Platelet-rich plasma

Introduction

Androgenetic alopecia (AGA) is the most common form of hair loss. It is characterized by progressive reduction and miniaturization of terminal hair follicles on the scalp. Caucasian men are a notably vulnerable population, with 50% of Caucasian men experiencing AGA by age 50. In women, AGA is referred to as female pattern hair loss (FPHL). FPHL may occur at any age with varying degrees of severity and becomes clinically detectable in about 3% of women by 29 years of age, 13% by 49 years, 19% by 69 years, and 25% among those over 69 years. The prevalence of FPHL has been shown to be lower among women of Asian descent. AGA typically occurs over many years but can progress more rapidly for some younger men with a strong family history. In addition to genetics, the presence of high levels of circulating androgens, specifically dihydrotestosterone (DHT), the end product of 5α-reductase enzymatic action on testosterone, contributes to this disease process. The typical distribution of hair loss in males with AGA involves the frontotemporal hairline and the vertex of the scalp, while women most often experience a widened hair part with relative sparing of the frontal hairline. These areas are the androgen-dependent areas on the scalp.

Although this condition is benign in nature and often considered part of the normal aging process, it is a familiar cosmetic concern encountered by dermatologists as it frequently poses significant psychological distress for patients. ^, Currently, the only FDA approved therapies for AGA are topical minoxidil for both men and women and oral finasteride for men only. Unfortunately, many patients report mixed outcomes and are either disappointed with treatment response or experience adverse drug events related to these agents.

Surgical hair transplantation is an option for a select number of patients; however, the invasive nature and financial commitment may be a significant limitation for most patients. Several studies evaluating various oral, topical, and minimally invasive alternative treatment options for AGA have been published. Off-label antiandrogenetic therapies such as oral dutasteride, oral spironolactone, topical ketoconazole, and topical finasteride have been shown to improve hair density with significant reduction in serum DHT concentrations. Additionally, minimally invasive treatment options including oral minoxidil, low level light laser, transdermal drug delivery via microneedling, and platelet-rich plasma therapy (PRP) have demonstrated promising results in randomized trials during the 2000s. In this chapter, we will discuss the pathophysiology and clinical features of AGA and the use of PRP for the treatment of AGA.

Pathophysiology of androgenetic alopecia

Elevated androgen levels in genetically susceptible individuals serve as a crucial predisposing factor for AGA. The key androgen involved in this pathway is DHT, which is the end product of testosterone acted upon by the enzyme 5α-reductase. There are three forms of this enzyme, with the two most notable being type 1 and type 2. Type 1 is found in the sebaceous glands and liver, and type 2 is found in the liver, prostate, and the scalp, beard, and chest hair follicles. Interactions between DHT and androgen receptors in scalp hair follicles results in shortening of the anagen phase, leading to follicular miniaturization and an increase in vellus hairs. In men, this occurs most commonly over the frontal hairline and vertex of the scalp, leading to the characteristic male patterned hair loss (MPHL). Conversely, in FPHL, some but not all patients may have elevated circulating androgens. Compared with men, the androgen receptors are fewer in number and the conversion of testosterone to estrogen in the scalp hair follicles occurs via increased activity of the cytochrome P-450-aromatase enzyme. It is the differences in the quantities of these key enzymes that are hypothesized to account for the diffuse central thinning along the hair part in FPHL rather than discrete areas of hair thinning seen in MPHL.