A prominent feature of photoaged skin is elastosis, a process characterized histologically by

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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responsible for sunburn, suntanning, and photocarcinogenesis following sun exposure,59

although UVA also contributes to these end points.60,61 UVA is suspected of playing a
proportionately larger role in photoaging because of its minimally 10-fold greater abundance in
terrestrial sunlight, far greater year-round and day-long average irradiance, and greater average
depth of penetration into the dermis compared with UVB. Moreover, human skin exposed daily
for only 1 month to suberythemogenic doses of UVA alone demonstrates epidermal hyperplasia,
stratum corneum thickening, Langerhans cell depletion, and dermal inflammatory infiltrates with
deposition of lysozyme on the elastic fibers.62 These latter changes have been interpreted to
suggest that frequent casual exposure to sunlight containing principally UVA, e.g., while
wearing a UVB-absorbing sunscreen, eventually may result in damage to dermal collagen and
elastin in ways expected to produce photoaging.
Although the clinical manifestations of aging and chronic sun damage differ, in many instances
these differences are subtle. Initially, histologic changes in elderly sun-exposed skin were
described by experienced investigators as differing only in degree from those in elderly sun-
protected skin at both the light microscopic and electron microscopic levels. Many of the age-
associated physiologic decrements, such as slowed wound healing and loss of
immunoresponsiveness, also appear to be accelerated in sun-exposed skin. Furthermore, cells
cultured from chronically sun-exposed skin sites differ from cells cultured from sun-protected
sites of the same donors in having shortened culture life spans, slower growth rates, lower
saturation densities, and altered responsiveness to retinoic acid,63 all changes also observed as a
function of advanced chronologic donor age. Only in recent decades have qualitative differences
in the dermal fibrous proteins and microvasculature of paired sun-exposed and sun-protected
sites been documented. On a theoretical level, several of the mechanisms known to be involved
in UV-mediated cellular damage are also postulated to underlie chronologic aging.32,64 These
include DNA injury and/or decreased DNA repair, oxidative damage, lysosomal disruption, and
altered collagen structure.
Molecular mechanisms for some of the degenerative changes observed in photoaged skin,
particularly the enzymatic breakdown of collagen,65 have been tentatively identified, consistent
with the overall clinical appearance of photodamaged skin. It was shown that modest physiologic
doses of UVB activate the transcription factors AP-1 and NF-κB in human skin.65 In intact
human skin, even a suberythemogenic dose of UVB transcriptionally upregulates and activates
extracellular matrix-degrading metalloproteinases that are regulated by AP-1, including
collagenase, stromelysin, and the 92K gelatinase, in both keratinocytes and fibroblasts.66 There
is also a concomitant upregulation of TIMPs that limits further matrix degradation, although
TIMPs presumably are not completely effective in blocking cumulative damage to dermal
collagen.
Degradation of matrix proteins is aggravated by NF- mediated induction of interleukin (IL)-1
and tumor necrosis factor (TNF), two proinflammatory cytokines, leading to recruitment of
neutrophils and secretion of neutrophil collagenase.66 UV irradiation also downregulates
procollagen transcription through an as yet unknown mechanism, leading to decreased levels of
both type I and type III procollagen.66 Presumably, over many years, these events in
combination reduce the collagen content of skin and promote wrinkling.
Other studies using UVA irradiation and the hairless mouse model showed decreased activity of
the enzyme prolyl-hydroxylase that participates in posttranslational modification of collagen.67
In contrast with UVB, which renders collagen more susceptible to enzymatic degradation,
irradiation with UVA rendered dermal collagen more resistant to degradation, in part as a result
of increased cross-linking of the fibers.