The aging of the skin is a complex process reflecting both intrinsic and extrinsic influences. It is clinically characterized as features of sagging skin, wrinkles, sunspots, and uneven skin tone. Many interacting factors influence the biology behind this process, namely, genetics, one’s environment, psychological changes, and social influences. For many years it has also been thought that ethnicity is also a key influencer of the aging process. It has been suggested that those of Afro-Caribbean descent are less susceptible to skin aging. The phrase ‘black don’t crack’ was coined at the start of the 21st century alluding to this phenomenon. This review aims to explore the validity of this premise by analyzing the biological processes behind skin aging and how they are influenced by ethnicity. Given that a large portion of the world’s population has ethnic skin, it is necessary that we better our understanding of the structural and functional variations between skin types, to effectively treat signs of aging across all populations.
1.Biology of skin aging
1.1 Skin aging
With continuous advancements in healthcare, the average life expectancy of the world population continues to rise. The clinical phenotypes of aging are predominantly seen in the skin as sagging lentigines, wrinkling, and increased laxity of the skin. Aging is influenced by intrinsic factors (chronological aging) and extrinsic factors, both contributing to a loss of integrity and physiological function. A review by Kammeyer et al identifies that no area of skin on the human body is aged by intrinsic factors alone. Extrinsic factors play an equally important role in the aging process.
1.2 Intrinsic aging
The theories behind intrinsic aging can be organized into evolutionary-based, damaged based, and program-based. This review focuses on the damage based theories behind aging skin. Reactive oxygen species (ROS) can be described as molecules consisting of oxygen with an unpaired electron, making them highly reactive with other molecules. These entities are continuously produced in small quantities, as byproducts of the electron transport chain during aerobic respiration. Around 1.5 – 5% of the oxygen consumed by keratinocytes and fibroblasts are converted into ROS.
In health, we have an equilibrium of ROS generation and removal – redox homeostasis. Low levels of ROS are important for cell signaling (insulin kinase receptor signaling) and vasodilation. In aging this equilibrium shifts and there is an observed increase in ROS production and a decrease in antioxidant defenses e.g superoxide dismutase (SOD). Evidence for this is provided by Ishii et al. who demonstrated accelerated aging in cytochrome B (succinate dehydrogenase) mutants. In concordance with this, antioxidants have been shown to extend lifespan. Reactive oxidative species cause harm to cells by oxidizing cellular proteins leading to a loss of function and aggregation, thus contributing to the aging phenotype e.g skin wrinkling.
At a cellular level, there is also a decline in the replicative ability of cells. This is termed cellular senescence and is due to the successive shortening of telomeres at every replication cycle. The haylick limit is the point in which cells can’t divide any further due to the complete erosion of the telomeres within that cell. Senescent cells are found in high levels within aged skin. A senescent cell is still viable but displays altered patterns of gene expression. Within the skin, this process affects keratinocytes, fibroblasts, and melanocytes.
Moreover, at the level of the tissue, there is observed degradation of the extracellular matrix (ECM). This is because senescent cells of the skin, particularly fibroblasts, show increased expression of matrix metalloproteinases (MMP) and decreased expression of MMP inhibitors. MMPs act to degrade the extracellular matrix and in health play a key role in tissue repair and remodeling. Inhibitors of these proteins act to regulate this process. Increased degradation results in reduced collagen, elastin, and proteoglycans, which contribute to the thin translucent appearance of aging skin.
1.3 Extrinsic aging
Extrinsic aging is induced by environmental oxidative factors such as UV radiation, cigarette smoke, and other pollution factors. Epidemiological studies by Yin et al. showed that long term exposure to tobacco smoke and UVA-exposure accelerated the aging processes in the skin. The main extrinsic factor responsible for aging skin is UV light. The cutaneous effects of photoaging include rhytids (deep wrinkles), mottled pigmentation, lentigines, and a generally thin, translucent appearance (due to atrophy). There are three tissue layers within the skin, the outer epidermis, the dermis, and the subcutaneous layer. The aged phenotype of photodamaged skin Is a result of the damage caused to the connective tissue of the dermis. UVA radiation is known to cause atrophy to elastin, collagen, and proteoglycans within the dermal layer. Darker skin types are less susceptible to the damage seen in photoaging (see later) so these clinical manifestations aren’t as severe in black skin and are seen 10 to 20 years later than fairer counterparts.
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2.The influence of ethnicity on skin aging
Vashni et al. (1) define ethnic skin as ‘the broad range of skin phenotypes and complexions that characterize persons with darkly pigmented skin including those of African, African American, Asian, and Latino/Hispanic descent ‘. This section compares the structure and function of Caucasian and ethnic skin.
2.1 Melanin production at melanosomes
The main determinant of skin color is the black pigment melanin. Melanin is synthesized in melanocytes of the epidermis within organelles called melanosomes. Darker skin types have a higher concentration of epidermal melanin. This is due to the observed difference in the melanosomal dispersion pattern across different ethnic groups. Lighter skin types consist of aggregated, smaller melanosomes containing less melanin. In contrast, darker skin consists of singly dispersed melanosomes containing higher quantities of melanin. The dispersion seen in darker skin is thought to protect against photoaging.
A study by Kaidbey et al using cadaveric skin demonstrated that the epidermis of black skin provides an SPF of 13.4 compared to 3.4 in white skin. However, darkly pigmented skin is lo more susceptible to dyspigmentation, thus a common characteristic of photoaging in black skin is large areas of hyper and hypopigmentation across the epidermis.
2.2 Pigmentation genes
At a molecular level, pigmentation genes such as melanocyte-stimulating hormone (MSH), melanocyte-stimulating hormone receptor, tyrosinase-related protein (TRP) family members, and the melanocortin-1-receptor are upregulated in dark skin. TRP1 expression correlates with increased tyrosinase activity, melanin synthesis, and melanosome size (5,27) and MSH directly enhances UV-induced DNA repair in keratinocytes
2.3 Progressive atrophy of the dermis
The aging phenotype of skin is also due to progressive atrophy of the extracellular matrix of the dermis resulting in folds and wrinkles. Black and Asian skin has thicker dermis that is more compact than white skin. . The thickness of the dermis is thought to be directly proportional to pigmentation. This explains the lower incidence of facial rhytids in black and Asian individuals to give a firmer, smoother appearance.
2.4 Fibroblasts
Fibroblasts are the main cell type of the dermis. Their role is to synthesize extracellular matrix proteins such as collagen, elastin, and Glycosaminoglycans (GAGs). Kidney et al reveal that Black skin contains more fibroblasts of a larger size that are multinucleated. Moreover, smaller collagen fibers and more macrophages are found in ethnic skin compared to Caucasian skin. This acts to preserve elasticity, however, does lead to an increased risk of hypertrophic scarring.
Furthermore, as described earlier, intrinsic aging results in the replicative senescence of fibroblasts, resulting in altered gene expression to promote ECM breakdown rather than production. As black skin has a higher number of fibroblasts initially, the effects of senescence are likely to be seen much later.
Summary
The literature suggests that overall individuals with a darker complexion have firmer, smoother skin than Caucasian counterparts of the same age. This is due to molecular and cellular differences seen in different skin types, which have a direct influence on the aging process. With regards to intrinsic aging, the differences seen are mainly attributed to fibroblast number and size. The lower quantity of fibroblasts in Caucasian skin amplifies the impact of cellular senescence. Concerning extrinsic aging, the high melanin content in black skin provides direct protection against photoaging.
The structural and functional variations across different skin types, outlined in this article, provide a reasonable explanation for the premise that black skin is resistant to the aging process. Thus, the theory that ‘black don’t crack’ is indeed a reality.
