Histology of Photoaged Skin

Several investigators have evaluated the histological changes associated with photodamaged skin in various racial groups and utilizing various techniques [45, 46, 47, 48]. Characteristics identified are different from those found in intrinsic or chronological aging [23]. In intrinsic aging, there is both epidermal and dermal atrophy, with flattening of the dermal-epidermal junction. Epidermal atrophy is due to the reduction of keratinocytes in the rete ridges, as well as melanocytes and Langerhans cells. There is loss of the undulating pattern of the dermal-epidermal junction. Dermal atrophy is attributed to loss of fibroblasts, elastic fibers, vasculature, and appendages. In adults, the amount of collagen decreases by 1% per year due to decreased collagen synthesis and increased collagenase mRNA [49, 50]. A loss of elastic fibers occurs with fragmentation of elastin fibers. The loss of skin appendages is due to a decrease in the number of hair follicles and in eccrine and apocrine gland size. There is also a decrease in the number of melanocytes in the hair bulb.

Montagna reported the histology of photodamaged facial skin of 200 Caucasian women ages 21–55 who resided in an area of intense sunlight: Arizona [45]. Changes were noted throughout all layers of the skin, including the stratum corneum, epidermis, and dermis. The stratum corneum of photodamaged skin was compact and laminated. The corneocytes were plump, with amorphous material between and at times inside the corneocytes. The transition between the stratum lucidum and the stratum corneum was often indistinct. The stratum lucidum was thicker compared with normal epidermis, with two or more cell layers. Large vesicles containing proteinous material were noted. Numerous changes were noted in the epidermis, as well. These included cell heterogeneity, vacuolization, dysplasia, and necrosis. The epidermal cells were noted to be in disarray, with atypical shape, size, and/or staining as well as loss of polarity. Necrotic cells were observed in the epidermis, with single dying or dead cells. The epidermis contained intercellular and intracellular vacuoles in the basal and spinous layers. These vacuoles distorted both basal cells and melanocytes.Large,pale, staining cells were present in the spinous layer. Fewer Langerhans cells were present in severely photodamaged skin compared with normal skin. Dyskeratotic or stem cells were present in the basal layer. The periodic acid-Shiff (PAS) positive basement membrane was distinctly crinkly as it followed the extensions of the basal cells. Empty vesicles formed a foamy layer beneath the basement membrane. In regard to pigmentary changes of photodamaged skin, basal and suprabasal keratinocytes contained more melanosomes in both photoaged and normal skin. In darkly pigmented areas of the skin, melanosomes were present in all of the keratinocytes and corneocytes. In the papillary and lower intermediate dermis, elastic fiber masses were noted. Areas with advanced elastosis were found to be next to areas with fewer elastotic changes. In areas with enlarged, knotted, elastic fibers and rounded elastotic masses, fragmentation of fibers was observed. The lower papillary and upper intermediate dermis of sun-exposed skin had numerous reticulin fibers accompanying the fibers of the elastotic masses. Small collagen fibers were noted in the papillary dermis. The grenz zone that replaced the papillary dermis consisted of small fibers horizontally oriented. Elastotic material appeared to crowd out the collagenous fibers.


Warren’s group also studied photoaging in Caucasian women [46]. They evaluated histology, actinic elastosis, and collagen in four groups of Caucasian women ages 45–51 with skin types I–III who resided in Arizona. The groups were divided according to age (younger versus older) and sun exposure (low versus high). Skin color, erythema, and darkness were evaluated using the CIE L*, a*, b* color scale. No differences in skin color with respect to skin redness and darkness were identified among the four groups. However, other histological characteristics of photoaging were identified. The older women had a statistically significant more elastosis than the younger women. Additionally, elastosis was more significant in the older women with high sun exposure compared with the older low-sun-exposure group. The older high-sun-exposure group had more elastin and decreased dermal collagen than the older lowsun- exposure group. A grenz zone was present in the dermis of all older women regardless of sun exposure. There were no changes in epidermal thickness related to solar exposure.

