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Physiology, Hair

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Last Update: July 26, 2021.


Hair is a component of the integumentary system and extends downward into the dermal layer where it sits in the hair follicle. The presence of hair is a primary differentiator of mammals as a unique class of organisms. In humans, it is a cherished and highly visible indicator of health, youth, and even class. It has a sensory function, protects from cold and UV radiation, and can have a significant psychological impact when its growth or structure is deranged. At a microscopic level, the variety in length, color, diameter, and cross-sectional shape of each hair creates the characteristic profiles seen across ethnic groups and among individuals. This article will discuss the physiology of hair, cellular components, mechanisms of growth and differentiation, and its clinical significance. [1][2][3]


Each hair is made up of two separate structures:

The hair shaft, which comprises the visible part outside of the skin.

The follicle which lies underneath the surface of the skin.

  • Inner root sheath
  • Outer root sheath

Hair is also made both of living and non-living components below and above the level of the epidermis. Above the level of the epidermis, the hair shaft is a thin, flexible cylinder of non-living, keratinized epithelial cells. Below, it is part of a living hair follicle which enlarges at the base and forms the hair bulb.

The hair shaft is made up of a cortex, surrounding cuticle cells, and sometimes a central medulla which is found in thicker hair. The bulk of this hair fiber belongs to the cortical layer which plays an important role in determining the physical and mechanical properties of the hair, such as strength, texture, and color. It is composed predominantly of macrofibrils, which are rods of microfibrils meshed together in a matrix.

The follicle is the primary structure from which hair can grow. The histological arrangement of the follicle is divided into outer and inner root sheaths.

The outer root sheath (ORS) has been recognized as a ready supply of multipotent stem cells which differentiate into several cell types including melanocytes and keratinocytes. More specifically,                 these stem cells are thought to reside in a distinct bulge area located between the insertion of the arrector pili muscle and the ductal opening of the sebaceous gland.

The inner root sheath (IRS) consists of the Henle layer, the Huxley layer, and the previously mentioned cuticle layer which also helps affix the growing hair shaft to the follicle, a task bolstered by the production of keratins and trichohyalin by the IRS cells. The cuticle is made up of flat overlapping cells that cover the hair shaft from the root until it exits from the epidermis. The cuticle is of considerable cosmetic importance as it is responsible for lending the hair an untangled appearance and shape.

The hair bulb is the region of the follicle which actively produces hair. It extends into the dermal layer of the skin and surrounds the dermal papilla, an important structure derived from mesenchyme, made of rich stroma, associated nerve fibers, and a loop of the capillary that supplies nutrients. The papilla is believed to be a primary orchestrator in the hair growth process, conducting the precise signals that determine the size and color of the hair shaft via a complex mix of essential growth factors including insulin-like growth factor, stem cell factor, keratinocyte growth factor, and bone morphogenetic protein. The hair bulb itself is divided into two regions by the Auber line. Below this line, cells are still undergoing differentiation. The immature cells below the Auber line comprise the germination center or matrix of the follicle where all cells are mitotically active and move in an upward direction where they enlarge, elongate vertically, and integrate into the hair shaft. 

Nerve supply to the hair follicles is similar to that of the surrounding network of dermal nerves in that it is composed of both sensory afferents and autonomic sympathetic nerves. Sensory information from hair stimulation enhances tactile ability. Autonomic nervous innervation primarily provides control of the arrector pili muscle. Contraction of these tiny muscles makes the hair “stand on end.” This is likely a vestigial function related to fur; erecting the shafts served to trap air and conserve heat in cold climates as well as cut a larger silhouette in an attempt to intimidate rivals or would-be predators.

Vascular supply is provided by small arterioles originating in the subcutaneous fat. The vessels are responsible for nourishing the hair follicle by delivering oxygen and nutrients, eliminating waste, and promoting growth. Subtle hair loss on the lower extremities can sometimes hint at the underlying peripheral arterial disease.

Hair that is darker and visible to the human is called terminal hair. Areas of the body that appear to be hairless, but have shorter, finer hairs that lack the medulla layer are called vellus hair. Neonates can be born with lanugo hair, fine hairs that get shed in utero or within the first weeks of life. Club hair is fully keratinized hair that is fully formed in the telogen stage of the hair cycle. The only parts of the external surface of the body that are truly hairless are the palms and soles of the hands and feet, lips, labia minora, and glans penis. [1][2][3][4]


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]

Clinical Significance

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]

Review Questions


Ocampo-Garza J, Griggs J, Tosti A. New drugs under investigation for the treatment of alopecias. Expert Opin Investig Drugs. 2019 Mar;28(3):275-284. [PubMed: 30642204]
Juhász MLW, Atanaskova Mesinkovska N. The use of phosphodiesterase inhibitors for the treatment of alopecia. J Dermatolog Treat. 2020 May;31(3):245-253. [PubMed: 30935254]
Breehl L, Caban O. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Apr 21, 2021. Physiology, Puberty. [PubMed: 30521248]
Martel JL, Miao JH, Badri T. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 26, 2021. Anatomy, Hair Follicle. [PubMed: 29261946]
Fernandez-Flores A, Saeb-Lima M, Cassarino DS. Histopathology of aging of the hair follicle. J Cutan Pathol. 2019 Jul;46(7):508-519. [PubMed: 30932205]
Ho A, Shapiro J. Medical therapy for frontal fibrosing alopecia: A review and clinical approach. J Am Acad Dermatol. 2019 Aug;81(2):568-580. [PubMed: 30953702]
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Saleh D, Yarrarapu SNS, Cook C. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 23, 2021. Hypertrichosis. [PubMed: 30521275]
Vinay K, Sawatkar GU, Dogra S. Hair manifestations of endocrine diseases: A brief review. Indian J Dermatol Venereol Leprol. 2018 Sep-Oct;84(5):528-538. [PubMed: 30027913]
Kawada T. Comment on "Association of alopecia areata with hospitalization for mental health disorders in US adults". J Am Acad Dermatol. 2019 Nov;81(5):e143. [PubMed: 31344378]
Cranwell W, Sinclair R. Common causes of paediatric alopecia. Aust J Gen Pract. 2018 Oct;47(10):692-696. [PubMed: 31195774]
Gamret AC, Potluri VS, Krishnamurthy K, Fertig RM. Frontal fibrosing alopecia: efficacy of treatment modalities. Int J Womens Health. 2019;11:273-285. [PMC free article: PMC6500869] [PubMed: 31118828]
Garg AK, Garg S. Donor Harvesting: Follicular Unit Excision. J Cutan Aesthet Surg. 2018 Oct-Dec;11(4):195-201. [PMC free article: PMC6371717] [PubMed: 30886473]
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