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Hair follicle
Hair follicle
Hair follicle
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Hair follicle
Hair follicle
A photograph of hair on a human arm emerging from follicles
Details
SystemIntegumentary system
ArterySupratrochlear, supraorbital, superficial temporal, occipital
VeinSuperficial temporal, posterior auricular, occipital
NerveSupratrochlear, supraorbital, greater occipital, lesser occipital
LymphOccipital, mastoid
Identifiers
Latinfolliculus pili
MeSHD018859
TA98A16.0.00.023
TA27064
THH3.12.00.3.01034
FMA70660
Anatomical terminology

The hair follicle is an organ found in mammalian skin.[1] It resides in the dermal layer of the skin and is made up of 20 different cell types, each with distinct functions. The hair follicle regulates hair growth via a complex interaction between hormones, neuropeptides, and immune cells.[1] This complex interaction induces the hair follicle to produce different types of hair as seen on different parts of the body. For example, terminal hairs grow on the scalp and lanugo hairs are seen covering the bodies of fetuses in the uterus and in some newborn babies.[1] The process of hair growth occurs in distinct sequential stages: anagen is the active growth phase, catagen is the regression of the hair follicle phase, telogen is the resting stage, exogen is the active shedding of hair phase and kenogen is the phase between the empty hair follicle and the growth of new hair.[1]

The function of hair in humans has long been a subject of interest and continues to be an important topic in society, developmental biology and medicine. Of all mammals, humans have the longest growth phase of scalp hair compared to hair growth on other parts of the body.[1] For centuries, humans have ascribed esthetics to scalp hair styling and dressing and it is often used to communicate social or cultural norms in societies. In addition to its role in defining human appearance, scalp hair also provides protection from UV sun rays and is an insulator against extremes of hot and cold temperatures.[1] Differences in the shape of the scalp hair follicle determine the observed ethnic differences in scalp hair appearance, length and texture.

There are many human diseases in which abnormalities in hair appearance, texture or growth are early signs of local disease of the hair follicle or systemic illness. Well known diseases of the hair follicle include alopecia[2] or hair loss, hirsutism or excess hair growth and lupus erythematosus.[3][2]

Structure

[edit]
Structure of a hair follicle.

The position and distribution of hair follicles varies over the body. For example, the skin of the palms and soles does not have hair follicles whereas skin of the scalp, forearms, legs and genitalia has abundant hair follicles.[1] There are many structures that make up the hair follicle. Anatomically, the triad of hair follicle, sebaceous gland and arrector pili muscle make up the pilosebaceous unit.[1]

A hair follicle consists of :

  • The papilla is a large structure at the base of the hair follicle.[4] The papilla is made up mainly of connective tissue and a capillary loop. Cell division in the papilla is either rare or non-existent.[contradictory]
  • Around the papilla is the hair matrix.
  • A root sheath composed of an external and internal root sheath. The external root sheath appears empty with cuboid cells when stained with H&E stain. The internal root sheath is composed of three layers, Henle's layer, Huxley's layer, and an internal cuticle that is continuous with the outermost layer of the hair fiber.
  • The bulge is located in the outer root sheath at the insertion point of the arrector pili muscle. It houses several types of stem cells, which supply the entire hair follicle with new cells, and take part in healing the epidermis after a wound.[5][6] Stem cells express the marker LGR5+ in vivo.[7]

Other structures associated with the hair follicle include the cup in which the follicle grows known as the infundibulum,[8] the arrector pili muscles, the sebaceous glands, and the apocrine sweat glands. Hair follicle receptors sense the position of the hair.

Attached to the follicle is a tiny bundle of muscle fiber called the arrector pili. This muscle is responsible for causing the follicle lissis to become more perpendicular to the surface of the skin, and causing the follicle to protrude slightly above the surrounding skin (piloerection) and a pore encased with skin oil. This process results in goose bumps (or goose flesh).

Also attached to the follicle is a sebaceous gland, which produces the oily or waxy substance sebum. The higher the density of the hair, the more sebaceous glands that are found.

Variation

[edit]

There are racial differences in several different hair characteristics. The differences in appearance and texture of hair are due to many factors: the position of the hair bulb relative to the hair follicle, size and shape of the dermal papilla, and the curvature of the hair follicle.[1] The scalp hair follicle in people of European descent is elliptical in shape and, therefore, produces straight or wavy hair, whereas the scalp hair follicle of people of African descent is more curvy, resulting in the growth of tightly curled hair.[1]

Terminal Scalp Hair Characteristics by Race [1]
Race diameter

(micrometers)

cross-sectional shape appearance
Blonde-haired white 40–80 elliptical straight or wavy
Dark brown/black haired/red haired white 50–90 elliptical straight or wavy
Black 60–100 elliptical and ribbon-like curly
Asian 80–100 circular straight
Terminal Scalp Hair Characteristics by Taxon [9][10]
Animal diameter

(micrometers)

cross-sectional shape appearance
Chimpanzee 101-113 circular straight
Orangutan 140-170 circular straight
Buffalo 110 circular straight

Development

[edit]

In utero, the epithelium and underlying mesenchyme interact to form hair follicles.[11][12]

Aging

[edit]

A key aspect of hair loss with age is the aging of the hair follicle. Ordinarily, hair follicle renewal is maintained by the stem cells associated with each follicle. Aging of the hair follicle appears to be primed by a sustained cellular response to the DNA damage that accumulates in renewing stem cells during aging.[13] This damage response involves the proteolysis of type XVII collagen by neutrophil elastase in response to the DNA damage in the hair follicle stem cells. Proteolysis of collagen leads to elimination of the damaged cells and then to terminal hair follicle miniaturization.

Hair growth

[edit]
Hair-follicle cycling
Hair follicle
See also: Human hair growth

Hair grows in cycles of various phases:[14] anagen is the growth phase; catagen is the involuting or regressing phase; and telogen, the resting or quiescent phase (names derived using the Greek prefixes ana-, kata-, and telos- meaning up, down, and end respectively). Each phase has several morphologically and histologically distinguishable sub-phases. Prior to the start of cycling is a phase of follicular morphogenesis (formation of the follicle). There is also a shedding phase, or exogen, that is independent of anagen and telogen in which one or several hairs that might arise from a single follicle exits. Normally up to 85% of the hair follicles are in anagen phase, while 10–14% are in telogen and 1–2% in catagen. The cycle's length varies on different parts of the body. For eyebrows, the cycle is completed in around 4 months, while it takes the scalp 3–4 years to finish; this is the reason eyebrow hair have a much shorter length limit compared to hair on the head. Growth cycles are controlled by a chemical signal like epidermal growth factor. DLX3 is a crucial regulator of hair follicle differentiation and cycling.[15][16]

Anagen phase

[edit]

Anagen is the active growth phase of hair follicles[17] during which the root of the hair is dividing rapidly, adding to the hair shaft. During this phase the hair grows about 1 cm every 28 days. A hair pulled out in this phase will typically have the root sheath attached to it which appears as a clear gel coating the first few mm of the hair from its base; this may be misidentified as the follicle, the root or the sebaceous gland by non-health care professionals. Scalp hair stays in this active phase of growth for 2–7 years; this period is genetically determined. At the end of the anagen phase an unknown signal causes the follicle to go into the catagen phase.

Catagen phase

[edit]

The catagen phase is a short transition stage that occurs at the end of the anagen phase.[18] It signals the end of the active growth of a hair. This phase lasts for about 2–3 weeks while the hair converts to a club hair, which is formed during the catagen phase when the part of the hair follicle in contact with the lower portion of the hair becomes attached to the hair shaft. A bulb of keratin attaches to the bottom tip of the hair and keeps it in place while a new hair begins to grow below it. A hair pulled out in this phase will have the bulb of keratin attached to it which appears as a small white ball on the end of the hair. This process cuts the hair off from its blood supply and from the cells that produce new hair. When a club hair is completely formed, about a 2-week process, the hair follicle enters the telogen phase.

