Epidermis

The epidermis is the outermost of the three layers that make up the skin, the inner layers being the dermis and hypodermis.[1] The epidermis layer provides a barrier to infection from environmental pathogens[2] and regulates the amount of water released from the body into the atmosphere through transepidermal water loss.[3] The epidermis is composed of multiple layers of flattened cells[4] that overlie a base layer (stratum basale) composed of columnar cells arranged perpendicularly.

This article is about human skin. For the outer layer of cells in plants, see Epidermis (botany). For other uses, see Epidermis (disambiguation).
Epidermis
Microscopic image of the epidermis, which constitutes the outer layer of skin, shown here by the white bar
Microscopic image showing the layers of the epidermis. The stratum corneum appears more compact in this image than above because of different sample preparation.
Details
Part ofSkin
SystemIntegumentary system
Identifiers
LatinEpidermis
MeSHD004817
TAA16.0.00.009
THH3.12.00.1.01001
FMA70596
Anatomical terms of microanatomy

The rows of cells develop from stem cells in the basal layer. Cellular mechanisms for regulating water and sodium levels (ENaCs) are found in all layers of the epidermis.[5]

The word epidermis is derived through Latin from Ancient Greek epidermis, itself from Ancient Greek epi, meaning 'over, upon' and from Ancient Greek derma, meaning 'skin'. Something related to or part of the epidermis is termed epidermal.

The human epidermis is a familiar example of epithelium, particularly a stratified squamous epithelium.

Structure

Cellular components

The epidermis primarily consists of keratinocytes[4] (proliferating basal and differentiated suprabasal), which comprise 90% of its cells, but also contains melanocytes, Langerhans cells, Merkel cells,[6]:2–3 and inflammatory cells. Epidermal thickenings called Rete ridges (or rete pegs) extend downward between dermal papillae.[7] Blood capillaries are found beneath the epidermis, and are linked to an arteriole and a venule. The epidermis itself has no blood supply and is nourished almost exclusively by diffused oxygen from the surrounding air.[8]

Cell junctions

Epidermal cells are tightly interconnected to serve as a tight barrier against the exterior environment. The junctions between the epidermal cells are of the adherens junction type, formed by transmembrane proteins called cadherins. Inside the cell, the cadherins are linked to actin filaments. In immunofluorescence microscopy, the actin filament network appears as a thick border surrounding the cells,[5] although the actin filaments are actually located inside the cell and run parallel to the cell membrane. Because of the proximity of the neighboring cells and tightness of the junctions, the actin immunofluorescence appears as a border between cells.[5]

Layers
Schematic image showing a section of epidermis, with epidermal layers labeled

The epidermis is composed of 4 or 5 layers, depending on the region of skin being considered.[9] Those layers in descending order are:[2]

Confocal image of the stratum corneum
Composed of 10 to 30 layers of polyhedral, anucleated corneocytes (final step of keratinocyte differentiation), with the palms and soles having the most layers. Corneocytes contain a protein envelope (cornified envelope proteins) underneath the plasma membrane, are filled with water-retaining keratin proteins, attached together through corneodesmosomes and surrounded in the extracellular space by stacked layers of lipids.[10] Most of the barrier functions of the epidermis localize to this layer.[11]
This narrow layer is found only on the palms and soles. The epidermis of these two areas is known as "thick skin" because with this extra layer, the skin has 5 epidermal layers instead of 4.
Confocal image of the stratum granulosum
Keratinocytes lose their nuclei and their cytoplasm appears granular. Lipids, contained into those keratinocytes within lamellar bodies, are released into the extracellular space through exocytosis to form a lipid barrier. Those polar lipids are then converted into non-polar lipids and arranged parallel to the cell surface. For example glycosphingolipids become ceramides and phospholipids become free fatty acids.[10]
Confocal image of the stratum spinosum already showing some clusters of basal cells
Keratinocytes become connected through desmosomes and produce lamellar bodies, from within the Golgi, enriched in polar lipids, glycosphingolipids, free sterols, phospholipids and catabolic enzymes.[3] Langerhans cells, immunologically active cells, are located in the middle of this layer.[10]
  • basal/germinal layer (stratum basale/germinativum).
Confocal image of the stratum basale already showing some papillae
Composed mainly of proliferating and non-proliferating keratinocytes, attached to the basement membrane by hemidesmosomes. Melanocytes are present, connected to numerous keratinocytes in this and other strata through dendrites. Merkel cells are also found in the stratum basale with large numbers in touch-sensitive sites such as the fingertips and lips. They are closely associated with cutaneous nerves and seem to be involved in light touch sensation.[10]

