Male androgenetic alopecia

Abstract

Male androgenetic alopecia (MAA) is quite common and worsens with age, with a significant impact on quality of life, and is increasingly a reason for consultation with a dermatologist. The etiopathogenesis of MAA is multifactorial and genetic and hormonal influences stand out. MAA starts with the process of follicular miniaturization in diverse phenotypic patterns. The diagnosis of MAA is basically clinical and currently corroborated by well-established trichoscopic findings. Despite this, therapeutic options are limited, especially when one considers medications with a high level of scientific evidence. This review aims to help the general dermatologist towards a better understanding of MAA providing a basis for good individualized and judicious therapeutic decisions.

Keywords: Alopecia; Dustasteride; Finasteride; Minoxidil; Therapeutics.

Fig. 1

Scalp follicular cycle: anagen phase (cell proliferation), catagen (involution) and telogen (resting). After successive cycles, the kenogen phase (without hair production) may occur.

Fig. 2

Androgen-dependent signaling pathway in the dermal papilla cells.

Fig. 3

Hamilton-Norwood classification. Stage I, No apparent hair loss or minimal loss in the temporal regions; Stage II, Slight bitemporal recession, showing a symmetrical triangular shape; Stage III, Significant loss with little or no hair coverage in the temporal regions; Stage III Vertex, Hair loss is more pronounced in the vertex and the recession in the temporal region does not exceed that described in stage III; Stage IV, Significant thinning in the temporal regions and in the vertex, leaving a dense band of hair separating the two areas; Stage V, Recession of the implantation line and more evident thinning at the vertex. The band of hair separating the two regions shows even more reduced density, making the transition area less evident; Stage VI, The frontotemporal and vertex regions unite through the complete loss of the band of hair that separated them; Stage VII: More extensive form of involvement, leaving only a narrow band of hair in the lateral and occipital regions.

Fig. 4

Clinical and trichoscopic comparison between father (right) and son (left): The images highlight the process of hair thinning and follicular variability characteristic of MAA, as observed in the image of the father (right).

Fig. 5

Horizontal section of a fragment of scalp skin in MAA (Hematoxylin & eosin, ×20) – 39 hair follicles at the level of the isthmus, 9 of which are vellus, and the others terminal and intermediate. Preserved follicular epithelium and sebaceous glands with enlarged lobules. All follicles are in the anagen phase, except one telogen germinal unit.

Fig. 6

Conversion of Minoxidil into its active form, Minoxidil Sulfate.