Dermnet Videos
Alopecia Videos
- Alopecia areata – Causes and Associated Conditions
- Alopecia Areata Information
- Alopecia Areata Treatment
- Course of Sudden Hair Loss Telogen Effluvium
- Evaluation and Treatment of Sudden Hairloss Telogen Effluvium
- Female Pattern Baldness and Hair Loss Causes
- Female Pattern Baldness and Hair Loss in Women
- Female Pattern Hair Loss Evaluation and Testing
- Female Pattern Hair Loss Treatment
- Hair loss and Alopecia Introduction
- Hair Loss Due To Hair Pulling – Trichotillomania
- Hair Loss Treatment and Male Pattern Baldness Medicine
- Loose Anagen Hair Syndrome
- Male Patern Baldness Causes and Hair Loss
- Male Pattern Baldness and Hair Loss Information
- Sudden Hair Loss Telogen Effluvium
- Traction Alopecia Hair Loss
- Traction Alopecia Hair Loss Treatment
- Central Centrifugal Cicatricial Alopecia
- Discoid Lupus Erythematosus – Clinical
- Discoid Lupus Erythematosus – Histology
- Discoid Lupus Erythematosus – Treatment
- Follicular Degeneration Syndrome
- Folliculitis Decalvans – Clinical
- Folliculitis Decalvans Treatment
- Hair Loss Alopecia With Scarring Information
- Lichen Planopilaris
- Lichen Planopilaris – Clinical Features
- Lichen Planopilaris Treatment
Video Topics
Male Patern Baldness Causes and Hair Loss
Male AGA results from the effect of androgens on susceptible hair follicles in men who are genetically susceptible to the condition. The role of androgens in male AGA was first appreciated by Hamilton in 1942. He observed that males castrated before puberty never developed patterned baldness. If these men were given exogenous androgens, baldness could develop. Testosterone is transformed to dihydrotestosterone (DHT) by the enzyme 5a-reductase. This enzymatic reaction occurs in the hair follicle in addition to other sites in the body. DHT binds to follicular receptors and results in follicular miniaturization in susceptible scalp follicles. The mechanism of the follicular miniaturization is unknown.
The follicles in men with AGA can be markedly reduced in size and resemble primary vellus follicles. The total number of follicles remains the same until late in the disease when there may be a slight reduction in follicular density. Susceptibility to developing male AGA may result from the genetic inheritance of the concentration of androgen receptors and the amount of 5a-reductase found in the follicle. The inheritance pattern of male AGA is not known, but it may be autosomal dominant with incomplete penetrance or polygenic.