NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Embryology, Lanugo
Brendon L. Verhave; Ali Nassereddin; Sarah L. Lappin.

Author Information and Affiliations

Last Update: October 10, 2022.

Introduction
Lanugo is fine, soft, unpigmented hair that is often present in fetuses, newborns, and certain
disease states. While lanugo is a normal finding in fetuses, its presence in an older person might
be an indication of underlying pathology. Many different cell types and molecular mechanisms
contribute to the development of lanugo, and it is an important tissue type necessary to ensure
normal fetal development.

Development
Lanugo plays an essential role in binding the vernix caseosa to the skin of fetuses. Vernix caseosa
is the viscous white covering on newborns that protects their skin, prevents water loss, plays an
important role in thermoregulation, and contributes to innate immunity. It protects the fetus from
damaging substances found in amniotic fluid, most notably urea and electrolytes.[1] Lanugo is
the first type of hair to develop in humans. The interaction of lanugo with the vernix is also
important in controlling the tempo of the fetal developmental rate during various times in the
gestation cycle. Lanugo arises about three months into development. Hair growth starts on the
scalp around the eyebrow, nose, and forehead area and proceeds in a cephalocaudal direction
from head to toe. It is shed at about 33 to 36 weeks gestation, when it becomes subsequently
incorporated into the amniotic fluid, eventually contributing to the composition of the meconium.
Lanugo is ultimately replaced by vellus (fine, thin hair) and terminal hair (thicker hairs found on
the scalp, axilla, and genitalia). Lanugo often remains present on 30% of newborns; this is a
normal finding.

After removal of the vernix, small amounts of lanugo can temporarily remain on the neonate.
Lanugo can thus be present on the neonate for the first few weeks of life. Its presence can,
however, indicate premature birth in a minority of cases. When present in an adult, lanugo can be
a sign of serious underlying disease states. These include, most notably, anorexia nervosa,
bulimia nervosa, various forms of malnutrition, and the presence of a teratoma.[2]

Cellular
Lanugo, like all types of hair, is derived from the ectoderm. The cell types present in the hair
follicle of lanugo hair include hair follicle stem cells (present in the bulge and matrix of the hair
follicle), germinal matrix cells (form the hair shaft), mesenchymal cells (form the hair papilla),
keratinocytes (form keratin in the epidermis), and fibroblasts (form collagen). While about 20
different cell types comprise the hair follicle of a lanugo hair, the cells mentioned above are the
most relevant ones to clinical practice.

Biochemical
Many biochemical processes involving signal relays from the dermal papilla to the hair follicle
occur to form lanugo hair. These processes result in the activation of downstream signaling
pathways and the activation of transcription factors. These biochemical pathways include, but are
not limited to, Wnt, Sonic Hedgehog, Notch, Ectodysplasin A, and Bone Morphogenetic Protein.

Molecular Level
The Sonic Hedgehog (SHH) pathway and its effectors are key to lanugo development and the
development of other hair types. Antagonists of Wnt and its effectors are also crucial. While
other mediators are necessary for the eventual production of lanugo, these two are the most
important. In either case, molecular messages initiating the process of hair development begin in
the dermis.[3] In the absence of a Wnt signal, cytoplasmic β-catenin is phosphorylated and
targeted for destruction by a protein complex. This complex includes axin, adenomatous
polyposis coli tumor suppressor protein (APC), and glycogen synthase 3-β (GSK3-β). In the
presence of an antagonistic Wnt signal, there is inhibition of the degradation complex, and β-
catenin moves to the nucleus. There it forms a transcription complex with DNA binding factors
of the lymphoid enhancer-binding factor/T cell factor family. This complex then activates the
transcription of various target genes. In the absence of an SHH signal, the actions of the Patched-
1 (PTC1) SHH receptor inhibit the activity of the smoothened (SMO) protein. In the presence of
SHH, the repression of SMO is removed, and target genes, including PTC1 and GLI1, are
transcribed through the actions of the transcription factors GLI1 and GLI2. After further
downstream processes, the formation of lanugo and other types of hair occurs.[4]

Function
Lanugo plays a vital role in binding the vernix to the skin; this protects the fetus from damaging
substances found in amniotic fluid. Lanugo’s interaction with the vernix also results in an
increased rate of fetal growth during mid-gestation and a decreased rate of fetal growth at the end
of gestation.

