INTRODUCTION
Androgenetic alopecia (AGA) is the progressive miniaturization
of the scalp’s terminal hair follicles that affects
over 50% of Caucasian men.1 Since hair is often associated with a person’s physical appearance, its loss can have a large psychosocial impact. Those who suffer from AGA have less self-esteem and impaired quality of life. A youthful appearance is often based on the presence of abundant hair and an intact anterior hairline. Studies have associated balding with overestimations of age.2 A study examining photographs of individuals with and without hair found that individuals with hair were perceived more masculine and younger.3
Despite the psychologic importance of hair preservation, FDA approved therapies for AGA is limited to topical minoxidil and oral finasteride. Topical minoxidil solution was developed as a treatment for AGA after its initial oral use for hypertension. Minoxidil increases hair weight through its primary effect of increasing the diameter of existing hairs.4 Finasteride, 5-a-reductase type II inhibitor, decreases levels of dihydrotestosterone
(DHT), which leads to increased hair diameter, growth, and hair counts.5 Since the approval of finasteride in 1997, there have been no FDA approved medications to treat AGA.6 The large unmet need for better treatments for hair loss has prompted both physicians and the pharmaceutical industry
to develop and pioneer new therapies for hair loss. This article reviews emerging medical, procedural, and surgical therapies for AGA.
Prostaglandins and Hair Growth
Prostaglandins (PGs) are lipid molecules derived from arachidonic
acid that regulate broad functions via autocrine and paracrine signals. Prostaglandins have been widely studied for their role in inflammation via the cyclooxygenase pathway.
Different PGs often have opposing biological functions. In the pulmonary system, PGE2 causes bronchial relaxation while PGD2 causes contraction.7 The effects of prostaglandins on hair growth were serendipitously discovered reminiscent to the discovery
of minoxidil. After the Food and Drug Administration (FDA) approval of bimatoprost, a prostaglandin F2α analogue, for ocular hypertension, a common side effect was increased eyelash hair growth. 8 This clinical observation spurred further studies ultimately leading to the FDA approval of the use of bimatoprost
0.03% solution (Latisse, Allergan Inc., Irvine, CA), for hypotrichosis of the eyelashes.9 The emergence of bimatoprost highlighted the importance of prostaglandins in hair follicle function.
In recent years, the effects on prostaglandins on the hair follicle have been further clarified. Prostaglandin D2, E2, and F2a have the ability to regulate hair growth. Mouse models and clinical data have demonstrated that PGD2 inhibits hair growth and PGE2/F2a promotes growth.10 Prostaglandin dysregulation may contribute to AGA pathogenesis offering potential therapeutic targets for its treatment. 11
Prostaglandin F2α Analogues
Prostaglandin F2α is thought to improve hair growth by extending
the duration of anagen phase. In a murine study using bimatoprost, treated mice demonstrated a significantly greater proportion of anagen follicles and a decrease in telogen and catagen follicles.12 Another murine study using a different prostaglandin F2α analogue, latanoprost, also documented induction
of telogen follicles into anagen phase.13 Since eyelash hair follicles are proportionally higher in the telogen phase, bimatoprost’s mechanism of action provides rationale for its effectiveness
for hypotrichosis of the eyelashes.
