The Hair Growth Cycle Explained: Anagen, Catagen, Telogen and the Dermal Papilla

Every hair on the scalp comes from a follicle that grows it, dismantles its own lower half, rests, releases the old hair and starts again. That repeating sequence is the hair growth cycle. It explains why shedding comes and goes, why hair length has a ceiling and why pattern hair loss means shorter growth phases and shrinking follicles.

This guide covers follicle anatomy, the dermal papilla, the hair growth phases and their signals, two cycle disturbances explained as physiology, laboratory models, and what peptide studies have and have not shown.

Inside the follicle: bulb, matrix, bulge and glands

A hair follicle is a small organ that regenerates itself, largely through interactions between its epithelial and mesenchymal cells (Stenn and Paus, Physiological Reviews, 2001). From the bottom up:

• Bulb and matrix. The bulb is the follicle’s growth centre. Its proliferating matrix cells build the hair shaft, and melanocytes among them supply pigment.
• Dermal papilla. Connective tissue tucked into the base of the bulb, rich in capillaries (see our guide to angiogenesis and VEGF).
• Root sheaths. Inner and outer root sheaths surround the shaft; the outer derives from the epidermis.
• Bulge. Where the arrector pili muscle meets the outer root sheath; home to the follicle’s stem cells, first proposed in 1990 by Cotsarelis, Sun and Lavker after they found label-retaining cells there.
• Sebaceous gland and arrector pili. The gland’s duct opens into the permanent upper follicle; the muscle, under sympathetic nerve control, makes the hair stand up when it contracts.

Only the lower follicle is dismantled in catagen; the upper segments persist, cycle after cycle.

The dermal papilla: the follicle’s signalling centre

The dermal papilla is a compact cluster of specialized fibroblasts at the base of the hair follicle that tells the surrounding epithelial cells when to grow and how much hair to make. It controls the number of matrix cells; during telogen its cells sit beneath the bulge and interact directly with the stem cells, which a 2022 review calls essential for starting a new cycle; and it carries the follicle’s androgen receptors and type II 5α-reductase. In catagen it resists apoptosis, partly through BCL-2, then condenses and moves up toward the bulge.

In 1984, Jahoda, Horne and Oliver showed in rodent experiments that serially cultured adult papilla cells induced hair growth when implanted into follicles that would not otherwise have produced hair. Human papilla cells lose much of that capacity soon after flat, two-dimensional culture, Higgins and colleagues found in 2013, but three-dimensional spheroids partially restored their signature and induced new follicles in human skin. In Canada, a 2009 study led from the University of Toronto and the Hospital for Sick Children reported that skin-derived precursors (SKPs) derive from hair follicle precursors and exhibit properties of adult dermal stem cells.

The phases of the hair growth cycle

Published figures differ between reviews, so the numbers below are approximate.

Anagen phase: growth

Anagen lasts about two to seven years on the scalp in one review, two to eight in another and about three in a third, with up to 85–90% of scalp hairs in it at any time. Because hair grows only in anagen, its duration caps hair length: in families with familial trichomegaly (extreme eyelash growth), Higgins and colleagues found FGF5 mutations, and affected individuals’ forearm hairs were longer than controls’, with more in anagen.

Catagen phase: regression

Catagen is an apoptosis-driven regression lasting about two to three weeks, with about 2% of scalp hairs in it at any time. Matrix and outer root sheath cells die, melanin production stops and the lower follicle shrinks, leaving the hair anchored but no longer growing.

Telogen phase: rest

Telogen lasts about two to three months, and estimates of its share of scalp follicles run from about 9% to 10–15%. The resting club hair stays in place while bulge stem cells stay quiet.

Exogen and kenogen

Shedding had been assumed to be part of telogen. In 2002, Milner and colleagues showed in mice that it is a distinct phase, exogen, which their data suggest is specifically controlled; it peaks with anagen and apparently involves a proteolytic process at the hair’s root. The same year, Rebora and Guarrera described kenogen (Greek for “empty”), the empty follicle seen on phototrichograms after shedding. In ten balding and non-balding men followed for 14 years, it lasted about four months, up to about seven, and featured in 80% of cycles; it was longer and more frequent in androgenetic alopecia.

The signals that move a follicle between phases

Into anagen: Wnt/β-catenin and Sonic hedgehog

In hair follicle stem cells, β-catenin activates LEF/TCF transcription and stem-cell activation, and overexpressing WNT10b in telogen can push follicles into anagen; mice engineered in 1998 to express a truncated β-catenin in skin formed new follicles de novo and developed hair tumours. Sonic hedgehog also drives the switch: in 1999, Sato and colleagues delivered the Shh gene by adenovirus to the skin of 19-day-old mice, which entered anagen early, with new hair within about two weeks and normal skin six months later.

Holding the rest: BMP

BMP signalling is a telogen brake that keeps stem cells refractory, and the BMP antagonist Noggin shortens that refractory period, a 2022 review notes, citing Plikus and colleagues’ 2008 work on cyclic dermal BMP signalling and stem-cell activation.

Ending anagen: FGF5 and TGF-β1

The 2014 trichomegaly study also showed FGF5 inducing regression of human follicles in organ culture; its authors called FGF5 a crucial regulator of hair growth in humans. TGF-β1 pushes the same way: it restrained growth in the first human follicle cultures in 1990, and in 2000 Foitzik and colleagues found TGF-β1-knockout mice still in early catagen on day 18, when wild-type littermates were in telogen, while adding TGF-β1 to normal mouse back skin induced premature catagen.

