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Journal of Cosmetology & Trichology Silva et al., J Cosmo Trichol 2019, 5:1
DOI: 10.4172/2471-9323.1000141
Jo

ISSN: 2471-9323

Review Article Open Access

Revisiting Hair Follicle Embryology, Anatomy and the Follicular Cycle

Laura Maria Andrade Silva1*, Ricardo Hsieh2, Silvia Vanessa Lourenço3, Bruno de Oliveira Rocha1, Ricardo Romiti4, Neusa Yuriko Sakai Valente4,5,
Alessandra Anzai4 and Juliana Dumet Fernandes1
1Department of Dermatology, Magalhães Neto Outpatient Clinic, Professor Edgar Santos School Hospital Complex, The Federal University of Bahia (C-HUPES/UFBa),
Salvador/BA-Brazil
2Institute of Tropical Medicine of São Paulo, The University of São Paulo (IMT/USP), São Paulo/SP-Brazil
3Department of Stomatology, School of Dentistry, The University of São Paulo (FO/USP), São Paulo/SP-Brazil
4Department of Dermatology, University of São Paulo Medical School, The University of São Paulo (FMUSP), São Paulo/SP-Brazil
5Department of Dermatology, Hospital of the Public Server of the State of São Paulo (IAMSPE), São Paulo/SP-Brazil
*Corresponding author: Laura Maria Andrade Silva, Department of Dermatology, Magalhães Neto Outpatient Clinic, Professor Edgar Santos School Hospital Complex,
The Federal University of Bahia (C-HUPES/UFBa) Salvador/BA-Brazil, Tel: +55(71)3283-8380; +55(71)99981-7759; E-mail: [email protected]
Received date: January 17, 2019; Accepted date: March 07, 2019; Published date: March 12, 2019
Copyright: © 2019 Silva LMA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The presence of hair follicles is one of the main characteristics of mammals. In each new follicular cycle, the
embryonic developmental steps are repeated to form a new hair. It is a complex structure, its functions ranging from
temperature regulation, physical protection, camouflage, and social interactions. In addition, it is also an endocrine
organ capable of producing and locally converting many hormones. In this review, we will describe the main
anatomical, embryological, and physiological properties of the hair follicle, as well as their clinical importance.

Keywords: Hair; Follicle; Embryology; Anatomy; Cycle Literature Review

Introduction Hair follicle embryology, anatomy, and molecular control

The presence of hair follicles is one of the main characteristics of Hair follicles begin to develop early during the fetal period, mainly
mammals. Their functions range from temperature regulation, physical around the 9th and 12th week of gestation. They originate because of
protection, camouflage, sensory and tactile activity, dispersion of the proliferation of the germinative layer of the epidermis and extend
sebum and sweat, in addition to being important in social interactions to the underlying dermis [5].
[1,2].
The primitive hair adopts a club shape and around the 14th
The psychosocial importance of hair in society is intense, many gestational week, the hair bulbs are already formed [5]. The
diseases that lead to hair loss, or hair over-abundance, generate epitheliocytes that form the hair bulbs will form the germinative
considerable morbidity, creating a demand for development of drugs matrix, which will later produce the hair shaft [6] (Figure 1).
that are capable of restoring hair growth and improving the
Subsequently, there is an invagination of the hair bulbs by the
appearance of hair [1].
mesenchymal papillae. Thus, the peripheral cells of the primordial hair
Human skin contains approximately 5 million hair follicles, of follicles form the root sheaths and the mesenchymal cells form the
which 100,000 are found on the scalp [3]. Hair is made by cells called dermal sheaths. The germinative matrix proliferates, pushing the cells
trichocytes, which form a filiform keratinized structure called the hair towards the surface, where they become keratinized, forming hair [7].
shaft. There are three main types of hair: lanugo hair, vellus hair, and Fetal hair does not appear in all regions at the same time, they may be
terminal hair. These differ in their pigmentation and structure, but first observed in the eyebrows, upper lip, and mental region [7,8]. At
follow the same principles of formation and development [3]. the 20th week of intrauterine life, the fetal body is lined with soft hair,
referred to as lanugo, which helps with the retention of the cheesy
Lanugo hair is present during fetal development and in the post-
vernix on the skin [9]. At this time, there is no difference in number of
natal period, and is structurally similar to the thin and lightly
fetal hair in women or men, secondary differences between them will
undeveloped hair found in adults called vellus hair. Terminal hair is the
happen later in puberty [8]. Hair follicles do not form de novo in adult
thick and pigmented hair found in the beard and the axillary and pubic
skin, as sweet glands the absolute number is establish in fetal period
regions [4]. Keratin is the main component of hair, being comprised of
and a density dilution occurs along the growth of body surface [8].
amino acids such as cysteine, arginine, and citrulline; citrulline is
exclusively found in humans [4].
The purpose of this review is to describe the most important aspects
of hair follicle development, anatomy, physiology, the relationship with
associated diseases.

