Similar to the skin, hair forms by rapid division and differentiation of stem cells which form keratinocytes that migrate, flatten, and die, forming keratinized cells. The final hair product that is exposed on the surface of the skin will be composed entirely of keratin. The growth of the hair follicle is cyclical. Stages of rapid growth and elongation of the hair shaft alternate with periods of quiescence and regression driven by apoptotic signals. This cycle can be divided into three phases: anagen (growth), catagen (transition), and telogen (rest).

Anagen growth is the active phase in which the hair follicle takes on its onion-like shape and works to produce the hair fiber. The anagen phase can be further broken down into proanagen and metanagen phases.

Proanagen sees the follicle proliferating hair progenitor cells and begins the process of differentiation.

The new hair shaft appears on the surface of the skin to mark the metanagen phase. The anagen phase as a whole can last for several years.

The catagen phase begins with the end of the anagen phase and is characterized by a transition into quiescence. During this phase, which can last a few weeks, the hair follicle undergoes apoptosis-driven regression and loses about one-sixth of its standard diameter. The formation of a club hair, an important prognostic indicator in assessing hair pathology, also occurs at this time. If many hairs form club hair at once and are subsequently shed, it can give the appearance of thinning. Some conditions that this may occur in include, but are not limited to hypothyroidism, hyperthyroidism, stress, vitamin deficiencies, and after childbirth.  

Next is the telogen or resting phase of the hair cycle in which the hair follicle is dormant, and growth of the hair shaft does not occur. About 10% to 15% of all hairs on the body are in this resting phase at any given time and can remain in this state for a variable amount of time depending on the location of the hair - from a few weeks for eyelashes to nearly one year in scalp hair. The exact mechanism that controls passage from one phase into the next is not fully known.

The bulge activation theory posits that growth factors produced in the dermal papilla stimulate bulge stem cells to proliferate and modulate growth-phase transitions. Because these cells are transient amplifying cells, they only can go through a limited number of mitoses, thereby setting the duration of anagen and onset of catagen phases. 

The hair follicle and its product are also one of the few areas of the body protected from immune surveillance in a phenomenon first described by Sir Peter Medawar in 1948 as an immune privilege (IP). IP is achieved via a number of major histocompatibility complex by the follicle, local production of immune modulators such as TGF-beta, and expression of Fas-Ligand to kill autoreactive T cells. Hair growth also is controlled by a number of hormonal signals, with androgens having the most prominent effect. The growth of hair on the face, trunk and extremities in the male and of axillary and pubic hair in both sexes is brought about by androgens, although with considerable ethnic variability: Chinese men, for example, exhibit less body hair than those from Europe. [1][2][3]

Hair has many areas of clinical significance which include diseases of hair loss, excess, alterations due to nutritional deficiencies, infectious causes, and effects of drug reactions.

The unwanted loss of hair, known as alopecia, is a widespread condition affecting both sexes, occurring in numerous patterns, and classified into non-scarring and scarring (cicatricial) subtypes.

The most common non-scarring type of alopecia is androgenetic or “pattern” hair loss which develops due to a combination of genetic predisposition and the action of androgen on hair follicles. While men commonly are associated with this condition, women can be affected as well and exhibit their own characteristic pattern. The hair loss typically begins in both temples and recedes to form an “M” shape.

This is not to be confused with traction alopecia which is seen in people who wear their hair and tight braids and ponytails. 

Alopecia areata is patchy hair loss, usually on the scalp, which often has the characteristic “exclamation point” hairs that are short and broken and appear to be floating exclamation marks. Alopecia totalis and universalis are the most severe forms of alopecia. Alopecia totalis eradicates all terminal scalp hairs alopecia universalis eradicates all body hairs. Former NBA athlete Charlie Villanueva displays this pattern of alopecia.

Scarring alopecia can arise from cutaneous manifestations of lupus or a bacterial inflammatory condition known as dissecting folliculitis. These patterns of alopecia exhibit patches of shiny, bare skin and result in permanent hair loss in the affected areas. 

Telogen Effluvium is when hair roots are pushed into the telogen resting phase. This usually occurs after some stress and can be acute or chronic.

A proliferation of fine lanugo hairs past the neonatal period can be a symptom of malnutrition and aid in the diagnosis of anorexia nervosa. Hair loss can also be due to an infection, like tinea capitis, a fungal infection that results in a patch of hair loss on the scalp. A kerion, fungal abscess, can sometimes form and also result in hair loss most commonly on the scalp and sometimes on the face, torso, and extremities. Hair transplantation has become a therapeutic option for those who fail to have hair growth with medication.

Excess hair or hair in abnormal locations is known as hypertrichosis. Hypertrichosis can be seen in the setting of porphyria cutanea tarda, where people experience photosensitivity blistering, and hypertrichosis. It can develop as an inherited condition or a drug reaction, for example after the use of phenytoin, cyclosporine, and minoxidil. [5][6][7][8][9][10][11][12][13][14][15]