The Malpighian layer (stratum malpighi) is both the stratum basale and stratum spinosum.[4]

The epidermis is separated from the dermis, its underlying tissue, by a basement membrane.

Cellular kinetics

Cell division

As a stratified squamous epithelium, the epidermis is maintained by cell division within the stratum basale. Differentiating cells delaminate from the basement membrane and are displaced outward through the epidermal layers, undergoing multiple stages of differentiation until, in the stratum corneum, losing their nucleus and fusing to squamous sheets, which are eventually shed from the surface (desquamation). Differentiated keratinocytes secrete keratin proteins, which contribute to the formation of an extracellular matrix that is an integral part of the skin barrier function. In normal skin, the rate of keratinocyte production equals the rate of loss,[4] taking about two weeks for a cell to journey from the stratum basale to the top of the stratum granulosum, and an additional four weeks to cross the stratum corneum.[2] The entire epidermis is replaced by new cell growth over a period of about 48 days.[12]

Calcium concentration

Keratinocyte differentiation throughout the epidermis is in part mediated by a calcium gradient, increasing from the stratum basale until the outer stratum granulosum, where it reaches its maximum, and decreasing in the stratum corneum. Calcium concentration in the stratum corneum is very low in part because those relatively dry cells are not able to dissolve the ions. This calcium gradient parallels keratinocyte differentiation and as such is considered a key regulator in the formation of the epidermal layers.[3]

Elevation of extracellular calcium concentrations induces an increase in intracellular free calcium concentrations.[13] Part of that intracellular increase comes from calcium released from intracellular stores[14] and another part comes from transmembrane calcium influx,[15] through both calcium-sensitive chloride channels[16] and voltage-independent cation channels permeable to calcium.[17] Moreover, it has been suggested that an extracellular calcium-sensing receptor (CaSR) also contributes to the rise in intracellular calcium concentration.[18]

Development

Epidermal organogenesis, the formation of the epidermis, begins in the cells covering the embryo after neurulation, the formation of the central nervous system. In most vertebrates, this original one-layered structure quickly transforms into a two-layered tissue; a temporary outer layer, the periderm, which is disposed once the inner basal layer or stratum germinativum has formed.[19]

This inner layer is a germinal epithelium that gives rise to all epidermal cells. It divides to form the outer spinous layer (stratum spinosum). The cells of these two layers, together called the Malpighian layer(s) after Marcello Malpighi, divide to form the superficial granular layer (Stratum granulosum) of the epidermis.[19]

The cells in the stratum granulosum do not divide, but instead form skin cells called keratinocytes from the granules of keratin. These skin cells finally become the cornified layer (stratum corneum), the outermost epidermal layer, where the cells become flattened sacks with their nuclei located at one end of the cell. After birth these outermost cells are replaced by new cells from the stratum granulosum and throughout life they are shed at a rate of 0.001 - 0.003 ounces of skin flakes every hour, or 0.024-0.072 ounces per day.[20]

Epidermal development is a product of several growth factors, two of which are:[19]

Function

Barrier

The epidermis serves as a barrier to protect the body against microbial pathogens, oxidant stress (UV light), and chemical compounds, and provides mechanical resistance to minor injury. Most of this barrier role is played by the stratum corneum.[11]

