KK Women’s & Children’s Hospital, Singapore, Singapore
People of skin of color comprise the majority of the world’s population and Asian people comprise more than half of the total population of the world. East Asia encompasses a subregion of Asia that may be defined in geographical or cultural terms. Geographically, it covers about 28 % of Asia and is populated by more than 1.5 billion people, just over one-fifth of the world’s population. Countries traditionally classified as being part of East Asia include China, Japan, North and South Korea, Mongolia, and Taiwan. Historically, many societies in East Asia have been part of the Chinese cultural sphere. However, with the increasing mobility of the world’s population over the past two centuries, people of East Asian descent have fanned out to not only other parts of Asia but also to all other continents.
KeywordsBiologyEast Asian SkinHairNailsPigmentationMelanosomesMelanocytes
Development and Biology of Pigmentation in East Asian Skin
Melanocytes migrate as neural crest cells to the epidermis where they reside within the basal epidermis and hair bulb matrix.
Difference in skin color is due to variations in number, size, and aggregation of the melanosomes.
Pigmentary skin disorders, e.g. post-inflammatory dyspigmentation, melasma, and lentigines, are commonly seen in East Asians.
The hallmark biological feature of people of skin of color is the amount and distribution of melanin in the skin. Melanin is synthesised by melanocytes within melanosomes [1, 2]. Melanocytes migrate as neural crest cells to the epidermis from the 18th week of gestation . In the skin, the melanocytes are resident within the basal epidermis and hair bulb matrix. Each melanocyte in the basal layer produces dendrites that are associated with approximately 36 epidermal keratinocytes . Tyrosinase, an enzyme critical to the formation of melanin, is formed within the Golgi bodies of melanocytes and transferred to melanosomes. Tyrosinase converts tyrosine to dopa, which is then converted to dopaquinone. Dopaquinone is further oxidised to form eumelanin, which is brown-black in color. In contrast, pheomelanin appears yellow-red and is formed by a shunt in the eumelanin pathway. Melanosomes are ultimately transferred to keratinocytes either as aggregated, complex particles or discrete, single particles .
The difference in skin color between different races is due to variations in number, size, and aggregation of the melanosomes found in melanocytes and keratinocytes . The absolute number of melanocytes does not vary between races. The melanosomes of East Asian subjects have been found to be in aggregates but have a more compact configuration compared to Caucasian skin, in which melanosomes are more grouped. In contrast, the melanosomes in Black skin are individually dispersed and not aggregated (see Tang N, et al. Chapter 2; Developmental Biology of Black Skin, Hair, and Nails) .
Sun exposure can also affect the grouping of melanosomes. Asian skin exposed to sunlight has been found to have more non-aggregated melanosomes compared to non-exposed skin, which have more aggregated melanosomes . In addition, the epidermal distribution of melanosomes has been shown to vary between races, with melanosomes distributed throughout the entire epidermis in black skin compared to white skin, where melanosomes are seen only in the basal and spinous layers . A study in Thai subjects showed melanosomes distributed throughout the entire epidermis with dense clusters in the basal layer and heavy pigmentation in the stratum corneum .
Melanin and melanosomes have been found to impact on photoprotection . Melanin offers protection from UV light by absorbing and deflecting UV rays . In addition, the more individually dispersed the melanosomes, the better the photoprotection . Minimal erythema dose (MED) has also been shown to be affected by melanin and melanosomes. Subjects with darkly pigmented skin have an average MED 15–33 times more than subjects with white skin . A study on 101 Japanese women, comparing skin color and MED, showed that the greater the epidermal melanin content, the less severe the reaction to sunlight . Despite this, however, significant photodamage can still occur in pigmented Asian skin in response to chronic ultraviolet light exposure, e.g. keratinocyte atypia, epidermal atrophy, dermal collagen and elastin damage, and hyperpigmentation . This may be partly attributed to the fact that melanin may not be an efficient absorber of UVA wavelengths. The incidence of skin cancers, e.g. basal cell carcinoma, squamous cell carcinoma, and melanoma, in East Asian individuals is relatively low compared to whites, but does occur.
The melanin content and dispersion pattern of melanosomes has been thought to be largely responsible for providing protection from the carcinogenic effects of UV radiation [14, 15]. Apart from incidence, differences in site distribution, stage at diagnosis, and histologic subtype occur in melanoma occurring in East Asians compared to whites. In particular, acral lentiginous melanoma is the most common form of melanoma occurring in Asians. Despite the low incidence, the prognosis of melanoma in Asians is not as good as in Caucasian populations, likely due to more advanced stages at diagnosis. This is due to a combination of factors like decreased individual skin surveillance and decreased suspicion of the disease in examining physicians. Differentiation of melanonychia, which is very common in adult Asians (e.g. Japanese), from acral lentiginous melanoma requires careful review of lesion width, coloration, dermoscopy, the presence of Hutchinson’s sign, and evolution of the lesion.
