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tangled masses of degraded elastic fibers that further deteriorate to form an amorphous mass
(Fig. 144-2). In addition, the amount of ground substance, largely composed of
glycosaminoglycans and proteoglycans, increases in photodamaged skin, whereas the amount of
collagen decreases, in part because of increased metaloproteinase activity and enhanced cytokine
release. In contrast with aged sun-protected skin that demonstrates hypocellularity,
photodamaged skin frequently displays inflammatory cells, including mast cells, histiocytes, and
other mononuclear cells, giving rise to the term heliodermatitis (literally, “cutaneous
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inflammation due to sun―) (Fig. 144-3). Fibroblasts are also more numerous than in sun-
protected skin. In contrast with chronologically aged skin, photodamaged epidermis is frequently
acanthotic, although severe atrophy also can be seen, displaying, in addition, loss of polarity and
cellular atypia. Also, there is a decrease in the number and function of Langerhans cells.
Additional changes are described in Table 144-3.
The relative severity of sun-induced cutaneous changes varies considerably among individuals,
undoubtedly reflecting inherent differences in vulnerability and repair capacity for the solar
insult. Photoaging occurs not only in fair-skinned individuals (skin types I and II) but also in
individuals with darker skin types III and IV with a history of ample past sun exposure. It usually
involves the face, neck, or extensor surfaces of the upper extremities most severely.
Interestingly, the gross appearance of photodamaged skin of individuals with skin types I and II
differs from that of individuals with skin types III and IV, the former generally showing atrophic
and dysplastic skin changes with actinic keratoses and epidermal malignancies rather than
hypertrophic responses such as wrinkling, lentigines, and coarseness. One study has noted that
patients presenting with basal cell carcinoma are less wrinkled than peers of similar complexion
and degree of photodamage,55 suggesting that different factors determine these two responses to
chronic UV exposure.
Wrinkling of photodamaged skin is exacerbated by cigarette smoking56 and possibly other
environmental factors. The apparent influence of sex on the prevalence of certain photoaging
features undoubtedly reflects different hair styles, patterns of dress, and nature of sun exposure
(occupational versus recreational) between men and women over the past several generations.
Other sex differences, such as epidermal thickness and sebaceous gland activity, and as yet
unrecognized effects of circulating sex hormones also may influence their development. The
characteristic distribution of different lesions is a complex function of relative sun exposure for
different body sites, anatomic distribution of the participating cutaneous structures (e.g.,
melanocytes and sebaceous glands), and other poorly understood factors.
The action spectrum for human photoaging has never been determined, and hence the relative
contribution of the various spectral bands within sunlight is unknown. There is no truly
appropriate animal model. In rodent skin, an elastosis-like condition can be produced by
prolonged intense irradiation with either a predominantly UVB or UVA source, but attempts to
determine the action spectrum for murine elastosis have yielded conflicting results.57,58 UVB
photons are on average 1000 times more energetic than UVA photons and are overwhelmingly
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