Solar Elastosis

Solar Elastosis

Todd Schlesinger

Clinton Favre


Skin aging is a complex, naturally occurring phenomenon that involves the accumulation of abnormal elastin (elastic tissue) and loss of collagen within the dermis. Skin aging may be classified as intrinsic aging and extrinsic aging. Intrinsic aging is predominantly the genetically determined loss of elastic tissue or other skin components over the passage of time.1 Extrinsic aging results from the environmental effects such as ultraviolet radiation (UVR).2 Ultraviolet rays are a part of the electromagnetic spectrum emitted by the sun and the primary cause of the damaging effects on the skin. Although cutaneous aging is inevitable, the addition of prolonged and excessive sun exposure accelerates the process of skin damage significantly, thus causing an expedited decline in skin function.2 Photoaging is the term used to describe premature aging of the skin through chronic sun exposure of UVR. Prolonged UVR exposure can lead to the development of many disorders that range in seriousness from benign to life threatening.

Solar elastosis, also known as actinic elastosis, is a condition that leads to a collection of abnormal elastin (elastic tissue) and loss of collagen in the dermis of the skin due to the harmful effects of UVR.3 Considered the most common disorder of sun damage, solar elastosis appears on areas that receive persistent sun exposure, such as face, back and sides of the neck, V area of the neck and upper chest, extensor arms, and dorsal hands. In its most common appearance, solar elastosis presents as heavily thickened, wrinkled, yellow skin, but it can
present in different forms, which cause the disease to be broad and elusive to diagnose.


The common cutaneous presentations of solar elastosis include increased thickness of the skin, yellow hue, irregular pigmentation, xerosis, and fissures. Often accompanying solar elastosis is the presence of rhytids (wrinkling/furrowing), lentigines, keratoses, and telangiectasias.


The etiology of solar elastosis is hypothesized to be due to the combined effect of chronic sun exposure with constant repetitive muscle movement. The chronic sun exposure creates the leathery and wrinkled appearance as stated earlier, and the constant voluntary muscle movement in the back of the neck causes deeper and more prominent wrinkles to be formed.

Constant and repeated muscle movement will cause wrinkles to be more prominent over time. When the muscle contracts, the overlying skin will stretch to be able to accommodate, and during this process, the connective tissue will begin to break. When connective tissue breaks, the skin becomes inelastic, resulting in a visible wrinkle. The combination of repetitive neck movement with chronic sun exposure (UV) accelerates the formation of these wrinkles. As stated previously, UV exposure decreases the amount of collagen and elastin found in the reticular dermis of the skin, causing the skin to become inelastic.6,9 In addition, collagen production naturally decreases with age, and with chronic UV exposure, there is a net loss of collagen and elastin within the dermoepidermal junction (DEJ), causing severe structural changes such as drooping and sagging skin. As more elastin and collagen are degraded, the DEJ continues to weaken, resulting in deeper and more prominent wrinkles. The loss of collagen also causes follicular ducts to become more open, and keratin can quickly fill in the ducts causing the formation of comedones.

The elastin quantity decreases over time; however, in areas of prolonged UV exposure, the elastin quantity increases corresponding with the amount of sun exposure.26 It remains unclear how the elastotic material is formed. However, researchers have suggested a few theories regarding this topic. UVR stimulates new elastin to be produced from fibroblasts.27 Other research suggests that new elastotic material found in solar elastosis is derived from pre-existing elastic fibers.28,29 An increase in inflammatory infiltrates, perivenular lymphohistiocytic infiltrate, has been hypothesized as a potential driver for the degradative process of elastin leading to new elastotic material to appear irregular, a condition termed chronic heliodermatitis.30 Although this hypothesis is unconfirmed, there is evidence to support this claim. Although the origin of the elastotic material is known, there is also an increase in elastotic material found in solar elastosis, and it appears that the newly formed elastin replaces the degraded collagen. Not only does the elastotic material take the place of the degraded collagen, but elastin produced from the UVR also has an abnormal, amorphous appearance compared with the original elastin found most prominently at the DEJ.30 The elastic fibers are thickened, distorted, and disorganized, forming a tangled mass in the papillary and reticular dermis, which causes a weakening of the DEJ, and thereby increasing the severity of wrinkles.

Studies have shown that in photoaged skin, there is an increase in the total population of cells, including the number of fibroblasts; however, in photodamaged skin, the affected fibroblasts appear more flattened than in nonphotoaged skin.29,31 Along with fibroblasts, the amount of Merkel cells and melanocytes seems to increase with prolonged sun exposure. Sites with chronic photodamage can see a moderate decrease in the size and total amount of blood vessels found in the upper dermis.29 The degree of severity for solar elastosis corresponds with the amount of chronic sun exposure over time.

The epidermis is also affected by chronic sun exposure. The epidermal layer is thicker in photoaged skin than in non-sun exposed skin.1 In addition, loss of polarity or atypia appears to be commonly expressed in many of the epidermal cells in photodamaged skin, which can lead to the development of skin cancers, such as basal cell carcinoma and squamous cell carcinoma.32,33 If left untreated, both cancers can be life threatening and locally destructive.

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Jun 29, 2020 | Posted by in Dermatology | Comments Off on Solar Elastosis
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