Characteristics
  • Physical barrier: Epidermal keratinocytes are tightly linked by cell–cell junctions associated to cytoskeletal proteins, giving the epidermis its mechanical strength.[3]
  • Chemical barrier: Highly organized lipids, acids, hydrolytic enzymes, and antimicrobial peptides[3] inhibit passage of external chemicals and pathogens into the body.
  • Immunologically active barrier: The humoral and cellular constituents of the immune system[3] found in the epidermis actively combat infection.
  • Water content of the stratum corneum drops towards the surface, creating hostile conditions for pathogenic microorganism growth.[11]
  • An acidic pH (around 5.0) and low amounts of water make the epidermis hostile to many microorganic pathogens.[11]
  • Non-pathogenic microorganisms on the surface of the epidermis help defend against pathogens by competing for food, limiting its availability, and producing chemical secretions that inhibit the growth of pathogenic microbiota.[11]
Permeability
  • Psychological stress, through an increase in glucocorticoids, compromises the stratum corneum and thus the barrier function.[21]
  • Sudden and large shifts in humidity alter stratum corneum hydration in a way that could allow entry of pathogenic microorganisms.[22]

Skin hydration

The ability of the skin to hold water is primarily due to the stratum corneum and is critical for maintaining healthy skin.[23] Skin hydration is quantified using corneometry.[24] Lipids arranged through a gradient and in an organized manner between the cells of the stratum corneum form a barrier to transepidermal water loss[25][26].

Skin color

The amount and distribution of melanin pigment in the epidermis is the main reason for variation in skin color in Homo sapiens. Melanin is found in the small melanosomes, particles formed in melanocytes from where they are transferred to the surrounding keratinocytes. The size, number, and arrangement of the melanosomes vary between racial groups, but while the number of melanocytes can vary between different body regions, their numbers remain the same in individual body regions in all human beings. In white and Asian skin the melanosomes are packed in "aggregates", but in black skin they are larger and distributed more evenly. The number of melanosomes in the keratinocytes increases with UV radiation exposure, while their distribution remain largely unaffected.[27]

Clinical significance

Laboratory culture of keratinocytes to form a 3D structure (artificial skin) recapitulating most of the properties of the epidermis is routinely used as a tool for drug development and testing.

Hyperplasia

Epidermal hyperplasia (thickening resulting from cell proliferation) has various forms:

  • Acanthosis is diffuse epidermal hyperplasia (thickening of the skin, and not to be confused with acanthocytes).[28] It implies increased thickness of the Malpighian layer (stratum basale and stratum spinosum).[29] Acanthosis nigricans is a black, poorly defined, velvety hyperpigmented acanthosis, usually observed in the back of neck, axilla, and other folded regions of the skin.
  • Focal epithelial hyperplasia (Heck's disease) is an asymptomatic, benign neoplastic condition characterized by multiple white to pinkish papules that occur diffusely in the oral cavity.[30].[6]:411
  • Pseudoepitheliomatous hyperplasia (PEH) is a benign condition characterized by hyperplasia of the epidermis and epithelium of skin appendages,[31] with irregular squamous strands extending down into the dermis,[32] and closely simulating squamous cell carcinoma (SCC).[31]
  • Acanthosis nigricans
  • Heck's disease
  • Pseudoepitheliomatous hyperplasia (PEH), low magnification, with acanthotic squamous epithelium with irregular thick finger-like downgrowths into the underlying dermis.
  • PEH, high magnification, with reactive-appearing squamous downgrowths with no significant cytologic atypia.

