Male pattern baldness is also known as androgenic alopecia. It is the cause of more than 95% of all cases of pattern hair loss; This includes baldness in men and thinning of hair in women.
The primary and hormones responsible for male pattern baldness are testosterone and dihydrotestosterone (DHT). The enzyme 5-alpha reductase regulates the conversion of testosterone to DHT. These elevated levels of DHD result in miniaturization of the half follicle, a shortened period of the growth phase of the half-cycle, known as the anagen phase, and eventual hair loss.
Hairs in the frontal, temporal, and vertex region of the scalp are particularly sensitive to testosterone. Conversely, hairs present on the back of the scalp and side of the head are not genetically predisposed to the influence of testosterone and are therefore not affected.
Consequently, hairs removed from the side and back of the scalp for use as donor hair will maintain that genetic predisposition and continue growing if they are transported to the top of the head where hair loss has occurred.
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The anatomy of the hair follicle
The hair growth cycle consists of three phases: anagen, catagen, and telogen. Anagen, known as the growth phase, lasts between three and 10 years. during this phase rapid cell division occurs in the hair bulb and dermal papilla. New hairs also begin to protrude from the scalp.
Following this, there is a transitional phase that lasts between two and three weeks. During this phase, called catagen, cell division stops, and pigment production from melanocytes ceases. Telogen is the resting phase and lasts approximately three to four months; during this period hairs are shed from the scalp.
Epidemiology of male pattern hair loss
The most common group affected by male pattern baldness are Caucasians, followed by Asians, and African Americans. The incidence is correlated with the age in Caucasian males, with 50% affected by the age of 50, and up to 80% affected by the age of 70. In females increase in incidence typically increases after menopause.
Pathophysiology of male pattern baldness
In the anagen phase, the activation of the androgen receptor shortens the anagen growth phase in the course of the hair growth cycle. Excessive activation, which may occur in androgenetic alopecia, leads to minimization of the follicle through a progressively shorter anagen phase is, resulting in thinner and shorter hair follicles. These thinner and shorter hair follicles may not be capable of penetrating through the epidermis. Pathological specimens show a decreased ratio of anagen to telogen hair, with a 5:0 ratio versus a 12:1 ratio in normal hair.
In most body sites, hair growth is mediated by the enzyme 5-alpha DHT. This is a potent metabolite of testosterone, that has a sevenfold higher sensitivity to the androgen receptor.
The enzyme 5-alpha reductase converts testosterone to DHT. There are two major isoforms of this enzyme. Both isoforms are responsible for the generation of DHT, however show a different biochemical and tissue-specific expression pattern.
Type 2 5-alpha reductase has a greater impact on male pattern baldness; this enzyme can be found in the outer root sheath of hair follicles, epididymis, vas deferens, seminal vesicles, and the prostate. Type 1 5-alpha reductase enzymes are present in sebaceous glands, keratinocytes, and sweat glands.
individual susceptibility to hair loss and its severity is determined by several factors. Intrinsic susceptibility of hair follicles to androgen gives a specific pattern of hair loss; as stated, occipital (; backs and sides of the head) hair is particularly resistant to the effects of and regions, even when it's transplanted to the vertex.
If not treated in the early stages, hair loss can progress, resulting in a complete loss of hair, particularly on the crown. Using a dermatoscope, which is a handheld epiluminescent microscope, two to five terminal hairs can be seen emerging from a single pore. the terminal hairs are noticeably different; they are typically longer and stronger compared to vellus hairs, which are much thinner, and maybe translucent – these are typically referred to as peach fuzz.
In a balding scalp, the terminal hair compound follicles are progressively replaced by fine and shorter vellus hairs. Eventually, only one or two terminals has can be seen emerging from a single pore in the affected area.
A reduction in the number of terminal hairs in a single pore is a useful feature in the early diagnosis of male pattern baldness, with the persistence of occipital hair even in the advanced stage.
Treatments for male pattern baldness
Oral minoxidil is a medicine initially indicated for hypertension in the 1960s. Hypertrichosis, excessive hair growth, is a commonly observed side effect and is reported to occur in 100% of users. These observations led to the development of topical minoxidil as a treatment for hair loss. A five-year follow-up study with topical minoxidil at 5% has shown a sustained effect on hair growth.
The mechanistic basis of action is thought to occur as a result of the upregulation of vascular endothelial growth factor (VEGF). VEGF is thought to maintain the dermo papilla vasculature and hair growth. It is thought that the binding of minoxidil to adenosine receptors A1 and A2 as well as the sulphonyl receptor activates adenosine signaling pathways and an increase in the releases of VEGF. This is thought to increase vascularisation of the tissue surrounding the follicle, resulting in accelerated hair growth.
An alternative and prevailing view are that minoxidil promotes hair regrowth via potassium channel openers. The opening of potassium channels is thought to initiate the onset of anagen and shorten the duration of telogen, prolonging anagen by delaying the initiation of the catagen phase. Excessive hair growth on the face and hands is a common side effect observed for topical minoxidil as well as increased erythema (skin rash) and excessive dandruff.
Finasteride is a 5-alpha reductase type 2 inhibitor that can reduce levels of DHT. Relative to minoxidil, finasteride can promote significantly more high growth. Side effects of finasteride include decreased libido, erectile dysfunction, and ejaculatory problems. Finasteride also affects the rate and grade of prostate cancer, with an overall reduction in the prevalence of prostate cancer by 25%. However, there is an increased risk of high-grade cancers, limiting its use in chemoprevention.
Dutasteride has similar characteristics to finasteride but is significantly stronger in its ability to reduce the levels of DHT in the scalp. Initially, dutasteride was approved for the treatment of benign prostatic hyperplasia. In phase two studies, there was a dose-dependent increase in hair growth after using dutasteride compared to finasteride.
Hair transplantation is another common treatment for male pattern baldness. It involves the removal of hair from the occipital scalp on subsequent reimplantation into the fold regions of the top of the head on the front of the scalp.
The procedure consists of strip harvesting, whereby a strip of scalp between 8 and 14 millimeters in width and 20 to 30 centimeters in length is removed from the occipital scalp under local anesthetic. Alternatively, follicular units can be harvested under local anesthesia with 1mm biopsies. Each of the harvested follicular units is then reinserted in bald regions of the head using a microblade. This is typically the preferred option as it does not leave any visible scars.
- Rathnayake D, Sinclair R. (2010) Male androgenetic alopecia. Expert Opin Pharmacother. doi: 10.1517/14656561003752730.
- Marchetti PM, Barth JH. (2013) Clinical biochemistry of dihydrotestosterone. Ann Clin Biochem. doi:10.1258/acb.2012.012159.
- York K, Meah N, Bhoyrul B, et al. (2020) A review of the treatment of male pattern hair loss. Expert Opin Pharmacother. doi:10.1080/14656566.2020.1721463.
- American Academy of Dermatology Association. What is male-pattern hair loss, and can it be treated? Available at: https://www.aad.org/public/diseases/hair-loss/treatment/male-pattern-hair-loss-treatment. Last accessed October 2021.
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Last Updated: Nov 17, 2021
Hidaya is a science communications enthusiast who has recently graduated and is embarking on a career in the science and medical copywriting. She has a B.Sc. in Biochemistry from The University of Manchester. She is passionate about writing and is particularly interested in microbiology, immunology, and biochemistry.
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