Chronological aging of the skin is a complex process that is associated with functional and structural changes within the stratified squamous epithelium (epidermis) as well as the underlying connective tissue of the dermis. When these changes are intensified by prolonged exposure to solar or ultraviolet (UV) radiation, the process is referred to as photoaging. Chronic sun exposure ages the skin at an accelerated rate, especially in exposed areas of the body such as the face, neck, dorsal surface of the hands, and fore-arms. Clinical signs associated with photoaging include dyspigmentation, freckles, deep wrinkles, increased laxity, and increased risk for cutaneous cancers. The most prominent changes in the dermis of pho-toaged skin are associated with connective tissue fibers. Decreased production of type I and type III collagen fibers is observed in normal aged skin; however, these changes are more pronounced in sun-exposed regions. Sunlight exposure affects collagen biogenesis by altering the cross-linking that occurs between collagen molecules during fibrillogenesis (page 168). These alterations result in for-mation of collagen fibers with abnormal stability and decreased resistance to enzymatic degradation. The overall number of elastic fibers also decreases with age; however, in photoaged skin, the number of abnormally thick and nonfunctional elastic fibers increases. Recent studies of fbrillin microfbrils from photoaged skin reveal that the microfibrillar network is affected by solar radiation. Excessive sun exposure causes the fibrillin microfibrils to undergo extensive changes. They became sparse and trun-cated, leading to the formation of aberrant nonfunctional elastic fibers ECM that finally degenerate into homogenous and amorphous elastin-containing masses. Photoaging is also characterized by abnormal degrada-tion of the connective tissue matrix associated with accu-mulation of nonfunctional matrix components. Fibroblasts and neutrophils residing in radiation-damaged areas of the skin secrete matrix metalloproteinases (MMP-1 and -9), elastases, and other proteases (cathepsin G). These enzymes are modulated by tissue inhibitors of metallopro-teinases (TIMPs) that protect extracellular proteins from endogenous degradation. In photoaged skin, TIMP levels are significantly reduced, which further contributes to photodamage of the skin. The best strategies to prevent photodamage caused by solar and UV radiation is the use of physical and chemical sunscreens to prevent UV penetration into skin. Other methods are also used in treating damaged skin. These include reducing skin inflammatory reactions with anti-inflammatory medications, inhibiting activities of elastase and other MMPs to prevent degradation of ECM, and stim-ulating natural or applying synthetic inhibitors of MMPs activities to control destruction of connective tissue ECM.
Elastic material is a major extracellular substance in vertebral ligaments, larynx, and elastic arteries.
In elastic ligaments, the elastic material consists of thick fibers interspersed with collagen fibers. Examples of this material are found in the ligamenta flava of the vertebral column and the ligamentum nuchae of the neck. Finer fibers are present in elastic ligaments of the vocal folds of the larynx.
In elastic arteries, the elastic material is in the form of fenestrated lamellae, sheets of elastin with gaps or openings. The lamellae are arranged in concentric layers between layers of smooth muscle cells. Like the collagen fibers in the tunica media of blood vessel walls, the elastic material of arteries is produced by smooth muscle cells, not by fibroblasts. In contrast to elastic fibers, microfibrils are not found in the lamellae. Only the amorphous elastin component is seen in electron micrographs.
Elastin is synthesized by fibroblasts and vascular smooth muscle cells.