Additional images
  • Epidermis and dermis of human skin
  • Cross-section of all skin layers
  • Illustration of epidermal layers
  • Optical coherence tomography of fingertip
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See also

References
  1. Young, Barbara (2014). Wheater's functional histology a text and colour atlas. Elsevier. pp. 160 & 175. ISBN 9780702047473.
  2. Marks, James G; Miller, Jeffery (2006). Lookingbill and Marks' Principles of Dermatology (4th ed.). Elsevier. pp. 1–7. ISBN 978-1-4160-3185-7.
  3. Proksch, E.; Brandner, J.; Jensen, J.M. (2008). "The skin: an indispensable barrier". Experimental Dermatology. 17 (12): 1063–1072. doi:10.1111/j.1600-0625.2008.00786.x. PMID 19043850.
  4. McGrath, J.A.; Eady, R.A.; Pope, F.M. (2004). Rook's Textbook of Dermatology (7th ed.). Blackwell Publishing. pp. 3.1–3.6. ISBN 978-0-632-06429-8.
  5. Hanukoglu I, Boggula VR, Vaknine H, Sharma S, Kleyman T, Hanukoglu A (January 2017). "Expression of epithelial sodium channel (ENaC) and CFTR in the human epidermis and epidermal appendages". Histochemistry and Cell Biology. 147 (6): 733–748. doi:10.1007/s00418-016-1535-3. PMID 28130590.
  6. James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.
  7. TheFreeDictionary > rete ridge Citing: The American Heritage Medical Dictionary Copyright 2007, 2004
  8. Stücker, M; Struk, A; Altmeyer, P; Herde, M; Baumgärtl, H; Lübbers, DW (2002). "The cutaneous uptake of atmospheric oxygen contributes significantly to the oxygen supply of human dermis and epidermis". The Journal of Physiology. 538 (3): 985–994. doi:10.1113/jphysiol.2001.013067. PMC 2290093. PMID 11826181.
  9. The Ageing Skin - Structure
  10. "Please update" (PDF). Archived from the original (PDF) on 2010-12-14. Retrieved 2015-01-07.
  11. Elias, P.M. (2007). "The skin barrier as an innate immune element". Seminars in Immunopathology. 29 (1): 3–14. doi:10.1007/s00281-007-0060-9. PMID 17621950.
  12. Iizuka, Hajime (1994). "Epidermal turnover time". Journal of Dermatological Science. 8 (3): 215–217. doi:10.1016/0923-1811(94)90057-4. PMID 7865480.
  13. Hennings, H; Kruszewski, FH; Yuspa, SH; Tucker, RW (1989). "Intracellular calcium alterations in response to increased external calcium in normal and neoplastic keratinocytes". Carcinogenesis. 10 (4): 777–80. doi:10.1093/carcin/10.4.777. PMID 2702726.
  14. Pillai, S; Bikle, DD (1991). "Role of intracellular-free calcium in the cornified envelope formation of keratinocytes: Differences in the mode of action of extracellular calcium and 1,25 dihydroxyvitamin D3". Journal of Cellular Physiology. 146 (1): 94–100. doi:10.1002/jcp.1041460113. PMID 1990023.
  15. Reiss, M; Lipsey, LR; Zhou, ZL (1991). "Extracellular calcium-dependent regulation of transmembrane calcium fluxes in murine keratinocytes". Journal of Cellular Physiology. 147 (2): 281–91. doi:10.1002/jcp.1041470213. PMID 1645742.
  16. Mauro, TM; Pappone, PA; Isseroff, RR (1990). "Extracellular calcium affects the membrane currents of cultured human keratinocytes". Journal of Cellular Physiology. 143 (1): 13–20. doi:10.1002/jcp.1041430103. PMID 1690740.
  17. Mauro, TM; Isseroff, RR; Lasarow, R; Pappone, PA (1993). "Ion channels are linked to differentiation in keratinocytes". The Journal of Membrane Biology. 132 (3): 201–9. doi:10.1007/BF00235738. PMID 7684087.