J Cosmo Trichol, an open access journal Volume 5 • Issue 1 • 1000141

ISSN:2471-9323
Citation: Silva LMA, Hsieh R, Lourenço SV, Rocha BO, Romiti R, et al. (2019) Revisiting Hair Follicle Embryology, Anatomy and the Follicular
Cycle. J Cosmo Trichol 5: 141. doi:10.4172/2471-9323.1000141

Page 2 of 8

Figure 1: Schematic figure shows hair follicle’s chronologic

development since undifferentiated epithelium, placode, hair germ,
hair peg/Bulbous peg and primitive hair follicle around 24 weeks of
gestational age (Autoral figure adapted from [5]).
Figure 2: A woman with alopecia due to Vitamin D-Dependent
Rickets type II (VDDRII), courtesy from University of São Paulo.
The key to the development of the hair follicle is the communication
between the epidermis and the mesenchyme, and this communication
is essential not only for hair formation, but also for the formation of all
other skin annexes as nails, teeth, and glands. Many epidermal-dermal Lanugo hair
signalling pathways are involved in these processes: the WNT/wingless
Lanugo hair is thin, soft, and slightly pigmented, and appears
family, the Hedgehog family, the TGF-β/BMP (transforming growth
around the 12th week of pregnancy, becoming abundant between the
factor beta and bone morphogenetic protein) family, the FGF
17th and 20th weeks. It is replaced by the thicker hair that remains
(fibroblast growth factor) family, and the TNF (Tumor Necrosis
throughout life, except for the inguinal and axillary regions where it
Factor) family. Different combinations of these signals dictate the
will be replaced at puberty by more pigmented terminal body hair [7].
development of each annex [9].
There is a genodermatosis called hypertrichosis lanuginosa
Dermal signalling which induces the vertical arrangement of
congenita in which lanugo hair persists from childhood through an
keratinocytes and their proliferation occurs in small epidermal
adult’s life (Figure 3). Since very little is known about the cause of this
invaginations in the dermis referred to as the placodes. Mesenchymal
condition the only treatment is through genetic counselling and hair
cells of different origins begin to interact and induce the regular
reduction therapies using lasers or electrolysis [11].
formation of inter-placode spaces. However, the molecular nature of
the early signalling from the dermis to the epidermis remains
uncertain [9]. Piloerector muscle and the sebaceous gland
Vitamin D-Dependent Rickets type II (VDDRII) results from a The piloerector muscle is derived from the adjacent mesenchymal
mutation in the Vitamin D Receptor gene (VDR), which is expressed in cells; it is attached to the hair Outer Root Sheath (ORS) and the dermal
several target organs, including the hair follicle. Full or partial alopecia papilla. It is present in all hair follicles except those in the axillae and
is a marker of a defect in the VDR and is often one of the first some areas of the face [12].
symptoms noted, occurring in 2/3 of cases (Figure 2). It has been The sebaceous gland is derived from the epidermis. The cell shoots
shown that inadequate differentiation of the hair follicle occurs in this arise from the epithelial cells in the ORS of the developing hair follicles
disease, and it is the reason why alopecia remains in patients treated by and invade the adjacent connective tissue and branch out to form the
replacement of vitamin D and calcium, however its mechanism has not primordial alveoli and associated ducts. Disruption of the central cells
been fully elucidated [10]. of the alveoli releases an oily secretion, the sebum, which together with
the desquamated epidermal cells form the vernix caseous [12].