Due to the biology of melanin and melanosomes in Asian skin, pigmentary disorders are much more common compared to white subjects. Post-inflammatory hyperpigmentation, melasma, and solar lentigines are extremely common pigmentation problems presenting in East Asian adults. Ultraviolet light-induced changes typical of young Caucasian children, e.g. spider angiomas and ephelides, are uncommon in East Asian children. These problems should not be treated as trivial cosmetic issues, as they can lead to significant psychosocial impairment in affected individuals.
Development and Biology of the Epidermis in East Asian Skin
In normal individuals, keratinocytes take approximately 4 weeks to be shed from the epidermis.
After birth, the skin barrier takes a few weeks to achieve maturity.
Skin lipids and filaggrin in the stratum corneum contribute to the integrity of the skin barrier.
The thickness of the human epidermis averages 50 μm and is made up of four or five layers, with the most superficial layer being the stratum corneum, followed by the stratum granulosum, stratum spinosum, and stratum basale. On the palms and soles, a layer known as the stratum lucidum is found between the stratum corneum and stratum granulosum. The keratinocytes that make up the bulk of the epidermis originate from the stem cell pool in the basal layer of the epidermis. The keratinocytes then undergo maturation as they move upwards towards the stratum corneum. On average, keratinocytes require 2 weeks to migrate from the stratum basale to the stratum granulosum, whereupon they lose their nuclei and differentiate into the corneocytes of the stratum corneum. In normal individuals, it takes approximately another 2 weeks for the corneocytes to shed from the skin. This duration can be shortened or lengthened in diseased states of the skin, e.g. psoriasis.
The epidermis is derived from the ectoderm in the human embryo. During the first month of gestation, the epidermis exists as a single layer, known as the periderm. Stratification of the epidermis begins about the eighth week of gestation and is mostly complete by the second trimester. Epidermal keratinisation begins during the second trimester and achieves maturation by the middle of the third trimester. The superficial keratinocytes undergo maturation as keratinisation progresses, with increase in the number of keratohyalin granules and lamellar bodies. By the mid-third trimester, the epidermal layers are morphologically similar to adult skin. However, skin barrier function only really achieves maturity a few weeks after birth [16, 17].
The data on racial differences in the structure and function of the stratum corneum have been conflicting, with even less studies performed on East Asian subjects. Some studies have shown the stratum corneum to be more compact in black compared to white subjects, with possibly more cornified layers and better epidermal barrier function [18, 19]. Corcuff et al., in a study comparing African Americans, white Americans, and Asians of Chinese descent showed increased spontaneous corneocyte desquamation in blacks compared to the Chinese and white group, which were almost similar . Studies on the thickness of the stratum corneum between races have shown conflicting results, with most of these studies comparing the epidermis in black and white subjects [9, 21]. There are a handful of studies documenting differences between East Asian skin epidermis and other racial skin types. In a very recent study, the epidermis of African skin was found to be thicker with deeper rete ridge projections than East Asian skin .
The barrier properties of the skin can be predicted by the structural integrity of the stratum corneum . The stratum corneum, being metabolically inactive, is penetrated by passive diffusion of substances. Penetration through cutaneous appendages, e.g. hair follicle wall, plays a smaller role [24, 25]. Studies on racial differences in the percutaneous absorption of various chemicals have produced conflicting results [26–30]. The susceptibility of the skin to irritants is also thought to be determined by the differences in the biological structure of the stratum corneum. However, the data from studies done to compare inter-racial skin susceptibility to irritants have also been somewhat controversial, with most studies done comparing white and black subjects [31–34]. A study by Goh and Chia evaluated skin irritation to 2 % sodium lauryl sulphate (SLS) by measuring skin water vapour loss (SVL) in 15 fair-skinned Chinese, 12 Malays with darker skin, and 11 Indians with very dark skin. No significant difference was found in mean baseline SVL values and SVL values after exposure to SLS between the three different groups . Kompaore et al. compared the barrier function of the stratum corneum between African blacks, white Europeans, and Asians. Baseline trans-epidermal water loss (TEWL) measurements were found to be significantly higher in Asian and black subjects compared to white subjects. The authors concluded that black and Asian skin may have a more compromised barrier function compared to skin of white Europeans, leading to greater susceptibility to irritants . However, Reed et al. found no significant differences in baseline TEWL among subjects with skin types II and III (Asian and whites) versus subjects with skin types V and VI (African American, Filipino, Hispanics). However, subjects with skin types V and VI demonstrated superior barrier integrity and recovery after exposure to skin irritants . Muizzuddin et al. found that, compared to African-American and Caucasian skin, East Asian skin had the weakest barrier properties and lowest degree of maturation . Both filaggrin and skin lipids in the stratum corneum are known to contribute to the integrity of the skin barrier. In addition, an optimal lipid composition is important to aid in this barrier function . Jungersted et al. have found significant differences in the ceramide/cholesterol ratios between different racial groups with Asians having the highest ratio compared to white-skinned individuals and Africans .