Telogen phase

[edit]

The telogen phase is the resting phase of the hair follicle, about three months.[19] When the body is subjected to extreme stress, as much as 70 percent of hair can prematurely enter the telogen phase and begin to fall, causing a noticeable loss of hair. This condition is called telogen effluvium.[20] The club hair is the final product of a hair follicle in the telogen stage, and is a dead, fully keratinized hair.[11] Fifty to one-hundred club hairs are shed daily from a normal scalp.[11]

Timeline

[edit]
  • Scalp: The time these phases last varies from person to person. Different hair color and follicle shape affects the timings of these phases.
    • Anagen phase, 2–8 years (occasionally much longer)
    • Catagen phase, 2–3 weeks
    • Telogen phase, around 3 months
  • Eyebrows:
    • Anagen phase, 4–7 months
    • Catagen phase, 3–4 weeks
    • Telogen phase, about 9 months

Clinical significance

[edit]

Disease

[edit]

There are many human diseases in which abnormalities in hair appearance, texture or growth are early signs of local disease of the hair follicle or systemic illness. Well known diseases of the hair follicle include alopecia or hair loss, hirsutism or excess hair growth, and lupus erythematosus.[3] Therefore, understanding the function of the normal hair follicle is fundamental to diagnosing and treating many dermatologic and systemic diseases with hair abnormalities.[3] Studies of Witka et al. 2020 has shown the role of microbiome in the biology, immunology and diseases of scalp hair follicle. Studies further shown that change in hair follicle microbiome result into scalp disease like; Seborrheic dermatitis of the scalp and dandruff, Folliculitis decalvans, Androgenetic alopecia, Scalp psoriasis and Alopecia areata.[21]

Hair restoration

[edit]

Hair follicles form the basis of the two primary methods of hair transplantation in hair restoration, Follicular Unit Transplantation (FUT) and follicular unit extraction (FUE). In each of these methods, naturally occurring groupings of one to four hairs, called follicular units, are extracted from the hair restoration patient and then surgically implanted in the balding area of the patient's scalp, known as the recipient area. These follicles are extracted from donor areas of the scalp, or other parts of the body, which are typically resistant to the miniaturization effects of the hormone DHT. It is this miniaturization of the hair shaft that is the primary predictive indicator of androgenetic alopecia,[22] commonly referred to as male pattern baldness or male hair loss. When these DHT-resistant follicles are transplanted to the recipient area, they continue to grow hair in the normal hair cycle, thus providing the hair restoration patient with permanent, naturally-growing hair.

While hair transplantation dates back to the 1950s,[23] and plucked human hair follicle cell culture in vitro to the early 1980s,[24] it was not until 1995 when hair transplantation using individual follicular units was introduced into medical literature.[25]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Hair follicle

View on Grokipedia
from Grokipedia
The hair follicle is a dynamic, tube-shaped of the that extends into the and sometimes the subcutaneous layer, forming a pocket that produces, nourishes, and anchors a strand of throughout its growth cycle. It consists of key components including the hair bulb at the base, which houses the dermal papilla responsible for nutrient supply, the inner and outer root sheaths that guide shaft formation, and the infundibulum at the surface opening. Embedded in mammalian as a specialized , the follicle not only generates the hair shaft but also facilitates essential responses such as , pigmentation, and immune surveillance. Hair follicles undergo a cyclical process of growth divided into three main phases: the anagen phase of active proliferation lasting 2–7 years, the brief catagen phase of regression, and the telogen phase of rest up to 4 months, ensuring continuous hair renewal. This cycling is regulated by intricate molecular signaling involving ectodermal-mesodermal interactions, with the dermal papilla acting as a central orchestrator of activation and differentiation. Beyond hair production, follicles contribute to , mechanosensory functions, and barrier protection against environmental pathogens, highlighting their role as multifunctional miniorgans. Human skin contains approximately 5 million hair follicles, distributed variably across the body with higher densities on the and sparse vellus hairs elsewhere, originating from embryonic around the 9th week of . Disruptions in follicle structure or cycling can lead to conditions like alopecia, underscoring their clinical significance in .