J Cosmo Trichol, an open access journal Volume 5 • Issue 1 • 1000141

ISSN:2471-9323
Citation: Silva LMA, Hsieh R, Lourenço SV, Rocha BO, Romiti R, et al. (2019) Revisiting Hair Follicle Embryology, Anatomy and the Follicular
Cycle. J Cosmo Trichol 5: 141. doi:10.4172/2471-9323.1000141

Page 3 of 8

process of holocrine secretion. The sebaceous glands are attached to

the top hair follicle through the infundibulum [12] (Figure 4).
Scarring alopecia results from follicular damage that is sufficient to
cause the destruction and replacement of the pilosebaceous structures
by scar tissue. When the sebaceous glands and the arrector pili muscle
are involved in hair follicle diseases they are generally associated with
irreversible hair loss not only in scarring alopecias, but also in
androgenetic alopecia where the loss of attachment to the arrector pili
muscle is associated with irreversible hair miniaturization in the final
stages of the disease [13,14].

Arrector pili muscle

The arrector pili muscle is a small muscle bundle that runs from the
hair follicle to the adjacent epidermis and dermis, contributing to the
regulation and secretion of sebum [12].
The arrector pili muscle attaches to the hair follicle at the isthmus,
in a region of stem cells called the follicular bulge. This muscle acts as
important factor in the integrity of the follicle, and the loss of contact
between the hair follicle and the arrector pili muscle is a predictor of
the irreversibility of hair loss [14]. The interaction between the dermal
papilla derived mesenchyme and the follicular matrix cells, as well as
the interaction between the follicular cells of the bulge and the arrector
pili muscle, are essential for hair follicle integrity [14].

Hair follicle
The hair follicle can be split into three main parts: the
Figure 3: Child with hipertrichosis lanuginosa congenita. Dr. Silva infundibulum, which goes from the follicular ostium to the duct that
photos-Federal University of Bahia. empties the sebaceous gland; the isthmus, comprising the area between
the sebaceous gland duct and the insertion site of the arrector pili
muscle, and finally the lower portion, which is located below the
insertion site of the arrector pili muscle [12].
The hair follicle can be divided into a permanent upper portion,
which surrounds the infundibulum and the isthmus, and a lower
portion that is continually renewed. The lower region of the isthmus,
referred to as the bulge, stores the epithelial and melanocytic stem
cells, and marks the end of the permanent region [12]. These cells have
a long, slow, life cycle and are able to differentiate into three structures,
namely, the epidermis, hair follicles, and sebaceous glands [12].
The lower region is where the metabolically active portion of the
follicle is located. The hair bulb contains the hair matrix and the
dermal papilla and a small portion of richly innervated and
vascularized connective tissue [12]. One of the most metabolically
active cells in an organism, the keratinocytes of the follicular matrix,
are found in the region of the capillary matrix in the bulb. These cells
Figure 4: Pilo sebaceous’s unit parts schematic draw. Permanent are found below the Auber line, at the largest diameter of the dermal
upper region and lower parts of hair follicle and its subdivisions papilla. These cells are capable of generating six different types of cells
(Autoral figure adapted from [3]). namely, the three layers of the Inner Root Sheath (IRS) and the three
layers of the stem itself (Figure 5). Between these cells are active
melanocytes, which, depending on the production of eumelanin or
Sebaceous glands can emerge in regions with or without hair and feomelanin, will color the hair in the shaft blonde or brunette. The
their size is inversely proportional to that of the hair present in the hair symmetry or asymmetry of the follicular matrix is one of the
follicle [12]. They are composed of several lobes with a layer of determinants of hair shape resulting in either straight or curly hair [4].
basophilic cubic cells and another central layer of cytoplasmic rich
cells that are not birefringent to polaroscopy. They are responsive to
androgenic hormones, but not to neural input, remaining undeveloped
until puberty. Sebum is secreted from sebaceous glands through the

J Cosmo Trichol, an open access journal Volume 5 • Issue 1 • 1000141

ISSN:2471-9323
Citation: Silva LMA, Hsieh R, Lourenço SV, Rocha BO, Romiti R, et al. (2019) Revisiting Hair Follicle Embryology, Anatomy and the Follicular
Cycle. J Cosmo Trichol 5: 141. doi:10.4172/2471-9323.1000141

Page 4 of 8

Figure 5: Hair shaft parts (IRS: Inner Root Sheaft; ORS: Outer Root
Sheaft; CTS: Conjutive Tissue Subcutaneous) (Autoral figure
adapted from [3]).

