Human Skin Adaptations and Functions Quiz

Our Skin Tone Rainbow

• Skin tone variations are a result of evolution.
• Folate, vitamin D, melanocytes, and melanin are crucial in skin pigmentation.
• Dark pigmentation (DP) and light pigmentation (LP) are observed.
• Aging and solar radiation (UV, visible, and infrared) influence skin.
• Photoaging affects elastin, collagen, and dermal-epidermal junctions.
• Photoprotection and treatments are available for DP skin.

Our Family Tree

• Humans (Homo sapiens) belong to the great apes.
• Humans evolved approximately 300,000 years ago, with larger brains and lighter skeletons than earlier humans.
• Fossils and DNA confirm humans are one of over 200 primate species.
• Humans are categorized within the great ape family, sharing characteristics with chimpanzees, gorillas, and orangutans.
• Neanderthals are the closest extinct relatives to humans, with Homo heidelbergensis being a common ancestor.

The Evolution...

• Humans have less body hair compared to other mammals; they are "functionally naked".
• Hair loss is believed to be an adaptation improving thermoregulation and heat dissipation during intense physical activity.
• Vellus hairs cover almost all the body surface.
• Humans retained body hair in areas such as the head, armpits, and groin.
• The loss of body hair led to enhanced thermoregulation.
• Disadvantages include reduced protection from abrasions and UV radiation.

The Evolution Continued...

• Accelerated keratinization and epidermal differentiation contributed to skin barrier functions.
• Genomic evidence links the evolution of permanent, dark eumelanin-rich skin pigmentation with reduced hair and increased eccrine glands.
• The strongest hypothesis suggests that eumelanin protected folate from photodegradation in the dermal vasculature, which is vital for fertility.
• Folate deficiencies lead to birth defects and infertility.
• Folate is important for DNA synthesis, repair, amino acid metabolism, melanin production, and thermoregulation.

What About Changes to Skin Pigmentation?

• If human evolution were compressed into a year, the change in skin pigmentation occurred this week.
• Migration of Homo sapiens occurred approximately 55,000 years ago and led to a vitamin-D deficiency.
• Vitamin D regulates calcium levels, bone development, and other physiological processes.
• Reduced UVB levels outside the equatorial regions hinders Vit-D synthesis.
• Darker pigmentation provides photoprotection.
• Near the equator, dark pigmentation is a crucial adaptation against photodamage.
• In regions further away from the equator, lighter pigmentation promotes vitamin-D synthesis.

Our skin is more than a protective barrier

• Skin provides a barrier against viruses, bacteria, and other foreign substances.
• It also prevents dehydration and is one of our five senses (touch).
• Skin regulates body temperature through sweating and heat retention.

A reminder of the cells in the epidermis

• Keratinocytes (95%), Langerhans cells (2%), and Merkel cells (0.5%) are primary components of the epidermis.
• Melanocytes account for approximately 3% of epidermal cells and have a 1:36 ratio with keratinocytes.
• This 1:36 ratio is referred to as the epidermal melanin unit.

Melanocytes & melanin

• Melanocytes reside in the basal layer of the epidermis.
• Melanocytes synthesise melanin and transfer it to viable keratinocytes.
• Pigmentary variations are due to both the number and melanin content of melanosomes (melanin granules) within melanocytes.
• Melanin consists of eumelanin (brown-black) and pheomelanin (yellow-red).
• Darker skins have higher eumelanin levels per granule and more melanosomes delivering melanin to keratinocytes.

Synthesis of melanin

• Melanin is derived from the amino acid tyrosine.
• Tyrosinase, tyrosinase-related protein 1, and tyrosinase-related protein 2 are the enzymes in melanin synthesis.
• Optimal melanin synthesis occurs at pH 6.8.
• Caucasian skin acidity hinders melanin synthesis, contrasting with darker skin acidity that facilitates it.
• Mature melanosomes migrate along dendrites and are incorporated into keratinocytes, forming supra-nuclear caps.

Melanocytes & melanin

• Melanocytes are involved in protecting keratinocytes by shielding them from UV damage.
• Eumelanin provides protection, while pheomelanin is potentially phototoxic, increasing risk of UV-related cancers in skin with high pheomelanin.
• Darker skin types have higher eumelanin levels, more melanosomes, and, thus, greater photoprotection.
• Higher melanin levels are observed in photo-exposed regions compared to protected areas.

Skin-typing: Fitzpatrick Skin Phototype Classification

• Fitzpatrick Skin Phototype Classification (FSPC) was developed in 1975 to determine appropriate UVA doses with psoralen treatments.
• Initial classification included skin types I-IV and was expanded in 1988 to include V and VI for darker skin tones.
• Insufficiently describing darker skin tones may lead to inaccuracies in skin classification.

Skin-typing: Individual Typology Angle (ITA)

• ITA assesses actual pigmentation based on colorimetry.
• ITA categorizes skin types from very light to dark based on a calculated angle (e.g., very light >55 degrees).
• Higher angles correlate with lighter skin, while lower angles correspond to darker skin.
• More objective method compared to Fitzpatrick scale.

Pigmentation and Photoprotection

• DNA damage from sun exposure is reduced in dark skin compared to light skin, by about a factor of three.
• Studies found higher rates of skin cancer in lighter-skinned individuals compared to darker-skinned individuals (e.g., Caucasian vs. African-American).
• Darker skin provides superior protection against solar radiation.
• Highly pigmented skin offers significantly higher photoprotection.

Non-pigmentary differences in DP and LP skin

• Differences exist in the dermal-epidermal junction, rete ridges (DP skin has more regular and pronounced ridges), and dermal protein composition.
• Monocyte chemotactic protein-1 (MCP-1) levels are higher in darkly pigmented skin, relevant to wound healing.
• Post-inflammatory hyperpigmentation (PIH) is more common in darkly pigmented skin, but is not the sole indicator of aging.

Aging - General

• Intrinsic aging reflects the natural effects of time on skin, noticeable even in areas shielded from the sun.
• Extrinsic aging is caused by environmental factors; for example, UV, visible light, and infrared light, causing premature skin aging most pronounced on the exposed parts of the body, including the face, neck, and hands.
• Chronic sun exposure greatly impacts aging, evident in one-sided darker-shaded facial skin due to prolonged sun exposure.

Aging - Intrinsic Caucasian Skin

• Intrinsic skin aging in Caucasians is tied to decreases in melanocytes and Langerhans cells, potentially leading to increased skin cancer risk.
• Darker skin types also exhibit reduced melanocytes but increased melanophages. This leads to less even skin pigmentation.
• Sebaceous gland size increases in Caucasians.
• Although sebaceous gland size in Caucasians increases, total sebum secretion reduces.
• MMP (matrix metalloproteinases) levels rise, as do degradation levels, and collagen type III/I ratios.

Solar radiation: UV

• UV radiation (UVA, UVB, UVC) is a critical aging factor.
• UVC is filtered by the ozone layer.
• UVB primarily affects the epidermis and upper dermis, while UVA penetrates deeper.
• Longer wavelengths have deeper penetration and higher energy.
• Shorter wavelengths have higher energy and greater penetrating ability.
• UVB, especially, is associated with tanning and skin cancer.
• UVA causes indirect DNA damage as part of aging.

Solar radiation: UV

• UVB is significantly more erythemogenic than UVA.
• Melanin effectively absorbs UV energy and dissipates it as heat.
• Without melanin, DNA, particularly thymine bases, could be damaged.
• UV exposure increases melanin in DP skin more than in LP skin, although the increments differ between skin tones.
• UV induces ROS and depletes endogenous antioxidants like glutathione, tocopherol, and ubiquinone.
• UV also leads to collagen degradation and inhibits collagen formation.

Solar radiation: visible light (VL)

• Visible light (VL), at 400-760nm, penetrates deeper into the skin compared to UV radiation.
• Melanin absorbs all visible light wavelengths, causing increased body temperature and a redness response.
• The vasodilation response to VL is more prominent in darker skin due to higher melanin concentrations.
• VL contributes to skin pigmentation, though less effective compared to UV in inducing pigmentation.
• VL can trigger reactive oxygen species and inflammation, especially in comparison to UV.

Solar radiation: infrared light (IR)

• Infrared radiation (760 nm-1 mm) penetrates deep into the skin.
• IRA, IRB, and IRC penetrate the epidermis, dermis, and subcutaneous tissue.
• Infrared radiation causes thermal effects, like vasodilation, leading to warmth and erythema.
• Unlike UV, any resulting pigmentation from IR is indirectly mediated through thermal effects.

Photoaging - Elastin

• Exposure to sunlight can cause elastosis.
• The accumulated elastin in the upper dermis of sun-exposed skin is morphologically abnormal, potentially occupying areas of lost collagen.
• Fibrillin-rich microfibrils involved in elastin deposition are susceptible to UV radiation.
• Darker skin effectively resists UV radiation's impact on elasticity.

Photoaging - Collagen

• Collagen type I and III levels decrease with sun damage.
• Collagen production decline with aging, more noticeably in sun-exposed skin.
• Sun exposure causes significant collagen reductions in the 1st to 9th decades.
• Sun-damaged skin shows roughly a 40% reduction in type III pro-collagen compared to non-damaged skin.

Photoaging - Dermal-Epidermal Junction

• The flattening of the dermal-epidermal junction (rete ridges) increases with photoaging, especially in skin exposed to the sun.
• Less contact between the vascular dermis and epidermis reduces nutrient supply, impacting skin health and increasing fragility.
• Increased regularity and prominence of rete ridges in DP skin can partly mask the impacts of aging compared to the epidermal thinning associated with LP skin.

Photoaging

• DP and LP skin exhibit different responses to solar radiation.
• LP skin exhibits effects predominantly from extrinsic aging (effects of sun exposure).
• DP skin shows delayed intrinsic aging effects.
• DP skin has a greater predisposition to dyschromias and more susceptibility to irregularities in pigmentation relating to aging.
• While LP skin shows faster extrinsic aging, DP skin may show this effect later by 20 years (or more).

Photoaging LP skin

• Two main extrinsic aging phenotypes are observed:
• HP (hypertrophic) is characterized by deep wrinkles, skin laxity, and impaired wound healing. This is common in LP skin.
• AP (atrophic) is characterized by smooth skin, fine wrinkles, frequent spider veins, depigmentation, and actinic keratosis. This is common in LP skin.

Photoprotection for DP skin

• The misconception that darker skin is resistant to skin cancer is inaccurate.
• Photoprotection methods can mitigate effects like dyspigmentation in darker skin from VL, or infrared radiation.
• Physical sunscreens are preferable to prevent negative effects of thermal absorption on VL exposure.
• Antioxidants help combat damaging free radicals (ROS).

Treatments for DP skin

• Treatments for uneven skin pigmentation in darkly pigmented skin include hydroquinone, azelaic acid, and kojic acid.
• Tretinoin can be used, however, hyperpigmentation can result from contact dermatitis.
• The potential benefits of these treatments include reductions in melanin, leading to more even skin tone. Improvement in fine wrinkles and collagen stimulation.

Conclusion

• DP and LP skin exhibit differences in their responses to factors like solar radiation, resulting in varied patterns of aging.
• DP skin features more pronounced rete ridges, promoting nutrient delivery.
• DP skin's prominent melanin content effectively protects against photoaging and skin cancer.
• DP skin may benefit from physical sunscreens due to its susceptibility to thermal effects of radiation (VL and IR).
• LP skin is more susceptible to extrinsic aging with two main phenotypes (HP and AP). This makes it important to use photoprotection.