Changes in the Skin
The facial skin is continually exposed to a variety of external conditions, such as wind, cold, heat, and ultraviolet radiation. The last factor is the principal agent causing extrinsic aging of the skin, with effects that are significant enough to warrant the term “photoaging.” This exposure extends throughout an individual’s life, although it is postulated that the ultraviolet exposure occurring early in one’s life is responsible for most of the changes in the skin decades later. Some authors have speculated that ~50 to 75% of a person’s total lifetime ultraviolet radiation exposure occurs before 20 years of age. ~People with fairer complexions are most susceptible to the harmful effects of ultraviolet radiation.
Sun-damaged epidermis is histologically disorganized and thickened compared with nonexposed skin. Keratinocytes lose their distinctive alignment, and a progressive flattening of the cellular architecture occurs. Dyskaryotic changes are seen in the superficial layers of the epidermis. In response to long-term exposure to sunlight, epidermal melanocytes enlarge, proliferate, and migrate to higher levels of the epidermis. This chronic stimulation of melanocytes leads to dyschromias, spotty hyper- pigmentation, and the proliferation of pigmented keratoses. These changes are reflected in the dull uneven texture and pigmentation of adult sun-ex- posed skin.
In the deeper layers of the skin, ultraviolet radiation causes different long-term changes in addition to those seen in the epidermis. In sun-damaged skin, the region immediately beneath the epidermis develops a band of densely packed collagen with little or no elastic content. Beneath this region is a broad zone of electron-dense, elastotic material. Here, curled entangled masses of the elastin-staining material are found among degenerated collagen fibrils. Elastotic degeneration of dermal architecture is a consistent histologic feature of cutaneous photo- damage. These occurrences are responsible for many of the changes seen as wrinkling.
Part of the aging of the skin is an inevitable degenerative process with changes that are superimposed on the external aging factors in each individual, thus producing the endless variety of problems that present. As part of the intrinsic skin-aging process, the skin varies in thickness. Skin thickness in women reaches a maximum at ~35 years of age and decreases gradually thereafter. In men, the curve is different, with the peak thickness occurring at 45 years of age. There is a diversity of cell size and shape. The der- matoepithelial abutment is flattened with the loss of rete ridges, rendering skin fragile and susceptible to injury from shearing forces. The dermis of senescent .skin is characterized by marlred cellular atrophy and a corresponding reduction in metabolic activity. The percentage of newly .synthesized collagen in the der – mis decreases. As a result, the skin is less distensible, poorly resilient, and prone to fine wrinkling. As the dermis thins, there is a decrease in collagen content. degeneration of elastic fibrils, decreased water content, and the gradual addition of stable cross-links between collagen fibrils.