Androgens, DHT and prostaglandin D2

Androgens stimulate follicles on the face, armpits, pubic area and chest but inhibit scalp follicles. The enzyme 5α-reductase converts testosterone into the more potent DHT, which binds androgen receptors in papilla cells and, in pattern hair loss, shortens anagen and lengthens telogen as scalp hair regresses to fine vellus hair: miniaturization. In 2012, Garza and colleagues found prostaglandin D2 (PGD2) and its synthase elevated in bald compared with haired scalp of men with androgenetic alopecia; PGD2 inhibited hair growth in explanted human follicles and in mice, through the G protein-coupled receptor GPR44.

When the cycle shifts: telogen effluvium and pattern hair loss

Both are changes in cycle timing. This is physiology for context, not diagnosis, and nothing here suggests that any research compound affects hair loss in people.

Telogen effluvium

Telogen effluvium is shedding caused by a cycle disturbance, seen as excess loss of normal club hairs. Headington’s 1993 review proposed five functional types, from immediate anagen release, in which a trigger tips many follicles out of anagen together, to delayed telogen release. Because club hairs are released only when telogen ends, shedding lags the trigger. Reported triggers include thyroid dysfunction, chronic inflammatory disease, psychological stress, rapid loss of body weight, low protein intake and some drugs.

Androgenetic alopecia

In pattern hair loss, successive cycles have a shorter anagen, so each hair is shorter and finer until terminal follicles produce only vellus-like hair, and kenogen lengthens. Balding scalp also shows raised PGD2 and, in miniaturized follicles and arrector pili muscles, more CXXC5, a brake on Wnt signalling.

How researchers study the hair cycle

Human hair follicle organ culture

In 1990, Philpott, Green and Kealey first kept microdissected human anagen scalp follicles growing in culture; they lengthened over four days by producing a keratinized shaft. A 2015 methods guide set out standard read-outs for serum-free organ culture, and the FGF5, PGD2 and AHK-Cu results here all used the model. Its limit: no surrounding skin, blood supply or immune system, and no way to follow years of anagen.

The mouse hair cycle

C57BL/6 mice cycle on a predictable early timetable (catagen in the second week after birth, telogen in the third, anagen in the fourth), and their skin colour changes with follicle activity. Depilation starts anagen on demand, wounding models measure wound-induced hair neogenesis, and whisker follicles can be cultured. But mouse cycles run in weeks, human scalp anagen in years.

Trichograms and phototrichograms

In people, methods range from the non-invasive phototrichogram to the semi-invasive trichogram and invasive approaches; a 2009 review notes that no single method is ideal. Phototrichograms follow the same follicles over time, which is how kenogen was noticed.

What peptide research has, and has not, shown

Every result below comes from cells, cultured follicles or rodents; none of the studies tested a peptide in people. Our guide to reading a peptide study explains why.

AHK-Cu: one study in cultured human follicles

AHK-Cu, the copper complex of L-alanyl-L-histidyl-L-lysine, carries alanine where GHK-Cu has glycine (see GHK-Cu vs AHK-Cu, and our histidine guide on why the middle residue binds copper). In 2007, Pyo and colleagues found that picomolar to nanomolar AHK-Cu stimulated elongation of human hair follicles ex vivo and proliferation of cultured papilla cells; at the highest concentration, apoptotic papilla cells fell (not significantly), the Bcl-2/Bax ratio rose and cleaved caspase-3 and PARP decreased. One study, one group, in culture.

GHK-Cu: thin hair-cycle data

GHK-Cu, discovered in 1973, has a wider literature (see our GHK-Cu research guide) but little on the hair cycle: a 2018 review co-written by Loren Pickart lists effects on hair and follicle size without citing a study for them.

Thymosin beta-4 in rats and mice

In 2004, Philp and colleagues at the US National Institutes of Health reported that thymosin beta-4, a 43-amino-acid peptide, accelerated hair growth in normal rats and mice. Bulge-derived keratinocytes expressed it in step with the cycle, and nanomolar thymosin beta-4 increased migration and differentiation of clonogenic keratinocytes from rat whisker follicles. The study has no human data; see our TB-500 (thymosin beta-4) research guide and thymosin alpha-1 vs thymosin beta-4.

PTD-DBM and the CXXC5 brake on Wnt

CXXC5 restrains Wnt/β-catenin signalling through Dishevelled. In 2017, Lee and colleagues found it raised in miniaturized follicles from human balding scalp and showed it reduced alkaline phosphatase activity and proliferation in cultured papilla cells; in mice, a peptide disrupting the CXXC5–Dishevelled interaction accelerated hair regrowth and wound-induced hair neogenesis. A 2023 follow-up from the same group studied PTD-DBM (protein transduction domain–Dishevelled binding motif), which interferes with CXXC5’s Dishevelled binding; the transduction domain is a cell-penetrating sequence. It linked DHT to CXXC5 through PGD2 and showed PTD-DBM reversing PGD2’s effects in mice and cultured mouse whisker follicles; against DHT, only a separate small molecule fully restored follicle elongation.

What’s established and what isn’t

Sourcing hair-cycle research reagents in Canada

Hair-cycle work raises the usual documentation questions for research peptides in Canada:

• Match the batch. The certificate’s batch number should match your vial; see our COA guide.
• Ask what identity testing covered. For AHK-Cu or GHK-Cu, whether the copper complex or only the peptide was characterized; for a fusion such as PTD-DBM, how the full sequence was confirmed.
• Store it cold, dry and dark, lyophilized until needed; see the peptide storage guide.

AHK-CuThe copper tripeptide tested on cultured human follicles in 2007View product PTD-DBMDisrupts the CXXC5–Dishevelled interaction; studied in miceView product GHK-CuGlycine in place of AHK-Cu’s alanine; hair-cycle data are thinView product TB-500 (Thymosin Beta-4)Thymosin beta-4, studied in 2004 rat and mouse hair workView product

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