Bouissou H, Pieraggi M T, Julian M, Savit T
Department of Anatomical Pathology, C.H.U. Rangueil, Toulouse, France.
Int J Dermatol. 1988 Jun;27(5):327-35. 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.
为了区分光化性损伤的变化与单纯衰老的变化，我们研究了不同年龄段正常受试者低日照皮肤和高日照皮肤中的弹性纤维。低日照皮肤仅表现出自然老化病变。这些病变在30岁时开始，表现为氧化弹性纤维消失以及网状真皮和深部真皮出现一些异常；40岁时，老化变化确立：无氧化弹性纤维，明显异常，弹性微原纤维和弹性纤维溶解。在高日照皮肤中，也会出现与年龄相关的病变，但与网状真皮和深部真皮中或多或少的早熟弹性组织变性有关。两种类型的老化纤维均可被抗弹性蛋白抗体HB 8显示出来，可被弹性蛋白酶分解，但能抵抗胶原酶。光化性弹性组织变性显然起源于弹性蛋白。这两种变化在电子显微镜下的表现不同：自然老化时，弹性纤维解体（纤维松散且多孔）；光化性损伤时，弹性组织变性纤维更粗，微原纤维致密团块更明显。与年龄相关的病变可能归因于成纤维细胞来源的蛋白酶的活性，而弹性组织变性可能是由于成纤维细胞受到光化性刺激所致。