Development and Biology of the Dermis in East Asian Skin
The cells of the dermis can be seen under the presumptive epidermis by 6–8 weeks gestation. Unlike the epidermis which is derived solely from ectoderm in the human embryo, the origin of the dermis is variable depending on the body site. Early fibroblasts found in the dermis are thought to be pluripotent cells that can differentiate into other cell types, e.g. fibroblasts and adipocytes. Early dermal cells are known to already be able to produce most types of collagen and the microfibrillar components of elastic fibres. However, these proteins are initially not fully assembled into large fibres. In reverse to the ratio seen in adult dermis, the ratio of collagen III to collagen I in embryonal skin is 3:1. By the early second trimester, the papillary dermis with its finer collagen weave becomes distinct from the lower reticular dermis with its larger, thicker collagen fibres. Elastic fibres become apparent around 22–24 weeks gestation. At birth, the neonatal dermis is thinner and more cellular than adult dermis. Subcutaneous fatty tissue begins to accumulate during the second trimester and throughout the third trimester, when the distinct lobules separated by septae become visible. Although the blood vessels in the dermis may be seen by the end of the first trimester, there is subsequent extensive remodelling that occurs not only throughout gestation, but also after birth . Nerves in the dermis are formed by the end of the first trimester and generally follow the distribution of the blood vessels [16, 17].
Although there has been no proven difference in thickness of the dermis between races, there have been differences shown at cellular level. Langton et al. showed that East Asian skin dermis was found to have less collagen I and collagen III than African skin but more than Eurasian (people of mixed Asian and European descent) skin. While fibrillar collagen confers tensile strength, the elastic fibre system in the dermis confers resilience and passive recoil. Fibrillin-rich microfibrils and the microfibril-associated protein fibulin-5 (found in oxytalan and elaunin elastic fibres of papillary dermis) were found to be reduced in both Eurasians and East Asians compared to Africans. However, glycosaminoglycan content was found not to be statistically different between the three races .
Development and Biology of the Dermal–Epidermal Junction in East Asian Skin
The dermal–epidermal junction (DEJ) is an important structure in the skin. It develops from a simple basement membrane in the embryo into a complex, multilayered structure during the second trimester. The embryonal DEJ contains molecules common to all basement membrane systems (e.g. type IV collagen, laminin, heparin sulphate, and proteoglycans). At the same time as stratification of the epidermis occurs during the mid-first trimester, the DEJ acquires specific skin-associated components, including hemidesmosomes, anchoring filaments, anchoring fibrils, type VII collagen, laminin 332, and BP180. During development, the rete ridge pattern and dermal papillae become more obvious. Langton et al. found that collagen VII was more widely distributed in East Asian skin compared to the more discrete distribution seen in African skin. In contrast, there was no significant difference in the distribution of laminin-332 and integrin β4 between East Asian, Eurasian, and African skin .
Development and Biology of Hair Follicle Units in East Asian Skin
Asian hair is round or circular and has the largest cross-sectional area compared to Caucasians and Blacks.
The hair cycle consists of anagen, catagen, and telogen, with hairs being shed soon after telogen.
The size of melanin granules in Chinese hair is smaller compared to Blacks.
Hair follicle development first occurs on the scalp and face, and progresses caudally and ventrally in the fetus. The formation of the hair follicle is initiated by signals from the dermis, directing the basal cells of the epidermis to focally aggregate, forming the follicular placode. The placode sends signals to instruct the underlying dermal cells to condense to form the presumptive dermal papilla. The dermal papilla then directs the cells of the placode to proliferate and extend deeper into the dermis. Two distinct bulges develop in the superficial part of the developing hair follicle. The more superficial bulge develops into the associated sebaceous gland, and the deeper bulge indicates the point of insertion of the future arrector pili muscle which also contains the presumptive follicular stem cells. The seven concentric layers of the hair follicle become apparent during the second trimester. From innermost to outermost layers they consist of the medulla, cortex, hair shaft cuticle, inner root sheath cuticle, the Huxley and Henley layers of the inner root sheath, and the outer root sheath. The lower portion of the hair follicle keratinises without forming a granular layer (trichilemmal keratinisation), while the upper portion of the hair follicle is continuous with the interfollicular epidermis and undergoes keratinisation similar to that of the epidermis, with a granular layer present. The hair canal is fully formed by the mid-second trimester. The hair cycle has three phases: anagen, the active growing phase, catagen, a short degenerative phase, and finally, telogen, the resting phase. The hairs are shed soon after the telogen phase and the entire cycle begins again. This hair cycle continues throughout the lifetime of the individual [16, 17].