Anatomy

Components

The hair follicle is a dynamic, tubular structure invaginating from the into the , comprising epithelial and mesenchymal elements separated by a . It forms the pilosebaceous unit, which includes the follicle proper, associated , and . The follicle is anatomically divided into three segments: the infundibulum (uppermost portion opening to the skin surface), the (middle constricted region), and the inferior segment (lower bulbous area). These segments exhibit distinct histological features, with the infundibulum lined by continuous with the interfollicular , the featuring a thicker outer root sheath, and the inferior segment containing proliferative matrix cells. Central to the follicle is the hair shaft, the visible keratinized filament produced by the follicle, consisting of three concentric layers: the medulla (central core of soft, loosely packed cells, often absent in finer hairs), the cortex (bulk of the shaft, providing strength and elasticity through tightly packed keratin filaments), and the cuticle (outer overlapping scales of flattened cells that seal and protect the shaft). Emerging from the base, the hair shaft is guided upward by the inner root sheath (IRS), a transient structure derived from epithelial matrix cells that encases the shaft and degrades as the hair emerges; the IRS comprises three layers—Henle's layer (innermost, cornified cells), Huxley's layer (middle, nucleated cells with trichohyalin granules), and the IRS cuticle (outer scales interlocking with the hair cuticle). Enveloping the IRS is the outer root sheath (ORS), a multilayered epithelium continuous with the basal layer of the epidermis, extending from the infundibulum to the follicle base and serving as a reservoir for stem cells. At the follicle's deepest point resides the hair bulb, a bulbous expansion of the inferior segment housing the germinal matrix—a population of rapidly proliferating that differentiate into the hair shaft and IRS during the growth phase. Within the concave base of the bulb sits the dermal papilla (DP), a specialized aggregate of mesenchymal fibroblasts and that acts as an inductive signaling center, regulating matrix and differentiation through paracrine factors. The bulge region, located in the upper near the arrector pili insertion, is a focal thickening of the ORS enriched with slow-cycling stem cells that contribute to follicle renewal. Supporting structures include the , a band of smooth muscle fibers extending from the dermal papilla to the bulge, enabling piloerection by contracting under sympathetic innervation to tilt the follicle and erect the hair shaft. The sebaceous gland, an acinar gland, ducts into the infundibulum and secretes sebum—a lipid-rich mixture that coats the hair and skin for lubrication and barrier function. In axillary and pubic regions, follicles associate with apocrine glands, which release their secretions into the infundibulum alongside sebum. Cellularly, the epithelial components—shaft, IRS, and ORS—are dominated by keratinocytes, which undergo programmed differentiation to produce keratins and structural proteins; these cells express specific keratins (e.g., K14/K5 in the basal ORS, hard keratins in the cortex). Melanocytes populate the upper , transferring granules to matrix keratinocytes for hair pigmentation. The DP comprises fibroblasts embedded in a collagen-rich matrix, expressing growth factors like VEGF and BMPs to orchestrate epithelial-mesenchymal interactions. Morphometrically, a typical scalp hair follicle measures about 4.16 mm in total length, with the infundibulum spanning 0.76 mm, the 0.89 mm, and the inferior segment 2.5 mm; shaft diameters vary by hair type, with terminal scalp hairs averaging 60–100 μm and vellus hairs under 30 μm.

Variations

Hair follicles exhibit significant variations across different body sites, reflecting adaptations to specific physiological needs. follicles are typically larger and produce terminal hairs with thicker shafts, capable of extended growth phases compared to those on other body regions. In contrast, body hair follicles generate finer, shorter hairs with more abbreviated cycles, often resulting in vellus hairs that are thin, unpigmented, and lack a medulla, covering areas like the face and limbs in a barely visible manner. During fetal development, follicles initially produce hairs, which are fine, downy, and cover the body but are shed shortly after birth, giving way to vellus and terminal hairs. Terminal hairs, characterized by their coarse texture, , and pigmentation, predominate in androgen-sensitive areas such as the , axillae, and pubic regions, while vellus hairs persist in less responsive sites. These distinctions arise from differences in follicle size, depth, and hormonal responsiveness. The shape of the hair follicle cross-section determines hair texture, with round follicles producing straight hair and asymmetrical or oval ones yielding wavy, curly, or kinky types due to uneven emergence and internal cellular asymmetries. Curly hair follicles, for instance, curve in multiple directions, leading to elliptical shafts with greater bonding asymmetry. Across species, hair follicles differ markedly from those in other mammals; scalp hair grows in independent, asynchronous cycles without seasonal synchronization, unlike the more uniform molting in many animals. In , vibrissae () feature specialized follicles that are larger, with blood-filled sinuses and dense neural innervation for tactile sensing, contrasting the simpler structure of human pelage follicles. Genetic factors, including polymorphisms in genes regulating follicle and sensitivity, influence hair , with scalp follicles typically numbering 150–200 per square centimeter in adults. Genome-wide association studies have identified variants affecting variations across populations, underscoring in follicle distribution. Sexual dimorphism is evident in facial hair, where male beard follicles activate post-puberty under androgen influence, developing into prominent terminal hairs absent in females due to lower testosterone levels and differing receptor densities. This pattern highlights follicle responsiveness to sex hormones, with minimal expression in pre-pubertal individuals of both sexes.