Mechanism
Lanugo fulfills its role by serving as a physical anchor between the skin and vernix. Lanugo
imparts an increased surface area to the fetus, allowing more interactions between itself and the
vernix, which strengthens the anchor. Without lanugo, the vernix would not remain affixed to the
skin and, therefore, would not be able to protect the fetus from harmful substances in the
environment.[5]

When it comes to regulating fetal developmental rate, oscillations of lanugo hairs surrounded by
the vernix during fetal movements in amniotic fluid activate sensitive mechanoreceptors
connected to unmyelinated C-afferent fibers. These afferents function to relay impulses
originating from all fetal skin dermatomes via the spinal cord and activate the vagal sensory
zone, hypothalamus, and insular cortex. This process results in the promotion of an "anti-stress"
effect through oxytocin release, which also results in the stimulation of fetal growth by the
incretin effect of various gastrointestinal hormones.

Testing
Lanugo is detectable on a physical exam, and it is fine, thin, soft, and depigmented hair. If the
suspicion is that lanugo is due to other diseases, a more thorough systemic workup is
necessary. This assessment includes psychiatric evaluation for anorexia and bulimia nervosa,
complete blood count (CBC), complete metabolic panel (CMP), and the search for other tumor
markers indicative of a teratoma. The clinician should note the degree of lanugo presence and its
distribution as well, as this can correlate with disease severity.

Pathophysiology
In disease states such as malnutrition and anorexia nervosa, where thermoregulation becomes
disrupted, lanugo grows to help insulate the body. This growth is a natural response to an
unnatural insult. Molecular signals from the dermal papilla are released following the detection
of temperature dysregulation and cause a series of signaling events (primarily via SMO, PTCH,
and other SHH components), leading to the formation of lanugo hair.

Clinical Significance
If the clinician recognizes the presence of lanugo in a newborn, it should raise suspicion for
prematurity; however, this is more often a normal variant than not. When lanugo is present in an
adult, this is a “red flag,” and an underlying systemic disease should be investigated and ruled
out.

Review Questions

Access free multiple choice questions on this topic.

Comment on this article.

References
1. Faist T. Vernix caseoza - composition and function. Ceska Gynekol. 2020 Winter;85(4):263-
267. [PubMed: 33562982]
2. Ahmed YA, Ali S, Ghallab A. Hair histology as a tool for forensic identification of some
domestic animal species. EXCLI J. 2018;17:663-670. [PMC free article: PMC6088218]
[PubMed: 30108469]
3. Hu XM, Li ZX, Zhang DY, Yang YC, Fu SA, Zhang ZQ, Yang RH, Xiong K. A systematic
summary of survival and death signalling during the life of hair follicle stem cells. Stem Cell
Res Ther. 2021 Aug 11;12(1):453. [PMC free article: PMC8359037] [PubMed: 34380571]
4. Zhou L, Wang H, Jing J, Yu L, Wu X, Lu Z. Regulation of hair follicle development by
exosomes derived from dermal papilla cells. Biochem Biophys Res Commun. 2018 Jun
02;500(2):325-332. [PubMed: 29654758]
5. Caro R, Fast J. Pregnancy Myths and Practical Tips. Am Fam Physician. 2020 Oct
01;102(7):420-426. [PubMed: 32996758]

Disclosure: Brendon Verhave declares no relevant financial relationships with ineligible companies.

Disclosure: Ali Nassereddin declares no relevant financial relationships with ineligible companies.

Disclosure: Sarah Lappin declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work,
provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article,
provided that you credit the author and journal.

Bookshelf ID: NBK526092 PMID: 30252348