[Normal and abnormal skin color]
- PMID: 23260521
- DOI: 10.1016/S0151-9638(12)70114-X
[Normal and abnormal skin color]
Abstract
The varieties of normal skin color in humans range from people of "no color" (pale white) to "people of color" (light brown, dark brown, and black). Skin color is a blend resulting from the skin chromophores red (oxyhaemoglobin), blue (deoxygenated haemoglobin), yellow-orange (carotene, an exogenous pigment), and brown (melanin). Melanin, however, is the major component of skin color ; it is the presence or absence of melanin in the melanosomes in melanocytes and melanin in keratinocytes that is responsible for epidermal pigmentation, and the presence of melanin in macrophages or melanocytes in the dermis that is responsible for dermal pigmentation. Two groups of pigmentary disorders are commonly distinguished: the disorders of the quantitative and qualitative distribution of normal pigment and the abnormal presence of exogenous or endogenous pigments in the skin. The first group includes hyperpigmentations, which clinically manifest by darkening of the skin color, and leukodermia, which is characterized by lightening of the skin. Hypermelanosis corresponds to an overload of melanin or an abnormal distribution of melanin in the skin. Depending on the color, melanodermia (brown/black) and ceruloderma (blue/grey) are distinguished. Melanodermia correspond to epidermal hypermelanocytosis (an increased number of melanocytes) or epidermal hypermelanosis (an increase in the quantity of melanin in the epidermis with no modification of the number of melanocytes). Ceruloderma correspond to dermal hypermelanocytosis (abnormal presence in the dermis of cells synthesizing melanins) ; leakage in the dermis of epidermal melanin also exists, a form of dermal hypermelanosis called pigmentary incontinence. Finally, dyschromia can be related to the abnormal presence in the skin of a pigment of exogenous or endogenous origin.
Copyright © 2012 Elsevier Masson SAS. All rights reserved.
Similar articles
-
Normal and abnormal skin color.Ann Dermatol Venereol. 2012 Dec;139 Suppl 4:S125-9. doi: 10.1016/S0151-9638(12)70123-0. Ann Dermatol Venereol. 2012. PMID: 23522626 Review.
-
The physiology of melanin deposition in health and disease.Clin Dermatol. 2019 Sep-Oct;37(5):402-417. doi: 10.1016/j.clindermatol.2019.07.013. Epub 2019 Jul 17. Clin Dermatol. 2019. PMID: 31896398 Review.
-
[Mechanisms underlying post-inflammatory hyperpigmentation: lessons from solar lentigo].Ann Dermatol Venereol. 2012 Nov;139 Suppl 3:S96-101. doi: 10.1016/S0151-9638(12)70118-7. Ann Dermatol Venereol. 2012. PMID: 23260525 Review. French.
-
The physiology of pigmented nevi.Pediatrics. 1999 Oct;104(4 Pt 2):1042-5. Pediatrics. 1999. PMID: 10506262
-
The biology of the pigmentary system and its disorders.Dermatol Clin. 1985 Apr;3(2):197-216. Dermatol Clin. 1985. PMID: 3913546 Review.
Cited by
-
Degraded melanocores are incompetent to protect epidermal keratinocytes against UV damage.Cell Cycle. 2018;17(7):844-857. doi: 10.1080/15384101.2018.1456601. Epub 2018 Apr 25. Cell Cycle. 2018. PMID: 29623762 Free PMC article.
-
Zebrafish phosvitin-derived peptide Pt5 inhibits melanogenesis via cAMP pathway.Fish Physiol Biochem. 2017 Apr;43(2):517-525. doi: 10.1007/s10695-016-0306-3. Fish Physiol Biochem. 2017. PMID: 28130732
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical