Alopecia

Disease/Disorder

Also known as: Hair loss, pattern baldness

Anatomy or system affected: Hair, head

Definition: Temporary or permanent hair loss.

Key terms:

anagen: active growth phase of hair follicles

catagen: transition between growth and resting phases of hair follicles

dihydrotestosterone: male hormone, a derivative of testosterone that plays a key role in androgenic alopecia

keratin: a family of fibrous structural proteins that compose skin, nails, and hair

telogen: the resting phase of hair follicles

terminal hair: thick, pigmented hairs found on the scalp and other parts of the body

vellus: short, fine, unpigmented hair that covers most of the person's body from childhood

Causes and Symptoms

During the ninth week of development, small patches of fetal skin cells aggregate in response to signals sent by the underlying dermis. These small, raised areas (epithelial placodes) grow downward, below the skin and elongate to become hair germs and then hair pegs. As the elongating hair peg grows further into the dermis, cells from the dermis accumulate at the growing end of the hair peg. The hair peg becomes a bulbous peg and outgrowths sprout from the sides to form the sebaceous gland, and connective tissue cells from surrounding tissue condense to form the arrector pili muscle that attaches to a bulge on the lower part of the bulbous peg. Dermis cells form the dermal papilla, which becomes the hair root and pigment cells (melanocytes) infiltrate the developing hair follicle to convey color to the growing hair shaft.

From about the third month of development, the fetus is covered with lanugo hair (Latin, “lana” meaning wool). The fetus sheds this lanugo hair about four weeks before birth, and begins to form the two types of neonatal hair: unpigmented and short (1–2 centimeters) vellus hairs that lack a sebaceous gland and do not produce another hair in their place, and terminal hairs that grow on the head and other parts of the body, have pigment, and initially appear rather thin and short.

Hair follicles progress through a series of growth and regression phases known as the hair cycle. The hair cycle consists of three phases: (1) an active growth phase called anagen; (2) a regression phase called catagens; and (3) a resting phase known as telogen. The length of time spent in each phase varies with ethnicity and the length of time spent in anagen determines the length of the hair. Anagen normally lasts from two to six years, telogen lasts approximately three months, and catagen lasts about three weeks. Some 85 percent of all hair follicles are in anagen, and 15 percent in telogen. Disruption of the hair cycle often results in alopecia or hair loss.

There are two types of alopecia: nonscarring in which hair loss occurs without scarring of the scalp, and scarring in which hair loss occurs with scarring. Some types of nonscarring alopecia occur as a secondary consequence of particular disorders or diseases. For example, nutritional deficiencies, in particular a lack of iron, can cause alopecia, as can an underactive thyroid gland (hypothyroidism), or syphilis. Other types of nonscarring alopecia include alopecia areata (AA), androgenic alopecia (AGA), telogen effluvium, anagen effluvium, traction alopecia, trichotillomania, and monilethrix. AA occurs when immune cells infiltrate the hair follicle, disrupt the hair cycle and cause programmed cell death of the hair follicle leading to hair loss and smooth, bald skin. Studies of inheritance patterns strongly argue for a genetic component to AA. AGA or male/female pattern hair loss involves the miniaturization of the hair follicle as a consequence of transforming the hair from terminal hair to vellus hair. The conversion of the circulating hormone testosterone into a derivative known as dihydrotestosterone or DHT in the hair follicle drives this miniaturization. AGA affects up to 70 percent of men and 40 percent of women in mid-adult life. Inheritance also plays a prominent role in AGA. Telogen effluvium results from physiological stresses such as high fever, severe illness, and drug-induced hair loss. These conditions cause anagen to prematurely stop growing and enter catagen; however, instead of renewing anagen the hair is shed. Environmental insults also cause anagen effluvium, in which the hair follicles enter anagen but do not grow and stay stuck in anagen without ever growing any hair. Hair weaves and ponytails that constantly pull on the hair can cause traction alopecia. Trichotillomania refers to the behavior of pulling one's hair out. Monilethrix results from inherited mutations in genes (KRT81, KRT83, or LFT86) that encode hair structural proteins known as keratins. The hair has a beads-on-a-string appearance and is also fragile.