Hair growth is directed and achieved by guiding structures and

cleavage planes and an inner and hard layer of differentiated
keratinocytes, referred to as the IRS, which guides and envelops the
hair shaft. The IRS is formed by three layers, the Henle layer, the
Huxley layer, and the cuticle. The hair shaft and the IRS move outward Figures 6a-6d: a) Woman with autossomic form of monilethrix b)
using a cleavage plane, the outermost portion of the outer root sheath Trichoscopy shows typical “ringed” hair bands form c) Woman with
as a companion layer. The ORS is formed by a single layer of flattened pili annulati with increase of fragility d) Trichoscopy shows typical
cells [4]. The ORS stretches from the epidermis to the lateral portions alternating light and dark bands (Dr. Silva photos-Federal
of the hair follicle, decreasing in thickness at greater depths. External University of Bahia).
to this sheath is a thin membrane called basal layer and in the dermis
there is an arrangement of thick collagen bundles around the root of
the hair follicle that constitute the fibrous root sheath [12]. While the
Phases of hair follicle formation
ORS is stationary, the IRS and its accompanying sheath move with the
hair shaft out of the channel [3] (Figure 5). The induction of hair follicle formation results in the placodes,
which is followed by organogenesis and cytodifferentiation of the
The hair shaft is composed of the external cuticle, the cortex, and
follicle; each phase has its specific molecular interactions. These three
the medulla. The cortex is composed of densely packed keratinocytes.
stages of development are split into eight phases [17].
The keratinocytes become keratinized to form the spindle, and
complexed a proteinaceous layer, these keratin filaments are In the first phase, the induction phase, a diffusion gradient between
surrounded by a matrix rich in sulfur, giving the stem resistance and inhibitors and activators is generated by creating a proliferative field:
elasticity. The cortex is covered by cuticle cells that are rich in sulfur- the pre-hair germ. During the first stage of the first phase of induction,
containing proteins arranged like rows of tiles. The cuticle is where the follicular germ is visible, the placodes is formed through the
responsible for maintaining the stem in the follicle. In the IRS and the action of molecules such as Wnt/β-catenin, EDA-A1, NF-κβ, Noggin,
capillary stem cells, the cells are strongly imbricated, which allows for and the surrounding area inhibited by Dκκ and BMPs [17].
hair adhesion. In the medulla, the keratinocytes are only loosely
Organogenesis, orientation of the hair follicle, occurs in the second
aggregated [3,12].
phase. The follicular germ proliferates vertically invaginating in the
Primary disorders of the hair shaft, referred to as genodermatoses, dermis and the dermal papilla is formed. Later on, several molecular
are associated with hair fragility, hair breakage, and thin hair, and are processes determine its polarization and the innervation of the
caused by mutations in cytokeratins and adhesion molecules such as trichocytes and germ formation. The organogenesis comprise phase 2
cadherins in some aetiologies but are not completely understood. to phase 5, hair follicle germ and peg phase. In phase 5, IRS and the
Monilethrix and pili annulati are examples of these conditions which bulge can be found, and at the phase 8 all hair follicle apparatus is
may be related to hair breakage [15,16] (Figures 6a-6d). completely formed. Cytodifferention comprise phases 6 to phase 8,
characterizing bulbous peg phase [3]. During cytodifferentiation, the
formation of the follicular lines occurs with the development of the
internal and external root sheaths and the pillar shaft, pigmentation,
and the formation of the follicular bulge and the sebaceous glands
[17-19].

J Cosmo Trichol, an open access journal Volume 5 • Issue 1 • 1000141

ISSN:2471-9323
Citation: Silva LMA, Hsieh R, Lourenço SV, Rocha BO, Romiti R, et al. (2019) Revisiting Hair Follicle Embryology, Anatomy and the Follicular
Cycle. J Cosmo Trichol 5: 141. doi:10.4172/2471-9323.1000141

