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Corneocytes are terminally differentiated keratinocytes and compose most if not all of the stratum corneum, the outermost part of the epidermis. They are regularly replaced through desquamation and renewal from lower epidermal layers, making them an essential part of the skin barrier property.


Corneocytes are polyhedral, anucleated cells without cytoplasmic organelles, interlocked with each other and organized as vertical columns of 10–30 cells and embedded within a highly hydrophobic lipid matrix to form the stratum corneum. Even if biologically dead they remain active, being filled with keratin, lipids, fatty acids and ceramides.[1][2]

Corneocytes in the lower part of the stratum corneum are bridged together through specialized junctions (corneodesmosomes). Those junctions disintegrate as corneocytes migrate toward the surface of the skin and result in desquamation.[1] At the same time, as those loosened junctions encounter more hydration, they will expand and connect together, forming potential entry pores for microorganisms across the stratum corneum.[2]

The corneocyte cell layer (stratum corneum) can absorb three times its weight in water but if its water content drops below 10% it no longer remains pliable and cracks.[3]


Corneocytes are keratinocytes in their last stage of differentiation. Keratinocytes in the stratum basale of the epidermis will multiply through cell division and migrate toward the skin surface. During that migration keratinocytes will undergo multiple stages of differentiation to finally become corneocytes once they reach the stratum corneum. As corneocytes are continually eliminated through desquamation or through rubbing, skin washing or detergents they are also continually formed through keratinocyte differentiation.[1]

Corneocytes, also referred to as squames (from Latin squama, meaning a “thin flake” or “scales”) are terminally differentiated, anucleated cells of keratinocyte lineage that constitute the majority of stratum corneum, the outermost layer of the epidermis. Size of a corneocyte is approximately 30-50 µm in diameter and 1 µm thick, and the average area of corneocytes at the surface of the skin reaches approximately 1000 µm2, but may vary according to anatomical location, age and external environmental conditions such as ultraviolet (UV) irradiation.[4][5] Major constituents of corneocytes are keratin intermediate filaments organized in parallel bundles to form a matrix to give rigidity to the overall structure of the skin.[6]


Layers of corneocytes produce high mechanical strength which allow epidermis of the skin to perform its function as a physical, chemical and immunological barrier. For example, corneocytes act as UV barrier by reflecting the scattered UV radiation, protecting cells inside the body from apoptosis and DNA damage.[7] As corneocytes are essentially dead cells, they are not prone to viral attacks, though invisible microabrasions may cause permeability. Colonization of pathogens in the skin is prevented via complete turnovers of corneocyte layer every 2–4 weeks.[8] Corneocytes are also capable of absorbing and storing small amounts of water to keep the skin hydrated and maintain its flexibility.[9]

Intracellular structures[edit]

Natural moisturizing factor[edit]

Corneocytes contain small molecules called natural moisturizing factors, which absorb small amounts of water into the corneocytes thereby hydrating the skin. The natural moisturizing factor is a collection of water-soluble compounds produced from the degradation of histidine-rich proteins called filaggrin, which are responsible for aggregating keratin filaments to form keratin bundles that maintain the rigid structure of the cells in stratum corneum.[10] When filaggrin is degraded, urea, pyrrolidone carboxylic acid (1,2), glutamic acid and other amino acids are produced.[11] These are collectively referred to as the ‘natural moisturizing factor’ of the skin. The components of the natural moisturizing factor absorb water from the atmosphere to ensure that the superficial layers of the stratum corneum stay hydrated. As they are water-soluble themselves, excessive water contact may leach them and inhibit their normal functions which is why prolonged contact with water makes the skin drier.[12] The intercellular lipid layer helps prevent the loss of natural moisturizing factor by sealing the outside of each corneocyte.[11]

Extracellular structures[edit]

Although stratum corneum is mostly composed of corneocytes, other supporting structures are present in the extracellular matrix to assist in the function of stratum corneum. These include:

  • Lamellar bodies
  • Intercellular lipids (lamellar lipid bilayer)
  • Cornified envelope
  • Corneodesmosomes