Development

Embryonic formation

The formation of hair follicles begins during around 8 to 12 weeks of , marking the initiation of epithelial-mesenchymal interactions that drive . Primary hair follicles, which give rise to the initial hairs covering the , emerge first in distinct waves starting on the and face, while secondary follicles develop later to form the denser vellus and arrays. By approximately 14 to 20 weeks, these processes extend across the body, establishing the foundational density and distribution of follicles before birth. This arises from reciprocal signaling between the ectodermal and mesodermal , where the thickens to form a placode—an early epidermal —over a condensing aggregate of dermal fibroblasts that precursors the dermal papilla. The placode subsequently induces downgrowth of the epithelial germ cells into the , elongating to shape the nascent follicle bulb and sheath, while mesenchymal cells migrate to envelop the growing structure, ensuring proper polarity and stratification. These dynamic interactions pattern follicle orientation and spacing, preventing overlap through inhibitory signals that regulate initiation sites. Key molecular pathways orchestrate these events: the Wnt/β-catenin pathway activates in the placode to induce follicle specification and dermal condensation, with its disruption blocking placode formation entirely. (BMP) signaling from the interfollicular inhibits ectopic follicle formation to refine patterning, while Sonic hedgehog (Shh) promotes epithelial proliferation and downgrowth in the emerging bud. (FGF) ligands, particularly FGF7 and FGF10 from the , further drive epidermal proliferation and germ elongation, sustaining the morphogenetic progression. As morphogenesis completes by late gestation, follicles transition into their inaugural growth cycle, entering the anagen phase in utero to produce the lanugo coat visible at birth, thereby linking embryonic patterning to postnatal hair dynamics.