Scarring or cicatricial alopecia results from inflammation of the hair follicle caused either by an autoimmune response against the hair follicle or by infection of the hair follicle by either fungi (tinea capitis) or bacteria (acne necrotica, folliculitis decalvans). Autoimmune diseases that cause hair loss include discoid systemic lupus erythematosis, dermatomyositis, and scleroderma. Lichen planopilaris results from abnormalities in fatty acid metabolism that causes a toxic buildup of fatty acids in the hair follicle that damage it, initiate inflammation, and cause hair loss. Central centrifugal cictricial alopecia causes a band of hair loss down the center of the scalp, and occurs most commonly in Black females. It seems to result from a combination of particular hair care practices and an inherited propensity for hair follicle inflammation. Perifolliculitis capitis abscedens et suffodiens or dissecting cellulitis mainly occurs in Black men. Obstruction of the hair follicle causes inflammation and painful nodules on the scalp. Bacterial infection of the hair follicle plays a role in hair loss, but it is unclear if infection causes the condition or it occurs secondarily. Brocq pseudopelade causes scarring alopecia, but its cause remains unknown.

Particular drugs can also cause alopecia (see Table 1), as can cancer. Alopecia mucinosa, for example, results from cancers of particular white blood cells called T-lymphocyte (T-cell lymphomas).

Table 1. Medications that Cause Alopecia

Treatment and Therapy

Alopecia remains a difficult condition to treat. Early intervention works best for both scarring and nonscarring alopecia. For nonscarring alopecia, oral finasteride, topical minoxidil, and injections of bimatoprost have shown some efficacy with some patients, but they must be used indefinitely and may lose effectiveness over time. Patient education and changes in hair care practices can reduce hair loss in people with traction alopecia. Trichotillomania may require psychiatric intervention, but some studies have shown that oral N-acetylcysteine reduces this compulsive behavior.

For scarring alopecia, treatments vary from one condition to the next. For autoimmune diseases that cause alopecia, drugs that suppress the immune response plus retinoids to promote skin health are typically used. For infectious types of scarring alopecia, oral antibiotics and topical corticosteroids help resolve these conditions, but the exact drug combinations vary according to each disease (see Table 2).

Table 2. Treatment of Scarring Alopecia

For alopecia mucinosa, the underlying cancer must be addressed.

Perspective and Prospects

The ancient Greek physician Hippocrates (460 BCE–379 BCE) originally called alopecia “Fox's disease” ("alopex" is classical Greek for "fox"). Centuries later in 30 CE, the great Roman scholar Cornelius Celsus described different types of alopecia. For many years no one had any idea what caused alopecia, but some proposed that parasite infestations caused it while others attributed hair loss to nervous conditions. Then in 1942, J. B. Hamilton demonstrated the link between the hormone testosterone and alopecia.

Hair transplantation procedures constitute the most permanent treatment for alopecia. Hair transplantation uses small patches of hair-bearing scalp and transplants them to a bald or thinning area. The number of grafts required to get proper coverage depends on the size of the grafts; minigrafts contain two to four hair follicles, micrografts, one to two hair follicles, slit graphs, which are inserted into slits created in the scalp, about four to ten hair follicles, and the long and thin strip graphs, about thirty to forty. Achieving satisfactory coverage usually requires several surgical sessions, and it usually takes about two years to see the final result.

Research studies on the causes of alopecia have been ongoing in the twenty-first century. One area of focus has been genetics, as scientists have worked to identify the disease genes found in those with alopecia in order to better understand the causes of the disease. Scientists have also researched how environmental factors, such as diet, stress, or microbes found in the human body, affect the disease. New treatments have also been investigated. Ongoing clinical trials during the 2020s included those testing a class of drugs called Janus kinase inhibitors, which can be taken orally or applied topically, and biologic response modifiers, a type of medication that has proven effective in decreasing inflammatory molecules in the hair follicles.

Bibliography

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Banka, Nusrat, Kristine Bunagan, and Jerry Shapiro. "Pattern Hair Loss in Men: Diagnosis and Medical Treatment." Dermatologic Clinics 31.1 (2013): 129–40. Print.

Breitkopf, Trisia, Gigi Leung, Mei Yu, Eddy Wang, and Kevin J. McElwee. “The Basic Science of Hair Biology: What Are the Causal Mechanisms for the Disordered Hair Follicle.” Dermatologic Clinics 31 (2013): 1–19. Print.

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Yamao, M., et al. "Restorative Effect of Hair Follicular Dermal Cells on Injured Human Hair Follicles in a Mouse Model." Experimental Dermatology 24.3 (2015): 225–27. Print.