Integumentary System Development - Vernix Caseosa: Difference between revisions
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* '''Applying a vernix caseosa based formulation accelerates skin barrier repair by modulating lipid biosynthesis'''{{#pmid:29217624|PMID29217624}} "Restoring the lipid homeostasis of the stratum corneum (SC) is a common strategy to enhance skin barrier function. Here, we used a ceramide containing vernix caseosa (VC)-based formulation and were able to accelerate barrier recovery in healthy volunteers. The recovery was examined over 16 days by monitoring trans-epidermal water loss (TEWL) after barrier disruption by tape-stripping. Four skin sites were used to examine the effects of both treatment and barrier recovery. After 16 days, samples were harvested at these sites to examine the SC ceramide composition and lipid organization. Changes in ceramide profiles were identified using principal component analysis. After barrier recovery, the untreated sites showed increased levels of ceramide subclass AS and ceramides with a 34 total carbon-atom chain length, while the mean ceramide chain length was reduced. These changes were diminished by treatment with the studied formulation, which concurrently increased the formulated ceramides. Correlations were observed between SC lipid composition, lipid organization, and TEWL, and changes in the ceramide subclass composition suggest changes in the ceramide biosynthesis. These results suggest that VC-based formulations enhance skin barrier recovery and are attractive candidates to treat skin disorders with impaired barrier properties." | |||
* '''Skin barrier in the neonate'''{{#pmid:29596733|PMID29596733}} "The purpose of this review is to focus on determinants of skin barrier function in neonates at molecular and cellular levels. The skin barrier is critical in terms of water and gas exchanges during fetal life and undergoes rapid changes at birth, followed by a progressive maturation. Consequences of skin barrier disruption can be extremely detrimental or lethal, as shown in severe genetic epidermal defects. In this context, the fine-tuned rapid adaptation from a liquid to a gaseous milieu is not fully understood. The stratum corneum provides an air-liquid barrier, tight junctions in the granular layer provide a liquid-liquid barrier, aquaporins represent a plumbing system for water-glycerol as well as gas exchanges, and Langerhans cells are central to the immunological barrier. Acid mantle formation is essential for appropriate interaction between the skin and microbial symbionts. Temperature and pH regulate the key enzyme activities responsible for the integrity of the stratum corneum. Skin barrier permeability can be assessed noninvasively and simply with miniaturized devices measuring transepidermal water loss, where water flow is faster in cases of a damaged or functionally premature barrier. New avenues for therapeutic skin barrier research in neonates include a better delineation of the maturation of aquaporins in water balance and gas exchanges from fetal to neonatal life and a better understanding of the role of vernix caseosa, in particular, for the implantation of a healthy microbiote. Practical applications should be derived for caring for infant skin, particularly in fragile zones, such as the diaper area." {{neonatal}} | * '''Skin barrier in the neonate'''{{#pmid:29596733|PMID29596733}} "The purpose of this review is to focus on determinants of skin barrier function in neonates at molecular and cellular levels. The skin barrier is critical in terms of water and gas exchanges during fetal life and undergoes rapid changes at birth, followed by a progressive maturation. Consequences of skin barrier disruption can be extremely detrimental or lethal, as shown in severe genetic epidermal defects. In this context, the fine-tuned rapid adaptation from a liquid to a gaseous milieu is not fully understood. The stratum corneum provides an air-liquid barrier, tight junctions in the granular layer provide a liquid-liquid barrier, aquaporins represent a plumbing system for water-glycerol as well as gas exchanges, and Langerhans cells are central to the immunological barrier. Acid mantle formation is essential for appropriate interaction between the skin and microbial symbionts. Temperature and pH regulate the key enzyme activities responsible for the integrity of the stratum corneum. Skin barrier permeability can be assessed noninvasively and simply with miniaturized devices measuring transepidermal water loss, where water flow is faster in cases of a damaged or functionally premature barrier. New avenues for therapeutic skin barrier research in neonates include a better delineation of the maturation of aquaporins in water balance and gas exchanges from fetal to neonatal life and a better understanding of the role of vernix caseosa, in particular, for the implantation of a healthy microbiote. Practical applications should be derived for caring for infant skin, particularly in fragile zones, such as the diaper area." {{neonatal}} | ||
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* [http://www.ijdb.ehu.es/web/contents.php?vol=48&issue=2-3 IJDB Vol. 48 Nos. 2/3 (2004) Skin Development] | * [http://www.ijdb.ehu.es/web/contents.php?vol=48&issue=2-3 IJDB Vol. 48 Nos. 2/3 (2004) Skin Development] |
Revision as of 11:30, 9 August 2018
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Introduction
The vernix caseosa consists of corneocytes embedded in a rich lipid matrix anchored to the fetal epithelium by hair. Prenatally, this thick slippery integumentary layer may protect the fetal skin from the watery environment, and at birth may aid the delivery process. Vernix has also many other known and potential functions.[1] The constituent components and their concentrations appear to differ between individuals and the sexes.[2]
Some Recent Findings
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More recent papers |
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More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Vernix Caseosa <pubmed limit=5>Vernix Caseosa</pubmed> |
Textbooks
- Human Embryology (2nd ed.) Larson Chapter 14 p443-455
- The Developing Human: Clinically Oriented Embryology (6th ed.) Moore and Persaud Chapter 20: P513-529
- Before We Are Born (5th ed.) Moore and Persaud Chapter 21: P481-496
- Essentials of Human Embryology Larson Chapter 14: P303-315
- Human Embryology, Fitzgerald and Fitzgerald
- Color Atlas of Clinical Embryology Moore Persaud and Shiota Chapter 15: p231-236
Integumentary Development Overview
4 weeks
- simple ectoderm epithelium over mesenchyme.
1-3 months
|
Integument Human Embryo (Week 8, Stage 22) |
4 months
Fetal human integumentary histology[6](Weeks in figure are from LMP)
- Basal cell - proliferation generates folds in basement membrane.
- Neural crest cells - melanoblasts migrate into epithelium. These are the future melanocyte pigment cell of the skin.
- Embryonic connective tissue- differentiates into dermis, a loose ct layer over a dense ct layer. Beneath the dense ct layer is another loose ct layer that will form the subcutaneous layer.
- Ectoderm contributes to nails, hair follictles and glands.
- Nails form as thickening of ectoderm epidermis at the tips of fingers and toes. These form germinative cells of nail field.
- Cords of these cells extend into mesoderm forming epithelial columns. These form hair follicles, sebaceous and sweat glands.
5 months
- Hair growth initiated at base of cord, lateral outgrowths form associated sebaceous glands.
- Other cords elongate and coil to form sweat glands.
- Cords in mammary region branch as they elongate to form mammary glands. These glands will complete development in females at puberty. Functional maturity only occurs in late pregnancy.
Embryonic and Fetal Epidermis
Electron Micrographs of the Developing Human Epidermis[7]
6 to 8 weeks (8-9 week EGA) |
7 to 9 weeks (9-11 week EGA) |
22 weeks (about 24 week EGA) |
Functions
Vernix has many different known and potential functions.[1]
- a highly variable coating of the fetal skin
- high water content (80%) largely compartmentalized within fetal corneocytes (cells forming the stratum corneum)
- develops cranio-caudally production coincides in utero with terminal differentiation of the epidermis and formation of the stratum corneum
- primarily composed of sebum, cells that have sloughed off the fetus's skin and shed lanugo hair
- can be absent in preterm infants
- dehydration and rehydration processes occur two to four times faster at 37 degrees celcius than at room temperature[8]
- towards term fragments of vernix can mix into the amniotic fluid resulting in (normal) turbidity
- fetal swallowing of amniotic fluid mixed with fragments of vernix can also occur
- cathelicidin LL-37, alpha-defensins, and LL-37 in neutrophils.[9]
Abnormalities
Vernix Caseosa Peritonitis
Vernix caseosa peritonitis is a very rare post caesarean section inflammatory response occurring maternally after birth.[10]
References
- ↑ 1.0 1.1 Pickens WL, Warner RR, Boissy YL, Boissy RE & Hoath SB. (2000). Characterization of vernix caseosa: water content, morphology, and elemental analysis. J. Invest. Dermatol. , 115, 875-81. PMID: 11069626 DOI.
- ↑ 2.0 2.1 2.2 Míková R, Vrkoslav V, Hanus R, Háková E, Hábová Z, Doležal A, Plavka R, Coufal P & Cvačka J. (2014). Newborn boys and girls differ in the lipid composition of vernix caseosa. PLoS ONE , 9, e99173. PMID: 24911066 DOI.
- ↑ Boiten WA, Berkers T, Absalah S, van Smeden J, Lavrijsen APM & Bouwstra JA. (2018). Applying a vernix caseosa based formulation accelerates skin barrier repair by modulating lipid biosynthesis. J. Lipid Res. , 59, 250-260. PMID: 29217624 DOI.
- ↑ Taïeb A. (2018). Skin barrier in the neonate. Pediatr Dermatol , 35 Suppl 1, s5-s9. PMID: 29596733 DOI.
- ↑ Fuchs E. (2008). Skin stem cells: rising to the surface. J. Cell Biol. , 180, 273-84. PMID: 18209104 DOI.
- ↑ 6.0 6.1 Coolen NA, Schouten KC, Middelkoop E & Ulrich MM. (2010). Comparison between human fetal and adult skin. Arch. Dermatol. Res. , 302, 47-55. PMID: 19701759 DOI.
- ↑ Dale BA, Holbrook KA, Kimball JR, Hoff M & Sun TT. (1985). Expression of epidermal keratins and filaggrin during human fetal skin development. J. Cell Biol. , 101, 1257-69. PMID: 2413039
- ↑ Rissmann R, Groenink HW, Gooris GS, Oudshoorn MH, Hennink WE, Ponec M & Bouwstra JA. (2008). Temperature-induced changes in structural and physicochemical properties of vernix caseosa. J. Invest. Dermatol. , 128, 292-9. PMID: 17671513 DOI.
- ↑ Yoshio H, Lagercrantz H, Gudmundsson GH & Agerberth B. (2004). First line of defense in early human life. Semin. Perinatol. , 28, 304-11. PMID: 15565791
- ↑ Stuart OA, Morris AR & Baber RJ. (2009). Vernix caseosa peritonitis - no longer rare or innocent: a case series. J Med Case Rep , 3, 60. PMID: 19208257 DOI.
Reviews
Visscher MO, Adam R, Brink S & Odio M. (2015). Newborn infant skin: physiology, development, and care. Clin. Dermatol. , 33, 271-80. PMID: 25889127 DOI.
Visscher M & Narendran V. (2014). The Ontogeny of Skin. Adv Wound Care (New Rochelle) , 3, 291-303. PMID: 24761361 DOI.
Chambers AC, Patil AV, Alves R, Hopkins JC, Armstrong J & Lawrence RN. (2012). Delayed presentation of vernix caseosa peritonitis. Ann R Coll Surg Engl , 94, 548-51. PMID: 23131223 DOI.
Singh G & Archana G. (2008). Unraveling the mystery of vernix caseosa. Indian J Dermatol , 53, 54-60. PMID: 19881987 DOI.
Visscher MO, Narendran V, Pickens WL, LaRuffa AA, Meinzen-Derr J, Allen K & Hoath SB. (2005). Vernix caseosa in neonatal adaptation. J Perinatol , 25, 440-6. PMID: 15830002 DOI.
Articles
Kalužíková A, Vrkoslav V, Harazim E, Hoskovec M, Plavka R, Buděšínský M, Bosáková Z & Cvačka J. (2017). Cholesteryl esters of ω-(O-acyl)-hydroxy fatty acids in vernix caseosa. J. Lipid Res. , 58, 1579-1590. PMID: 28576934 DOI.
Checa A, Holm T, Sjödin MO, Reinke SN, Alm J, Scheynius A & Wheelock CE. (2015). Lipid mediator profile in vernix caseosa reflects skin barrier development. Sci Rep , 5, 15740. PMID: 26521946 DOI.
Visscher MO, Utturkar R, Pickens WL, LaRuffa AA, Robinson M, Wickett RR, Narendran V & Hoath SB. (2011). Neonatal skin maturation--vernix caseosa and free amino acids. Pediatr Dermatol , 28, 122-32. PMID: 21504444 DOI.
Tollin M, Jägerbrink T, Haraldsson A, Agerberth B & Jörnvall H. (2006). Proteome analysis of vernix caseosa. Pediatr. Res. , 60, 430-4. PMID: 16940245 DOI.
Rissmann R, Groenink HW, Weerheim AM, Hoath SB, Ponec M & Bouwstra JA. (2006). New insights into ultrastructure, lipid composition and organization of vernix caseosa. J. Invest. Dermatol. , 126, 1823-33. PMID: 16628195 DOI.
Tollin M, Bergsson G, Kai-Larsen Y, Lengqvist J, Sjövall J, Griffiths W, Skúladóttir GV, Haraldsson A, Jörnvall H, Gudmundsson GH & Agerberth B. (2005). Vernix caseosa as a multi-component defence system based on polypeptides, lipids and their interactions. Cell. Mol. Life Sci. , 62, 2390-9. PMID: 16179970 DOI.
Akinbi HT, Narendran V, Pass AK, Markart P & Hoath SB. (2004). Host defense proteins in vernix caseosa and amniotic fluid. Am. J. Obstet. Gynecol. , 191, 2090-6. PMID: 15592296 DOI.
Yoshio H, Tollin M, Gudmundsson GH, Lagercrantz H, Jornvall H, Marchini G & Agerberth B. (2003). Antimicrobial polypeptides of human vernix caseosa and amniotic fluid: implications for newborn innate defense. Pediatr. Res. , 53, 211-6. PMID: 12538777 DOI.
Hoeger PH, Schreiner V, Klaassen IA, Enzmann CC, Friedrichs K & Bleck O. (2002). Epidermal barrier lipids in human vernix caseosa: corresponding ceramide pattern in vernix and fetal skin. Br. J. Dermatol. , 146, 194-201. PMID: 11903227
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Integumentary Development
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Cite this page: Hill, M.A. (2024, April 23) Embryology Integumentary System Development - Vernix Caseosa. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Integumentary_System_Development_-_Vernix_Caseosa
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