  18. Tu, CL; Oda, Y; Bikle, DD (1999). "Effects of a calcium receptor activator on the cellular response to calcium in human keratinocytes". The Journal of Investigative Dermatology. 113 (3): 340–5. doi:10.1046/j.1523-1747.1999.00698.x. PMID 10469331.
  19. Gilbert, Scott F (2000). "The Epidermis and the Origin of Cutaneous Structures". Developmental Biology. Sinauer Associates. ISBN 978-0-87893-243-6.
  20. Weschler, Charles J. (April 8, 2011). "Squalene and Cholesterol in Dust from Danish Homes and Daycare Centers" (PDF). Environ. Sci. Technol. 45 (9): 3872–3879. Bibcode:2011EnST...45.3872W. doi:10.1021/es103894r. PMID 21476540.
  21. Denda, M.; Tsuchiya, T.; Elias, P.M.; Feingold, K.R. (2000). "Stress alters cutaneous permeability barrier homeostasis". Am J Physiol Regul Integr Comp Physiol. 278 (2): R367–372. doi:10.1152/ajpregu.2000.278.2.R367. PMID 10666137. S2CID 558526.
  22. Tsai, Jui-Chen; Guy, Richard H.; Thornfeldt, Carl R.; Gao, Wen Ni; Feingold, Kenneth R.; Elias, Peter M. (1996). "Metabolic Approaches To Enhance Transdermal Drug Delivery. 1. Effect of Lipid Synthesis Inhibitors". Journal of Pharmaceutical Sciences. 85 (6): 643–648. doi:10.1021/js950219p. PMID 8773963.
  23. Blank, IH (1952). "Factors which influence the water content of the stratum corneum". The Journal of Investigative Dermatology. 18 (6): 433–40. doi:10.1038/jid.1952.52. PMID 14938659.
  24. C. W. Blichmann, J. Serup: Assessment of Skin Moisture, Acta Derm. Venereol. (Stockli) 1988; 68: 284–290
  25. Downing, DT; Stewart, ME; Wertz, PW; Colton, SW; Abraham, W; Strauss, JS (1987). "Skin lipids: An update". The Journal of Investigative Dermatology. 88 (3 Suppl): 2s–6s. doi:10.1111/1523-1747.ep12468850. PMID 2950180.
  26. Bonté, F; Saunois, A; Pinguet, P; Meybeck, A (1997). "Existence of a lipid gradient in the upper stratum corneum and its possible biological significance". Archives of Dermatological Research. 289 (2): 78–82. doi:10.1007/s004030050158. PMID 9049040.
  27. Montagna, William; Prota, Giuseppe; Kenney, John A. (1993). Black skin: structure and function. Gulf Professional Publishing. p. 69. ISBN 978-0-12-505260-3.
  28. Kumar, Vinay; Fausto, Nelso; Abbas, Abul (2004) Robbins & Cotran Pathologic Basis of Disease (7th ed.). Saunders. Page 1230. ISBN 0-7216-0187-1.
  29. M. S. Stone; T. L. Ray (September 1995). "Acanthosis". DermPathTutor. Department of Dermatology, University of Iowa. Archived from the original on 29 May 2012. Retrieved 17 May 2012.
  30. Tenore, G.; Palaia, G.; Del Vecchio, A.; Galanakis, A.; Romeo, U. (2013-10-24). "Focal epithelial hyperplasia (Heck's disease)". Annali di Stomatologia. 4 (Suppl 2): 43. ISSN 1824-0852. PMC 3860189. PMID 24353818.
  31. Chakrabarti, Suvadip; Chakrabarti, PreetiRihal; Agrawal, Deepak; Somanath, Shreyas (2014). "Pseudoepitheliomatous hyperplasia: A clinical entity mistaken for squamous cell carcinoma". Journal of Cutaneous and Aesthetic Surgery. 7 (4): 232–4. doi:10.4103/0974-2077.150787. ISSN 0974-2077. PMC 4338470. PMID 25722605.
  32. Lynch, Jane M. (2004). "Understanding Pseudoepitheliomatous Hyperplasia". Pathology Case Reviews. 9 (2): 36–45. doi:10.1097/01.pcr.0000117275.18471.5f. ISSN 1082-9784.
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