Among the various factors contributing to hair loss, Androgenetic Alopecia (AGA), manifesting as male pattern baldness, stands out as the most prevalent. The prefix “Andro” alludes to hormones, specifically testosterone and dihydrotestosterone, crucial in initiating male pattern hair loss. Simultaneously, the term “Genetic” underscores the hereditary aspect indispensable for the manifestation of hair loss.
AGA
Androgenetic Alopecia (AGA) is distinguished by the miniaturization of androgen-sensitive hair follicles, culminating in the conversion of normal hair into fine, nearly imperceptible strands marked by pigment loss (vellus hair follicles). This transformation is coupled with the apoptosis of certain follicle cells, denoting a process known as follicle cell death. Notably, it is hypothesized that a significant portion of affected hair follicle cells survives, albeit incapable of generating terminal hair.
During the initial phases, it’s common to witness a receding hairline in the temporal areas of mature Caucasian males, affecting 96 percent of them, including individuals not slated for significant hair loss advancement.
The prevalent male pattern entails hair loss in the frontal, mid, and vertex/crown areas, preserving the hair on the sides and back. Follicles in the postero-lateral regions exhibit resistance to androgens (hormones), allowing continuous hair growth throughout a man’s lifespan. In contrast to women, men may experience the complete loss of follicles in the affected areas over time.
The androgenetic loss of hair seems to be a hereditary condition, traceable through either parental lineage or both. Current knowledge points to a heightened form of the male sex hormone (testosterone) known as the instigator of this alopecia type. This hormone is identified as Dihydrotestosterone (DHT).
DHT binds to the androgen receptors within hair follicles, setting off a series of events that result in the miniaturization of the follicles through successive growth cycles.
DHT is produced through the interaction of the enzyme 5-alpha-reductase (5aR) with testosterone. Among the two isoenzymes of 5aR (type I and II), the latter is implicated in the conversion of testosterone to DHT within the hair follicle. A medication specifically designed to inhibit 5-alpha-reductase type II exists, known as Finasteride (1 MG), utilized for over two decades in treating AGA. Fundamentally, the singular solution to impede the miniaturization of hair inherent to male AGA entails a continuous reduction in blood levels of DHT.
Androgenetic Alopecia accounts for 90% of male hair loss, impacting around 50% of individuals over 40. Dr. Hamilton’s observation over 50 years ago, revealing the absence of AGA in castrated men, indicates that hair follicle growth in specific areas is androgen-dependent. In contrast, hair behaves differently in other regions. The mechanism behind why androgens (hormones) exert paradoxical effects on hair growth in various body zones remains elusive.
Following puberty, hair follicles sensitive to hormones require continuous exposure over time before hair loss initiation. The age at which these effects become evident varies among individuals, correlating with genetic makeup and testosterone levels in the bloodstream.
Hair loss in men doesn’t happen abruptly; it follows a distinct cyclic pattern. Those facing hair loss experience alternating phases of gradual and rapid loss, including periods of stability. While many factors affecting the pace of loss remain unidentified, it’s understood that with aging, the overall volume of hair diminishes.
Androgenetic Alopecia (AGA), observed in both men and women, involves a disruption in the natural hair cycle, characterized by a gradual shortening of the anagen phase and progressive follicular miniaturization.
Baldness in men typically adheres to a recognizable pattern, categorized into progressive degrees (II – VII) for enhanced interpretation. This classification, identified as the Hamilton-Norwood Scale, precisely defines these regular patterns.
Diffuse Patterns in Men
Two types of genetic hair loss in men, often disregarded by many professionals as they fall outside the Norwood scale, are Diffuse Patterned Alopecia (DPA) and Diffuse Unpatterned Alopecia (DUPA). Both present a substantial challenge in terms of diagnosis and the approach to medical and surgical treatment. Grasping these conditions is paramount for evaluating hair loss, particularly in the case of younger individuals, where diagnoses might be easily overlooked, signifying that a patient may not be an ideal candidate for surgery.
DPA
Diffuse Patterned Alopecia (DPA) represents a manifestation of androgenetic alopecia marked by diffuse thinning in the distinctive regions of a common male pattern (frontal, mid, and crown), while maintaining stability on the sides and back (donor region). In DPA, the entire upper scalp undergoes a gradual process of miniaturization (thinning) without conforming to the typical stages of Norwood.
The frontal hairline commonly exhibits subtle recession, enabling these patients to effectively conceal their alopecia in the initial stages, akin to the pattern observed in women.