Page 5 of 8

The Wnt/β-catenin signalling pathway is the main pathway that

defines the fate of the hair follicle, and its deficiency results in the
absence of placodes. The epithelial placodes generates a signal to the
mesenchyme so that it condenses and forms the dermal papilla. The
Sonic Hedgehog signalling pathway is the major driver for the
maturation and growth of the dermal papilla. The dermal papilla itself
becomes an area of secretion and interaction with the mesenchymal
cells that will eventually generate signals for the development of many
follicular layers [17-19].
Not every keratinocyte becomes a trichocyte, so there are local
inhibitory systems that allow for the regular and orderly distribution
and development of placodes. While Wnt/EDA-A1 and Noggin are
well described inducers of follicular development, the pathways
involved in blocking this process have yet to be clarified. Studies in
mice have shown that BMP is able to inhibit the development of
placodes but not their formation [17-19].
Cytodifferentiation is characterized by development of all the
compartments of the HF. Various signalling molecules are related to
this process. IRS differentiation is regulated by the Gata3 and Cutl
transcription factors, while BMP signalling and transcription factors
such as Msx2, FoxN1 and Hoxc13 regulate hair shaft differentiation.
Other factors controlling differentiation include the Dlx3 transcription Figure 8: Schematic description of the hair growth cycle: anagen,
factor that controls differentiation of IRS and hair shaft. Dlx3 is a catagen and telogen phases (Autoral figure adapted from [2]).
direct target of Lef1 and up regulates expression of Hoxc13 and Gata3
transcription factors, regulators of hair shaft differentiation [17,20]
(Figure 7).
Anagen phase
The anagen phase is the period of the follicular cycle where the
lower portion of the follicle regenerates alone, producing a new pillar
shaft [20-22]. It can be induced by a variety of factors, including
trauma and healing, although its area of stimulation is limited, and it
can only stimulate the area around the trauma. Other substances that
are also capable of inducing the anagen phase, include the drugs
cyclosporin A, minoxidil, FK506, norepinephrine depleting agents,
estrogen receptor antagonists (in mouse), and tretinoin. Many growth
factors and neural mediators such as tumor promoting factor,
keratinocyte growth factor, hepatocyte stimulating factor, Sonic
hedgehog, substance P, capsaicin, parathyroid hormone antagonists,
Figure 7: Schematic figure of hair follicle morphogenesis. Placode
ACTH, and the degranulation of mast cells are able to induce anagen,
formation is facilitated by promoting signals, prevented in
although the pathways and its participation in the spontaneous
neighbouring epithelial cells by inhibitory signals. Signals from the
induction of the signal is still unclear [20-22].
epithelium induce the clustering of mesenchymal cells to form a
dermal condensate. The dermal condensate signals to the follicular The anagen phase is divided into six sub-phases. The durations of
epithelium to proliferate and grow down into the dermis. The the first five stages differ little on different scalp sites, although only the
dermal condensate becomes enveloped by follicular epithelial cells duration of the last phase is the determining factor for hair length. The
to form the dermal papilla (Autoral figure adapted from [17]). first changes observed in the initial anagen phase are changes in the
papilla and in the follicular germ. Epithelial cells in the follicular germ
descend towards the dermis as an epithelial finger, guided by a fibrous
tract called the stela. This tract is created by the first mature follicle
Follicular Cycle formed and when they reach the desired depth, they change direction
The hair follicles are constantly renewing themselves. Growth, and rise to form the radicular sheath and the pillar rod. The highest
regulation of growth, cellular death and destruction and tissue mitotic rate occurs at the height of the Auber line. The matrix cycle
repairing are not clearly understood at other biological systems as they lasts 23 hours in humans and has a mitotic index of 4.3%. Cylinder
are in hair follicle [8]. They are alternating between biologically active formation is not seen in anagen phase 1 and can only be seen at the
phases of growth, the anagen phase, the involution phase, the catagen end of anagen 3 when the hair follicle layers begin to form [20-22].
phase, and the rest phase, telogen. There is also a shedding phase called Anagen I down growth shows no cylindrical layer differentiation. At
exogen [2,17-22] (Figure 8). anagen III, the IRS/ORS are identifiable. At the point that the finger of
epithelium reaches its deepest level and before anagen III, the layers of
the follicle begin to form [22].

