There are three types of excessive hair loss, clinically known as alopecia. They are discussed in detail below.
1. Auto-immune Conditions
Alopecia areata is an autoimmune disease in which hair falls out from areas of the body, usually from the scalp, due to the body’s failure to recognize its own cells. The immune system subsequently destroys the hair follicles as though they were invaders.
The hair typically falls out in small, round patches about the size of a quarter. In many cases, the disease does not extend beyond a few bare patches. Often it causes bald spots on the scalp, especially in the early stages. In 1%–2% of cases, the condition can spread to the entire scalp (alopecia totalis) or to the entire epidermis (alopecia universalis).
Conditions resembling alopecia areata, and having a similar cause, occur also in other species.
There are two types: Scarring alopecia, where there is fibrosis, inflammation and loss of hair follicles, and Nonscarring alopecia, where the hair shafts are gone but the hair follicles are preserved, making this type of alopecia reversible.
No matter how widespread the hair loss, most hair follicles remain alive and are ready to resume normal hair production whenever they receive the appropriate signal. In all cases, hair regrowth may occur even without treatment and even after many years. It does not reduce life expectancy and it should not interfere with going to school, playing sports and exercising, pursuing any career, working, marrying and raising a family.
Alopecia areata is thought to be a systemic autoimmune disorder in which the body attacks its own anagen hair follicles and suppresses or stops hair growth. For example, T cell lymphocytes (white blood cells) cluster around affected follicles, causing inflammation and subsequent hair loss.
A few cases of babies being born with congenital alopecia areata have been reported, but these are not cases of autoimmune disease because infants are born without fully developed immune systems.
Alopecia areata is not contagious but it occurs more frequently in people who have affected family members, suggesting heredity may be a factor. Strong evidence of genetic association with increased risk for alopecia areata was found by studying families with two or more affected members. This study identified at least four regions in the genome that are likely to contain these genes. In addition, it is slightly more likely to occur in people who have relatives with autoimmune diseases.
Endogenous retinoids metabolic defect is a key part of the pathogenesis of alopecia areata. In 2010, a genome-wide association study was conducted that identified 129 single-nucleotide polymorphisms that were associated with alopecia areata. The genes that were identified include those involved in controlling the activation and proliferation of regulatory T cells, cytotoxic T lymphocyte-associated antigen 4, interleukin-2, interleukin-2 receptor A and Eos (also known as Ikaros family zinc finger 4) as well as the human leukocyte antigen. The study also identified two genes — PRDX5 and STX17 — that are expressed in the hair follicle.
Alopecia areata commonly involves hair loss in one or more round spots on the scalp.
Hair may also be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata.
Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head.
Alopecia areata multilocularis refers to multiple areas of hair loss.
Ophiasis refers to hair loss in the shape of a wave at the circumference of the head.
The disease may be limited only to the beard, in which case it is called alopecia areata barbae.
If the patient loses all the hair on the scalp, the disease is then called alopecia totalis.
If all body hair, including pubic hair, is lost, the diagnosis then becomes alopecia universalis.
Alopecia areata totalis and universalis are rare.
2. Adrogyn genetic-mediated conditions
Approximately 1.7% of the population will experience episodes of alopecia areata during their lifetime
Female-pattern hair loss, also known as androgenetic alopecia, is the most common type of hair loss in women. There is no known prevention for it.
In FPHL there is diffuse thinning of hair on the scalp due to increased hair shedding, a reduction in hair volume, or both.
Another condition, chronic telogen effluvium, also presents with increased hair shedding and is often mistaken for FPHL. It is important to differentiate between these conditions as management for both conditions differ.
FPHL presents quite differently from the more easily recognizable male-pattern baldness, which usually begins with a receding frontal hairline that progresses to a bald patch on top of the head. It is very uncommon for women to bald following the male pattern unless there is excessive production of androgens in the body.
In general, baldness occurs when the hair follicle shrinks over time, resulting in shorter and finer hair. Eventually the follicle does not grow new hair. The follicles remain alive, which suggests that it is still possible to grow new hair.
The reason for female-pattern baldness is not well understood but may be related to the following:
Changes in the levels of androgens (male hormones). For example, after reaching menopause, many women find that the hair on their head is thinner, while the hair on their face is coarser.
Family history of male- or female-pattern baldness.