Stem cells and regeneration

Hair follicle stem cells (HFSCs) reside primarily in the bulge region of the follicle, where K15+ slow-cycling cells maintain quiescence and self-renewal, serving as a reservoir for tissue homeostasis. These bulge cells, marked by keratin 15 (K15), exhibit multipotency and contribute to all epithelial lineages during the hair cycle. Adjacent to the bulge, hair germ cells act as progenitor-like intermediates, rapidly proliferating to initiate anagen and bridging the slow-cycling bulge population to the actively growing matrix. In the lower follicle, Lgr5+ matrix cells function as transient amplifying progenitors during anagen, undergoing multiple divisions to produce the differentiated hair shaft before depleting and re-entering quiescence. Regeneration of hair follicles involves HFSC activation, particularly during , where bulge-derived cells migrate and form new follicles through wound-induced hair neogenesis (WIHN), a process conserved in select mammals but limited in adult humans. De novo follicle formation occurs robustly in embryonic development but is restricted in adults to sites, relying on epithelial-mesenchymal interactions to recapitulate . Recent advances highlight microRNA-205 (miR-205) as a key regulator, where its upregulation reduces actomyosin contractility in aged HFSCs, promoting bulge activation and regrowth in models. Similarly, Wnt agonists enhance β-catenin signaling to reactivate quiescent HFSCs, optimizing tissue mechanics for regeneration as demonstrated in 2025 studies on epidermal mechanotransduction. Recent research has shown that hair follicle stem cells can adapt to nutrient stress, such as dietary restriction of serine, by prioritizing skin repair over hair growth during wound healing, as observed in mouse models. For details on this functional adaptability and therapeutic implications, see the Physiology section. Biomaterials have advanced follicle neogenesis by providing scaffolds that mimic the , supporting HFSC engraftment and differentiation. Hydrogel-based scaffolds, such as matrices co-embedded with skin-derived precursors, promote de novo hair formation by sustaining progenitor proliferation . Recent techniques utilize gelatin-alginate hydrogels to fabricate multilayer constructs that replicate follicle architecture, enabling vascularized equivalents with functional hair germs. In 2023 innovations, multicomponent hydrogels incorporating and ions activate HFSCs within bioprinted scaffolds, enhancing neovascularization and hair shaft production in preclinical models. Aging impairs HFSC function through progressive exhaustion, where cells escape the bulge niche into the , leading to depleted reservoirs and shortened hair cycle durations. This exhaustion manifests as reduced regenerative capacity, with fewer anagen initiations and follicle miniaturization over time. The (SASP) from aging dermal cells exacerbates this by secreting pro-inflammatory factors that induce neighboring HFSC , disrupting niche signaling and accelerating depletion. Hair follicles can remain dormant for years, or potentially decades, without fully dying or undergoing complete atrophy or replacement by scar tissue or fibrosis. Studies on androgenetic alopecia demonstrate that hair follicle stem cells often persist even in long-bald scalps, maintaining the structural integrity of the follicle in an inactive state with theoretical potential for reactivation through appropriate signaling or therapeutic interventions. Therapeutic strategies leverage HFSC for alopecia treatment, including transplants of bulge-derived cells to repopulate denuded scalps, though challenges like low rates persist in clinical translation. JAK inhibitors target inflammatory signals that suppress HFSC activation, promoting regrowth in by restoring and signaling, as evidenced in 2025 phase trials showing sustained hair coverage.

Physiology

Functions

Hair follicles contribute significantly to through the mechanism of piloerection, in which the arrector pili muscles contract to erect the hair shafts, thereby trapping a layer of warm air close to the skin for insulation during exposure. Associated sebaceous glands produce sebum that coats the hair and , providing to prevent heat loss in humid or wet environments. Beyond temperature control, hair follicles enable protective functions by serving as a physical barrier; the hair shaft shields underlying from ultraviolet radiation, mechanical trauma, and invading pathogens. Follicles themselves function as reservoirs for commensal microbes, fostering interactions within the microbiome that modulate local immune defenses. Hair follicles also play a key role in , with bulge stem cells migrating to the wound site to promote reepithelialization and tissue regeneration. Sensory capabilities arise from mechanoreceptors embedded in the follicular structure, which detect tactile stimuli such as touch and , often in association with Merkel cells that convert mechanical deformation into neural impulses for fine touch discrimination. Hair follicles exhibit endocrine roles, including responsiveness to androgens like , which binds to receptors in dermal papilla cells of and follicles to regulate growth and patterns. Follicular express receptors, enabling responsiveness to that regulates and hair , contributing to calcium . Evolutionarily, hair follicles evolved in mammals primarily for and protection via dense coverage, but in humans, density reduced dramatically—likely adapting to enhanced sweating for cooling—while and follicles were retained to shield against solar exposure and manage .

Hair Follicle Stem Cells in Wound Healing

Recent research has elucidated the adaptability of hair follicle stem cells in prioritizing wound healing over hair growth under conditions of nutrient stress. A 2025 study from Rockefeller University, published in Nature Cell Biology, demonstrated that restricting dietary serine—an amino acid found in common foods—triggers these stem cells in mice to shift metabolic pathways, enhancing their stress response and accelerating skin repair. In experimental findings using mouse models with induced skin wounds, low-serine conditions led to 30-50% faster wound closure compared to controls, as the stem cells migrated more efficiently to the injury site and promoted reepithelialization without compromising hair regeneration long-term. This adaptability highlights the role of serine in modulating stem cell fate, where its limitation activates protective mechanisms that favor tissue repair during stress. The therapeutic potential of this discovery lies in developing interventions to accelerate wound healing in chronic conditions, such as diabetic ulcers, by targeting serine metabolism; however, as the findings are preclinical (based on mice), further human trials are needed to translate these results. Future directions include exploring clinical applications and understanding broader implications for stem cell-based regenerative therapies.