J Cosmo Trichol, an open access journal Volume 5 • Issue 1 • 1000141

ISSN:2471-9323
Citation: Silva LMA, Hsieh R, Lourenço SV, Rocha BO, Romiti R, et al. (2019) Revisiting Hair Follicle Embryology, Anatomy and the Follicular
Cycle. J Cosmo Trichol 5: 141. doi:10.4172/2471-9323.1000141

Page 6 of 8

The term anagen effluvium refers to the abrupt loss of hairs in their Telogen phase
growth phase due to an event that impairs the mitotic or metabolic
activity of the hair follicle (Figures 9a and 9b). Chemotherapy, The telogen phase is where the follicle is found in the dermis
radiation, toxic chemicals, and sometimes inflammatory diseases such covered by quiescent epithelial cells, the papillary fibroblasts forming
as alopecia areata and pemphigus are also capable of diminishing the an epithelial sac. Later, this adopts a rod format that is adherent to the
metabolic activity of hair follicles resulting in anagen hair loss. Anagen ORS. Even though it is widely known as a resting phase, it is speculated
effluvium is reversible, and hair regrowth occurs after a delay of 1-3 that it is a much more active phase than we are able to identify today
months [23]. [20-22]. The telogen phase is the third phase of hair’s cycle, occurring
after both the anagen phase and catagen phase. It typically lasts
between three to five months. During this final stage of hair cycle the
hair ceases to grow any further and becomes fully keratinized. The
dermal papilla enters a resting stage and does not supply any nutrition
to the hair; which is fully grown and no longer needs sustenance. This
hair is called club hair and it has matured and no longer has access to
the blood supply because there is no longer a need to grow. The hair
bulb is made of keratin is ready to make an exit off the scalp [20-22].
Telogen Effluvium (TE) is the most common cause of hair loss; it is
a heterogeneous disorder that can be classified into three main
categories: premature teloptosis, collective teloptosis, and the
premature entry into telogen induced by drugs. TE can also be caused
by dietary deficiencies and an “autoimmune” response. It is a self-
limited condition such that hair regrowth occurs after 3 to 9 months
[24].
Figures 9: (a and b) Woman with anagen effluvium due to
Chemotherapy-Trichoscopy shows black dots and broken hairs Exogenous phase
(Courtesy from Dr. Anzai University of São Paulo). In animals, it is common for hair to grow before the previous hair
falls out, mainly for protective reasons. In humans, the anagen and
telogen phase are events that are independent of the exogenous phase.
Catagen phase This requires an innate control of hair falling out process and a local
apparatus responsible for this. In mammals, temperature, nutrition,
The catagen phase begins when the anagen phase ends. It is a highly genetic, and systemic factors are all involved in hair fallout. The
controlled phase where there is coordination between cellular adhesion of the hair follicle in the canal is influenced by the presence
differentiation and apoptosis, resulting in a cessation of cellular growth of many factors such as desmogleins, enzymes such as cathepsin L, and
and in pigmentation. At this stage, the papilla is released from the bulb; lipids. Mouse with specific deficiencies in any of these factors, and
there is a loss of differentiation of the lower follicle layers, a patients using the protease inhibitor class of drugs, suffer from hair
remodelling of the follicle matrix, and shrinking of the distal portion of loss. Problems at this stage lead to the retention of many strands,
the follicle through an apoptotic process [20-22]. causing dilation of the infundibulum, a condition seen in a pathology
Although the spontaneous signals leading to this phase are not well called trichostasis spinulosa. In androgenetic alopecia the opposite
characterized, the many stresses that precipitate the catagen phase are occurs, there is an early exogenous phase, with one strand falling out
well-known and include environmental and chemical factors such as before the next anagen phase starts. Although it is believed that the
trauma and dexamethasone as well as hormones such as ACTH and anagen and exogenous phase are separate events they are connected in
17-β-estradiol [20-22]. The catagen phase can be divided into eight some way, but the exact mechanisms of how this occurs is not yet
sub-phases beginning at the late anagen phase and ending with the known [20-22].
initial telogen phase [22]. The first sign is the loss of the cellular In each new cycle a new hair is formed, and its formation depends
projections from fibroblasts in the basement membrane of the dermal on the activation of epithelial stem cells found in the bulge. The hair
papilla. The extracellular matrix ceases the supply of substances and follicle is sensitive to many cytokines, growth factors, neuropeptides,
the papilla shrinks, cell division in the bulbar matrix ceases, and and hormones that are often produced by the hair follicle itself,
massive apoptosis occurs in specific regions of the regressing follicle although the pillar cycle is an autonomous phenomenon capable of
[3]. Changes also occur in cytoskeletal proteins and in the adhesion continuing alone in the culture of isolated cutaneous follicles [2,20-22].
molecules trichohyalin, transglutaminase I, and desmoglein that stop The basis for this continuous regeneration is the interactions between
being produced. Concomitantly, the lower follicle shrinks and becomes the follicular unit and the mesenchyme. Some molecular signals have
an epithelial cord [20-22]. Catagen is a highly regulated event. Its already been defined as follicular cycle markers and regulators such as
purpose is to delete the old hair structure and to bring up a new follicle fibroblast growth factor, transforming growth factor, and Wnt
utilizing the stem cells from bulge and from papilla. As catagen signalling, Sonic Hedgehog, neurotrophins, and homeobox proteins
regression occurs by apoptosis, understanding the controls of [22].
apoptosis will be central to understanding catagen control [22].
The reasons why the hair follicle cycles are obscure, but it is
speculated that cycling controls the size of the hair in each place, to
promote the fall of the rods to help maintain skin cleanliness,
adaptation to climatic conditions, social conditions, and incorrect

