The elastic tissue of the skin. A comparison of spontaneous and actinic (solar) aging

• Published in: International journal of dermatology Vol. 27; no. 5; p. 327
• Main Authors: Bouissou, H, Pieraggi, M T, Julian, M, Savit, T
• Format: Journal Article
• Language: English
• Published: England 01.06.1988
• Subjects: Adult; Aged; Aging - pathology; Aging - radiation effects; Elastic Tissue - pathology; Elastic Tissue - radiation effects; Elastic Tissue - ultrastructure; Humans; Microscopy, Electron; Middle Aged; Skin - pathology; Skin - radiation effects; Skin - ultrastructure; Ultraviolet Rays - adverse effects
• ISSN: 0011-9059; 1365-4632
• DOI: 10.1111/j.1365-4362.1988.tb02363.x

In order to separate the changes of actinic damage from those of simple aging, we studied the elastic fibers in low and high sun-exposed skins of normal subjects at different ages. Low sun-exposed skin shows chronologic aging lesions only. These begin at age 30 with a disappearance of oxytalan fibers and with some abnormalities in the reticular and deep dermis; at age 40, aging changes are established: no oxytalan fibers, marked abnormalities, and lysis of elaunic and elastic fibers. In high sun-exposed skin, age-related lesions also occur but are associated with more or less precocious elastotic degeneration in reticular and deep dermis. Both types of aging fibers are revealed by the antielastin antibody HB 8, disappear with elastase, but resist collagenase. Actinic elastosis clearly originates from elastin. The two types of change differ in electron microscopic appearance: with spontaneous aging, elastic fibers are disintegrated (loose and porous fibers); in actinic damage, elastotic fibers are thicker and have accentuated microfibril dense masses. The age-associated lesions could be due to the activity of protease of fibroblastic origin whereas the elastotic degeneration is probably due to the actinic stimulation of fibroblasts.