Desquamation
Desquamation | |
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Other names | Skin peeling |
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Specialty | Dermatology |
Desquamation,orpeeling skin,is the shedding of dead cells from the outermost layer ofskin.[1]
The term is fromLatindesquamare'to scrape thescalesoff afish'.
Physiologic desquamation
[edit]Keratinocytesare the predominant cells of theepidermis,the outermost layer of the skin. Living keratinocytes reside in the basal, spinous, or granular layers of the epidermis. The outermost layer of the epidermis is called thestratum corneumand it is composed of terminally differentiated keratinocytes, thecorneocytes.In the absence of disease, desquamation occurs when corneocytes are individually shed unnoticeably from the surface of the skin.[2]Typically the time it takes for a corneocyte to be formed and then shed is about 14 weeks but this time can vary depending on the anatomical location that the skin is covering. For example, desquamation occurs more slowly at acral (palm and sole) surfaces and more rapidly where the skin is thin, such as the eyelids. Normal desquamation can be visualized by immersing skin in warm or hot water. This induces the outermost layer of corneocytes to shed, such as is the case after a hot shower or bath.[citation needed]
Corneocytes are held together by corneodesmosomes. In order for desquamation to occur these corneodesmosome connections must be degraded.[2]Keratinocytes residing in the stratum granulosum produce corneodesmosome-degrading kallikrein family members, especiallyKLK1,KLK5,andKLK7.[3]Kallikreins are serine proteases. They are packaged within lamellar bodies and released into the intercellular space between the keratinocytes as they transition into becoming corneocytes.[2]To prevent premature desquamation, granular layer keratinocytes also produce kallikrein-inhibitory proteins.[3]At acral surfaces, desquamation occurs more slowly because granular layer keratinocytes downregulate expression of KLK1 and KLK7 and upregulate expression of protease inhibitors, including the KLK5-specificSPINK9and the cysteine protease inhibitors CSTA and CST3.[3]Slowing the process of corneocyte desquamation allows acral (palm and sole) skin to form a thick protective stratum corneum.[3]
Abnormal desquamation
[edit]Scale forms on the skin surface in various disease settings, and is the result of abnormal desquamation. In pathologic desquamation, such as that seen in X-linked ichthyosis, the stratum corneum becomes thicker (hyperkeratosis), imparting a "dry" or scaly appearance to the skin, and instead of detaching as single cells, corneocytes are shed in clusters, which forms visible scales.[2]Desquamation of theepidermismay result from disease orinjuryof the skin. For example, once therashofmeaslesfades, there is desquamation. Skin peeling typically follows healing of a first degreeburnorsunburn.Toxic shock syndrome,a potentially fatalimmune systemreaction to abacterial infectionsuch asStaphylococcus aureus,[4]can cause severe desquamation; so canmercury poisoning.Other serious skin diseases involving extreme desquamation includeStevens–Johnson syndromeandtoxic epidermal necrolysis(TEN).[5]Radiation can cause dry ormoist desquamation.[6]Desquamation is also abnormal in patients with immune-mediated skin diseases such as psoriasis and atopic dermatitis.[3]Abnormal desquamation often results in scale formation on the skin's surface.[3]Lipid composition alterations in scale have been used to construct diagnostic models for human skin disease.[3]
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Desquamation of skin on hands, caused byscarlet feverinfection
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Desquamation of skin on fingertips, caused by scarlet fever
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Desquamation of skin on the finger, caused by the popping of anacute paronychia
Eyes
[edit]Certain eye tissues, including theconjunctivaandcornea,may undergo pathological desquamation in diseases such asdry eye syndrome.[7]The anatomy of thehuman eyemakes desquamation of thelensimpossible.[8]
See also
[edit]- Desquamative gingivitis
- Exfoliation joint
- Moist desquamation
- Pityriasis—flaking of the skin
- Spalling
- Sunburn
References
[edit]- ^Miller, Claire; Crampin, Edmund; Osborne, James M. (August 2022)."Multiscale modelling of desquamation in the interfollicular epidermis".PLOS Computational Biology.18(8): e1010368.arXiv:2107.08575.Bibcode:2022PLSCB..18E0368M.doi:10.1371/journal.pcbi.1010368.ISSN1553-7358.PMC9462764.PMID36037236.
- ^abcdJackson, Simon M.; Williams, Mary L.; Feingold, Kenneth R.; Elias, Peter M. (1993)."Pathobiology of the Stratum Corneum".The Western Journal of Medicine.158(3): 279–85.PMC1311754.PMID8460510.
- ^abcdefgMerleev, Alexander A.; Le, Stephanie T.; Alexanian, Claire; Toussi, Atrin; Xie, Yixuan; Marusina, Alina I.; Watkins, Steven M.; Patel, Forum; Billi, Allison C.; Wiedemann, Julie; Izumiya, Yoshihiro; Kumar, Ashish; Uppala, Ranjitha; Kahlenberg, J. Michelle; Liu, Fu-Tong (2022-08-22)."Biogeographic and disease-specific alterations in epidermal lipid composition and single-cell analysis of acral keratinocytes".JCI Insight.7(16): e159762.doi:10.1172/jci.insight.159762.ISSN2379-3708.PMC9462509.PMID35900871.
- ^Dinges, MM; Orwin, PM; Schlievert, PM (January 2000)."Exotoxins of Staphylococcus aureus".Clinical Microbiology Reviews.13(1): 16–34, table of contents.doi:10.1128/cmr.13.1.16.PMC88931.PMID10627489.
- ^Parillo, Steven J; Parillo, Catherine V. (2010-05-25)."Stevens-Johnson Syndrome".eMedicine.Medcape.Retrieved2010-09-06.
- ^Centers for Disease Control and Prevention (2005-06-30)."Cutaneous Radiation Injury".CDC.Retrieved2011-05-15.
- ^Gilbard, Jeffrey P. (November 1, 2003)."Dry Eye: Natural History, Diagnosis and Treatment".Wolters Kluwer Pharma Solutions. Archived fromthe originalon January 30, 2013.RetrievedFebruary 3,2012.
- ^Lynnerup, Niels; Kjeldsen, Henrik; Heegaard, Steffen; Jacobsen, Christina; Heinemeier, Jan (2008). Gazit, Ehud (ed.)."Radiocarbon Dating of the Human Eye Lens Crystallines Reveal Proteins without Carbon Turnover throughout Life".PLOS ONE.3(1): e1529.Bibcode:2008PLoSO...3.1529L.doi:10.1371/journal.pone.0001529.PMC2211393.PMID18231610.
External links
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