Electron microscopic characteristics of photoaging in white skin were evaluated by Toyoda [48]. He demonstrated both qualitative and quantitative differences between photoaged and intrinsically aged facial skin. There were several characteristics of sun-exposed facial skin that were statistically significant compared with sun-protected skin. Some of these differences included increased keratinocyte and melanocyte heterogeneity, electron lucent degeneration of epidermal and peri-infundibular keratinocytes, melanocytes with vacuolar structures, dermal melanophages, reduplication of the basal lamina of the epidermis, degenerated microfibrils, solar elastosis, active mast cells, and decrease in normal microfibril bundles. Regarding melanocyte damage, irregularly shaped nuclei and electron-dense cytoplasm in sun-exposed skin compared with sunprotected skin were noted. Semiquantitative evaluation revealed a significant increase in melanocytic heterogeneity in sun-exposed skin. Vacuolar structures in melanocytes were identified, and the degree of vacuolization was commensurate to the severity of the degeneration of keratinocytes. It is likely that these changes are responsible for the development of pigmentary changes and cancerous changes.

Histological evaluation of photoaged black and Asian skin has also been performed [47, 51]. Compared with white skin, striking differences were noted in individuals with black skin. In one group of Asians from Thailand, marked similarities were noted between white skin and Asian skin [47]. Montagna performed a histological analysis of sun-exposed skin of 19 black and 19 white women [51].He reported dramatic racial differences in the skin of whites and blacks after long-term sun exposure. Overall, the epidermis of black skin showed only minor changes compared with the profound alterations that occurred in white skin. Histological analysis of the skin of many of the 19 black women analyzed revealed an entirely normal epidermis. In the others, vacuoles and dyskeratosis were present in the keratinocytes of the malpighian layer. These alterations were reported to be similar to those observed in white skin. However, white epidermis showed more dramatic changes, with many focal areas of atrophy and/or necrosis. In contrast, atrophy was observed in only one of the 19 black women ages 22–50, and it was mild in that case. The stratum lucidum in undamaged skin, white or black, consisted of one or two thin layers, and the stratum granulosum rarely exceeded three layers. However, in white skin, on exposure to UV light, the stratum lucidum was distorted. It was swollen, with increased cell layers. In contrast, the stratum lucidum in black skin rarely showed any sign of alteration and remained compact and unaltered.

Montagna’s data demonstrated that the entire epidermis of blacks, including the stratum granulosum, lucidum, and corneum, contained melanosomes in both the younger and older age groups. In white skin, only a few melanosomes were seen in the basal layer. Melanophages in black dermis were more numerous and larger that in white dermis.Melanophages were observed to become progressively smaller in the deeper dermis. The melanophages in black skin contained membrane-bound complexes of melanosomes.

Black skin reportedly has a thick and compact dermis with an indistinct intermediated layer in contrast to the distinct layer in white facial skin. In black dermis, there was close stacking of the collagen bundles, which ran parallel to the surface of the epidermis. Collagen fiber bundles in the dermis were smaller than those found in white skin. In contrast to white skin in which they were sparse, there were many collagen fiber fragments in the dermal interstices.


Elastosis, a hallmark of photoaging in white skin, was not observed in the specimens of any of the black subjects. In contrast, in white skin, variable amounts of moderate-to-extensive elastosis were observed.White skin always had more elastic fibers in the dermis compared with black skin. Dermal changes were observed in the older black subjects. There was an increase in the number and thickness of elastic fibers in the reticular dermis. Elastic fibers, configured in single strands in younger black subjects, appeared in thicker braid-like configurations in 50-year-old subjects. Elaunin fibers in black skin did not form the candelabra-like structures found in white skin but were configured in a parallel or angular array to the epidermis. Oxytalan fibers in older black women were intact in contrast to those of older white women.

Kotrajaras studied photodamage and the effect of topical treatment in a population of 61 Asian women of Thai descent. These women, with skin type IV, had a history of substantial UV exposure [47]. Histology revealed epidermal atrophy, atypia, and dysplasia. The keratinocytes in the basal layer of the skin had dense clusters of highly melanized melanosomes. There was an overall increase in melanin in the keratinocytes. Many large, pigment-laden melanophages were identified in the dermis, including the reticular dermis, of the majority of the women.Additionally, in the dermis, marked elastosis presenting as twisted fibers in various stages of amorphous degeneration were noted. Elastotic tissue almost completely replaced the collagen network.