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Solar elastosis, also known as actinic elastosis, is a condition in which there is chronic sunlight-induced damage to the skin, particularly the upper and middle dermal layers which are especially vulnerable to this kind of degeneration.
The pathology is that of disorganization of the elastic fibers due to photodamage in aging skin. These tropoelastin fibers are separated from the epidermis by a band of collagen called the grenz zone which has no gross abnormality. The amount of abnormal elastic fibers deposited in the dermis depends on the cumulative damage suffered by the skin as a result of ultraviolet exposure.
The appearance of solar elastosis is as patches of thick coarsely furrowed skin with a bumpy rough surface. It occurs most often over the sun-exposed areas of the face, lips, hands and forearms, ears and neck.
The normal collagen and elastic fibers in the skin are degraded by ultraviolet rays, with the fibroblast responding to photodamage by oversecreting new tropoelastin. This elastic tissue is hyperplastic but has lost its normal orderly appearance. This is accompanied by the action of matrix metalloproteinases which degrade the surrounding tissue.
The disruption of collagen and elastic tissues in the dermis causes the normal cellular structure to be lost, with excessive deposition of residual material which eventually results in vasodilatation. The normal dermal architecture is thus lost in the damaged region.
Ultraviolet radiation is part of the solar spectrum. Its impact on the skin leads to neutrophil infiltration which release neutrophil elastase. These enzymes break down elastic fibers. This is one reason for the photodamage seen in solar elastosis.
The second effect is the oxidative stress caused by the generation of reactive oxygen species in excess. This cannot be buffered by the normal antioxidant systems of the body resulting in damage to the DNA of the mitochondria and cell nuclei of the skin. Mutations may also be a result of DNA damage by ultraviolet radiation, which could contribute to the process that culminates in solar keratosis.
The resulting fibroblast secretion of this condition causes accumulation of abnormal tropoelastin clumps rather than orderly arrays, in the dermis. The fibers are not only hyperplastic but abnormally coarse, branched and crosslinked. They are visible as a basophilic zone in the papillary and upper reticular dermis.
The grenz zone just below the epidermis is thought to be the region where collagen fibers synthesized by the overactive fibroblasts collect as they are pushed up by the elastosis. The greater the elastosis, the higher the degree of photodamage. The elastotic material comprises tropoelastin, microfibrillary proteins, and a little collagen in between the elastin fibers. Fibrillin, vitronectin and amyloid P are also present in these lesions.
The final phase consists of elastic fiber digestion by proteolytic enzymes which is the destructive stage. This may be due to the release of mast cell mediators and matrix metalloproteinases which break down the collagen and elastin in the affected dermis. This degradative phase denotes severe solar elastosis.
Though solar keratosis is a condition that may affect anyone after prolonged solar exposure, the following factors may increase the risk: