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Burke. Plast Aesthet Res 2020;7:59 I http://dx.doi.org/10.20517/2347-9264.2020.154 Page 3 of 16

Figure 1. Subclinical photodamage in a 45-year-old female. No photodamage of hyperpigmentation can be seen unless examined with
a Wood’s light (λ = 367 nm), revealing hyperpigmentation from previous sun exposure. VISIA ultraviolet photograph. (Printed with
permission by Canfield Imaging Systems, Parsippany, NJ 07054.)

Individuals with light, sun-sensitive skin (Fitzpatrick phototypes I and II) are at high risk for UV-induced
photoaging and skin cancer. The pheomelanin synthesized in response to UV actually produces reactive
oxygen species (ROS), leading to increased photoaging and skin cancers, especially in red-heads. Also,
damaging DNA photoproducts are produced by chemo-excitation of melanin derivatives, even long after
[4]
UV exposure . In addition, most red-haired individuals have dysfunction of their melanocortin-1 receptor
(MC1R) which hampers the possibility of developing a tan.

Studies with confocal microscopy have demonstrated that individuals of Fitzpatrick skin types I and II not
only have lower melanin but also significantly fewer dermal papillae than those with higher Fitzpatrick skin
[5]
types and darker skin . With age, there is an even greater disparity between light and dark skin in density
of dermal papillae, with increasingly fewer in light-skinned individuals as they age. This is a less-recognized
manifestation of photoaging, probably contributing to the crepe-like texture of extrinsically aged skin in
light-skinned phototypes.

UV radiation
Only about 5% of solar terrestrial radiation is UV radiation. Of the UV component, 95% is UVA and 5%
is UVB. The primary chromophore of UVB (λ = 290-320 nm) radiation is DNA which suffers specific
[6]
“UVB fingerprint mutations” resulting in intrastrand pyrimidine dimers . Further mutations are incited
by the generation of ROS. With cumulative UVB damage and natural aging, there is a decreased ability
for nucleotide excision repair so that mutations persist, directly leading to pre-cancerous actinic keratoses
and skin cancers - basal cell carcinomas (BCCs), squamous cell carcinomas (SCCs), and malignant
[6]
melanomas (MMs) - of which SSCs and MMs are potentially lethal.