strategies, which aim to halt disease progression. Inflammation and erythema may be controlled with topical corticosteroids, although hair growth may be limited [17]. Injections of intralesional corticosteroids have been used successfully to treat inflammation [18]. Several systemic treatments have been found to be effective in treating FFA patients, including hydroxychloroquine and doxycycline [19].

There is evidence that retinoids, such as isotretinoin, regulate the proliferation of keratinocytes while finasteride, an inhibitor of 5-alpha-reductase, may act against the proposed hormone component of FFA.[20]. Recent studies have shown that Janus kinase (JAK) inhibitors like tofacitinib and ruxolitinib can inhibit mechanisms involved in T-cell immunity, making them potential therapeutics [21].

Hair transplantation is a surgical option with variable results in stable patients who have been well-selected [22]. Their use, however, is complicated by the risk of recurrence and involvement of donor sites [23].

Conclusion
Postmenopausal women are primarily affected by Frontal Fibrosing Alopecia, a complex PCA. Despite the lack of clear pathogenesis, genetic factors, hormones, and autoimmunity appear to play a role. Research into the underlying mechanisms of FFA is needed in order to develop more effective therapeutic options for this disease. Current management strategies aim to control inflammation, stop disease progression, and stimulate hair regrowth. These patients may benefit from novel therapeutics, such as JAK inhibitors, in the future as more research is done on FFA.