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ISSN:2471-9323
Citation: Silva LMA, Hsieh R, Lourenço SV, Rocha BO, Romiti R, et al. (2019) Revisiting Hair Follicle Embryology, Anatomy and the Follicular
Cycle. J Cosmo Trichol 5: 141. doi:10.4172/2471-9323.1000141

Page 7 of 8

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melatonin, and ACTH, as well as hormones produced by the
13. Ioannides D, Tosti A (2015) Alopecias - Practical Evaluation and
pilosebaceous unit itself namely, corticotropin releasing hormone, beta management. Curr Probl Dermatol 47: 1-9.
endorphin, and alpha melanocyte stimulating hormone [22,25]. 14. Sinclair R, Torkamani N, Jones L (2015) Androgenetic alopecia: New
Physical and psychological stresses may lead to disturbances in the insights into the pathogenesis and mechanism of hair loss. F1000Res 4:
585.
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(2009) Pili annulati: refinement of the locus on chromosome 12q24.33 to
canities subita phenomena seen in Marie Antoinette syndrome, and a 2.9-Mb interval and candidate gene analysis. Br J Dermatol 160:
the abrupt hair fall out in a severe telogen effluvium are examples. Beta 527-533.
adrenergic receptors can be found in the bulge region in the early 16. Redler S, Pasternack SM, Wolf S, Stienen D, Wenzel J, et al. (2015) A
anagen phase and substance P can induce both anagen and catagen novel KRT86 mutation in a Turkish family with monilethrix, and
phases [22,25-27]. identification of maternal mosaicism. Clin Exp Dermatol 40: 781-785.
17. Oh JW, Kloepper J, Langan EA, Kim Y, Yeo J, et al. (2016) A guide to
Immune system studying human hair follicle cycling in vivo. J Invest Dermatol 136: 34-44.
18. Hardy MH (1992) The secret life of the hair follicle. Trends Genet 8:
It is possible that changes in the location and amount of immune 55-61.
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when they attack the isthmus and bulge (cicatricial alopecia). involved in hair follicle morphogenesis and development. Int J Mol Sci 15:
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phase whereas corticosteroids induce the catagen phase in rodents 21. Paus R (1998) Principles of hair cycle control. J Dermatol 25: 793-802.
[22]. Mast cell activity also has relevance in the follicular cycle, where 22. Stenn KS, Paus R (2001) Controls of hair follicle cycling. Physiol Rev 81:
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Conclusion
25. Paus R, Peters EM, Eichmuller S, Botchkarev VA (1997) Neural
The hair follicle is a fantastic mini organ with structural, endocrine, mechanisms of hair growth control. J Investig Dermatol Symp Proc 2:
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other components of the skin are. Numerous studies have tried to follicle: Hunting the “hair cycle clock”. J Investig Dermatol Symp Proc 4:
338-345.
understand its physiology in order to find possible therapeutic targets,
but currently so little is known that we expect this to be a significant 27. Stenn KS, Paus R (1999) What controls hair follicle cycling? Exp
Dermatol 8: 229-233.
area of research in the future.

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J Cosmo Trichol, an open access journal Volume 5 • Issue 1 • 1000141

ISSN:2471-9323
J Cosmo Trichol, an open access journal Volume 5 • Issue 1 • 1000141
ISSN:2471-9323