Growth cycle

The hair follicle undergoes a continuous cyclic process known as the hair growth cycle, which consists of three primary phases: anagen, catagen, and telogen. This cycle regulates hair production throughout life, with each follicle independently progressing through the phases, though the overall process ensures renewal of the hair shaft. The anagen phase is the active growth period, during which the hair follicle's matrix cells proliferate rapidly to elongate the hair shaft, and melanocytes produce pigment for coloration. On the , this phase typically lasts 2 to 7 years, allowing hairs to reach lengths of up to 1 meter, while approximately 85-90% of scalp follicles are in anagen at any given time. The catagen phase follows as a transitional regression stage, lasting about 2 to 3 weeks, in which ceases, the follicle detaches from its blood supply, and leads to the formation of a club-shaped . Only 1-2% of follicles are in this phase simultaneously. In the telogen phase, the follicle enters a resting state for roughly 3 months under normal conditions, during which the old hair remains anchored until shedding occurs, often coinciding with the onset of a new anagen phase in the same follicle; this shedding is termed exogen. About 10-15% of follicles are in telogen, contributing to the daily loss of 50-100 hairs under normal conditions. However, in conditions like androgenetic alopecia, follicles can remain dormant for years (or potentially decades) without fully dying or undergoing complete atrophy or replacement by scar tissue/fibrosis; studies show hair follicle stem cells often persist even in long-bald scalps, meaning the structure is intact but inactive with theoretical reactivation potential. Human scalp follicles exhibit asynchronous , forming a pattern across the skin rather than synchronized waves, unlike in some mammals; follicles also display asynchrony but with shorter cycles overall. The full cycle on the spans 4-5 years, dominated by anagen, whereas eyebrows complete a cycle in about 4 months due to a briefer anagen phase of 2-3 months. Cycle durations and phase transitions can vary with external factors such as seasonal changes, which may subtly influence growth rates, and nutritional status, where deficiencies can shift more follicles toward telogen.

Pathology

Disorders

Disorders of the hair follicle encompass a range of conditions that disrupt normal follicular structure and function, leading to hair loss or inflammation. These pathologies often involve genetic, autoimmune, infectious, or mechanical factors that alter the hair growth cycle or cause irreversible damage to the follicle. Common manifestations include non-scarring alopecias, where follicles remain intact but produce thinner or absent hair, and scarring alopecias, which result in permanent follicular destruction due to fibrosis and inflammation. Androgenetic alopecia, the most prevalent form of , involves progressive of hair follicles due to and sensitivity, affecting up to 50% of men by age 50 and a significant proportion of women. This leads to a reduction in the size of terminal hairs, transitioning them to vellus-like structures, primarily on the . In this condition, affected follicles can remain dormant for years or potentially decades without fully dying, as studies show hair follicle stem cells often persist even in long-bald scalps, maintaining the structure intact but inactive with theoretical reactivation potential. , an autoimmune condition, targets the hair follicle , causing patchy, with a lifetime prevalence of approximately 2%. In non-scarring alopecias like alopecia areata, follicles similarly retain intact stem cells, allowing for potential reactivation absent scarring. Cicatricial alopecias, such as lichen planopilaris, are inflammatory scarring disorders characterized by lymphocytic infiltration around the follicular bulge, resulting in irreversible follicle destruction and epidermal replacement by fibrous tissue. Infectious disorders include , an inflammation of the hair follicle often caused by bacterial agents like or fungal pathogens such as species, presenting as pustules or papules around affected follicles. arises from overproliferation of mites (D. folliculorum and D. brevis) residing in hair follicles, potentially triggering inflammation and contributing to through mechanical blockage and immune responses. Other conditions include , a compulsive hair-pulling disorder that induces through repetitive mechanical trauma to follicles, leading to breakage and patchy loss. Chemotherapy-induced effluvium, often manifesting as , results from cytotoxic drugs disrupting the hair cycle, causing widespread shedding due to premature entry into the resting phase. Systemic associations with hair follicle disorders involve conditions like dysfunction, particularly , which prolongs the telogen phase and causes diffuse non-scarring alopecia. , the most common nutritional shortfall, is linked to by impairing follicular proliferation and hemoglobin synthesis essential for growth. of hair follicle disorders relies on clinical evaluation supplemented by tests such as the hair pull test, where grasping 40-60 hairs yields more than 10% telogen or anagen hairs in active shedding conditions like . biopsy is confirmatory, revealing findings like perifollicular in or lichenoid infiltrates with fibrosis in cicatricial alopecias.

Treatments

Pharmacological treatments for hair follicle-related conditions primarily target androgenetic alopecia and alopecia areata through mechanisms that modulate hormone levels or immune responses. Topical , a vasodilator approved by the FDA in 1988, prolongs the anagen phase of the hair growth cycle and increases blood flow to follicles, leading to modest hair regrowth with an average increase in hair density of 8-20% after 6-12 months of use. Oral , a type II approved in 1997, reduces scalp levels by up to 64%, halting progression in 86% of men and promoting regrowth in 66% after one year, while , a dual inhibitor, shows similar but potentially stronger effects in . Both drugs are more effective in combination, with studies reporting superior outcomes compared to monotherapy. For immune-mediated , (JAK) inhibitors represent a major advance; (Olumiant), approved by the FDA in 2022 for severe cases, inhibits JAK1 and JAK2 to suppress inflammatory signaling, achieving significant hair coverage in 36% of patients after 36 weeks in phase 3 trials. Other JAK inhibitors like , approved in 2023, offer oral alternatives with response rates up to 23% for substantial regrowth. Common side effects of and include such as decreased or erectile issues in 1-2% of users, though most resolve upon discontinuation. Procedural interventions focus on surgical and minimally invasive methods to restore follicle density. employs (FUE), which harvests individual follicles without linear scarring, or (), involving strip excision for higher graft yields; both achieve graft survival rates of 80-90% in qualified candidates, with visible density improvements in 6-12 months. () injections, prepared from autologous blood and rich in growth factors, enhance these procedures by promoting follicle survival and accelerating regrowth, with meta-analyses showing 20-30% greater hair density when used adjunctively compared to transplantation alone. Emerging therapies leverage regenerative biology to address follicle dormancy. Various autologous stem cell-based therapies, derived from adipose or dermal sources, aim to repopulate depleted follicles and are under investigation in early clinical trials (phase 1/2) as of 2025. Topical PP405, developed by Pelage Pharmaceuticals, reactivates dormant stem cells by elevating lactate levels to boost mitochondrial energy, demonstrating statistically significant follicle stem cell activation in phase 1 trials; phase 2a trials completed in 2025 showed increased hair density in approximately 31% of participants, with phase 3 studies planned for 2026. Microneedling combined with growth factors like VEGF creates micro-injuries to stimulate regeneration, with randomized trials reporting 15-25% hair count increases when applied weekly. Gene editing approaches, including targeting follicle-specific genes like those in the Wnt pathway, remain preclinical but show promise in animal models for reversing genetic predispositions to loss. Adjunctive options include (LLLT), which uses red light wavelengths (630-670 nm) to enhance cellular metabolism in follicles, with controlled trials demonstrating a 20-35% increase in hair density after 16-26 weeks of thrice-weekly sessions. Nutritional supplements such as are often promoted but lack robust for efficacy in non-deficient individuals, with reviews finding no significant benefit for hair growth beyond correcting rare deficiencies. Overall outcomes vary by treatment and condition severity; hair transplants yield 60-80% patient satisfaction for natural appearance and permanence, though they require stable donor areas and carry risks like temporary shock loss or in 5-10% of cases. Pharmacological agents like maintain benefits long-term in 80% of users but necessitate ongoing use, with discontinuation leading to reversal within 12 months. Emerging therapies hold potential for higher efficacy but await larger trials for safety confirmation.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK470321/
  2. https://www.ncbi.nlm.nih.gov/books/NBK499948/
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