Lamellar bodies[edit]

Lamellar bodies are tubular or ovoid-shaped secretory organelles derived from the Golgi apparatus of keratinocytes in the upper part of stratum spinosum.[13] From the site of production, lamellar bodies migrate to the top of the stratum granulosum and then into the intercellular domain of the stratum corneum to extrude their contents, which are predominantly lipids. The lipids ultimately form the lamellar lipid bilayer that surrounds corneocytes and also contribute to permeability barrier homeostasis of the stratum corneum.[11] The homeostasis function is regulated by the calcium gradient in the epidermis.[14] Usually the calcium level is very low in stratum corneum, but high in stratum granulosum. Once the permeability barrier is disrupted an influx of water occurs in the stratum corneum, which in turn increases the calcium levels in the stratum corneum but decreases it in the stratum granulosum. This perturbation induces lamellar bodies to undergo exocytosis and secrete lipids such as glycosylceramides, cholesterol and phospholipids to retrieve the permeability barrier function of stratum corneum.[7]

Intercellular lipids (lamellar lipid bilayer)[edit]

Corneocytes are embedded in a matrix of specialized lipids that constitute approximately 20% of the stratum corneum volume.[6] The major constituents of the intercellular lipids in stratum corneum include ceramides (30-50% by mass), cholesterol (25% by mass) and free fatty acids (10-20% by mass), mostly produced by lamellar bodies.[7][15] These hydrophobic components fuse together to form multiple bilayers of lipids between corneocytes to act as the principal barrier to the transcutaneous movement of water and electrolytes.

Cornified envelope[edit]

The cornified envelope is a protein shell that surrounds each corneocyte. Its thickness varies between 15 and 20 nm.,[16] and is formed during the transition stage of granular keratinocytes into corneocytes The three proteins that form the scaffold of the cornified envelope include involucrin, envoplakin and periplakin. These proteins are highly insoluble and extensively cross-linked to each other, giving the insoluble property of the cornified envelope and contribute to the mechanical resistance of the skin.[17]

Corneodesmosomes and desquamation[edit]

The overall integrity of the stratum corneum is maintained by specialized intercellular proteins called corneodesmosomes. Three adhesive proteins desmoglein-1, desmocollin-1 and corneodesmosin compose the corneodesmosomes and provide the cohesive forces to connect the adjacent corneocytes.[18] The components of the corneodesmosomes are gradually degraded by the enzymes that digest proteins,[18] as the corneocytes are pushed towards the surface of the skin. As a result of the weakened corneodesmosomes in the outer skin surface, the uppermost layers of corneocytes get exfoliated through frictional forces such as rubbing or washing. This process is a normal protective mechanism of the skin to prevent pathogens from colonizing the skin, and is referred to as desquamation. In healthy skin, desquamation is an invisible process and the stratum corneum is turned over completely within 2–4 weeks, while maintaining the tissue thickness.[8]


Dry skin (xerosis)[edit]

Dry skin (xerosis) involves increased thickness of stratum corneum (hyperkeratosis), which may occur due to various reasons including aging, humidity of the environment or UV irradiation. The accumulation of corneocyte clumps on the surface of the skin may lead to abnormal detachment of squames as visible clusters. Xerosis is common, especially in elderly individuals [19] which may be due to decreased quantity of free amino acids, a constituent of natural moisturizing factor.[20] Consequently, many moisturizers in the markets incorporate the components of the natural moisturizing factor as well as keratin and elastin.


Main article: Epidermis (skin)

Corneocytes are part of the stratum corneum of the epidermis and contribute the barrier function of the skin.

See also[edit]


  2. ^ a b 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. 
  3. ^
  4. ^ Pierard, G.E., Courtois, J., Ritacco, C., Humbert, P., Fanian, F. & Pierard-Franchimont, C. (2015) From observational to analytical morphology of the stratum corneum: progress avoiding hazardous animal and human testings. Clin Cosmet Investig Dermatol, 8, 113-125.
  5. ^ Ya-Xian, Z., Suetake, T. & Tagami, H. (1999) Number of cell layers of the stratum corneum in normal skin - relationship to the anatomical location on the body, age, sex and physical parameters. Arch Dermatol Res, 291, 555-559.
  6. ^ a b Harding, C.R. (2004) The stratum corneum: structure and function in health and disease. Dermatol Ther, 17 Suppl 1, 6-15.
  7. ^ a b c Proksch, E., Brandner, J.M. & Jensen, J.M. (2008) The skin: an indispensable barrier. Exp Dermatol, 17, 1063-1072.
  8. ^ a b Wilhelm, K.P., Saunders, J.C. & Maibach, H.I. (1990) Increased stratum corneum turnover induced by subclinical irritant dermatitis. Br J Dermatol, 122, 793-798.
  9. ^ Rawlings, A.V., Scott, I.R., Harding, C.R. & Bowser, P.A. (1994) Stratum corneum moisturization at the molecular level. J Invest Dermatol, 103, 731-741.
  10. ^ Steinert, P.M., Cantieri, J.S., Teller, D.C., Lonsdale-Eccles, J.D. & Dale, B.A. (1981) Characterization of a class of cationic proteins that specifically interact with intermediate filaments. Proceedings of the National Academy of Sciences of the United States of America, 78, 4097-4101.
  11. ^ a b c Robinson, M., Visscher, M., Laruffa, A. & Wickett, R. (2010) Natural moisturizing factors (NMF) in the stratum corneum (SC). I. Effects of lipid extraction and soaking. J Cosmet Sci, 61, 13-22.
  12. ^ Warner, R.R., Boissy, Y.L., Lilly, N.A., Spears, M.J., McKillop, K., Marshall, J.L. & Stone, K.J. (1999) Water disrupts stratum corneum lipid lamellae: damage is similar to surfactants. J Invest Dermatol, 113, 960-966.
  13. ^ Tarutani, M., Nakajima, K., Uchida, Y., Takaishi, M., Goto-Inoue, N., Ikawa, M., Setou, M., Kinoshita, T., Elias, P.M., Sano, S. & Maeda, Y. (2012) GPHR-dependent functions of the Golgi apparatus are essential for the formation of lamellar granules and the skin barrier. J Invest Dermatol, 132, 2019-2025.
  14. ^ Feingold, K.R. (2007) Thematic review series: skin lipids. The role of epidermal lipids in cutaneous permeability barrier homeostasis. J Lipid Res, 48, 2531-2546.
  15. ^ Squier, C.A., Cox, P. & Wertz, P.W. (1991) Lipid content and water permeability of skin and oral mucosa. J Invest Dermatol, 96, 123-126.
  16. ^ Jarnik, M., Simon, M.N. & Steven, A.C. (1998) Cornified cell envelope assembly: a model based on electron microscopic determinations of thickness and projected density. J Cell Sci, 111 (Pt 8), 1051-1060.
  17. ^ Sevilla, L.M., Nachat, R., Groot, K.R., Klement, J.F., Uitto, J., Djian, P., Maatta, A. & Watt, F.M. (2007) Mice deficient in involucrin, envoplakin, and periplakin have a defective epidermal barrier. J Cell Biol, 179, 1599-1612.
  18. ^ a b Caubet, C., Jonca, N., Brattsand, M., Guerrin, M., Bernard, D., Schmidt, R., Egelrud, T., Simon, M. & Serre, G. (2004) Degradation of corneodesmosome proteins by two serine proteases of the kallikrein family, SCTE/KLK5/hK5 and SCCE/KLK7/hK7. J Invest Dermatol, 122, 1235-1244.
  19. ^ Reamy, B.V., Bunt, C.W. & Fletcher, S. (2011) A diagnostic approach to pruritus. Am Fam Physician, 84, 195-202.
  20. ^ Horii, I., Nakayama, Y., Obata, M. & Tagami, H. (1989) Stratum corneum hydration and amino acid content in xerotic skin. Br J Dermatol, 121, 587-592.